 Good morning and welcome everyone on behalf of Dr. Simpson, who is out today, welcome to Grand Rounds. It's that time of year when we are wowed by our medical students. Keep in mind the four talks you're about to hear have had more preparation than any four talks anyone else will give the rest of the year. They of course are excited and ready to put their best foot forward and we're all excited as well. One announcement for our faculty, we are doing beta testing of our yellow sheets and these are the virtual yellow sheets. There's an iPad with a yellow cover. We still want you to continue to use the regular yellow sheets if you do have feedback. You can funnel that feedback to me if you just need a quick email to send it to and I can get it to Ann. You can also send that to Ann Brady or Judith Warner as we go through the beta test process. So I'll be turning it time over to Ashley, who will be our resident Ashley Polsky, who will be doing our introductions and moderating our session. Thanks Dr. Petty. Thank you everyone for coming to Grand Rounds today. We have four really awesome medical students who are going to be presenting. First up is Anakit Ramshaykar. Anakit is a fourth year MD PhD student at University of Utah School of Medicine and a fun fact about Anakit is that he loves to garden and if you stick around to the end of his presentation, you may or may not be seeing some photos of some of his favorite plants. So Anakit is going to be presenting some of his PhD research titled the role of erythropoietin receptor signaling in choroidal neobascularization. Thank you Ashley for that wonderful introduction. Can people on Zoom hear okay if they can drop a chat and then can people in the audience hear me okay? Excellent. With further ado, this project was one of the projects I did during my graduate phase of my training and it focused on age related macular degeneration, which is a leading cause of central vision loss worldwide. Project specifically focused on two advanced forms, atrophic and neobascular. Shown here are some color fundus images representing neobascular on the left and atrophic AMD on the right. The question that we asked looking at these fundus images is how do we prevent progression of AMD to these advanced forms? At the time of this project, when it was still in the design phase, erythropoietin was being explored as a potential therapeutic target to slow progression of atrophic AMD. Erythropoietin or EPO is a hematopoietic hormone and it has known neuroprotective ability on retinal neuronal cells and vascular cells in the eye. EPO also has antioxidant and anti-inflammatory effects, which are key signaling cascades implicated in AMD pathology. A retrospective pilot study conducted in 2014 found that off-label use of intravitural EPO slowed progression of geographic atrophy expansion and vision loss in AMD. Taken together, EPO was postulated to be a potential therapeutic target to reduce the progression of atrophic AMD. However, when we reviewed literature, we also found evidence to support the notion that erythropoietin is also implicated in neovascular AMD. One study found an elderly patient with active CNV had increased serum EPO levels compared to age-matched patients with inactive CNV. Studies have also demonstrated erythropoietin signaling primarily through its receptor, erythropoietin receptor or EPO-R is implicated in angiogenesis. Erythropoietin receptor canonically signals through the jack-stat signaling cascade and looking at single cell RNA-seq data from eyes from Rob Mullins' lab, erythropoietin receptor was expressed in coriocapillaris. Taken together, this supported the notion that EPO-EPO-R signaling is involved in the progression of neovascular AMD and raises the concern regarding the use of EPO in atrophic AMD. So this led us to postulate, is erythropoietin receptor signaling increasing the development of coroidal neovascularization by direct effects on coroidal endothelial cells that line the coriocapillaris? To put it in a graphical abstract, we postulated that EPO by binding to erythropoietin receptor on coroidal endothelial cells leads to downstream stat activation to ultimately lead to coroidal neovascularization. The first question we wanted to address was, is EPO-R functional in coroidal endothelial cells? To address this, we isolated coroidal endothelial cells from adult human donor eyes from Utah Lions EyeBank. We ensured that there are endothelial origin by ensuring endothelial marker expressions such as CD31 and Bonn-Villibrand factor. And we repeated experiments using coroidal endothelial cells isolated from three different donors to enhance the rigor of our study. The first experiment we performed using these isolated coroidal endothelial cells was treating controlled coroidal endothelial cells with saline, PBS, vascular endothelial cell growth factor as the positive control and then erythropoietin. In control cells, we, and then we measured phosphorylation of stat 3 as a downstream outcome. What we found was, as we would expect, PBS did not activate relatively as much stat 3 compared to the positive control vascular endothelial cell growth factor, but then erythropoietin did also increase stat 3 activation supporting the notion that Epo, EpoR signaling exists in coroidal endothelial cells. To enhance the rigor of this finding, we knocked down expression of erythropoietin receptor, which reduced Epo induced stat 3 activation. We quantified that across independent experiments using cells from different donors, and we did find a significant reduction in Epo induced stat 3 activation in cells that had EpoR levels reduced. Returning back to the hypothetical framework, our results from cell culture supported that EpoR was expressed and is functional in coroidal endothelial cells. And now what our question was, what is the role of EpoR in coroidal neovascularization? To address this part of the project, we use two models in the mouse model. One was a laser induced coroidal neovascularization, and the other was a transgenic knockout mouse, and I'll walk through both those models coming up here. So the murine laser induced CNV model or coroidal neovascularization model allows us to perform laser induced injury to the back of the eye, specifically at the RPE Brooks membrane, which stresses those surrounding cells to release angiogenic inflammatory and oxidative factors to ultimately lead to pathology similar to what is seen in neovascular AMD patients term coroidal neovascularization. And as mentioned, it recapitulates the inflammatory and oxidative angiogenic factors, and it's a relatively rapid development of CNV, making it an ideal translational model to study coroidal neovascularization. And now the second model we use in the coroidal neovascularization were transgenic mouse models, wherein it was an endothelial specific erythropoietin receptor knockout. So I'll first walk through the bottom row here, which is our experimental animal. And these animals express Cree recombinase, which is an enzyme that specifically deletes genes that are flanked by locksp sequences. And this Cree recombinase was conjugated to estrogen receptor, so that it's inactive until tamoxifen is administered. And it's under the guidance of a CDH5 promoter so that Cree recombinase is only expressed in endothelial cells and no other cells. So when we go ahead and inject tamoxifen to activate Cree recombinase, it deletes essential axons in erythropoietin receptor so that it knocks out erythropoietin receptor in endothelial cells. And then as a positive outcome of Cree recombinase activity, we also had a TD tomato reporter to show the fluorescence in cells that had positive Cree recombinase activity. Our control animals lack Cree recombinase and therefore continue to express erythropoietin in endothelial cells, even after tamoxifen. And shown here are some fluorescent fundus images demonstrating that our experimental animal had the TD tomato fluorescence in endothelial cells lining the retinal vessels here, whereas our control did not. Combining the two models, what we found was that animals that had erythropoietin receptor knocked out in endothelial cells had significantly reduced carotoneavascularization volume compared to littermate control animals that continue to express erythropoietin. Returning back to our central framework, it supported the notion that erythropoietin receptor is necessary for the development of carotoneavascularization. So to summarize, our data suggests that erythropoietin receptor signaling is involved in the development of carotoneavascularization and it raises an important point in that balance of future treatment to prevent not only the progression of atrophic AMD, but also neovascular AMD. Some ways in which this might be possible is perhaps or self specific treatment wherein we only activate signaling cascades and specific cell types. In the case of erythropoietin, perhaps only activating erythropoietin signaling and retinal neuronal cells or even perhaps co-treatment with the gold standard for neovascular AMD anti-vegeth agents in combinations with EPO, for example, for atrophic AMD. With that, I have a lot of people to think, but especially Dr. Hartnett and her lab for providing me the opportunity to perform this project, collaborators who perform essential reagents to make this project possible. My MD, PhD advisors, especially Dr. Bernstein, other academic advisors, Dr. Petty and Dr. Jardine, and of course, the Moran Eye Center and Chandler for allowing me the opportunity to present today at Grand Rounds and organizing our sub-eye. With that, thank you all for listening and I'm happy to take any questions about the project or the pictures of plants that you see here. This question may not make sense, but with the you showed a positive you showed a control where you were with anti-vegeth, that it was also knocked when you did EPO, you knocked that. So what's the crosstalk and what happens if you knock out or what happens to the VEGF pathway? What's the interaction really between VEGF and EPO? That's an excellent question to sort of repeat the question to those who are on Zoom. The question was why does VEGF treatment also not induce death reactivation when EPO-R was knocked down? When looking into literature, there are receptor like beta-common receptor, that link VEGF receptor with EPO-R receptor. And we postulate that might be a connection between two different receptor signaling cascades and why we might be seeing this data. There are ongoing research to knock out or knock down beta-common receptor, for example, and see if that could be a possible link. But those experiments are still ongoing. And if you knock out the VEGF receptor, does EPO work? What happens on that? That's an excellent question. We haven't tested that and I'm not sure of literature that has looked at that quite yet. If I were to postulate based on the data, it might still be a reduction. We do know when we knocked down VEGF receptor 2 or KDR, we do see that VEGF induced death reactivation is reduced. But the EPO part of it I would postulate would also be reduced. Any other questions? Okay. Great job. Anna Kitt. Next up is Michael Jensen. Michael is a fourth year medical student also at the University of Utah School of Medicine. And before Michael was a medical student and aspiring ophthalmologist, he actually danced for ballet West as a kid. So if you stick around to the end of his presentation, he may show you some dance moves. No, just kidding, Michael. Michael is going to be presenting a case titled bilateral giant cell arthritis. Right. Good morning, everybody. As I actually said, I'm Michael Jensen, fourth year student here at the U. Really excited to present this case to you today that came through our console service. So let's go ahead and jump right in. 80 year old white male with history of polymyalgia rheumatica presents to his primary ophthalmologist at an outside hospital with complaint of intermittent dyplopia. He says that it started a few days ago and that it comes and goes. He's not sure if it's horizontal or vertical and it's associated with grain vision, especially when looking up at traffic lights. Our review of systems reports a severe by temporal headache and scalp tenderness for the past month and states that it's partially responsive to opioids. He also has proximal proximal muscle pain and weakness decrease or increased malaise, night sweats, throat and ear pain, though he denies jaw or tongue pain, no fever and no weight loss. As mentioned, he has polymyalgia rheumatica. This was diagnosed in January of 2023 and recently started tapering his steroid dose. His coronary artery disease, heart failure, hypertension and had a stent placed in October of last year and he was in a car accident of April 2023 and head CT was normal. This past medical history plays an important part in. Ultimately deciding to seek care later on that we'll talk about. He's also pseudo fake it and has age related macular degeneration. On exam, he has scalp tenderness and prominent temporal arteries bilaterally. His eye exam is pretty baseline and our remarkable is visual acutes 2040-2050, which is baseline for him. There's no Diplopia, no APD, the visual field are full and extra as well as the extra ocular movements and there's no optic nerve pallor or edema noted on exam. At this point, given the patient's age, history of PMR, temporal headaches, scalp tenderness, prominent temporal arteries and some vision changes, most likely diagnosis was thought to be giant cell arthritis, though other causes in the differential could be like in the Joe cranial lesion, a master hemorrhage or migraine or in AIO and with that most likely diagnosis in mind, ESR, CRP and CBC were ordered. A referral was placed ocular plastics for an emergent temporal artery biopsy and the steroid dose was increased to 80 milligrams. So so far, pretty straightforward routine case of giant cell arthritis, most likely. On day two, the patient goes to get a temporal artery biopsy that morning and reports that he had a sudden decrease in vision last night, the night prior after taking his steroids. On exam, his vision is now counting fingers with both eyes. He has mild optic nerve pallor and edema. His ESR, CRP and playlets are both elevated. It was at this point that the patient was transferred to the University of Utah Hospital for further work up and management. And while being seen by our team here, being admitted, temporal artery biopsy came back positive confirming the diagnosis of giant cell arthritis. Below is a picture of an example, biopsy. On the left is a normal temporal artery. You can see an intact internal elastic lamina, normal thickness of the various layers of the vessel wall and a nice wide lumen. On the right, you can see that the internal elastic lamina is almost completely obliterated. There's pretty impressive hyperplasia of that intima layer and the lumen is much more narrow. In the picture below are some examples of the optic nerve pallor and edema that you might expect to see in giant cell arthritis. In terms of epidemiology and etiology, giant cell arthritis is primarily a disease of aging with 80% of cases occurring in adult 70 years or older. Women are a slightly greater risk than men. And highest incidence in those of Scandinavian descent, though the diagnosis can be made in any racial group. The etiology is not totally understood, but it's a large demeaning vessel vasculitis, thus its association with PMR and saw that some kind of antigen triggers dendritic cells leading to an inflammatory cascade, the release of multiple cytokines, ultimately leading to the intima hyperplasia and narrow lumen causing the symptoms and vision loss. Workup is fairly straightforward. We want to get a CRPSR and platelets, both are very sensitive markers for inflammation and the temporal artery biopsies, the gold standard for diagnosis, the sensitivity 77%, the specificity of 98%. There are several different diagnostic criteria and calculators you can use, both from rheumatologic side and ophthalmologic side. The ethylene GCA prediction model is a pretty good one. It includes a lot of the systemic and ocular clinical presentation findings as well as labs and helps risk stratified patients when the clinical pressure isn't quite as clear and can possibly reduce the need for temple unnecessary temporal artery biopsies. It's one of the few that also includes Diplopia in the workup, which is something that the rheumatologic ones don't do. Standard of care, steroids, IVRPO, there's no strong evidence either way, but common practice is to start IV treatment if there are signs of threat and vision as was done in our patients. Regardless of route, early treatment has the greatest impact on outcomes. And this played a pretty significant role in our patient's ultimate outcome that we'll see. Some other things to keep in mind that are important to think about when considering Giants of Arteritis, the systemic symptoms, headache, that temporal headache, jaw claudication is very common and very specific, though wasn't seen in our patient. The history of PMR, throat, tongue pain, even tongue necrosis can be seen. Constitutional symptoms like malaise and fever our patient had, weight loss and anorexia also can be seen in a temporal artery beating or prominence. On the ocular side, APD is common, the Chalky-White disc edema that we saw, hemorrhages can also be seen, depopia, decreased color vision, transient vision loss, cranial neuropathies and visual field defects can all be seen and should be considered and tested when working up Giants of Arteritis. So back to our patient, he was admitted and started on IV steroids as well as several adjuvant therapies, including IV heparin, which had to be transitioned to lobenox injections due to a supratherapeutic PTT. He's also started on pitoxypilene and brahmannadine drops. Despite three days of this maximal treatment, his visual acuity continued to decrease from counted fingers to NLP, which in both eyes, which as you can imagine is very devastating outcome for the patient and his family and also for the team. In the aftermath of this diagnosis and outcome, and as this patient was kind of grappling with his new reality, both him and his wife use the phrase shoulda coulda woulda multiple times as they thought about the month, leading up to being diagnosed and the multiple times that they thought about seeking care, but ultimately did not. All of their symptoms, all of his symptoms, they kind of excused away due to some other aspect of his medical history. So like the headache and dyplopia they thought might be from the headache or from the car accident, which the head CT was normal, so they thought everything's fine. This is just a temporary thing. The gradient vision they thought might be from his AMD, the systemic symptoms are from his PMR, maybe going to low on the opioid or from the steroid dose. And then the fact that opioids helped relieve his headache a little bit also led to delays in care when they were considering going to the emergency department. All these things highlight the fact that educating patients on some of these red black symptoms is critical importance. I want to take these last couple of minutes to talk about the role of anticoagulation in the treatment of giant cillarderitis. The rationale somewhat straightforward, thrombocytosis is common giant cillarderitis. Elevated anti-cardiolipin antibody is also seen, which can lead to hypercoagulable state. And just the fact that 30% of eyes treated with IV steroids still lose two or more lines of visual acuity, suggesting that perhaps steroids aren't providing adequate coverage. The decision to start heparin in our patient in part was based on a case study from Buono and others in 2004. This is a case where a patient had biopsy proven giant cillarderitis and the right eye was on steroids for three days, was NLP, then started heparin with bridge to warfarin. And then by day 15 his visual acuity was back almost to baseline. His optic nerve pallor and edema also improved and the pulsatility index also improved. Pulsatility index is a measurement of the resistance of flow in a blood vessel. And here they looked at the central retinal artery. So you can see after they started heparin around day five or six and then warfarin on day eight, the pulsatility index decreased dramatically indicating that blood flow was had returned to that central retinal artery. Ultimately, warfarin was not started in our patient due to unfavorable risk benefit ratio. And just the fact that despite three days of anticoagulation, his visual acuity decreased did not improve like the patient in the case study. And finally, he was discharged on an oral steroid, tokylizumab and brumonidine and we'll have follow-up with our normal ophthalmology team as well as rheumatology here at the university. So in summary, this is an extremely potentially devastating diagnosis that we all need to be aware of. Older adults with classic symptoms of temporary headache, claudication, then the just distribution of the carotid arteries and history of PMR are all high suspicion for giant cell arthritis. Simple but powerful begin steroid treatments before the results of the temporary biopsy come back, clinical suspicion is strong enough and you can consider therapy with adjuvants as appropriate and then always, always, always take the time to educate our patients on red flag symptoms that they need to be aware of so there aren't delays in seeking care. Special thanks to Dr. P and the rest of the neural ophthalmology team, Jordan and Dr. Mike Burrow and Dr. Jardine for this really interesting case. I'm happy to take any questions if there are any. Any questions? All right, thank you so much, Michael. OK. Next, we have Andrew DeLaurier. Andrew is a fourth year medical student who's coming here all the way from University of Vermont Larner College of Medicine. And Andrew here used to have, I think, one of the coolest jobs I've ever heard of. He was a member of a hot air balloon chase crew, which involved catching ropes thrown over by the pilot in order to safely bring balloons to the ground. Very cool. Andrew's presentation is titled Eyes in the Crowd, Early Identification of Retinal Disease with Fundus Camera Based Nurse Driven Screening Programs in Kumasi, Ghana. Thanks, Ashley. So my name is Andrew DeLaurier. I'm a fourth year medical student at the University of Vermont, and I just completed a research year working on global health initiatives with the Himalayan Cataract Project under the mentorship of Dr. Jeff Taban. Today I'll be discussing one of the projects that I worked on, which was developing a fundus camera based screening program for diabetic retinopathy and sickle cell retinopathy in Kumasi, Ghana. These are my disclosures. So I spent 10 months living in Kumasi, Ghana over the past year, and most days I would go into the Kampanoche Teaching Hospital Eye Center, which is on the bottom right here. And I'd like to mention that this eye center probably would not exist had it not been for the initial connection formed by Dr. Alan Prandol and all of the incredible work that he did in Ghana. So I feel very fortunate to be rotating at the institution where he practice. On the bottom left is myself and Dr. Akwesi Ahmed. He was my primary in-person mentor over the course of the year, and I worked very closely with him. He is a vitro retinal surgeon in Kumasi and the only vitro retinal surgeon north of the capital city of Accra. At the top is some of our team. Dr. Jeff Taban is right of center in the green scrubs. He was my mentor for the year and then Arthur Brandt is next to him. He's a resident at Stanford with whom I worked very closely over the course of the year. So this is a patient who I met early on during my time in Ghana. He's a 31-year-old male who is a single father and he came in about a month after a complete loss of vision in one eye. He actually presented to his local eye care provider and optometrist just a few days after losing vision. However, it took him a month before he reached Konfinate Teaching Hospital where there are retina specialists who could evaluate his pathology. He was diagnosed with proliferative sickle cell retinopathy in both eyes and a combined tractional and regentagenous retinal attachment in the eye in which he had lost vision. He came in thinking he would receive some sort of treatment that would restore his vision, but he was told not only was it unlikely he would regain vision in the eye that he had lost vision in, but his only remaining eye was now at risk of vision loss from proliferative disease. He was devastated by this news. He is the sole caregiver for his daughter, who is under the age of 10. And he said if he lost vision in what is now his only eye, there's no way in which he could support himself and his daughter. They really had no safety net. So how could this have been prevented? Unfortunately, I met many patients like this man during my time in Ghana. Patients with diabetic retinopathy, sickle cell retinopathy and a host of other conditions who would really only present once they had developed a decreased vision to a point that it severely interfered with their daily activities. And in many cases, this was after they had developed irreversible vision loss. I discussed this with Dr. Kwesi Ahmed, Arthur Brant, the resident from Stanford and Dr. Tabin. And Arthur Brant and Dr. Kwesi Ahmed had already sort of discussed the idea of fundus camera based screening for diabetic retinopathy in Kumasi. And we felt that while I was in Ghana for a year and had time to work on this project, this would be a good opportunity to implement a screening program for diabetic retinopathy and to see if we could do so for sickle cell retinopathy. So diabetes and sickle cell disease probably represent the two leading causes of retinal blindness in Ghana for which there are prophylactic treatments. Diabetes affects 6.5% of the population and sickle cell disease affects 2% of the population. And there are no screening programs for retinal screening programs for retinal complications of either disorder. About 50% of patients with sickle cell disease developed some form of retinopathy. And we conducted a retrospective chart review in Dr. Kwesi Ahmed's retina clinic looking at 100 consecutive patients coming into the clinic. About 75% were returned, 25% were new patients. And for each patient, we looked at best corrected visual acuity over the course of an entire year from presentation. And in that sample of 100 patients, sickle cell retinopathy was actually the leading cause of both bilateral and unilateral blindness. Now, we are currently expanding on that to a larger sample size and focusing just on new patients to get a little bit of a cleaner picture. But it certainly is evident right now that sickle cell retinopathy is a major cause of blindness and Ghana and is worth screening for. So how to screen? Focusing on diabetes, the catchment area for Konfo Noche Teaching Hospital is 10 million patients. That's over a half a million patients with diabetes, which is far too many for the two retinot tendings in Kumasi to screen. There are about 20 trainees at Konfo Noche Teaching Hospital, residents and intern level trainees who could potentially help with screening, but that's still far too many patients. Deep learning and AI models have gained a lot of traction and we are excited to work with something like this in the future at some point, hopefully, however, at present we felt that human grading is at least on par with these models and it was really too expensive for us to implement in a screening program of our scale. So is there anybody else? The one group that there are a lot of in Ghana actually are nurses due to the economic situation in the country right now. Many nurses are either working part time and looking for more work or currently looking for work and there have been a number of studies in Canada, the UK and elsewhere looking at training nurses to essentially run every component of a screening program for diabetic retinopathy. So we felt we could develop a screening model where nurses who are trained to image and grade would form really the backbone of the program. So there are a lot of steps that went into developing this model. I've sort of summarized them into six steps here. And the first of those was to develop the model, get by in and find personnel. So we met with administration at Kofanoche Teaching Hospital and we were given permission to use a space actually in the diabetes clinic to set up a camera and image patients, which is very convenient. We're focusing a lot on diabetic retinopathy initially and this allows us to screen patients at their normal diabetes center visits. We're even able to charge patients a small amount about what they'd pay for diabetic foot care. And the hospital will take a portion of that, but we'll actually get some of that back as well to continue funding this screening site, which is excellent because it should help with long term, long sustainability and longevity. We then had to acquire the cameras. So the cameras we're using are three Nethra Classic HD cameras, which we felt represented the most affordable and reliable option for us to use. And then we had to train our photographers and imagery. So we trained two nurses from the diabetes center. They both had additional time in their schedule and we're very excited about this program. We imaged with them for a while and then and now they've been imaging on their own and we review the quality of the images and they're both very good. And then we also had them take a grading course offered through the NHS. And this course provided them with a certificate after completing an exam at the end of the course. And it just allowed us to make sure that there was a certain standard of grading before we started having them grade images. Currently, all the images are still being overgraded by the retina specialists in Kumasi. The nurses and the retina specialists are using the form on the right. But right now, what we're doing is comparing nurse grading to the retina attendings grading with a study in including 500 patients. We've already imaged these patients and at present the nurses are grading the images. We'll compare them with the retina attendings grading and hopefully if we're able to show that the nurses are proficient in grading, they'll be able to take over first pass grading in the future. Sickle cell retinopathy is a little bit less straightforward than diabetic retinopathy. There currently are no screening protocols available or fundus camera based screening protocols. Many authors in the literature suggest using wide field cameras. The initial lesions in sickle cell retinopathy occur in the periphery. So a wide field camera is optimal to pick up those lesions. However, many places with a high burden of sickle cell disease may not have funds available to purchase a wide field camera, especially not just for screening purposes. In Kumasi, there is no wide field camera available for imaging for academic purposes or anything else. So we thought we could develop a protocol by which a standard field camera could be used to screen for sickle cell retinopathy. And we based this protocol off of a paper describing imaging peripheral lesions with a standard field camera for fluorescein angiography in sickle cell patients and felt that based on that evidence that it can essentially can get far enough out into the periphery, we decided to try this for ourselves. We developed a gaze target for patients to look at that attaches to the camera can be easily recreated. And in a small sort of case series of patients, we found that we were indeed able to pick up early lesions of sickle cell retinopathy using a protocol involving two shots of the posterior pole and then images in all eight directions of gaze. The sensitivity and specificity were quite good for this small sample and we were even able to retain most of the sensitivity and specificity when focusing just on the temporal periphery which speeds up the imaging process quite a bit and maybe what we moved towards in the future. So we felt like that was good enough evidence to run a larger study. So far we've enrolled 70 and image 79 out of 200 patients and we will be comparing grading from our 10 field protocol to the gold standard which is a dilated fund this exam and indirect exam by a retina specialist in Kumasi. So I wanted to mention briefly that we've also done a lot of work with increasing awareness and developing referral network. This is really what we're focusing right now and have plans for the future and our next steps are to monitor make sure the quality is good enough and hopefully to scale and expand. We've actually opened a second imaging site which allows us to refer patients from the community. They don't it's a little hard to get patients into Konpo-Noche Teaching Hospital Diabetes Center unless they're already patients there and this is actually our imager at the first independent site and then we formed a Ghanaian NGO called Africa Eye Imaging Center which is run by Dr. Akwesi Ahmed and this will oversee the creation of further sites and hopefully at some point a treatment center. These are my acknowledgements. Dr. Jeff Tabin was my mentor for the year. Dr. Akwesi Ahmed also mentor for the year. Arthur Brandt at Stanford who I worked very closely with and then many others in the U.S. and then many in our on our growing Ghanaian team. Take any questions? Thank you to talks have all been exceptional. So yeah, I have a few questions. Do they have any sense right now of how many patients that go through the diabetic clinic are getting eye exams? So we don't know what percentage are getting eye exams with to a varying degree they're being referred for eye exams. However, at least in we ran one small study looking at high risk diabetics was about 100 patients and we asked the endocrinologist to refer to us. Their high risk patients and we found eight with proliferative diabetic retinopathy within that group and none had received PRP treatment or prophylactic laser treatment which they would have received have they been referred either to the Kompanoche Teaching Hospital Eye Center or somewhere else? You know, and then another question there's you know, I'm really interested in the implementation of this. We see a lot in global eye health a lot of screening programs there's still a lot of talking buzz around AI and it's potential for scalability. And, you know, you're working in one site with one single, you know, incredible and capable retina specialist. But as you now look at the funneling of patients and the potential volumes that would be coming in, what do you see as the challenges to implementing this program in the next one to two years? And do you feel that AI will ultimately have to be implemented to be able to scale the screening? Or do you feel like in this model you've gotten a human resources of nurses where you can do the screening without that? So in this model assuming that the nurses are able to grade proficiently and continue imaging proficiently and that future nurses that we train will be able to do the same. We feel that for the foreseeable future, paying the nurses competitively in Ghana is actually probably less expensive than the cost of AI implementation. We weren't able to find any models where it would be less than a dollar per patient and without paying the nurses a lot more than they would make otherwise, they were able to we should be able to expand the program and pay people fairly but also keep the cost low to patients. The goal is sustainability and so we'd like to have the cost that patients pay for imaging and eventually for treatment if we're able to open a treatment center to continue funding the program. So you talk a lot about aware of lack of awareness of these diseases there. How are you going to try to combine this with screening either a hemoglobin A1C or sickle cell screening? You know, how would that how would that fit together with your with your photographic screening as well? Thanks. So we've considered at least we've focused on screening for sickle cell disease because many patients may not be aware whether or not they actually have sickle cell disease and the cost of mass screening is is likely for sickle cell disease and then also for hemoglobin A1Cs is probably more expensive than it would cost for us to image patients and it's sort of a larger problem that we're hoping to see some progress made towards in the future. We're considering school based screening for sickle cell disease in which we would try to get essentially grant funding to fund a pilot project where we may be doing genotype screening. However, that's all still very preliminary at this point. You may have mentioned this but how does it function once the photos are showing that someone has diabetic retinopathy or sickle cell retinopathy? How is the system working to getting the patient actually to see the high specialists? So right now, what we're doing is we have contact information for all of our patients and cell phone contact does work pretty well in Ghana. And so patients who need treatment or more regular follow up are being referred to the Confono J. Teaching Hospital Eye Center. At present, the volume has not substantially kind of overwhelmed that clinic. However, as soon as possible, we're exploring the idea of creating an independent center that is able to offer treatment that'll be run by Dr. Quacy Ahmed and hopefully other ophthalmologists. And for the time being potentially retina fellows will help there as well and trainees under the guidance of Dr. Quacy Ahmed. Similarly to how the eye center functions. We have a comment on chat. So the question is, does Kath or Confono J. Teaching Hospital have an established protocol for follow up and treatment of identified sickle cell retinopathy? And. I'm not aware of a protocol that's sort of written in the books anywhere. However, Dr. Quacy Ahmed and Dr. Amos Aikens, who's a medical retina specialist at Kath, essentially determine the follow up period based on the pathology that they see. So for patients requiring urgent treatment, they try to deliver that treatment as soon as possible. For patients with currently non-treatable disease, they'll probably they'll scale the follow up to the degree of pathology. Thank you very much. Great job, Andrew. OK. All right. Last but not least, we have Olau Luwa Omatoa. Ola is a fourth year medical student also here at University of Utah School of Medicine. A fun fact about Ola is that he can solve a Rubik's cube and he's working towards a goal of being able to solve it in under a minute. Olau is going to present a case titled bilateral exudative retinal detachment in a pediatric patient. So I did bring my Rubik's cube with me. So if there are any professionals in the audience, I would love to exchange any tips, tricks that you may have to get me to my under a minute goal. Right now I'm at two minutes, so I have a ways to go. So this case came our way back in January. There was a four year old patient who was presented to an outside hospital with progressive ataxia, bilateral facial weakness and ptosis consistent with Bell's Palsy and she was found mostly drinking fluids. Outside hospital CT showed ventricomegaly and a brain stem glioma prompting an urgent referral to primary children's neurosurgery consult service. Lifelike documentation revealed that she was normal intensive with a blood pressure of 9458 and she was noted as having a normal mental status. Upon arrival to primary children's, her gate became progressively ataxic. She developed right ear pain and had occasional episodes of emesis prompting an urgent MRI when she laid flat to prepare for her MRI. Her blood pressure spiked to with systolic in the 180s. Blood pressure was controlled following an 18 milligram dose of IV libata law and a 1.5 microgram per kilogram per hour drip of necarpene which normalized her blood pressure to 138 over 100. She was subsequently intubated and taken for an emergent external ventricular drain placement. Ocular findings of bilateral retinal hemorrhages often findings of bilateral retinal hemorrhages prompted a consult from the ophthalmology service. Upon further questioning, past medical history revealed placental abruption were resulting in an extended stay in the neonatal intensive care unit. While she was in the NICU, she had a seizure. She was a demodus and she was hypertensive requiring anti-hypertensive medications. In addition, she was found to have hypothyroidism, a diagnosis of Bell's Palsy at the age of one and suspected albinism as well. Furthermore, her home blood pressure medications were required in order to maintain her blood pressures between the 130s and the 140s. Pertnit eye exam findings revealed that her visual acuity, she was not blinking to light bilaterally. Additionally, visual fields showed that she had not reacted to visual stimuli in the periphery of either eye. Her dilated fundus exam apologies, her dilated fundus exam showed that she had an irregular contour with peripapillary sub-retinal creamy infiltrates and her maculas were detached bilaterally. Additionally, her vessels were detached bilaterally as well. And the periphery showed that she had bilateral diffuse exudative retinal detachments. An extensive lab workup was conducted to try and get to the bottom of this patient's overall presentation. However, the lab workup was largely unremarkable. Imaging obtained showed from the OCT on the following day of the right eye demonstrated an inferior serious retinal detachment sparing the macula with optic discadema. And in the left eye, we see serious retinal detachment with macular involvement also with optic discadema. Color fundus showed bilateral serious retinal detachments, peripapillary cotton wool spots with full detachment of the macula in the left eye, as well as l-shnick spots in the periphery bilaterally as well. And a B-scam was also obtained. The fluorescence angiograph showed patchy caroidal filling with scattered non-specific hypofluorescent lesions with late hyperfluorescent lesions seen bilaterally as well. Looking at exudative detachment in general, there are three different flavors. You can have a retinogenous retinal detamages. Retin, apologies. You can have a tractional retinal detachment. You can have an exudative retinal detachment. And then you can have a regipamidus retinal detachment as well. Retinal detachments can have, when they are tractional, they occur because of a fibrous vascular scar occurs that pose traction on the retina. When it is exudative in nature, fluid accumulates between the neurosensory layer as well as the retinal pigment epithelial as well. The causes of bilateral exudative detachments in the exudative flavor happens when fluid accumulates between the neurosensory layer for one of three reasons. Either you have too much fluid being produced or not enough fluid being excreted by the retinal pigment epithelium. Or you can have a combination of one of the first two reasons. After difficult follow-up, she was seen once later at a Nevada pediatric office and it was noted that her retinas were reattached. And there was a resolution of her creamy infiltrates. Notably, her right eye had 2,300 vision and her left eye had 2,200 vision with optic nerve pylor bilaterally. In general, what this case demonstrates is the need for eye care providers to consider rare causes of retinal detachments in patients with bilateral exudative retinal detachments. Increase awareness of malignant hypertensive sequela, malignant hypertension sequela amongst healthcare professionals is essential to ensure timely interventions and to prevent irreversible vision loss in children with bilateral exudative attachments. The authors have led to believe that because her retinals were found reattached after the aggressive and prompt control of her blood pressure, her retinal detachments were most likely due to malignant hypertension. These are my overall resources for this presentation. And I would truly like to acknowledge the authors who contributed to this presentation, reviewed this presentation, and were able to help finalize this overall report. And most of all, I want to give a big thank you to all of Moran. Thank you to the faculty who gave me patience as I honed in on my salient exam skills. Thank you to the staff who helped me navigate this building. And thank you to the residents who allowed me to take call, who allowed me to learn from you all in the early morning lectures, and let me use your loops in the operating room. And thank you, everybody, here for the most phenomenal rotation in all of medical school. Thank you. Just more a comment. Often we have a problem in our specialties where we think of the pediatric cases as just little adults. It's just way more complex than that. And a lot of these things that can have very important impact on vision can be relatively subtle and often amiss. And we shouldn't expect the average pediatrician will necessarily see this. So we're really fortunate to not only have great retina but have pediatric retina. And now we have pediatric neuroophthalmology because that's even more difficult often to figure out exactly what's going on. So we do a great service by helping our pediatric colleagues because in my career I've seen some, I mean, severe retinoblastoma that had clearly been missed in well-patient exams for multiple times until it was already a significant problem. So anything we can do to help them, they need it. They're like most ophthalmologists. We used to joke or most general medical care, primary care that in the old days before electronic medical record when they put double E and T down, they put W and L. And we used to joke it really meant we never looked.