 All right, good morning, everyone. We're gonna get started here. Welcome to another Moran Ice Center Grand Rounds. I'll be moderating today. Say we have a lot of great discussions and topics from our medical students and also oculoplastics. First up will be Amy Amoy. She's a rising second year medical student from the University of South Florida. Talking about improving compliance to follow up eye care for children. Welcome. Good morning, everyone. Thank you for the introduction. So as previously mentioned, my name is Amy Amoy and I'm a rising second year medical student from USF Morsani College of Medicine. Today I'll be providing background information and an introduction to a research project that I started during my time here at the Moran in collaboration with Dr. Asari, who's my research mentor. The aim of our project is to ultimately identify, summarize and disseminate strategies to improve follow up eye care for children after failed vision screenings in primary care studies. So we're gonna start off with a case presentation. Our patient is a 13 month old girl who presents to the Ophthalmology Clinic at Riverton for a follow-up evaluation after a failed vision screen with her primary care provider. She failed her vision screen due to NSO metropia. Upon further examination, she was found to have myelinated retinal nerve fibers in her right eye. She also had high myopia in her left eye and was a refractive embliopia suspect. Her mom was counseled to have her wear glasses full time. In subsequent visits, patching of the right eye was recommended for NSO metropic embliopia of her left eye. Cases like these underscore the importance of vision screening and follow-up eye examination early in life as they're crucial for preventing of wittable vision loss in children. So vision screenings and follow-up eye examinations enable early detection and prevention of vision loss from a myriad of conditions like embliopia. Ambliopia is a leading cause of preventable and reversible vision loss in children and the prevalence among U.S. children under three is about two to 3%. There's also a narrow window of opportunity to detect and treat embliopia as well as its risk factors. And after about the age of eight, the effectiveness of embliopia treatment declines and visual loss can become irreversible. As a result, the U.S. Preventive Services Tax Force recommends vision screening at least once in all children age three to five years old. Other associations like the American Association for Pediatric Ophthalmology and Strabismus recommends vision screenings to start at birth. So vision screenings can be performed by primary care providers as well as trained lay persons at schools and as well as community-based screening programs. Vision screenings function as quick tests to flag potential eye conditions that a child may have. In primary care settings, visual acuity test and instrument-based screening, either using a photo screener or an auto refractor are the primary methods of assessing vision in children. When a child does not pass a component of the vision screen, timely referral for a comprehensive exam in order to enable diagnosis and treatment of vision problems are crucial. Despite the importance and benefits of vision screening, the literature shows that children are not getting the necessary eye care due to poor follow-up compliance. For example, authors of the following study from the Journal of American Association of Pediatric Ophthalmology and Strabismus surveyed the parents of children who failed a vision screen in order to determine the rate of follow-up and identify barriers to follow-up exams. Of the 57 surveyed parents, 29% of them were not aware of their child screening failure. Of the 40 parents who were aware of their child screening failure, 17% of them did not schedule a follow-up appointment and 5% of them missed their child's follow-up appointment. So this study found that parental unawareness of their child screening failure due to possible miscommunication, in addition to parental unawareness of the need for follow-up and logistical challenges like forgetfulness and scheduling conflicts were the main causes of poor follow-up compliance. For the sake of time, I will skip over this study, but again, it shows different barriers to follow-up compliance. So as noted, reasons for poor follow-up include a combination of provider system and patient factors. Several studies have reported on interventions to improve follow-up compliance after failed vision screenings, but these studies have primarily focused on schools and community-based screening programs. An example of such interventions involve providing assistance in scheduling a follow-up appointment with an eye specialist after a failed vision screening. In an initial review of the literature, we found that not as many studies investigated improving follow-up from primary care providers to eye care providers. So the aim of our scoping review is to summarize existing strategies to improve follow-up compliance for children after abnormal vision screenings in primary care settings, as well as identifying gaps in the literature. So a scoping review is a preliminary assessment of the potential size and scope of the available research literature. They allow us to investigate broad research questions, examine the extent and nature of research activity, summarize research findings, and identify gaps in the existing literature. For our scoping review, we plan to include articles that have children from three to five years of age and its target population. We also plan to include articles that are published in peer-reviewed journals and that report strategies to improve compliance to follow-up eye care from primary care providers to eye care providers. We will exclude articles that are reviews, case reports, or opinion pieces, and articles not written in English. We will also exclude articles that do not have strategies to overcome barriers to follow-up. So this is our initial search strategy. It's broken down into four main concepts or keywords. And this search strategy took a couple of weeks to develop and required looking up relevant medical subject headings as well as synonyms for our four main concepts. After running this search strategy through PubMan, we got 149 hits or potentially relevant articles to our topic of interest. So in terms of the next steps, we are currently in the process of writing a protocol for our scoping review and plan to have that registered. We've also had a research librarian analyze our search strategy and she's helping us refine that as well. Once our search strategy is finalized, we plan to run it through the relevant databases such as Medline, M-Base, Synol, Psych, Info, Web of Science and Scopus and then we'll screen the articles. Screening will be done in two teams. Each team will have a medical student as well as a faculty member with expertise in our topic and then it will be done in two levels. So the first level will be a review of the titles and abstracts and then the second level of review would be a full-on review of the evidence. So I plan to continue working on this research project remotely even after my time ends at the Moran. Okay, so these are my references and I would first like to thank Dr. Asari for her guidance and support during my time here at the Moran and allowing me to join her on this research project. I would also like to thank Dr. Vagunta for her support and helping me to refine my presentation. I would also like to thank all the physicians that allowed me shadow them and the residents that I worked with that just made me feel welcome during my time here. And finally, I would like to thank the Moran for giving me the opportunity to learn and gain exposure to the field of ophthalmology. So this concludes my presentation and I'm open to any questions. Great job and thank you for the great presentation. Any questions right now? Go ahead. That's not a great question. The ambliopia is so dependent on what the cause is. Deprivation of ambliopia is so sensitive. Refractive, I've had patients who were in their teens who had never been treated and gained several lines after being in the proper correction and with patching. So there's been some studies that have shown that if you don't have a history of patching that actually the eyes are pretty responsive to glasses and patching even later in life. But I think given the degree of anisomatropia and the depth of the ambliopia, it has a pretty wide range. What's interesting is that we're seeing tons of kids coming in now with these auto refractors is as like eight months old or eight month olds or even up to two and three, there's a big influx. And so we're catching more early, which has been good but sometimes it's probably a little over sensitivity in that screening. But that was a great presentation, Amy. And I think it's pretty impressive to the number of people who aren't coming in. I mean, that for the last dead end, I think looking at those barriers is gonna be a really big deal, but I hope I answered your question, Bob. And I think again, Amy. In a clinical setting, we see unilateral ptosis, they're ambliopic, and then a frontalis sling doesn't work well unless you're recruiting the frontalis. So the question in my mind is, at what point in time would you be able to regain or say to develop single binocular vision? I don't think that's a more early life sort of. Yeah. Isn't it? The binocularity is really sensitive. So if that, if it's, I mean, especially with something like severe ptosis that's causing, you know, if they're not fusing with both eyes in that first year, sometimes even the first six months, you know, for patients who have like congenital strabismus, that seems to be the most, one of the most sensitive short windows. I find a lot of those patients with ptosis, I'm amazed how many of them compensate with just a giant chin-up head position and seem to still maintain it because that drive for binocularity, if it's an option at all, is powerful. I mean, kids will touch their ear to their shoulder just to get their fourth nerve palsy diffused. They're pretty good at finding it. Yeah, no, when we see chin-up head position, that's great news. We know that'll work then. Right. Okay, thank you. Thank you both for the great discussion. Next up, we'll have Junae Ascartes, a fourth-year medical student from Florida State University, presenting from Holy Terror to Ideal Recovery. Please welcome. Thank you. Ethan, can I do a present of you? Alrighty, thank you everyone. So my name is Junae Ascartes. I'm a fourth-year medical student at Florida State University and this talk is titled From Holy Terror to Ideal Recovery. So when we had orientation, Dr. Jarjean said that he would rather be bored to death for eight minutes than to have his mind blown in 15. So our objective today is actually just to blow your mind in eight minutes alone. So we're gonna start with, well, financial disorders and under-report. So we'll start with a case presentation. So we have a 71-year-old pseudophagic woman with a history of type II diabetes presenting a complaining of decreased vision in her left eye for six months. On an ocular exam, she had the best corrected vision of 2100 in that eye in 2020 in her Pella Y. Silt lamp exam, her anterior segment was unremarkable and then fundus exam revealed a chronic stage four full thickness macular hole in the left eye and it was confirmed by OCT and showed a diameter of 519 micrometers. And you can see the wise ring on the left-hand side over there. And so treatment plan for this patient was a PPV with ILMPL 12% C3F8 gas tamponade and face down positioning, which she did for two weeks and then followed up, hole was still open. And so we had her face down for two more additional weeks and again, still open. So this is an OCT four weeks post-op reveals that the hole still open has a diameter of 307 micrometers at this point. And despite discussing re-operation, which is kind of the go-to strategy for cases like this, she declined and didn't wanna go through another operation. So she was just instructed to follow up with routine surveillance appointments. And again, this is just six weeks post-op showing a hole still open. And then two months post-op, she presented urgently to clinic with acute pain, conjunctival injection, photophobia in the left eye. Slant lamp exam showed one plus cellular reaction in the anterior chamber and the OCT revealed CME. And as you can see, the hole is actually closed up now. And so due to timing, she was diagnosed with idiopathic post-op iritis with macular DMA and she was treated just to get rid of some of that swelling with trimescent alone 40 milligram injection. And this was one month after that injection so you can see that the hole's closed up now and there's a little central cavity in the outer retinal cavitation. And again, reiterating this is four months after that trimescent alone injection and when she returned and her final vision here was 2080. But again, you can see the holes closed up now. So how did I acquire this case? This was actually presented to me or referred to me from Dr. Riley Sanders who's a vitria retinal surgeon at the University of Arkansas Medical Center. And he reached out in February of 2023 and we've submitted this case for publication this past month. And while I'm not the world's leading expert on macular holes, I do dabble in them. And so this was kind of the harbinger for why he reached out to myself and Dr. Brooks. This is a paper that we published in June, 2022. And so I just like to give a little overview on this case itself. So this was a 70 year old pseudophagic woman who presented with an 18 month history of a central scatoma and reduced vision to 2200. Imaging revealed a stage three chronic macular hole shown in that first image with a diameter of 506 micrometers. And so treatment for her was PPV with ILMPL 30% SF6 gas and she did excellent face down positioning for two weeks. However, when she came back for her two week post appointment, you can see that the surgery failed, the hole still open and the diameter was 337 micrometers at this point. She didn't have any edema here, but she again, this was another patient who didn't wanna go back to the operating room. She'd already been having these visual changes for a year and a half now. So for her, she felt like it wasn't worth going back to another surgery. And so at this point, my research mentor, Dr. Brooks, who's the co-author on this paper with me, had this idea that, you know, maybe if we can induce edema that could bring the edges of this hole together and possibly lead to some sort of co-optation. So after her metform consent, we decided to put her on Latanna Frost twice daily for six weeks. And when she followed back up, the third image shows that that was able to induce CME. And so at that point, she had a C3F8 injection into the vitreous cavity and was instructed to face down for five days. And when she followed up two weeks later, that was her OCT and that final FIGAS figure four. And it shows that the hole closed and her visual acuity eight months later was 20 over 50. So pathogenesis of idiopathic holes are not fully understood and there's multiple theories, but one of the most common factors in all the different theories is the involvement of vitreoretinal interface forces. And recently there's been some discussion about medical management for full thickness holes associated with CME, especially for smaller holes. And the treatments here usually include anti-inflammatories like NSAID drops with or without carbonic anhyzeres inhibitors. And those have been proposed as potential treatments for smaller holes with CME. And it's believed that these treatments can dehydrate the hole if they're CME present. And that'll allow for closure. But kind of what we've been proposing in these two cases is that the reverse process of increasing edemia via leutanoprost or in the first case that I presented by some sort of idiopathic iridus has been shown to aid and closure of a large chronic hole that's failed primary surgery. And so this is kind of a nice figure that demonstrates how that happens. So you got a hole leaking and you just want to induce some edema. I think this is a really good schematic to kind of go through with this idea present. So the top picture, this is from a paper in 2004 by Dr. Smitty and Flynn and they talk about the pathogenesis of holes. The top figure you can see that's the early stages of a macular hole and there's glial cell proliferation which is that layer of cells that are a little more oblong and they extend to form a bridge and that can actually aid in a self closure. So by extending the edges of the hole, you can inhibit the further formation and create a seal to actually repair it. However, if posterior hyaloid detaches then you lose that glial bridge and you've kind of got this hole and eventually it can progress to that bottom picture. As the glial cells contract, you can see that the hole actually kind of gets that characteristic appearance where the edges have blunted and the slope is increased at the bottom portion. And so the theory that these two cases show if we can go back from this chronic hole closure back to the original state that can maybe aid in the formation. So really by inducing edema, you can bring the edges of the hole back closer together and then re-allow for this glial bridge formation to form. So while this report, the original report had idiopathic post-op CME, both cases that I've described demonstrated a potential effect of CME for larger holes persisting, especially after surgery. In both cases, the rehydration increased the volume of the edges of the regular hole and helped approximate the edges of the hole for co-optation. That process brings the glial cells closer together and it decreases the degree of obstacles for cell migration and bridge formation. And subsequent treatment, as in the first case with the trimestallone afterwards, helps to dehydrate the CME, allowing for kind of a final resolution. And other methods for macular hole surgery, rescue are more invasive compared to this theory that we've reported here. So I'd like to acknowledge the following people, hear my references, and if this video will play, this will kind of go back to our objective. Oh, you're crazy. Am I? Or am I so sane that you just blew your mind? So thank you, and I don't take any questions. Yes, sir. Dr. Dardin, sorry. My question to you is, well, remind me again what the visual acuity change was pre and post whole closure. And then do you have any comment on their subjective description of their vision, change if it improved, if there's a survey done on that? So in the first case, I believe she presented 2080 or 2100 and her final vision was 2080. And that one was not as exciting just because she'd already failed surgery. We weren't expecting to have a much better vision and she didn't even care for future surgery. And that was the idiopathic cause where she had the iridus that closed it. And then in the second case, she presented with 2200. And then after surgery, which had failed, she presented with 2400. But then after inducing with the TANF process, her final vision was 2080 or 2050, I believe. So it had increased. And then, sorry, what was the second part? I'm not sure. Don't care about that. Yes, sir. How often do you know does Latinopros cause CME? Is that frequent or are you just really, really lucky? From what I've read, it's kind of similar to the gas Irvine syndrome. So it's still up for debate a little bit. There's been some cases that show that it does cause it and others that show that it does not, but usually it's gonna be after an inflammatory stage. So either post cataract surgery, in the second case, like a post, or sorry, in the first case, like a post iridus. So I think from clinical experience and some of the studies that had been read by my research mentor with that Latinopros-induced case, his theory was that for his patients, it normally does induce it. And whether it's the actual Latinopros or the preservatives, like the benzoyl chloride in the Latinopros, what's causing the edema, I think that's still kind of. So would one consider that as a therapeutic trial in somebody with macular hall? That's kind of the situation in that original case that I presented that was published. That was the first time that that had been reported. Thanks. Yeah. I'm gonna pull Wayne. Yes, thank you all. Great job. Next up, we have Christopher Lee from the University of Colorado School of Medicine presenting a rare masquerader. Thank you. Morning, everyone. My name's Chris. Like Chris Lee, like Brandon said, I'm a visiting fourth year medical student from the University of Colorado. And I'm gonna present a case this morning. Special thanks to doctors Hanson, Kohler and Kohler for helping me to put this together. I have no disclosures. Talking a little bit about our patient, we had a 14 year old male with no significant past medical history who presented to the ED with three days of the splurred vision from his left eye, a red eye, eye pain, fever, body aches, and a facial rash. He described his vision as being blurry and dark and reported being able to see objects that were close to him and in the bottom of his field of vision. On examination of this patient, he was noted to have a visual acuity of light perception only from that left eye and was positive for an APD. He had three plus conjunctival injection and pretty significant anterior chamber and vitreous cell. On fundus exam, his disc was hyperemic. The macula was detached with yellow intra-retinal and sub-retinal exudative material. And on peripheral exam, he was found to have a multifocal exudative retinal detachment with a yellow whitish appearance of sub-retinal exudative material, as well as retinal whitening and emerges peripherally. In terms of a differential diagnosis for this patient, presenting with this pan-euvietic picture with an exudative retinal detachment, some of the things that we thought about were seated in an infectious and non-infectious category, such as syphilis, bacterial endophthalmitis, varicella, pan-euvietis, sarcoidosis, and BPH. Other things to consider are vascular causes, such as Coates disease and neoplastic causes, such as lymphroproliferative disorders and retinoblastoma. This patient had a pretty extensive workup on presentation. In the emergency department, he underwent a TAP and injection, which yielded a dry, vigorous TAP, a successful AC TAP. He also had a respiratory viral panel, a broad uveitis workup, and was also seen by the uveitis team here, who recommended that you get a vitreous biopsy done. So that being said, the patient underwent an exam under anesthesia and also a vitrectomy with a vitreous biopsy, as well as intravitrile injection of several antimicrobial agents. In terms of the results for this broad workup, most of it was negative. Of note, he was positive for rhinovirus on PCR, and the vitreous culture came back growing a pan-sensitive staph capitis. And importantly, this patient had a negative carious panel. So given the result of this negative carious panel, it was thought that the vitreous culture coming back growing staph capitis was likely a contaminant. And so after this patient's initial vitrectomy, they were able to get an exam. And this fondest photo on the left side of the screen here was taken after that vitrectomy. And it shows lung ectatic vessels with bulbs and associated yellow, white sub-retinal exudates, as well as a multifocal exudative retinal detachment. Also, he had a wide field FA or fluorescein angiography done in the clinic after this initial vitrectomy showing, again, diffused to lung ectatic vessels with these terminal light bulb aneurysms, capillary non-perfusion, and showing perivascular leakage as well. And so given these findings, this patient was diagnosed with Coase disease stage three. So Coase disease masquerading as a uveitis is a rare but reported entity in the literature. Our patients had a very unusual presentation given this adamant sudden change in his vision and the history of a dilated exam a year prior that was reportedly normal. He also had these strange prodromal symptoms of fever, chills. He also had a lesion near his lip resembling a cold sore. This in association with an exam concerning for a pan-uveitis kind of make this a strange presentation with this disease masquerading as a uveitis. In this case, the key was obtaining the wide field fluorescein angiography following the patient's vitrectomy in order to basically see the pathonomonic findings and characteristic findings in this disease. So uveitis masquerade syndromes are ocular and systemic pathologies that present with intraocular inflammatory cells in an inflammatory picture but aren't secondary to immune mediated or infectious processes. Some of the things that we think about in this category of diseases are classically intraocular lymphomas and other non-malignant causes such as Coase disease and retinitis piglimtosa. So Coase disease was first described by George Coase in 1908. It's a congenital non hereditary idiopathic disorder of the retinal vasculature that leads to this intra-retinal and sub-retinal exudation. It's typically diagnosed in the first or second decades of life in males and is the unilateral disease affecting one eye in a patient. To briefly go over the pathophysiology and clinical features of Coase disease, it's essentially a defect in the endothelial cells and abnormal parasites of the retinal vasculature that leads to the development of these telangioptatic vessels, retinal ischemia and this leakage of this lipid-rich exudative material. Symptoms that presentation can be variable, but the ones commonly reported are vision loss, strabismus and leukocorea. I wanna highlight the key exam findings that should be looked for in patients with concern for Coase disease. And this includes the telangiocatic retinal vessels with capillary non-profusion as well as this diffuse exudation that has a yellow-white appearance. The treatment of Coase disease, the main state of treatment is laser photocoagulation with the goal of treatment being to address the abnormal vasculature and to control this exudative process. Recent literature has suggested that anti-veges and intravitriol steroid injections can serve as an adjuvant therapy and help to control the exudation and macular edema. It's also worth noting that a lot of these patients develop exudative retinal detachments and may necessitate vitriol retinal surgery such as vitrectomy and external drainage of that exudative material. So a month after initial presentation, our patient presented for treatment with laser, but on exam was found to have diffuse vitreous hemorrhage and a now total retinal detachment. And so because of this, the patient was taken for a vitrectomy and scleral buckle with external drainage and adjuvant therapy with a vasculin intravitriol injection. The picture at the top of the screen here was taken shortly after that vitrectomy. And now after several months of treatment with multiple exams under anesthesia, laser treatments and a vasculin or subtenants, catalog injections, the photo on the bottom of the screen here highlights an improvement of the patient's exudative retinal detachment but its persistence as well as improvement but persistence of the diffuse exudative material and also with some residual fibrosis interaction involving the retina, the mahula, excuse me. This patient's visual acuity recovered to count fingers and he's developed no signs of glaucoma. Thank you all for having me. It's been a great time getting to know the team here at the Moran and look forward to the rest of my rotation. I can take any questions now. Any questions for Chris? Good job. All right, more. There's one thing. Yeah, I remember when this case came in. It's a super, super interesting case, good job. All right, a little bit more UVitis here for our last medical student discussion. So please welcome Krishna Malim from Drexel University discussing a geodemographic analysis of travel time to UVitis specialist in the United States. All right, good morning, everyone. My name is Krishna Malim. I'm a fourth year medical student from the Drexel University College of Medicine. And today I'll be talking to you about an original research project, the title of which is a geodemographic analysis of travel time to UVitis specialist in the United States. I have no financial disclosures. So travel time to a patient's medical provider represents a significant component of access to care. There's a growing body of evidence in medicine that shows that increased travel times are associated with poor compliance and adverse outcomes for patients. I'd like to go through some of the studies that have been done to demonstrate this. So Kelly et al, they performed a systematic review of 108 papers in primary and secondary care specialties that suggested that increased travel times lead to poor outcomes across a variety of specialties. The dialysis outcomes and practice pattern study or DOPS showed that greater travel times for patients requiring dialysis resulted in increased mortality with reduced health related quality of life. Single center studies in bariatric and vascular surgery have showed that greater travel times are associated with poor post-op compliance and in fact served as independent predictors of decreased long-term survival. And multiple studies in oncology have shown that increased travel times are associated with higher cancer stage at the time of diagnosis as well as potentially increased cost and reduced access to care. So what about in ophthalmology? There are a small number of studies that have looked at the role of travel time within ophthalmology. Examination of the role of travel time in ophthalmology has been limited to general ophthalmology and glaucoma. Lee et al performed a study in which they looked at the average driving distance for travel time for the American population to their nearest eye specialist which they defined as an ophthalmologist or optometrist and found that 90% of the American population lives within a 25.2 minute drive of their nearest eye specialist. Rothman et al performed a similar study looking at Florida's elderly population and their travel time to the nearest glaucoma specialist and they found that 88.4 of Florida's elderly population lived within a 60 minute driving distance of their nearest glaucoma specialist. However, a similar study had not previously been performed in uveitis which is a relatively small subspecialty in ophthalmology and has a smaller number of fellowship trained doctors who are trained to treat it. So in this study, we examined the travel time to the nearest uveitis specialist for the American population and characterized its potential impact on access to uveitis care. So addresses of fellowship trained uveitis specialists were collected from the American uveitis society and ocular immunology and uveitis foundation websites and using ArcGIS 2.9 Pro, these addresses were geocoded and a map was constructed with all of the locations in the map for the United States. We then constructed 60 minute drive time service areas around each of these specialist location using ArcGIS cloud-based software. And to standardize, we set the parameters as the average driving distance on a weekday at midday to simulate patient conditions. We then imported demographic data into our map using the American Community Survey and American Census Bureau. So variables that we imported included racial groups, household poverty levels, population in dependent groups which was people who were younger than 18 or older than 65 for the American Community Survey and health insurance status which were all overlaid at the census tract level. And then this data was aggregated for census tracts that fell within and outside of service area coverage, creating two groups. And these groups were compared across these variables using chi-square analysis. This table summarizes our results. So on the left hand, we have the variables that we looked at. The left-sided column is for populations that fell within service area coverage, so within that 60 minute drive time. And on the right hand side, we have the population that falls outside of service area coverage. So we found that just about 63.3% of the American population lives within an hour driving distance from their nearest UVIDA specialist. People within service coverage were 12%, there were 12% of them in households with the total income below poverty level versus 15% outside of service area coverage. Only 8% were uninsured within coverage versus 9.5% outside of service coverage. Only 37.4% of people within coverage belong to a dependent age group versus 40.4% outside of service area coverage. And we looked at every ethnic group in the Census Bureau but the major ones that we looked at in our analysis were white and non-Hispanic which was 55.9% within service area coverage versus 66% outside. Black or African American which was 14.7 versus 10% outside and Hispanic which was 19% within but 16.6% outside of service area coverage. And all variables that we compared were found to be statistically significant. This is the map that we constructed with all of the UVIDA specialists and their service areas. So in red, we have UVIDA specialist locations and the green clouds represent the 60 minute drive time service areas around each of their locations. So immediately what you can see is up here in the northeast we have a relative saturation of UVIDA specialists especially in large cities and at large tertiary care centers. So we're looking at New York, Boston, Philadelphia, Baltimore. But as you move out further west we can see that become relatively less dense. And once we get to the Midwest all of a sudden it's like there's no one. So we come here that's us right now. So at the Moran we have now I believe four UVIDA specialists so the doctors Vitaly, Shakur, La Rochelle and Craven and they are caring for all of them. So just three or four states that have no UVIDA specialists or very few within state boundaries which represents a large number of people who have no easy access to UVIDA care. So in conclusion we found a significant travel burden at the nearest UVIDA specialist for a large proportion of Americans just under 37%. This is much greater than what was previously reported for comprehensive ophthalmology or glaucoma. We found that people outside of service area coverage were more likely to belong or more likely to live under the poverty line be uninsured or belong to a dependent age group all of which may further independently impact their ability to access care. We also found a relative saturation of UVIDA specialists in metropolitan areas and all this together we believe highlights the importance of increasing the number of fellowship trained UVIDA specialists in areas especially the fall outside of existing service area coverage and practically for providers I believe it's important to assess how travel time might impact patients and their ability to access care and in the future attempting to quantify the effect that travel time can have on patient compliance and outcomes specifically in UVIDAS and ophthalmology in general. Thank you all for listening and for taking the time and I'd like to acknowledge my research mentors at the Wilmer Eye Institute specifically Dr. Meg Burke and stock for helping me with this project and I'll take any questions. Thanks, that was great. So just a quick question. How do you determine an hour I guess of travel time because an hour traveling in New York City I think can look a lot different than an hour in Montana. Yeah, so great question. So ArcGIS it has a function within it called Esri and it's linked to an Atlas of the United States with all of the road systems in the United States and it algorithmically calculates how long travel time is going to be dependent on traffic and other conditions in specific locations. So that kind of standardizes. So you can see as you move out west like you can't see it on a zoomed out view necessarily but when you zoom in an hour in New York would be exactly as you said much smaller it might be like Queens to Manhattan versus if you go to Montana it could be, I don't know very far in Montana. I don't know towns in Montana. So yeah, so that is how it standardized using the software and the reason we use 60 minutes specifically is because I forget the exact government agency but there's a published metric that says that 60 minutes represents if you fall outside of 60 minutes that represents low access to care based on travel time. So that's why we use that as our dividing metric. Thanks, yep. Come down from Montana, drive eight, 10, 12 hours and say nothing of it. Yeah, absolutely. No, I was in Dr. Vitale's clinic this Monday and there was a patient from, I wanna say Idaho who said she had driven seven hours for her appointment and she was very nonchalant. Yeah, I'm driving back right after this. So we tried to get her out of there as fast as we could but. Other questions? Great job, Christina. Great job to all of our medical students. I think Dr. Kirsten or Dr. Olson's going to introduce the last speaker, is that correct? I am. Awesome, thank you everybody. So everybody, I'm gonna keep it brief because you don't wanna hear from me, you wanna hear from Dr. Kim. It's an honor to have Dr. Kim here and then just four things I wanna say, you got to her CV so I don't need to reiterate any of that. Number one, I can tell you that peers and colleagues say that she's an absolutely outstanding oculoplastic surgeon. Is number two, is that she has special interest in pediatric oculoplastics. And number three, is that I can tell you that she's also highly regarded for out tending teaching skills and very much appreciated for that which we'll get a chance to experience here in just a second. And number four, everyone who knows her says she's just a wonderful person. So what else can I say other than welcome Dr. Kim we're ready for your lecture. Thank you. Well, good morning everyone. I am so happy to be here and grateful for this opportunity to present to you all this morning. And I'm especially thrilled to present on this topic of new innovations in oculoplastic surgery because while I've only been in practice for about 11 years, I think by far for me this is the most exciting time in oculoplastics for two main reasons. Two treatment options that are relatively new that I have surfaced in the last few years that have gone mainstream. So in the medical arena, I believe Teproteumab is one of the most exciting drugs that I've seen for our thyroid eye disease patients. And the surgical arena, corneal neurotization for our neurotrophic keratitis patients. And I'll discuss both today. So Teproteumab, the most successful drug launch ophthalmic drug launch in history. And for a good reason, it is a revolutionary treatment option for thyroid eye disease. It has transformed practice patterns for thyroid eye disease. And not only that, it has really restructured our understanding of thyroid eye disease and forced us to question kind of our traditional beliefs and allowed us to gain a deeper understanding of disease process. That does not work. Shift things just a little bit. So just some background information. Thyroid eye disease is a progressive autoimmune eye disease. Incidence is about 19 per 100,000 per year. Most patients with thyroid eye disease have hyperthyroidism, remainder are either you thyroid or hypo. And to look at it from a different perspective, about 20 to 50% of patients with hyperthyroidism develop eye disease. And clinical findings stem from oral inflammation and subsequent tissue swelling. As far as risk factors, we know it is much more common in women, but much more severe in men. And smoking worsens it in every regard, increases the risk of developing the disease, increases the severity, as well as prolonging the duration of it. With each decade, the severity increases as well. And radioactive iodine can increase the risk of developing or worsening the existing disease. As far as soft risk factors, selenium and vitamin D deficiency can contribute as well as stress. And you're all familiar with the clinical findings of the eyelid retraction, certainly one of the most characteristic findings in our thyroid eye disease patients that affects about 90% of them. And in the acute phase, they can also have eyelid edema and erythema. Ocular surface changes include conjunctival injection, chemosis, caruncular edema, as well as exposure to keratopathy that can stem from about 60% of patients that end up with proptosis and lack of thalamus. And lastly, about half the patients are affected by diplopia from restrictives to business. And about 5% of patients end up with compressive oponeuropathy that can impact their vision. And the pathogenesis of thyroid eye disease is complex. We don't fully understand it, but we know there is an overexpression and activation of insulin-like growth factor one receptors in orbital fibroblasts and B cells and T cells. And with this activation and interaction with thyroid tropon receptors, we see an increase in cytokine production and Halyrona accumulation that increases edema and inflammation in the orbital adipose tissue as well as muscles. And so with all of this, the way I've always traditionally thought about thyroid eye disease and how I teach thyroid eye disease to my residents is to think of thyroid eye disease in terms of disease activity and disease severity. Just because they look severe doesn't necessarily mean that they're acutely active and vice versa. So in order to determine the disease activity, there's lots of versions of the clinical activity score. This is kind of fading out as well, but this is the simplest one that I like to teach my residents because it really focuses on just the basic signs of inflammation that we see in pretty much all inflammatory conditions, which is pain, redness and swelling. And on the initial visit, we concentrate on the external findings, on subsequent visits, more of the orbital findings that can impact vision, proptosis and motility. And four or greater positive components indicate active phase of the disease. And of course neuroimaging will show oftentimes hypertrophy of the muscles and I'm sure the residents are all familiar with the mnemonic for I am slow, I think is the common one that indicates that infurrectus is most commonly involved and lateral rectus is the least commonly involved muscle for thyroid eye disease. You can also see fat hypertrophy, lacrimal gland enlargement. And of course anytime we're obtaining neuroimaging, we're especially interested in seeing whether there's apical crowding or optic nerve compression. And based on this information, we can determine disease activity, the acute phase or active phase lasts about one to three years where the orbital signs are progressively worsening or the chronic phase where the inflammation has pretty much subsided or applied it down, but you see kind of resulting permanent damage from it. And the disease severity, it just basically stratifies the findings that I've pointed out to mild, moderate, severe and a small subset of patients that have site threatening disease as well. And once we have both of that information, then we determine kind of the treatment algorithm. What do we do if they're in the acute phase? Well, the first goal is to kind of put out the fire because they are inflamed. And then the goal is to reduce the damage by controlling the inflammation. We know it's relatively self-limiting disease. So sometimes if it's mild, we wait it out. And if needed preserve vision and really the traditionally the only recommended surgery in the active phase used to be orbital decompression. And if you deem that they're in the chronic phase, then you assume, well, the fire has been put out, now it's time to restore. It's more performing the elective surgeries, such as your business surgery and eyelid surgery. And the traditional belief was that we had, you know, not great options for controlling inflammation. And certainly we didn't think that we could alter the course of the disease. And a lot of medications have been tried that targeted different aspects of the inflammatory cascade. And really, I didn't really see them work that well for our thyroid patients, which is why I think we are still hugely dependent on prednisone with all of its side effects. Until temperature map surface, this is a fully human monoclonal antibody inhibitor of IGF-1R, which then turns off downstream signaling, thereby reducing inflammation. It is an infusion though, it is an infusion every three weeks for a total of eight infusions. So it's about a six month commitment for the patients. And at the height of the pandemic in 2020, this original article came out that looked at temperature map in patients with active thyroid eye disease. And we were seeing results that we had never seen before with any medical management for thyroid eye disease. We were seeing about close to 80% overall response to the therapy, as well as about 60% of patients that achieved a clinical activity score of zero to one from four or greater. And as you can see in the photo, it certainly looked as though we were able to possibly alter the course of the disease because again, we were not, we had never seen results like this before with any other medical management. And so the modified belief came that maybe we do now have an effective option for controlling inflammation. And maybe we can in some patients, alter the disease course. Another belief originally was that surgery really is the best option for improving proptosis, made preserving vision for patients with a compressed optoneuropathy and for minimizing severe diplopia as well as eliminating eyelid retraction. And so for whether it's for proptosis, compressive optoneuropathy, stretch optoneuropathy, orbital decompression was the answer. But again, going back to the study results showing that 80% of over 80% of patients responded to tumenbab in terms of proptosis. And we were seeing greater than three millimeters of improvement from tumenbab as seen in the photo. Again, numbers that we only saw previously with surgical intervention. And as far as diplopia, if it's mild, we were able to maybe treat them with prisms. It's still controversial. I think it's very institutional dependent whether we liked radiotherapy for this or not, but certainly severe, a lot of them requires your business surgery. But study showed with tumenbab, about 70% of patients saw improvement in diplopia and neuroimaging that confirmed actually reduction in size of the muscles that were involved. And lastly, eyelid retraction. Certainly surgical correction of these patients. Once again, when the fire was put out, they're quiet, they're stable. We perform surgery to achieve results like this. This is a patient of mine that before treatment looked like this. After treatment, suppressing didn't have that great a response to proptosis, but as you can see, retraction greatly improved and she was happy. She did not want anything else after this. So now potentially a medical management that can achieve all of these findings that traditionally only surgery could achieve. But this is not a perfect drug. This is not what I'm saying. I always approach everything with a healthy dose of skepticism. And nor is it a permanent fix either. The original study showed about 30% flare within two years of cessation of medication. And so there's a follow-up study that was published in 2020, the called the optic X study. And with this study, they looked at three groups. One was a longer duration of active disease group. The original study, the patients only had thyroid eye disease for about six months. This study looked at those with 12 months. And those patients that didn't respond to the first round of treatment and then patients that had a flare up. As far as the longer duration group, pretty much the same outcome as the shorter duration group, excellent results in every regard. Those that didn't respond to the first round of medication, as expectedly they didn't respond to another round either. And those with flare, actually they responded very well to another round of temperatumab. But again, this is not a cheap drug. And it's certainly not an easy one to get insurance approval from. It has added a lot of administrative burden on our staff and myself. It's $400,000 per infusion. So you can see why there's a lot of resistance to approving this drug. So we have to, correct, for the entire treatment course. Yeah, so we have to also take that into account as well. And last traditional belief that I think this medication is now starting to more and more debunk is that inflammation only exists in the active phase. That was kind of our traditional thinking and medical management certainly was ineffective in the chronic phase. We didn't really even try it. That was time to do surgery. Two months ago, Horizon, the company that produced a temperatumab came out with a phase four clinical trial in patients with chronic thyroid eye disease, two to 10 years with very low or zero clinical activity score. So basically people that we would never really treat with medical treatment in the past. And this study showed greater than 60% improvement in proptosis and greater than two millimeters of improvement in proptosis, which was a very big surprise. So maybe we can treat these patients in the chronic phase as well and still anticipate improvement. But another thing to consider, of course, like any other medication, it has side effects. And so you have to take that into account for somebody with very mild disease, do you wanna potentially risk hearing loss, which is the biggest side effect that patients always worry about, but common ones like muscle cramps, alopecia, they do get better after cessation of the drug, but something to also consider when considering maybe even the repeat treatments. And so this is certainly a drug that physicians are excited about, but not only that, it's also a drug that patients are incredibly excited about. And it's the first I've seen that actually. And I think it's because it's spoken to their quality of life. And I'm sure you guys have seen this commercial, this is Genie, most of my patients know Genie, refer to her by name as if it's her friend. And it's because I think this company did a wonderful job of marketing this drug of really kind of honing it down to what really bothers patients about this condition, which is the terrible proptosis that they see as a deformity. And so Genie has kind of gained a reputation that's close to flow for progressive. Everybody kind of knows her in the thyroid community. And as you can see, quality of life, huge difference between the placebo group and those treated with Tepertumabab. And especially the orange line indicates change in appearance that has led to increased quality of life. As you can see a big difference for this group that's received Tepertumab. And we forget how this impacts them on a day-to-day basis. As you can see studies have shown that patients with thyroid eye disease, they have worse quality of life than those with heart failure, pulmonary emphysema, diabetes. And that's really hard to believe but you could understand why because it's such a visible condition. So I'll tell you, this is one of my patients. This is a patient that came right before Tepertumab came out. I've been seeing her for a while. She had seen two to three other surgeons beforehand. She also has a clotting disease that prevented her from getting any surgery because she couldn't come off her anticoagulants and she cried at every visit. And clinically, she's not that bad. She has some attraction, some proptosis but she was miserable and so unhappy with how her appearance has changed. She brought me a stack of her photos from how she used to look and she was reasonable. It's not like she wanted to look like how she did 21 years ago but she just wanted me to know the changes that she had undergone. She was on the brink of divorce so literally cried at every visit and March of that year that I was seeing her this is when Tepertumab was FDA approved. She completed it and this is how she looked afterwards without any surgery. Still to this day, she is my happiest patient because it has improved her quality of life so much. So how has Tepertumab impacted my practice? It's kind of transforming how I think of the disease. It's certainly shifted my management from surgical to medical about 30 to 40% reduction in surgery actually. And for the first time, I can offer a non-surgical option for improving their appearance. So just like that previous patient who thought, you know, I can't have surgery, I'm never gonna be normal again. This drug has finally actually given them that potential which is why I think it's one of the most amazing drug launches in history. And now shifting gears is something that's just been as impactful in the surgical renaissance, corneal neurotization. You don't need to hear about the cornea from inoculoplastics first, since I'll keep it brief. This is a degenerative condition, neurotrophic heritopathy, characterized by decrease or loss of corneal sensation where the trigeminal nerve is involved. Incidence is about 50 to 100,000. And pathophysiology of neurotrophic herititis is that the corneal surface is prone to injury, decrease, there's decreased reflex hearing, decreased epithelial healing that results in persistent epithelial defects, corneal ulcers and possibly perforations. Three stages of treatment. Stage one, oculoplastics usually is not involved because they're mainly lubricating. Stage two is when you usually get our calls from our corneal colleagues asking for usually a temporary tarsorophy, maybe a gold weight or an eyelid spacer graft if there's facial nerve paralysis, especially associated with it. Stage three is when they're now asking for that permanent tarsorophy because nothing is working and they're worried about continuous perforation. And there is a medical option that also recently surfaced, but I don't know about your experience here, but it just has not worked well for us. It's an incredibly expensive drug. Again, it's I think about $10,000. And we're not seeing the 65% resolution that the studies have shown. Now, studies have shown that maybe decreasing the frequency to four times a day, they've seen better improvement with that. So maybe it's a compliance issue, I'm not sure. But we just weren't impressed with the with observate. So then came corneal neurotization. And there's a lot being published right now in the literature about corneal neurotization, surgical technique, the graph materials, duration to sense a cornea and the success rate. So I'll go over a little bit of it. So the direct method for corneal neurotization actually surfaced in 2009. And I'll tell you, I was not aware of this. Bob, were you aware of this in 2009? Yeah. The direct method is basically dissecting out the super orbital super trochlear nerve that's intact and directly laying that around the anesthetic cornea on the limbus. I think 2015 is when the indirect method came out. And this is when I think more and more people became aware of the surgical technique. And the indirect method is just placing a nerve graph at the time it was a serial nerve graph from the intact super orbital and or the super trochlear and laying the serial nerve around the limbus of the anesthetic cornea. And now there's just so many different variations of this. There's an endoscopic method, a minimal incision method. So there's a lot of that. And as far as graphs, the initial autograph that was used was a serial nerve graph. Now, some people are using greater auricular nerve, which is just as effective. And now there's a catarveric option as well that has shown great promise. And it gets really nuanced in terms of the technique. How do you attach the serial nerve to the intact super orbital super trochlear? Do you do it end to end into size? So methods of co-aptation are even being discussed and argued. And if you're interested in knowing all about this, this is actually a fantastic review. I'm not gonna go through each one, of course, but it was done by the Mass Eye and Ear group. And so it goes over all the advantages and disadvantages of the different techniques if you're interested in learning more about it. So at Emory, we do a team-based approach. We've pretty much done the indirect method the entire time. And I do adults as well as Pete, so I've done both. And the cornea folks do the actual laying down the nerve around the cornea itself. And the plastic surgeons harvest a serial nerve for us. So this is the plastic surgery team harvesting the serial nerve posted to the lateral malleolus is where the incision is made. And they obtain about a 15 centimeter length of the graft. And then I'm doing this portion where I either make a sub-brow incision bilaterally or a lit crease incision and then isolate either super orbital or super trochlear. I traditionally like super orbital because the caliber of the nerve is a better match for the large serial nerve. And the serial nerve is tunneled across the nasal bridge with a hemostat. And then, I apologize, this is not the best photo, but that's an end-to-sci co-optation of the serial nerve to the super orbital. On the anesthetic side, I use a right needle to pass the serial nerve to the superior fornex and then incisions are closed. And this is when the cornea specialist takes over and I'll speed through some of this. This is probably the most tedious portion of the surgery where we have to open up the perineurium, I mean epineurium, I'm sorry. And then divide out all the fascicles. So I'll fast forward through some of this. So the epineurium is being opened and the individual fascicles are teased out. We can usually get about six fascicles. So I'm trying to fast forward here. And once that's done, then sometimes he uses a gas hook or just forceps and each fascicle is passed around the limbless. Okay. And again, we're seeing results that were completely unexpected. This patient, multiple failed corneal transplants had pretty much a permanent tarsorophy in place, went from light perception. After a few months after a successful corneal neurization and the scar started improving, went to hand motion. Once she achieved a sensei cornea, was able to get a corneal transplant and refracted to 2020. So at this point, it's the cornea service that follows these patients. So I thought my work was done. I'm feeling pretty good and it's an amazing surgery. Thought I was done. But apparently when you do enough of these and patients do really well, they find their way back to you for additional services or other services, actually other specialties. And so I'll go over a few cases where we've done some interesting things for these patients after a successful neurotization. So back to this patient that had 2020 vision after her successful corneal transplant. She still can't see. That was her complaint. Well, obviously because she has terrible ptosis from everything that those eyes have endured. And so I realized, oh, ptosis is already the bane of every oculoplastic surgeon. But it's a love-hate relationship for sure. But having a seronal nerve graft there certainly didn't make things easier. So it's amazing how the seronal nerve, I thought I placed it really high in the superior pharynx, somehow migrated much more inferior than where I thought it was. So I found it much lower than where I expected it. So the location of the nerve graft was a surprise. Dissection is of course a little tougher because there's more scarring. And I've learned that the eyelid contour is a little bit more challenging to achieve the ideal contour because where the graft is there's always a little bit of ptosis. And I've traditionally only done anterior approaches for these patients. I'm curious to see if anyone would be brave enough to try a posterior approach. And if you're not the one doing the surgery you certainly want to warn whoever is going to be doing it that there is a graft there. I received a phone call from a colleague that practices kind of out in the middle of nowhere, Georgia. So if you're familiar with Georgia, there's Atlanta and then there's the rest of Georgia. And he was unaware of this procedure, did not know the patient underwent this procedure, patient failed to mention it to him. I got a call saying this patient needs a biopsy. I found this lesion I've never seen before during my ptosis repair. I'm sending her to you right away. And I said, thank you so much for not cutting it. We know exactly what that is. But yes, please send the patient back to me. So warn the surgeon that this graft is there. So this is her one month post-op. As you can see right side still has a little bit more swelling than the left. And immediately I couldn't raise it as high as I wanted just as I just matched the other side to that contour. So second case, this is a 41 year old female. She has phenoid wing meningioma resection involving the right cavernous sinus that resulted in cranial nerve three, five and six palsy. Ended up with count finger vision in that eye with kind of the similar story as the previous patient of recurrent epithelial defects from stromal scarring. Ended up with a permanent tarsorophy. She underwent a successful corneal neuratization and her vision improved to 2050. Then what happened? She ended up with debilitating diplopia. And she was sent to our pediatric colleagues and it turns out the strabizma surgery is a little bit more challenging as well due to where you have to make the incisions. And so this was a publication by our pediatric group. Natalie Wild is no longer with us. She joined Louisiana. So we're very sad about that. But before she left, she was part of this group. And basically their pearls for the pediatric specialist was try to make a paralimbol incision as small as possible with relaxing incisions to avoid tearing of the congenitiva because the congenitiva is very fragile and friable. Avoid, if you can, the supranasal quadrant and supererectus muscle altogether because of the placement of the nerve graft and be prepared with an amniotic membrane graft in case you can't primarily close the congenitiva. So last case, 31 year old female underwent a craniotomy for assist. We had no records, but she resulted in a craniotomy in her five and seven palsy. Vision was 2150. She also had a gold weight placed by an outside surgeon due to the facial nerve palsy. And this is what bothered her the most. And this was her motivation for getting the neurotization surgery in hopes that maybe she could have the gold weight removed. Underwent a successful neurotization, went from 2150 to 2060, but she still had the exposure issue from her facial nerve palsy. So we actually sent her to our scleral lens specialist who struggled because of this large nerve around the limbus. And we learned now to actually try to leave about a two millimeter margin between the limbus and the nerve graft in the event that patients need something like a scleral lens. And this patient did get a successful scleral lens fitting, corrects to 2020, now planning on the gold weight removal, which has made her so happy because she never thought that was actually possible beforehand. And so again, another patient that thought that thought she wouldn't ever be normal again, we're able to get her close. And hence, I think the two most exciting things in oculoplastic currently. Thank you. Yes. That was an outstanding presentation, June. Thank you. Make a quick comment about Tepituma map. First of all, Ray Douglas is driving a really nice car now. I bet he is. But it's interesting, the history on that, that was initially developed as an anti-cancer drug. Didn't really work for that, but they found a little piece in the literature that said, oh, it also may decrease fibrosis and inflammation and put a lot of money into it, getting a lot of money back out of it. The other side effect, I know you couldn't go over everything, is inflammatory bowel disease. But just to underline how happy these patients are, I had a patient who developed de novo ulcerative colitis while on it and she did not want to stop. She said, I don't care. I want to finish this. So it's really remarkable. The other thing I make a real quick comment on, and I have to always do this when we talk about thyroid eye disease, we all talk about Rundle's curve. And I would say that it's real, but it's a minority of patients. The large majority of patients, in my experience, present without any inflammation at all. We interestingly had a five-year-old non-smoker last week who presented with lid retraction, von Grafis sign, a little bit of proptosis, no inflammation whatsoever. So we don't understand what's going on with this disease. If you look at insulin-like growth factor one titers, they're usually not elevated in these patients as opposed to thyroid immunity, immunoglobulin, which usually is. And in fact, the higher, the ones who do have it, the higher their titer, the less inflammation they have. So we don't know for sure what's going on, but that drug works great. And that was an outstanding presentation. Thank you. Yeah, I see a lot of pediatric thyroid eye disease. And I would say only about maybe 5% of them present with inflammation. And the younger they are, the less inflammation they have. And the only change that I see as I follow them is that their proptosis worsens. And that's it. And it gets better as their thyroid levels improve. And so why children are able to temper the inflammation that adults can't? Yeah, there's so much we still don't know about thyroid eye disease. But I think Teproteumab is forcing us to actually think about it a little bit more, which is also nice. Yes, I think. Mm-hmm. And then publish back. Right. Right. You have two patients. Yeah. You can publish back in a day. Yes. So the initial studies with Teproteumab specifically excluded patients with optic neuropathy. Correct. So have you had any experience with sort of, I guess it would be somewhat off-label use of Teproteumab for the acute phase with optic neuropathy? How quickly it works? Is it fast enough to avoid decompression and steroids? So it's interesting you mentioned that there's actually a study that going on right now looking at that. And it's not so much does the drug work fast enough? It's can we get approval fast enough for the drug to get them started? No, and practically speaking, that's been our barrier to try this more quickly in patients with optic nerve involvement. But yes, I have seen it. I have a handful of patients that I've tried it because I've also learned that you can get two doses right away without approval for urgent use. And so you're able to at least get them two doses. But if it's going to take a while, I still resort to decompression to make sure that their vision is preserved. But we are seeing promising results. And I believe this study will probably presented our fall ACE-oppers meeting and subsequently will be published. But I think we're seeing actually very good results in patients with compression as well. So it's interesting. I think because this is so good in so many ways, financial is going to be the biggest barrier. And sadly, that's a battle for a lot of new things coming down the pipe that the price tags are so high, yet the impact is huge. How do we handle that? So it just seems amazing to me that you can just pull a nerve down out of the leg, you know, and you just kind of hook it to the opposite side. I mean, you know that there's no axonal connection at that point. And you just kind of slap it around the limb of the cornea. I mean, if you ask me, what are the odds of success? If you came to me as a corneal specialist 10 years ago, hey, we're going to do this and this. I'd say, you're out of your mind. That's not going to work. So it shows you how often we've got to think outside of the box and prepare to consider what has always been for corneal specialists, the worst of all diseases, bad neurocopic keratitis, just is horrendous. Yes, yes. You actually don't want any axons in the nerve. And when you get a cataviric transplant, there's no nerve in there. It's just the neural sheaths. Because when you cut a nerve, it undergoes while they're in degeneration. It dies all the way back. So you don't need the axons. You just need the sheath to direct. It's remarkable. Yeah, and there's a lot of focus of the research right now is how does this actually work? Is it direct sprouting from the nerve that's laid around the limbus, which I think is probably less likely, or is it that it is stimulating the native nerves to regenerate? And that seems more likely. But still, it's incredible how it works. Very exciting. Got any other questions? Bob. You know, if herbs have people that treated patients doing muscle surgery on them has changed. Yes. And the experience of the terribly swollen adematous tight orbit, it's different. The muscles look normal. Yes. And so when we still have to do muscle surgery, the other side benefit is that technically the surgery is a lot more straightforward. Yes. I've been impressed with that. It's a big difference. Yes. So this is a game changer. Yeah, thank you for pointing that out because that's also why it's shifting our timeline for performing some of these quote unquote traditionally elective surgery where we waited and waited and waited until they were quiet and stable. But now we're asking, should we just go ahead and do these surgeries while they're on treatment? Mm-hmm. Mm-hmm. Yes. Question back here. Can we see any damage? Oh, thank you. In the leg, like post-operatively, any loss of sensation or function or anything like that? So temporarily, they do have some decreased sensation. But so far, we have not had any issues with the harvest site. And I think one patient developed a little bit of a saroma, and that was it. Yes. Thank you for the talk, Dr. Kim. I had a question along the same lines. Have there been studies harvesting nerves from different locations? Also, you mentioned like six fascicles needed from the, or you get six fascicles or so from the serial nerve. Have you ever tried like less or more? There were studies looking into those differences at all. So in terms of different autographs, a greater auricular nerve graft is also being used. And the fascicles, I leave that up to the cornea specialist. And so six is average. But certainly if you have a huge serial nerve, you're going to get like 9 to 11 sometimes, or less if you have a much smaller serial nerve. And so I think in terms of if I remember correctly, he mentioned he needs at least four. And we have no problems getting that from the serial nerve or the catarveric. Not that we're aware of. As long as you have complete coverage of the limbus, it doesn't seem to impact the overall, because you cut away the rest anyways. Yes. Here. Thank you so much for your presentation, Dr. Kim. I was just wondering, are there certain patients for whom the graft would not be an option just going into it? You know that you wouldn't be able to do it? Yeah, I mean, there's still a lot to consider. A lot of times these patients are really sick. There's a reason why they're neurotrophic to begin with. Maybe they had a huge brain tumor that was resected. And so comorbidities and age. And we know that the older they are, the less successful the surgery is. So I recently had an 85 year old and, you know, the coordinator special and I discussed it for a while. And he's also a very sick patient. So we decided against it. Do you think that's just because the relative regenerative potential of their nerves goes down as an age? Yeah, it just, you know, as we get older, we know. It's not the same. I know, it just, you know, thank you so much, guys.