 Great. Okay, so hi everybody. Welcome to Grand Rounds. Today we have some really great presentations from our University of Utah fourth year medical students and then these are currently rotating with us to be respectful of everybody's time. I'm just going to give everybody maybe like a 30 seconds one morning if you're kind of coming up to the 10-minute mark and then we'll have an additional five minutes for everybody for questions. So to start off we have Caitlyn Cooper. She is from Minnesota and currently on the neuro ophthalmology rotation. Something interesting about Caitlyn is that she recently hiked through the peek-a-boo and spooky slot canyons in southern Utah and the heat of southern Utah was sort of a very eventful trip and ended up ending with her party having to call the search and rescue. So definitely ask her about that the next time you see her. Her presentation is titled virtual reality as a screening mechanism for glaucoma. So take it away, Caitlyn. Thank you so much for the introduction, Dr. Hu. Let me share the screen All right. I am so excited to speak with you guys today and discuss glaucoma screening. Okay, it's working. So what I'm discussing is a clinical research study that was designed by Dr. Olson, Dr. Simpson and myself that we've been working on for the last two and a half years. So as far as financial disclosures, I have none. So I'd just like to start by saying that I am intimidated to be speaking on glaucoma in front of a group where every single person on this call is definitely more of an expert than I am. So bear with me. We'll start from the basics. Primary open angle glaucoma prevalence is 2.85% and a population of 50 plus. The incidence is 0.38 per 100 person years at 50 plus and the population is 44.7 million worldwide. When discussing screening for glaucoma, right now the USPSTF recommendations is that you don't do it. The studies that they looked at to make these recommendations were a combination of IOP visual fields and fundus exams. Those were what were used for screening and they said most tests that are available in a primary care setting do not have acceptable accuracy to detect glaucoma. And of course when we talk about most tests available in a primary care setting, we're talking about a ton of pen, a rudimentary fundus exam and visual fields by confrontation. They stated that the evidence of effectiveness of screening for glaucoma on clinical outcomes is lacking and that the balance of benefits and harms therefore cannot be determined. They noted that early screening and treatment might help to prevent small visual field defects, but we're not clinically detected by the patients, but no huge outcomes on vision overall. So why should we care about screening? I'm going to kind of go from here and build a case for glaucoma screening. First study I want to talk about is the early manifest glaucoma trial, 255 patients with primary opening ankle glaucoma that was already diagnosed. Two groups, one they received trabeculoplasty and betaxyl all the second no treatment. Over six years they were followed up every three months and there was a 53% progression rate when you look at visual field. At the end of the study they noted that the treatment group had half the disease progression as compared to the control group. So that's great for early glaucoma treatment, but why would we want to find and treat glaucoma suspect patients before they develop glaucoma? So second study that I'm going to talk about, ocular hypertension treatment study, 1636 patients that did not have primary opening glaucoma at the beginning of the study did have ocular hypertension. There were two groups, one was treated with ocular hypotensives, the other one with no treatment. They were followed for an average of 60 months, every six every six months, excuse me, and there was a 7% progression rate to glaucoma in this group. So what's cool about this study is that the treatment group had less than half the rate of progression to glaucoma as compared to the control group. It was a point for hazard ratio with a 95% confidence interval of 0.27 to 0.59 and a P of less than 0.001. So while you could argue that perhaps the number needed to treat, considering we're talking about 1636 patients, right, the number needed to treat might be pretty high, so it might not be super clinically significant, although I do believe it is, but you might argue that, but you definitely couldn't argue that this isn't a statistically significant study. So why not use IOP for screening then? So next study that I want to talk about is a Swedish drive model. There are 32,918 subjects that they looked over 10 years to create a prediction model based off of age and IOP alone. The IOP cutoff that they used for this study was 25 millimeters mercury. There were 406 glaucoma diagnoses in this time in this population. 57% of these diagnoses had an IOP of less than or equal to 21. So they found with this model that they created that they had a 32% sensitivity with a 99% specificity. So it was great in the fact that it had very few false positives, but a lot of missed cases. In fact, there are a lot of missed cases of glaucoma worldwide. There it was a meta analysis done that they estimated that out of the glaucoma population, greater than 50% of them were undiagnosed and specifically they did one in Thessaloniki, Greece, where it was 57% what they found and these are in developed countries and I know the map has Italy, I just didn't know how to change the figure. So that kind of brings me, hopefully I kind of built this case here for why screening might be important. So that brings me to the screening test that was developed. So this was developed by Dr. Kidari who as I understand did his residency here at the University of Utah and Jonathan Olson and Dr. Kyle McDermott who works in the company that Dr. Kidari started in and in discussing with them what they considered important in this screening test that they were developing through virtual reality for glaucoma. These are the characteristics that they thought were important. The first one was a detection of visual field defects kind of obvious, right? Also contrast sensitivity, velocity sensitivity and that it was less uncomfortable in time in terms of been Humphrey, right? So this video that I took of myself because of COVID and I don't really have any friends anymore. So this video you can see putting on the headset and it's not too bulky, not very uncomfortable, pretty easy to adjust to different patient settings. That piece in the front gives a 120 degree field view and what I'm looking at is kind of targets and I'm targeting them with my vision. If I were to stand up and turn around I would have a 360 degree view almost like a spear, right? This was the first time I'd done virtual reality was this game. So just kind of explain it for anyone like me who's never done it before. And what the patient sees. So when you put this headset on this is the first screen that you come to this is kind of the instruction screen and right over target you'll see a hollow circle. That hollow circle is my visual target. So that represents the center of my vision right now. It's right on the horizontal permitting right in the center of the screen as I move my head that circle moves with my head and I use that circle to target different objects. So right here you see the this circle with a cross on it and that is when I rest my vision on it for a second or two it blips and it goes out of screen and you move on to the next portion of the game. So here's an example of one of the screens that you would see on the game. You see one circle with the cross on it and then the other circles don't and they're moving they move at different velocities. So this gives you velocity and contrast sensitivity and as you keep playing the game the contrast changes so it becomes harder and harder to distinguish the one circle with the cross on it from the other circles. And then later on in the game there is kind of an X in the middle of your screen and you keep your target right on that X and from your peripheral vision a circle will start to come in and as soon as you see it you move your head to target it. So that's how the visual fields are tested and again that's 120 degrees of visual field testing. So study design we have three patient groups a control group with no evidence of glaucoma a glaucoma suspect group and this is through chart search the patients that were actively being managed as glaucoma suspect and then the glaucoma group and specifically looking at primary open angle glaucoma. The measures that we all the patients needed to have a current in the last six months IOP for both eyes OCT, RNFL and Humphrey visual fields. So inclusion criteria and based off of the initial data that Dr. Kidarian his team collected we kept our inclusion criteria from 40 to 70 that was just for the IRB and statistical analysis because that was the initial data that we had and then a visual acuity of 20 over 40 or better. For exclusion criteria the first one was extensive video gameplay. We arbitrarily set a limit of five hours per week for extensive video gameplay which probably unsurprisingly was not an issue in this age group and population and that's an interesting point is that the data that we're collecting probably would only be accurate for this generation or this group of people because once you have extensive video gameplay that probably does change your parameters of what you would consider you know a cut off or sensitivity and specificity. We also excluded prosthetic eye or unilateral vision. We excluded pregnant women which again has not been an issue in this age group and individuals with corneal or optic nerve pathology or retinal dystrophy. As far as so just this is just kind of a side note doctors Olson and Simpson are incredible because as I was chart searching I would see these these diagnoses and I wasn't quite sure you know if these would affect the study or not so just keep this running tally of diagnoses and then text or email them every couple of days and they were so nice and this is kind of this running list you can see they got a lot of texting emails these are acceptable and these are the unacceptable comorbidities. Risk for the study you there's a slight risk of nausea playing virtual reality and apart from that there weren't really any other risks that we could think of to put on the IRB. So for preliminary data there aren't enough patients enrolled to say how how good this screening model is but I can say that I've had the glowing combination of it is way better than the blinking light test so the patients don't hate it as much as they hate the visual fields. As far as next steps for this test or for this study really manpower since 30 years started and fourth year's kind of shaping up to be pretty similar I haven't had a lot of office hours to devote to this study when I could be recruiting patients. So if you guys get any emails of medical students or pre-med students or anyone that's looking for a project send them my way this is super awesome a very fun project to work on. So we references huge thanks to Dr. Wilson and Simpson to the fourth floor research team and all the techs and doctors who let me steal their patients before they were dilated. Do you guys have any ideas any questions about this study? Awesome thank you so much Caitlin. Right now we'll open it up to questions you can feel free to raise your hand or and we can unmute you or even throw in some chat questions. All right well we'll just move along if there are any questions of course for Caitlin feel free to put them in the chat and we can also go back. Our next presenter is William West he is from Sandy Utah and went to BYU for undergrad. We've had some fun seeing kids in pediatric ophthalmology with Dr. Jardine during his rotation. His hobbies include climbing, water sports and quilting you can think that last one to coronavirus and he is presenting a case report on unilateral epitheliopathy after lesic. So we'll get him up on the screen perfect. Okay let me get my screen shared here so I appreciate the opportunity to share this case that we were able to see in the corneal clinic. We saw a case of unilateral epitheliopathy after the case consists of a 36 year old male who returned to our corneal clinic was referred to us back to our corneal clinic for epitheliopathy about six months after we performed an uncomplicated lasic procedure bilaterally for correction of myopia. The patient complained of worsening vision in in his left eye exclusively as well as an increasing sense of irritation and foreign body sensation. His past medical history was negative for any trauma to the eye however he did have a history of redness and episodic irritation in the left eye. He had also been diagnosed with a single episode of contact lens induced keratitis that was seen to affect just the superior aspect of the cornea. He denies any family history of ocular disorders. He was seen during the interim period in the first six months of his lasic recovery by his local optometrist and we had no follow-up with the patient until he returned via referral for this epitheliopathy. In the two weeks following the lasic procedure he was seen to have perfect vision with no complications with a visual acuity in both eyes of 20 over 15. At one month however he returned to clinic with a sense of irritation and slight loss of vision. He was seen at that time to have a visual acuity in the left eye of 20 over 30 while the right eye continued to have a visual acuity of 20 over 15. On physical exam at that time a plaque was seen to develop from the superior aspect of the cornea and a three week taper of prednisone was started for presumed interface inflammation. The prednisone gave him symptomatic relief only without improving his visual acuity or the appearance of the plaque. At four months the plaque was seen to have grown significantly and now involved the superior aspect of the lasic flap. At that time a second trial of steroids were performed and again gave symptomatic relief only. From the period of four months to six months the plaque continued to grow and a second plaque was seen to develop from the inferior aspect of the cornea. In both cases the plaques started at the limbis and moved progressively toward the the visual axis. At the time of the development of the second plaque the patient was referred back to us for exam. The patient denied any trauma or chemical exposure between his lasic procedure and when we saw him back in clinic. However on careful questioning he was found to have a history of acutane use as a young man as well as a possible history of battery acid exposure to the left eye when he was a young child after a battery exploded. This was not seen by any medical provider at that time and never caused him any problems that he knew of. He also had a history of military service with work around chemicals however no direct contact with those chemicals and as a hobby he performed he was a barbequeer and brewed his own alcohol but again denies any thermal or chemical exposure. The physical exam is pictured here with a well demarcated wave-like coarse plaque progressing from the superior limbis and inferior limbis. Both of these plaques were seen to involve the lasic flap without any invasion underneath the flap. The flap additionally was well approximated without any sign of dislocation or interruption. A sub epithelial haze was visible and on fluorescein staining a punctate staining pattern was seen. There was also slight injection in the superior congenitiva. For our differential diagnosis we included epithelial ingroth, diffuse lamellar keratitis, and central tautic keratopathy as likely in the period surrounding his lasic procedure. These were considered with a grain of salt however because of the lack of any invasion of epithelial cells underneath the lasic flap as well as the lack of visible white blood cells in the corneal stroma. Additionally this pathology that we saw progressed from the limbis whereas these three diseases tend to initiate and grow from the lasic flap edges itself. We also considered limbal stem cell deficiency to be very likely as the limbis was the source of the beginning of this plaque and we also considered OSSN and CIN as necessary parts of our differential. These were less likely in the context of recent lasic surgery being so closely related to the development of the pathology. Other considerations included acutane associated keratopathy also somewhat less likely due to the distant past of only six months worth of acutane use and knowing that acutane keratitis tends to resolve after cessation of the drug. Herpes keratitis was also considered but also less likely due to the lack of a branching pattern in the plaque and due to the fact that it did not get any worse with the use of steroids. A diagnosis of advancing wave-like epitheliopathy was made. This is a subcategory of partial limbal stem cell deficiency. In the normal eye, the limbal stem cells are responsible for the generation of healthy epithelium that covers the cornea. In a limbal stem cell deficiency, the balance, the delicate balance that maintains these epithelial cells and the growth of the corneal epithelium is disrupted. This results in neovascularization and inflammation and often causes conjunctival invasion of the cornea as seen in these photos. In this case, in advancing wave-like epitheliopathy, this is considered likely to be an unusual presentation of limbal stem cell deficiency, whereas normally we would see this corneal conjunctivalization. We instead see the normal growth pattern of epithelium with unusual abnormal epithelial cells creating the wave-like plaque for which the pathology is named. Any limbal stem cell deficiency is known to be caused by trauma or irritation or toxic exposure to the limbus itself and can be partial or complete depending on the extent of the damage to the limbus. Patients tend to present with the classic wave-like appearance of this plaque that was shown earlier and classically it starts at the superior limbus. There are also cases of this plaque being caused by contact lens use or topical medications. In addition to the classic appearance of the physical exam here, the diagnosis was considered much more likely and made due to the multiple chemical and toxic exposures in addition to lasik that this patient had. The patient also had contact lens history which made the diagnosis much more likely. In management of advancing wave-like epitheliopathy, we focused first on maximizing the ability of the cornea to heal itself as well as to minimize inflammation of the cornea. Often, however, these interventions have been seen to be ineffective. Surgical management shows more promising results with superficial carotectomy or corneal epithelial debridement. This tends to give temporary relief with initial regrowth of smooth epithelium, however, almost universal recurrence of the pathology. Use of silver nitrate in addition to epithelial debridement has been known to prevent the recurrence of the pathology. Other things that have been tried include the topical interferon, vitamin A and topical cyclosporine. These all have been used in other limbal stem cell pathologies, however, the data is poor in this pathology. Lymphal stem cell transplant can also be effective. In our specific case, we first attempted medical management, which classically was ineffective. We then tried corneal epithelial debridement with, again, classic results, initial success followed by recurrence of the pathology. The patient has been on a three-month topical interferon trial with vitamin A and has seen some improvement. His visual acuity is now 20 over 50, where it was at worst 20 over 80. Our plan going forward is to attempt a simple limbal stem cell transplant, however, the patient is currently resistant to that course of action. So take away points for advancing wave-like epitheliopathy. It is a partial limbal stem cell deficiency that results in this classic plaque and wave-like pattern, often progressing from the superior limbus. Treatment consists of medical therapy, first attempting to minimize inflammation followed by surgery with silver nitrate, causing the most durable results. These are the sources that I used to research this pathology, and I would like to thank my mentors, Dr. Majeed Moshafar and Dr. Griffin Jardine. Are there any questions that anybody has about this pathology? I have a question. Thank you for the presentation. That was excellent. So for anyone that doesn't know SLET, that acronym, that is where you take from the fellow eye some of the limbal stem cells. And thankfully, you don't have to take a lot. You actually just cut them up into small pieces and then distribute them around the limbus. Anyone from cornea? Correct me if I've led anyone in error. The question I had in your review had you come across any allogenic limbal stem cell transplant from the fellow eye that then caused limbal insufficiency in the donor eye. Again, I would assume that this would run together if you've got some level of limbal stem cell insufficiency in one eye that you'd potentially have some in the other. That's certainly always a risk with this pathology. Clearly the patient is predisposed to having a limbal stem cell deficiency. In this case, this would be a case where those concerns would be slightly less due to the history of a unilateral battery acid exposure as a kid as well as preoperatively this patient complained of recurrent irritation in the left eye only. Had this patient consented to moving forward with a simple limbal stem cell transplant, we likely would have been very comfortable proceeding with that procedure knowing that the same symptoms weren't present in that right eye. But it's certainly always a risk and can definitely occur with removal of limbal stem cells from the opposite eye. Great. Any other questions? Okay. And of course, if anybody thinks of any, we can put them in the chat window. And so we'll probably move on to our last presenter. So last but not least, we have Rhett Thompson. He is from Spanish Fork, Utah. He majored in American Sign Language and undergrad at Utah Valley University. And something interesting about Rhett is that he took a leave of absence during medical school to create a medical education company called physio.com. And today he is presenting on deep anterior lamellar keratoplasty. So Rhett, take it away. Awesome. Thank you, Dr. Hu. So are you seeing my screen? Just want to make sure. Yeah, we are. Cool. Okay. So I'm really thankful to be here. I'm going to be talking about a doc, deep anterior lamellar keratoplasty. So interestingly, the first successful cornea transplant was reported in 1905 by Dr. Edward Zerb. It's an interesting fact. And we've come a long way since then. And right now, in the modern day, there's two broad categories of corneal transplants. There's the full thickness penetrating keratoplasty, which most of us are familiar with, PK. And then there's a partial thickness lamellar keratoplasty. It's just another category. And some of the more familiar ones, some of the conditions that you're usually going to treat with a lamellar keratoplasty or a partial thickness keratoplasty would be something like fuchs dystrophy, in which is just like a posterior pathology. And this would be often treated with a desec or a DMEC. Now, when it comes to anterior pathology, that's where the deep anterior lamellar keratoplasty comes in to play. So let's dive into that now. So a doc is a condition, a doc is a procedure in which you remove the native epithelium, the bowman's layer, and the stroma. And you leave behind decimates membrane and the endothelial layer. So if you look at this image on the right, you can see a space between the inferior stroma and decimates membrane to kind of highlight the idea of what you're trying to do. You're only transplanting that top part. So the technique is in broad strokes listed here. And I don't want to read them all to you. I would rather explain them to you as I watch a video together of one of Dr. Mifflin's surgeries. So this is a kind of truncated version of the surgery. So here he's trefinating. Oh, I think you have to, we can't see the video. I think you have to actually reshare your screen to that panel. Oh, thank you so much. Here's what we'll, so Dr. Hugh, I thought I would just share my whole screen. So is it sharing it now? I don't see it. No. Okay, that's okay. I'll just explain it. I apologize. It was a good video, but this is Dr. Petty. What you can do just briefly is unshare your screen and then reshare your screen, but select the video and make sure it's optimized for video as you select. And in the meantime, I'll just just queue up a little bit about your company just to let everyone know. So this is something that Rhett created to help medical students in study for their step exams. I'll probably get some of the stats wrong, but as I understand, I mean, it's really one of the top one, two or three resources now utilized by medical students across the country and has become widely known and a well-used resource. And now with that, I'll let you continue on. You'll probably have to do the same thing to get back to your power point. Gotcha. Thank you so much, Dr. Petty. Okay, so now that we're here, so this is again a truncated version of Dr. Mifflin's surgery of a successful doc. And here we've got, we see the trefination and then manual dissection of the stroma, like the top 50% or so of the stroma is what you'd remove. And you're actually going to leave the deeper layers of the stroma because you want to be careful once you're getting closer to the decimates membrane. And so here you can see injecting air into the anterior chamber. And then now this is where we're introducing or Dr. Mifflin's introducing the big bubble and using air to actually separate the remaining stroma from decimates, you create this gap that way and it's a little bit safer. Now here's some viscoelastic that he's putting on here now because as he's going to puncture into the stroma, then it creates that positive pressure where the decimates membrane can actually pop up and hit the instrument that you're using, which is not ideal. You don't want to damage the decimates membrane that way. And now he's dissecting the stroma because there's enough space. It's a little bit safer now that there's this air gap between decimates membrane and that stroma. So as you can see, cutting it into quadrants and then carefully dissecting that. And of course, laying on the new suture and then with suture that in place. So that's the basic overview of how to perform a dolk. Now it's important that we understand the context of a dolk in the current environment because PK or penetrating keratoplasty is typically what's done in order to treat anterior pathologies, even in a situation in which you could potentially use a dolk. So my only point in making this is that the only point I'm trying to make here is that a dolk is really compared and the outcomes of a dolk are compared against a PK. So the reasons that a PK might be more commonly used than a dolk is that the PK is well-established. The very steps and the procedure is very well-established and there's decades of research supporting its use. And also with a dolk, it's actually difficult, at least historically, to manually dissect off the stroma and leave behind uniform tissue. If you can't achieve that, then there's poor visual outcomes. And so a PK is typically has been used. And also it's technically challenging in the sense that it's really easy to puncture decimates membrane. So I want to dive into this idea a little bit more. So this on the right, you can see an image just taken from a snapshot of that video I showed you. And I want you to appreciate just those anterior chamber bubbles that were injected and how it really highlights this superficial or how thin this decimates membrane is. And it's so easy to puncture. And so there's actually evidence that it's been punctured at several different steps during the surgery, like from the beginning with trefination and even at the end when you're just suturing on the donor graft. So traditionally, when this occurs, when there's a decimates membrane puncture, the surgeon would just convert to a PK. And that's still what's typically done. What I want to point out is that there's a couple of studies that I found in which the surgeon actually used a more conservative measure like fiber and glue or something and then proceeded with the surgery as normal and didn't convert to a PK. And so in those outcomes were actually compared to situations in which a delt was performed as normal without any puncture. And it looks so far that the outcomes were similar, which is good. So a more conservative treatment if you end up puncturing decimates membrane may be appropriate, but the basic idea is that you would generally convert to a PK. So having said all that, there are some advantages to a doc over PK. And the biggest thing to keep in mind is that there would be decreased risk of graft rejection. And that makes sense because the endothelial layer in a corneal graft is usually the target of host immune attack. And if you're not transplanting a foreign endothelial layer, then graft rejection overall is very, very much decreased. And so the patient that you want to be thinking about would be young patients in whom you would expect to have a high immune response. So a young otherwise healthy patient would be a good candidate for a doc. Now there's evidence, there's some evidence that the wound is potentially a little bit stronger with a doc, which may be helpful in trauma patients. It's not super clear yet with whether or not that will hold true. The evidence is not necessarily robust for that idea. But something really interesting is that a doc can be performed successfully even with lower quality grafts. So this can be really useful in situations or even areas in which a hospital doesn't have access to healthy tissue readily. And so in those situations, they may have access to, you know, just the anterior layers of the cornea. So and sometimes eye banks will actually even donate these eyes, which can be helpful. And at least no situations can lower the cost of the surgery. Now this is a patient, this is a picture taken from a patient last week. And this is a post-op doc, patient of Dr. Mifflin's. And I want you to appreciate the neovascularization that's coming in, especially superiorly. And if you can follow that along, you can see just how far down it descends. And so I want to point this out because, yes, there is decreased endothelial graft rejection. But, you know, things like this can still occur. So that was just an interesting patient case there. You know, there was a lot of studies that have a lot to say on comparing docs in PK. And the one that I liked the most was actually the most recent and it was performed, it was published earlier this year, it's a systematic review and meta analysis. And in that study, the included 530 doc surgeries and 560 PKs, and the visual outcomes overall were comparable between the two. And then the graft rejection risk was, as you would expect, lower overall with a doc. And then the complication overall was also decreased with a doc, with doc surgeries. And this is the end of my presentation. And here's some of the references. Here's some more references. And I just want to give a special, I just want to thank Dr. Mifflin for his help with this. And Dr. Petty, I want to thank you for covering for me during that awkward moment, which I was trying to get my screen to work. It was helped me a lot. So thank you. Great job, Rudd. And then we also have a question from faculty. It just says iPhones. I'm actually not sure where this question came from. But it just says, can Rhett repeat what he was saying about another method using fibrin glue? They didn't quite catch that part. So yeah, so there's evidence that fibrin glue, there's some several other more conservative measures as well that that some surgeons, I guess, experimented with. This was in the Middle East. And they were able to, so in that situation, they punctured the decimates membrane. And instead of converting to a full PK, which you might expect they actually used fibrin glue and just tried to restore the cohesion of the decimates membrane. And then they just proceeded with the surgery as normal. And there were, there was a five case studies that they studied. And each one of them, according to their reports, actually had the same visual outcomes when compared to docks that proceeded as normal without any puncture and decimates membrane. So the idea that was trying to make is that, or the point I was trying to make is that that is potentially a way to proceed in the surgery, even though that's not really commonly done. And traditionally, you just move to a full PK. Hope that answers the question. So, Rhett, I don't know if you'll be able to answer that, and Ethan, you may need to keep an eye to see if any of the other cornea faculty can answer this. So having trained a lot of residents, I've seen a number of decimates membrane tears, significant tears. I even had a case in an outreach setting where I personally had a small tear. And when I put some visco elastic back into the eye to check something that looked odd, I actually managed to completely separate decimates membrane from the rest of the cornea with visco elastic. Patient did well in the end, but it took me a minute to figure out what exactly had happened. It does seem like decimates is a lot more resilient than perhaps we initially thought. And I'd just be curious if in, in, you know, our cornea, our cornea faculty's practice, they feel like in the future, in these, you know, really technically difficult surgeries, Mark, you made it look easy. If again, with these, you know, tears that invariably will happen, if you think we're going to more and more continue to just proceed with the dalk rather than conversion to PK. So I think that's a good question. And I'll defer to your professionals who have more practical experience with this. But I can't say that I was only able to find two studies that really examined that and they were minimal in their sample size, sort of. We'll unmute you, Brian. Brian Zog has a comment. We'll unmute you here and have a sec, Brian. Good to go, Dr. Zog. Am I unmuted now? There we go. We can hear you. All right. I thought I was unmuted and then I'm not. Okay. So in some of those cases where you have like a really small decimase tear when you're trying to do a dalk, you can actually continue it. The challenge is, is that once you commit to a dalk, then you're stuck because you take your donor tissue and you actually destroy or wipe off decimase membrane. And then you essentially put that on top of the host decimase membrane and suture it in place. And so in our situation in the U.S., if I am concerned that I've torn decimase membrane and I don't feel like I can keep it in place, which sometimes you can do with an air bubble after you've sutured on your PK, then I'm just going to do a PK because I know I've got really good tissue with endothelium that's very healthy. In other countries, so where this kind of fiber and glue idea came in is they may not have tissue that is viable for a PK. So their only option when they're doing that surgery is to do a dalk. And so if they rupture decimase, host decimase membrane, they don't have tissue that is healthy enough to do a PK. And so they're just, they've got to make do with what they have. And so in some of those situations, they'll just try to reattach decimase once they kind of suture on that dalk tissue. So we're pretty lucky in the U.S. that in most cases surgeons will just convert to a PK if they're concerned, whereas in other countries they may not have that option because of tissue availability. And there's some really cool things that are happening with this where they'll take, they'll take tissue that's PK worthy and they'll actually strip off endothelium and do a DMAC or even a desec on a patient. And then they'll use that anterior lamellar essentially donor tissue to do a dalk. And so they're kind of splitting one donor cornea into two different surgeries to help patients with different pathologies. So kind of different situations where that might come up, but for us it's usually just go on to PK. Great. Thank you, Dr. Zog. Does anybody have any other questions for Rhett? Otherwise, we also did want to circle back to a question for Caitlin. So this was from Dr. Petty. It said, a question we can come back to at the end, but how would you design a study that you could evaluate a subject's experience with gaming? Young healthy gamers will likely score higher than older healthy non-gamers. Yeah. So this is actually a thought that I've been kind of ruminating non for a couple of years now. I think it would be very tricky. I think in 20, 30 years, it will be a lot easier because we would have video gamers in this age range that have been playing since they were little. Right now, even in the 40 to 70 year old age range, the people who have been playing for 20 years, I would hypothesize that their gameplay is fundamentally different from someone who started playing when they were five or six versus someone who started playing when they were 20 or 30. So I think it would be super hard. I think the best that you could do is kind of start with an age group and then study gamers versus non-gamers or start with gamers versus non-gamers and then try to allow for age, try to create a model for age. I'm not 100% sure how it would work. Well, thank you for that. No, it is really tough. I do wonder if, you know, in a large enough study, you could use a multivariate analysis and then, tease that out in the end. Certainly, there will be a learning curve, right? And we even know that with just typical visual fields, there's a learning curve for those who have done them for a number of years versus those who are just starting. But this, thinking about this as a screening device, I think that'll be an interesting element. What thresholds are you putting or perhaps eventually having a different threshold depending on the amount of gaming experience that really does play out as something significant? And I mean, since it is such a complex system, they can build algorithms in. So I mean, the patient, the first thing that they do is they say, this is my age, these are more comorbidities. And I do think that eventually the algorithms, the AI learning models, could account for all of that, which is probably take an end of much higher than what I'm doing with this study. And then final question, are the games fun? Fun enough that people would actually just play them and perhaps auto screen themselves as they're playing a fun game? I will say no, but okay, here's, there's a no but. So this game that was developed, this was kind of, this was developed specifically for glaucoma screening and kind of less time was put into this game than the other games that Dr. Kidari developed. I played those ones. Those ones I would play for just fun. This one. All right, well, great job everybody to all our presenters today. I think if there are no other questions, we'll wrap up here and we'll see you guys all next week.