 All right, I'm gonna get started today. We have three very amazing presentations by our residents. First up is Dr. Reinhart, who will be presenting an interesting case on Diplopia. And he's one of our excellent pediatric neurology residents. Can everyone hear me? Okay, so I've unimaginatively detailed this the cause of Diplopia. So this case, the patient is 21 years old. He's right-handed and he's presenting for chronic and progressive Diplopia. He first noticed it when he was about 16 years old. He told us that he would turn his head over his shoulder to look at something and he'd see double. And that was the main time that it happened. He also noticed it during latent times of stress. He was relatively stable until around the age of 22. He was on a mission trip in South America, at which point he noticed more consistent Diplopia in multiple directions of gaze. Sometime between the age of 16 and 22, he also started seeing some very slight ptosis. Of note, his dad also has very mild ptosis, but doesn't have the Diplopia symptoms that his son has. He also endorsed the somewhat vague symptoms of fatigue and hip, knee, and ankle pain bilaterally. The onset of this wasn't exactly clear. So I don't have a picture of my patient, but this would be a representative picture, just noticing that there's relatively symmetric ptosis. And it's kind of hard to appreciate in this, like just on a front on view, but there's a chin up posture that this patient is demonstrating. So moving into the exam, the visual acuity was relatively normal. This is uncorrected. His pupils were normal and reactive. And then there was symmetric limitation in right gaze and down gaze. There was more limitation of adduction of the right eye than the left. When you look to the left is apparent that his right eye cannot adduct at all. His right eye is also slightly more limited in superduction than the left. This resulted in a exotropia and a right hypertropia, which I'll show you the, this is the slide for the strabismus exam. And then for the slit lamp exam, just notable for ptosis, it's a little worse on the right than on the left. And then we did take some pictures. And so it's notable for pigmentaries, peripheral pigmentary streaks. And it might be hard to kind of appreciate in the setting, but you can kind of look, it's almost like a little bit of a circular type darkening here. And then in the same approximate region over here, there's some pigmentary streaks that a little bit abnormal as well. Oh yeah, and then on this slide, you might not be able to appreciate it, but there is some temporal paler on the optic disc that was reproduced on the RNFL. More obvious on the right than on the left. This patient came to us having been worked up to some extent for this condition. So we had some coronal MRI in slices, like with an orbital sequence. So this is the patients. And then I kind of have this normal control the left side of the screen. And again, it might be hard to totally appreciate just because it's not exactly the same cut, but I think it's relatively obvious that these are nice and bulky and juicy. These are not. Another thing to appreciate about our patient's presentation is that the muscles are relatively symmetrically atrophied. Again, he came to us with a couple of labs. He had had a mycine agravis workup that had been negative on antibody testing. He hadn't had any EMGs done. He had an AST of 102, but the remainder of the CMP was normal, as was his CBC, CRP, ISR and TSH. So that kind of summarizes most of the information we had going into this case. So just to summarize, this is a 21 year old man with chronic slowly progressive diplopia, ptosis, retinal pigmentary changes and mild optic atrophy. He also has fatigue, joint pain and a family history of progressive ptosis, specifically in his father. So for this presentation, this is like a limited or kind of like a grouped differential. So in this kind of presentation, you can think of a neuromuscular junction disorder. So mycine agravis was obviously on the previous ophthalmologist's mind. You could think of what it might be called neurogenic causes of a phomoplegia if you'll pardon that term. So like multiple sclerosis, Kean-Barre syndrome, Miller-Frisher variant, those types of things, mitochondrial disorders could also cause this type of presentation. And of course, thyroid eye disease would also be a possible cause. So for this patient, we felt that his presentation most closely resembled mitochondrial chronic progressive external ophthalmoplegia. I will be calling this CPEO moving forward. So like I said, there was some testing that had been completed prior to the patient's arrival by his other ophthalmologist. This is a limited gene panel that was negative. It was sent through this Athena diagnostics. This patient came from Texas. I'm not sure this is the one that their ophthalmologist used. Emily Spath is one of our genetic counselors. She works in neurology as well as ophthalmology. Discuss this case with her and I asked her what type of genetic testing would you do? So looking at this panel and then compare it to this panel that Emily thought would be more appropriate. Hopefully you can probably can't see the injo-injo ones but the idea is it's a lot more than what they tested for. This is the site that she tends to refer people to. There is a move is in mitochondrial testing as well as many other genetic testing just to go towards whole genome or a whole mitochondrial genome sequencing. It just is more of a matter of money and technical limitations. So at some point we might just be doing whole genomes on everything. And I'll talk a little bit more about the genetic testing that you can also do at the end of the presentation. But first I wanna kind of talk about this syndrome. So remember a syndrome is a collection of clinical and historical findings that together point to a particular set of diagnoses. So for the syndrome of chronic progressive external ophthalmoplegia, CPEO, you want progressive ptosis. You want impaired ocular motility in both eyes. It should again be bilateral involvement. Defected muscles should be innervated by more than one muscle or by more than one nerve. The people should be spared. There should be gradual progression over years and there typically shouldn't be any remissions or exacerbations. So the differential I gave, you can think of CPEO as the syndrome. You can look back to that differential I gave and kind of work through those things as you're working your patients with this condition. So I wanna talk a little bit about mitochondrial CPEO. So you can think of CPEO as being mitochondrial ophthalmoplegia as being on a spectrum. You have the simplest, most limited form, which is CPEO. You have CPEO plus, and then you have these more classic syndromes. I think many of us are probably aware of Perrin Sayer's syndrome from med school. And again, you go from one end with limited involvement to the other end where everything's involved. There's been a recent reclassification accorded by the mitochondrial North American Consortium that CPEO can include limb myopathy, dysphagia and exercise intolerance. Previously, CPEO plus would have been, would have like subsumed basically anyone who had any other findings other than the eye findings. So you might see some differences in nomenclature in that area. And for time sake, I won't go and get into all the things that CPEO plus can involve, but this is just a picture of representing, obviously anywhere there's a mitochondria, there can be a problem. And there's many, many systems and presentations, including neurologic, psychiatric, endocrine, MSK, joint involvement. It's basically, it's a huge, huge list. So thinking about, so I just wanna keep this on your minds as ophthalmologists. There is, there's always a concern that something beyond the eyes could be involved when you have mitochondrial CPEO as your differential. So this article looked at all the cases of mitochondrial disease in North America. So there's about 666 genetically confirmed cases. I think this is in 2015, 2018. I put arrows next to the ones that have ophthalmologic, primary ophthalmologic manifestations. If you count up this number, it's roughly 100. And then if you look at CPEO, that's like 18. So about 20% of patients that have a mitochondrial ophthalmoplegia will have an isolated mitochondrial ophthalmoplegia. So what I'm just trying to get across is, if you think they have mitochondrial disease, you really have to be thinking beyond the eye in most cases. So if you're thinking beyond the eye, what would you do as part of your workup? So thinking back to that differential diagnosis, obviously if you have this progressive ophthalmoplegia, you don't want to just necessarily jump right to mitochondrial disease. You want to think of other things such as mimics. So you want to get typically an ESR, CRP, TSH, T4, TSH receptor antibody disease. Myosinogravus antibody panel. You want to get MRI brain with orbits. And then we recommend you get an EKG as well. I'm going to turn and say you're syndrome in a number of other of these mitochondrial disease present with cardiac arrhythmias. So that's like a good don't miss thing. Other tests that you could obtain, but probably would, you can just leave it probably to the neurophthalmologist as you can talk about getting lactate, prioryvate, CK, acylcarnitine, urine, organic acids, glucose, echo, EMG, all that type of stuff. Kind of depends on your practice situation. I will say probably of these kind of italicized ones, CK is probably the more accessible one that you could all order. And then if you're a general ophthalmologist, obviously referring to a neurophthalmologist is a good idea. Neuromuscular doctors also handle this type of thing. If you are relatively convinced that this is a mitochondrial disease, you could just jump to making referred to a metabolic clinic that deals with mitochondrial disease. And then if you're happened to be here at the U, as I imagine you are, if you're watching this, you could also email Emily Spath, who is a, like I said, our genetic counselor, and she kinda give you some tips about genetic testing. If you want to place these orders for genetic testing, that's okay, but obviously they're gonna need to be seen by a neurophthalmologist. So you might as well, you could also just wait for them to see the patient. So that is all I have for today. Are there any questions about this topic? Yes, ma'am. So I guess just the term like CPEO, so that's like a clinical syndrome, right? And then you could have like CPO due to curnsayer, which is more like a genetic, that's like a specific genetic cause of CPO plus other stuff. Is that right? Yeah, so the question, I don't know if anyone can hear that. The question is, is CPEO a clinical syndrome or is it a diagnosis? I think it's kind of both. So like you have mitochondrial CPEO and that's like a diagnosis, but this constellation of bilateral findings, multiple renal nerve involvement, progressive ptosis, that would be like a syndrome. You could think of that as a syndrome as well. So like, oh, wow, that's a lot louder. Does CPEO, that's like associate with a specific gene, like isolated CPEO is like a specific genetic syndrome or so mitochondrial CPEO has like multiple genes that could cause it. I didn't look in depth into that answer. One particular paper I read showed that there was poor association with particular mutations and particular phenotypes. That's like the rule in mitochondrial disease. It's so heterogeneous because there's so many things like heteroplasmy in play. Okay, so you could have like the, I guess the gene doesn't necessarily make the diagnosis of like mylas or myrrh or whatever. It's like, you're just looking at like the clinical picture of like what specific manifestations does the person have or? I would say I'm not 100, 100% sure of the answer to that but like there might be one gene that's always associated with this particular syndrome. But from my reading, generally speaking, there's not one gene that causes one syndrome. And there's many different phenotypes that are associated with each syndrome and gene. Okay, thank you. What are you gonna do to get rid of his double vision? Oh, sorry, I was supposed to mention that. So the question, what are we gonna do to get rid of his double vision? So in this patient, we did send, basically repeated some of the workup. We sent him to neuromuscular for a consultation. We also sent him to the pigment retina specialist. We're kind of waiting and then we're gonna repeat genetic testing. We wanted to wait to do any interventions till we had a little more data but the plan is potentially to do surgery to correct his ptosis and to try to fix his ocular misalignment. So it's your business surgery, ptosis. When you're gonna do, have somebody do the surgery, it needs to be focused on what's going on in primary position, not what's going on off to his left having operated on many of these patients. And I agree, the clinical spectrum of this, having done this long before anybody did genetic testing for it and figured out what was going on is very interesting and I've seen this both from the standpoint of showing up with motility issues which is fascinating to me with this patient or the patients who show up with unexplained decreased vision and then it dawned on me that they had optic nerve power and vessel narrowing and pigmentary retinal changes. And then we kind of went down that road and that's what they turned out to do that they had other changes that kind of led us down that path. This is cool, good presentation, thanks, thank you. All right, next up we have Dr. Mohamed who's one of our top four PGY-3s presenting on an excellent case of Ubiadec La Coa. Top four, man, I've been waiting for so long. I finally made it. But yeah, so it's a little bit of an audible on the title that I'm presenting Ubiadec La Coa and I saw an interesting case in the Ubiades Clinic that was interesting in the sense of just kind of this patient's unfortunate force and just wanted to kind of have a discussion about if that was okay with us at the end. I don't have any disclosures, but I was pretty naive when I started residency, all the lunches and dinners that we had from these drug reps, I didn't realize like anytime they made a sign in that we would be in the CMS like open payments database. So I do have to disclose my list of free lunch providers and Johnson and Johnson, Vashalom and Genentech are the top players here. As far as this case presentation, very unfortunate course and I'll probably spend the first half kind of talking about his clinical course, second half talking about Ubiadec La Coa and then if we have time, maybe a quick case discussion in regards to kind of the decision-making. Absolutely, that would be fantastic. So we have a, well that would be great if I can take a look here too. So a 28 year old male, no past medical history is presented to an outside ophthalmologist in Idaho, back around June of 2022, reporting three months of haze and vision and floaters in both eyes. His examination at this time showed normal IOP visual acuity of 2025, normal anterior segment examination. His posterior segment examination was notable for trace cells, vitreous debris in both eyes and snowball is inferior in both eyes. And then Mac OCT showed mild CME. He declined laboratory workup for presumed intermediate Ubiadec and he was diagnosed with idiopathic parisplanitis. This patient was started on Durazol and Catolec BID with planned for follow-up in six months to see how his inflammation was going. He presented one month later here, visual acuity is decreased to 2040. His IOP is 16 and 12. He still has persistent vitreous debris in both eyes. He had worsening CME in the right eye and mild morson CME in the left eye. He was offered increasing Durazol and Catolec versus Ozardx versus Subtenon's Kenilog. He opted to increase topical therapy and he was started on COSOFT because at the last visit, he had mildly elevated IOP after starting topical steroids. Plan was to follow up in two months. Late November of 2022, he reports that his vision is getting blurrier. His visual acuity now is 80 and 2050 in the left eye. IOP is in the high teens. He still has persistent vitreous debris, new and fierce snowballs that were last seen in his last exam and improving CME. He had been having trouble obtaining Durazol, so he had actually been using Predforte as well as Catolec. Given his persistent inflammation as well as the decreased visual acuity, it was offered to either increase his Predforte versus Ozardx versus SDK versus Vtrek to me at this visit and he opted to increase topical therapy. He had continued the IOP lowering medication as well as Catolec. Next month, his visual acuity now is 2400. He's 20 in the right eye, 2100 in the left eye. His IOP is 14 and 16. He now has a little bit of anterior chamber inflammation. He still has persistent vitreous debris, no CME. At this time, he was offered to try obtaining the Durazol prescription that he had done previously versus Ozardx versus SDK. He elected to try seeing if his insurance would pay for Durazol if not pursuing SDK. January of 2023, he was unable to get the Durazol and he underwent a subtenance catalog in the right eye, planned for follow-up in one month. At this visit in February, his visual acuity is 2400 in the right and 2800 in the left. His IOP is elevated. Now, it's 25 and 26. Yes, trace cells and persistent vitreous debris, no CME. He was offered a contralateral subtenance in the left eye. One month later, he's 2800 in the right eye, 2400 in the left. His IOP now is in the mid-30s. Antersegment examination shows trace cells, new microcystic corneal edema and still persistent vitreous debris. MACO CT was unable to be obtained in the right eye due to the poor view. No CME in the left eye. He was started on dimox in the clinic and then BID at home, as well as Latenaprost and then was offered to continue the COSOFT plan was for one week follow-up. March of 2023, his IOP is a little bit better but still high, 28 and 30 in the right and left, respectively, he did not get visual acuity at this visit. Dimox was continued as well as the Latenaprost and COSOFT the plan was to follow up in two weeks. At this visit in April of 2023, his visual acuity now is 2800 and the right eye, 2400 in the left. IOP now is in the 40s. He has microcystic corneal edema. They do a fundus examination with the elevated cup to disc ratio now 0.6 unable to get the MACO CT in the right, no CME in the left. Again, received dimox in the office, was instructed to continue the dimox at home, continued the Latenaprost and COSOFT and then urgent referral to a glaucoma specialist where he underwent sequential perbeculectomy that next month. And then that's when he was referred to the Moran Eye Center in the UVitis Clinic for this bilateral intermediate UVitis. So as far as a case summary, a gentleman who was 29 years old, no prior medical history, inflammation was not controlled in topical steroids underwent sequential bilateral subtenance catalog injections. In January of 2023, his course was subsequently complicated by severe steroid response with IOPs in the 40s, who underwent bilateral perbeculectomy the next month. When the UVitis service saw him, his visual acute was kind of fingers in the right eye pinhole to 2040 in the left. Of note, he had had the perbeculectomy more recently in the right. I believe I think he was like post-op a week too. No evident APD, as far as his anterior segment examination had the superior trap, blebs as well as thin fear catalog, lacy flap, and then his optic nerves were extremely cupped, 0.9. This is his Arnafell, which you can appreciate severe thinning more notable on the right. At this initial visit with the UVitis, he was quiet. He will start on IMT methotrexate, given his history of chronic inflammation and the steroid response as well. He did finally get a laboratory workup as well. And then you had, I did not mention, but in his examination, he had diffused PSC, likely the x-equally of his perbeculectomy as well. And we had recommended deferral of cataract surgery until he was at least quiet for three months. Plano was to fall up in two months with a follow-up with his glaucoma provider. One month later, his infectious inflammatory workup came back normal. He's still quiet, visual acute, he continues to be counting fingers in the right eye, 20, 30 in the left. His IOP now however is low, three and four by aplenation. Mac OCT did not show any signs of hypotenomeculopathy. He's continued on the methotrexate. He had been on low to max as kind of his post-operative medication from the Trab and Plano was to start at forte BID to increase his IOP with follow-up in two to three months in UVitis clinic and then the glaucoma specialist in six weeks. October 2023, he's still quiet, visual acute remains stable, but he still continues to have very low IOP. There is now mild hypotenomeculopathy in the right eye which you can see here. Plano's to continue methotrexate increases spread forte to QID follow-up in two to three months as well as a continued follow-up with his glaucoma provider. And then this was his most recent visit and this when I saw him, he's quiet in both eyes, visual acute, he's counting fingers in the right eye. He's 2,500 in the left eye. IOP remains low, five and three. Mac OCT shows significant hypotenomeculopathy in the left eye. And this is his Mac OCT. He had elected to continue his methotrexate as well. He had been placed on door resolved by the outside provider. We had recommended increase to QID dosing. He had been actually planning to undergo cataract surgery in the left eye in late January of 2024 upcoming. And at this visit, we had recommended closure of his trabeculectomy at the time of cataract surgery as well as preoperative oral steroid taper. Plan is to follow up in six weeks post-surgery. So I don't know how you felt, but I almost had a visceral reaction with kind of that clinical course, particularly a 29 year old male going from 20, 25 visual acuity to kind of fingers in one eye to 2,500 in the left eye. So just wanted to kind of give a quick overview particularly in glaucoma and uveitis. It's certainly a complex intersection between two disease processes, but we're lucky to be in an academic institution. So I'm hopeful to just kind of go over a quick overview and then maybe have a case discussion in regards to both uveitis and glaucoma and maybe some people can find a way in regards to what they would have done differently in this case. But as far as pathophysiology, the mechanism that determine IOP increases in uveated glaucoma and steroid response are pretty diverse and complex. They're often simultaneously present in the same patient up to one third of patients treated with uveitis have elevated IOP. It's sometimes hard to tell if the elevated IOP is secondary to like a steroid response versus the actual inflammation here. We can likely guess it's steroid response given he had inflammation pre and post and when he had received a subtenance kind of like as well as the topicals he had on elevated IOP. Some history of glaucoma, rheumatoid arthritis, diabetes, and younger age are risk factors for a steroid response. As far as the open-angle and closed-angle mechanisms, you can have both in uveitis. Certainly we know about the secondary angle closure that comes off from scenic closure, a new vascularization as well as the seclusion pupillae. And then as far as the open-angle mechanisms, you just kind of get clogged up in the trabecular mesh work. As far as a steroid response, we don't really know the exact mechanism but you do have increased resistance to outflow and how the trabecular mesh work. And then less common of angle closure is when inflammation and endemic causes the ciliary body to kind of rotate forwarding off times you see that in BKH. Glaucoma occurs in about 20% of patients with chronic uveitis and the incidence and clinical appearance is different according to disease ideologies. It's gonna go real quick, kind of six specific ideologies, particularly in uveated glaucoma, fuchsiaederochromic uveitis which we know is a triad of uveitis, fuchsiaederochromic cataract unilateral chronic low grade inflammation. Recent studies have shown that about 40% of eyes are CMV positive. PSS has unilateral recurrent episodes of myocytitis. Myope is usually normal between attacks and there was a seminal paper by I think Dr. Posner that kind of showed or graphed the IOP attacks with a quiescent periods in between. And again, many of these patients are CMV positive as well. Herpetic uveitis, which certainly a lot of the residents have seen on call. Most common complication of patients with herpetic uveitis usually unilateral. You have inflammation of the trabecular mesh work. Oftentimes you can see iris atrophy as a sequelae of this disease process and cervical carotid uveitis is a hallmark of this disease. JIA, associated uveitis as well up to 42% of patients can have elevated IOP and you can have low grade inflammation. Oftentimes patients don't have any symptoms. So hence why screening is important and oftentimes you see a lot of these patients in the pediatric clinics as well. IMPT therapy is necessary to treat this. BKH, which I haven't seen but presents the bilateral pet and uveitis. What's pretty interesting is in this disease process is there's an anterior rotation of the ciliary body here. And then postoperative uvetic glaucoma which I think we've all seen can be secondary to retained nuclear cortical lens fragments. They can have malposition of subluxation of intraocular lenses. Oftentimes presenting as UGG syndromeing. Here you have a scan here looking at an IOL kind of shaping the posterior surface of that iris on the nasal side of this patient. As far as diagnosis, routinely we do get RNVL OCTs. It's important to know that uveitis is a confining factor in assessing RNVL thickness. Substantial thickening can happen in inflammatory eyes. And this is thought to be due to a breakdown of the blood-random area as well as the production of prostaglandin analogs. And then importantly, you should be screening for glaucoma as RNVL changes during quiescent periods in patients that are to have uveitis. And you can have continued thinning of the RNVL despite good IOP control. And you should note that that can be due to resolution of the edema rather than actual progression. UBM and anterior segment are helpful, particularly in cases where you can't have kind of a good view to look in the back and you can see different types of angle closure. UBM is very helpful in cases of chronic octahipotin as well as looking for anterior, anterior rotation of the ciliary body. And then you can use anterior segment OCT to look at two placement in glaucoma drainage devices. As far as the management of uvea glaucoma, obviously it's a very complex disease, requires kind of a multidisciplinary approach. Knowing the etiologic diagnosis is important for treatment. Anti-inflammatory treatments, we know that corticosteroids are first line in many cases. And since I've been shown to be helpful in uvea glaucoma and can actually partially block the hypertensive effects of sub glaucoma medications, which I did not know. And then certainly, immunosuppression can be needed, particularly in cases where you either have a lot of inflammation or non-responsive to corticosteroids or you have corticostero induced elevated IOP, hence coordination with the uvea to specialists or rheumatologists is advisable in these cases where these immunosuppressive drugs could have systemic effects on the body. As far as the anti glaucoma drugs, they can vary in the presence of inflammation as far as efficacy. And less topical medication may be absorbed. Traditionally, topical beta blockers as well as carbonic and hydrous inhibitors can have been considered first line. And then certainly in our case, we know that systemic carbonic and hydrous inhibitors have to be used if the IOP is not controlled. These are just a quick overview. I think we know all of these disease or classes of medications, but obviously caution with prostaglandins and herpetic acrytitis, carbonic and hydrous inhibitors can be helpful in particular cases where CME is coexistent. And then I've seen case reports at least for alpha two adrenergic agonists where you can have this granulomidus anterior uveitis that has been described after use of apoclonidine and brmonidine. And the inflammation typically succeeded in allergic response and faded after stopping the medication. As far as surgical management with the uvea glaucoma, about 30% of eyes with uvea glaucoma may require surgery. So the course of success rate is lower in eyes with uvea glaucoma compared to poag and oftentimes it's because of the inflammatory response. Significant risk factors for surgical failure include male sex, aging within 45, non-granulomidus uveitis as well as a prolonged postoperative inflammatory period. This is gonna go over a quick overview before I've at least seen here in residency that I've been used in management of glaucoma. Drainage devices often considered first line, especially in ideologies with active inflammation. Studies have shown all three common types. The Ahmed, Barbelle, and Multino are effective in lowering intraclopressure. I haven't seen any studies that have compared valve versus non-valved. Drainage devices that are preferable in uvea glaucoma. And oftentimes the Ahmed can be more convenient because of its unidirectional valve mechanism and possibly helping prevent postoperative hypotony, particularly in our case here. These are kind of some of the short-term complications as far as encapsulated blood, transit, hypotony, hyphaema. Barbelle's trabeculectomy historically has been the procedure of choice in treating UG with the exception of aphiagic snubathorization and poor visual function. Current standard of care is to use adjuvant and type proliferatives just because the rates as far as success have been lower without their use. And there is a higher risk of progression of cataracts with trabeculectomy with mitomycin C. In our case, we did see the pretty dense PSCs after his bilateral traps. As far as goniatomy, often offered for refractive glaucoma, particularly chronic childhood uveitis, the largest series I've saw was 54 goniatomies and 40 eyes. Overall success rate was 72%. A recent series by Chen and Al at Coli Institute showed that goniatomy did demonstrate favorable efficacy and safety and steroid induced and uveated glaucoma eyes. And these were 24 eyes and 22 patients that are not goniatomy and they had sustained IOP and glaucoma medication burden at 24 months. And I think success was determined by IOP lowering by 20%. And then as far as cycle ablative procedures, we know that they can exacerbate inflammation, high risk of postoperative hypotomy and thysis, often used in refractive glaucoma, particulate in eyes with poor visual potential and where conventional drainage or surgery has failed. SLT has been suggested by some as an alternative treatment and many of us might kind of have trepidation, particularly due to the risk of IOP increase or intraocular inflammation. There were a couple of case series by these two authors, Searsadique and Zhao that showed efficacy of SLT and steroid induced glaucoma with greater response and lower failure rate than actual POAG and pseudo exfoliation, which I found interesting. Certainly steroid response IOP like rises higher than pseudo exfoliation and glaucoma, that might be one of the confounders of the study but interesting nonetheless and then uveated glaucoma had similar results to pseudo exfoliation as well as POAG. So that's my quick overview. I just wanted to do a quick case summary and timeline. I think the most beneficial, at least for me, would be just to kind of hear what the audience thinks of kind of this course of this patient, particularly if anything that they would have done differently in maybe any pearls in terms of their practice. Well, Mark, thanks for your presentation. Great, great overview. It's these are tough cases. The therapeutic window for uveated glaucoma is very, as Norm likes to say, is a razor's edge. The difference between doing too much or too little. My general presence, it's easy for me to sit back and make comments in hindsight here on this case, but I do think that an earlier involvement in terms of glaucoma control and a mitigation plan would have been better instituted. I think we oftentimes feel that uveitis needs to be under control before you can actually do something surgically, but I would actually argue against that. In this case, I think the patient lost a significant amount of vision and optic nerve tissue because of not being more aggressive with actually intervening sooner on the surgical side. And rather with the delay in managing the IOP, I think this patient suffered a tremendous amount of optic nerve damage that could have been prevented, I think. If the glaucoma specialist had been involved a little bit earlier. In terms of the choice of surgical treatment, Dan Bettis and Grant Moschetti, some of our prior fellows, did a review of our cases here at the Moran in like 2015 and looked at those cases that went under when a Trab versus an Ahmed valve. And both were successful, but the Ahmed valves won out a little bit at about 12 months in terms of success rate. So I would say it's not a party line rule that you put an Ahmed valve for everybody with uveated glaucoma, but I would say that it's a reasonable choice. Number one is that these patients are often gonna be receiving a ton of steroids already. And we know that steroids are not only gonna increase the IOP potentially from the steroid response, but they also can delay encapsulation of the plate. And ultimately that is what serves as the biological valve of the success rate for any valve. Whether you put a non-valve tube in or a valve tube in, it's often the tenons, it's gonna predict how that patient's gonna do with that particular intervention. Something that we're doing now is actually doing a hybrid. We want the safety of an Ahmed valve, just in case the patient does start to become aqueous suppress and not produce enough aqueous. So some of us are now tying off the Ahmed valve. So treating it as if it's a non-valve device and essentially allowing it to open up in stages so that hopefully we can get a better capsular response in a more permeable capsule over the long run. So we don't have any date on that, but it's just something that we're trying to do to mitigate against significant hypotony. And we have had a few cases of hypotony even after an Ahmed valve that technically should protect against that. So there's no absolute guarantees. These are tough cases. And I think you have to be prepared. Cole has a great case. If you guys ever wanna see our Tim, I believe has a really interesting case of how we revised an Ahmed valve three different ways on a patient who had UVA at glaucoma. Initially we put the Ahmed valve in as she became hypotonist. And then we attenuated the tube. And on the table, just simply attenuating the tube, you could still see that she was over filtering. So then we actually ended up putting a stent in, a stent suture where we took, I believe it was 4L Proline and we flanged it like we do a Yamani haptic. And then we stuffed it in the lumen of the tube inter-camerally in order to shut down the tube completely. And then about four to six weeks later when we could see that her aqueous production was starting to pick up, we went back in and then pulled the stent out. So there's no definitive treatment. You have to be prepared to revise these procedures. In this case for this patient, I do think now you have to address this hypotomaculopathy. And that's much more difficult in a trabeculectomy case. So I probably would have leaned towards a tube shot based on the patient's age and the severity of the disease course and being able to go in and actually shut off the tube if you needed to easily. With shutting down a trabeculectomy, it's very difficult to titrate that to know exactly how much fluid to let out. So going in to revise it may completely shut the trap down and now you're gonna have to put a tube in. So I think most of us in our group here would probably lean towards a glaucoma drainage device for this particular patient based on age and the long-time course in complexity. Do you wanna have Tyler's presentation up? So if we're running on time, I think we should because Tyler has a very interesting presentation as well. All right, thanks Dr. Mohamed for that excellent presentation. Next up we have Dr. Ethridge, one of our chief residents, also a top four chief resident. He's gonna be presenting on cognitive enhancing supplements in resident physicians. Mubarak, I'll leave your presentation up just in case there are any questions. All right, thank you for the introduction. I thought that I didn't have any conflicts of interest but apparently I have many. So cognitive enhancement is technically defined as taking supplements or medications to improve memory, boost levels of energy and wakefulness as well as increased mental alertness or concentration. The mechanism of action of these supplements and medications is inconclusive. Some work to increase circulating adrenaline to help with wakefulness while others modulate neurotransmitters such as dopamine. Our initial study conducted here at the University of Utah showed that over 78% of all residents take caffeine, more than 19% take amphetamines and over 11% take medaffinil for cognitive enhancement even though nearly 50% of those users reported experiencing side effects specifically with the medications. This study showed that male residents in surgical subspecialties who were not married and did not have children were more likely to take those medications and supplements. Those who took cognitive enhancers were more likely to feel pressure to perform well, feel like, or I should say feel afraid to be left behind by their peers or think that they could not have reached their current level of training without them. Medications and supplements taken for cognitive enhancement by ophthalmology residents in the United States has never been explored, at least to my knowledge. Ophthalmology residents I think are a pretty unique study population with multiple stressors that influence the likelihood of taking them. Some of these include long work hours and call which contribute to chronic fatigue that personal and debt incurred from medical education costs, decreasing confidence in the job market with optometry scope of practice expansion as well as decreasing reimbursements and an increasing effort to master this rapidly expanding knowledge base in a more litigious medical landscape. Therefore, we sought to evaluate the prevalence, motivations and side effects of cognitive enhancing medications and supplements among United States ophthalmology residents. We distributed an anonymous cross-sectional voluntary survey on cognitive enhancing medications and supplements to all United States ophthalmology residents using the web-based platform Qualtrics between March and June of 2023. Residency program coordinators were asked to distribute the survey to their residents via email on two separate occasions. The first was directly from the researchers themselves and the second was through AUPO sponsored email slash survey. No incentive was provided and respondents were asked to complete the survey only once. Survey sections included demographic information such as related medical diagnoses like ADHD and narcolepsy. We included additional questions such as whether or not the resident matched into their top three residency program. The residency program's geographic region as well as their call structure and the resident's most recent OCAP score and their intended subspecialty. Sections on cognitive enhancing medications and supplements included type, duration, frequency, side effects as well as motivations. We focused particular attention on amphetamines, methylphenidates, medaffinil and the supplements NUEPT and RACITAMS as these are explicitly taken for cognitive enhancement. Here are our results. According to the SF match ophthalmology resident results over the preceding four years, the total number of possible residents surveyed was a 2003 of those 267 or about 13% responded to our survey. This table shows unweighted descriptive statistics summarizing participant demographics. So among respondents, 28% were female, 48% were male, 24% did not specify a gender, 38% were married, 16% had children and 56% matched into one of their top three residency programs. All US geographic regions were represented, 58% of respondents selected home call as their residency program call structure. All OCAP score quartiles were also represented but unfortunately 24% of respondents did not select a geographic region, 24% did not select a residency program call structure and 56% did not specify an OCAP score quartile. Most respondents indicated they intended to pursue comprehensive ophthalmology at 24%. The next most common was unknown at 16% followed by vitro retinal surgery at 13%. 4% of respondents were diagnosed with ADHD and about 2% with shift work sleep disorder. This table shows the weighted prevalence for supplements. We estimate based on our survey results that about 79% of ophthalmology residents use caffeine in some way, shape or form, which is the most common among all the supplements. About 18% do not use cognitive enhancing supplements and about 4% of residents use other supplements, the most common being nicotine, creatine and ratom keratom. It's a really scary one if you ever read about it. This table shows the weighted prevalence for medications. Based on our data, we estimate about 15% of ophthalmology residents take amphetamines, 3% take methylphenidate and 6.5 to 7% take medaffinol. When we asked respondents when they started taking supplements and medications and how often they take them or took them, this table shows the weighted prevalence of amphetamines. So we estimate that about 31% of residents started taking them in college and 55% started in medical school. However, 57% said that they no longer take them. These bar graphs show the reasons for taking supplements on the left and for taking medications on the right. The answer, yes, is represented in teal. The most common reason for taking supplements and medications, not surprisingly, were to improve concentration memory or alertness and to increase studying or working time. Reported side effects for supplements were low, I think only one person reported. This table shows the weighted prevalence of medication side effects with the most common being a change in appetite, sleeplessness and anxiety or paranoia. We asked whether residents who took cognitive enhancing supplements or medications had ever been asked to share or distribute them to their colleagues. We estimate that about 3% of residents have been asked to share their supplements and about 23% have been asked to share their medications. Represented in this figure, is the logistic regression for taking supplements. It seems like having an in-hospital call system or a night float system and being diagnosed with ADHD were associated with a higher likelihood of taking supplements and then being from the Northeast and considering comprehensive ophthalmology or possibly glaucoma as a subspecialty were associated with a lower probability, again for supplements. Represented in this figure is the logistic regression for taking medications. Scoring in the 51st to 75th percentile on the most recent OCAP exam and being diagnosed with ADHD were associated with a higher likelihood of taking medications and then being married was associated with a lower probability. I wouldn't be a millennial if I didn't have a photo of myself but when I reached this point in creating this presentation, I really had to ask myself, why do I care about this project and why did I care about the one that preceded it? And as many of you know in medical school like many of my peers, I felt immense pressure to perform well and I succumbed to that pressure by on one occasion taking Adderall to prepare for a shelf exam which was given to me by a friend. In residency that pressure persisted and through my encouragement I received a diagnosis of shift work sleep disorder and was given a prescription for medaffinil from my physician which I used periodically throughout residency to be at my best when I was sleep deprived mainly after call. Given I'm no longer taking primary call and the side effects that I experienced I no longer take medaffinil but I realized that I started these research projects to see if I was alone in feeling pressure to perform at or above the level of my peers and respond as I did. With that in mind, I wanna focus on a unique group of ophthalmology residents that are highlighted in these data. I wanna focus on residents who self-medicated with cognitive enhancers when they started and why they did it. So considering that 4% of respondents had received a diagnosis of ADHD yet over 17% had taken amphetamines or methylphenidates both of which are prescribed to treat ADHD. We could conclude that about 13% of ophthalmology residents self-medicated with amphetamines or methylphenidates. Similarly, considering 2% of residents had received a shift work sleep disorder diagnosis yet 6.5% take medaffinil which is prescribed to treat that disorder we could conclude that about 5% of ophthalmology residents self-medicate with medaffinil. The majority of these residents started taking these medications in either college or medical school and they did so with the express purpose of improving their memory, alertness or concentration and to increase their studying or working time. In addition, and I think a good thing many no longer take them possibly because of the side effects they experienced as it turns out I'm not alone. Our study had several obvious limitations. Our survey was relatively newly developed and could exhibit measurement errors. There's no validated instrument to capture these data however we did follow best practices in survey development. This was a self-reported survey with the possibility of misreporting. Although we distributed the survey multiple times through various means we had an overall low response rate and poor response to numerous questions. Given that little is known about the survey non-responders we of course cannot rule out the presence of non-response bias. And finally we included limited demographic information to protect the anonymity of respondents. I'll leave today with a quote by the American author Nora Zeal-Hurston. Research is formalized curiosity. It is poking and prying with a purpose. These are my references. There are many people to acknowledge at least of whom are listed here and I will take any questions. Thank you, Tyler. You know, on many fronts you've taught all of us a tremendous amount. It was really shocking early on to see how little was known. I know you think a lot about the root causes that would lead someone to use cognitive enhancers or you know, on another level perhaps have periods of burnout. You know, periods where they're not well in medical training. And now that you've matched you're nearly out the door. Just wonder if you could give us some perspectives on how we train in medicine in general and recommendations you would have at the undergraduate GME level and then our graduate GME level for improving the environment for learners. Yeah, I think that's a great and complex and multifaceted question. And I think it has to go way back like high school, college. I think a lot of the driver that I experienced in my training was the increasing performance or the improved performance. I mean, you know, you think about like USMLE step one scores and 10, 20 years ago like a 230 was a good score and then now we're declining people not now, but previously with 260s, you know, 270 scores that I didn't even know existed. And you see applications now and the first response is, oh my gosh, they're so, they have so many achievements. They have 30 publications and they're only a third year medical student. And we think that in a positive light, but it also has a negative connotation or it came with consequences. And I think some of those consequences are isolation. You know, I always think of medical training as like the perfect learn helpless as model. I mean, you're one of the most stressful periods in an adult's life is changing a job and we're having learners change jobs almost daily, if not every half day with a new boss, new expectations, new location, new staff and personnel. I think that's a big component, but that's largely driven by ACGME having the requirements and we're, you know, trying to fill holes and that means residents have to go all over the place and train all over the place. The match system is in and of itself the basis of learn helplessness, which is I use that term learn helplessness because that's like the framework for how we think about anxiety and depression is like if things are happening to you and you have no control over the response, then that's kind of a recipe, especially if you have a genetic predisposition and then medical training kind of highlights like perfects that. I think the financial aspect is certainly something that you can't bat an eye at. You know, if you're coming out of medical school and you have $300,000 in student loan debt and you're going and you wanna be and all you can get into is a general pediatrician program or pediatric residency where your expected income is 90,000. You know, that can be really anxiety provoking and you know, from a financial perspective it makes no sense, which is not why we did this but I think a lot of us hope that at the end we would be financially stable enough that we could provide for ourselves and our family. I think those are, yeah, it's easy to identify the problems. It's hard to identify the solutions, right? We all like to complain and probably not come up with great solutions. Yeah, to get married and have kids. Children were apparently protective, which is interesting but I know when I had both my kids in residency it's because I gave up. And then I just didn't care anymore about being a great resident and I was just trying to survive. So maybe not the path to go. It's a change in perspective though. I mean, I think that's really what it highlights is like when you're, at least for those of, I mean, we all did medical school but man, it is so selfish. You are just like locked in on yourself and your daily achievements. And I remember coming out of an exam and like going to the mall and just walking around and be like, all of these people have this life that my life is getting up, studying, eating breakfast, studying lunch, study, dinner, study, go to bed, repeat. And it's like, wow, this is like a whole big world. And I was coming away from, living abroad for three years and working for a year. So I can't imagine going straight through like you don't know anything else. So having kids, having a relationship like those, I think it makes sense that they're protective because it changes your perspective. Sorry, I wish I could have just like dropped a big knowledge bomb and blown everybody's mind. So Dr. Nakatsuka asked, why are prospective glaucoma docs? Why do they have a lower likelihood of taking supplements? Maybe it's perspective again. I don't know. Oh, everything's fintile and it's up. It's like you're making it up. I mean, we're all making it up but it's maybe glaucoma providers acknowledge that. And that's probably a good thing. That was the only question. Yeah, thank you everyone. I have one more quick question comment. Great job, Tyler. One thing that I thought about a lot with this study is that how it's higher in surgical subspecialties and the use of like caffeine or other medications or supplements you think would increase tremor. So it makes me wonder like if people are taking uppers or they're also taking downers or taking things to sleep and also just performance in general. So I'm not sure there's any data out there but I think that's just like an interesting thought. Yeah, there's some data in the retina fields measuring tremor and taking beta blockers and caffeine and basically caffeine can lead to a tremor which is measurable but those results are like negligible for attending levels. So it's kind of like the study that there's a recent study in the retina field where and Erica words can talk about this probably better than I can but basically like sleep deprivation affects trainees more than it does people who have been in the field and practicing for a substantial period of time and the results of like beta blockers was similar. It helped trainees with tremor but it didn't have any effect on attendings. Caffeine was more likely to affect trainees as far as tremor than attendings.