 I can have everybody's attention. Got it. So I think everybody here knows me. But if not, I'm Randy Olson. I'm a chair of ophthalmology. And I'm really excited for today. We've got a good showing of people. That's fantastic. We like everybody here because it's so much great work has gone on to the effort of these talks. But in particular, we're honored to have Ike Ahmed here with us. And I think we've probably got a few of the faces here because Ike. So just to give a little idea about Ike, who trained here with Alan and the Glaucoma Fellowship and has gone on to just be a superstar, is that he and I had a chance to be speaking at the ANSI meeting here about 18 months ago. And they have a couple of keynote speakers. And he was a keynote. And I was a keynote. And I saw Ike off over to the side. And there was just this crowd hanging around Ike. And I'm looking at this and I'm saying, holy mackerel, this is like a rock star with his groupies going around there. They were all going on. I'm trying to go over and say hello to Ike. Ike being the warm, humble guys. He finally broke out of this group, came over, gave me a big bear hug and go on. I said, Ike, it's the first time in ophthalmology. I feel like I'm in the presence of a rock star. So Alan knows what I'm talking about. Ike always takes it good naturally. But it is amazing how his career has gone on. He's going to talk about some of the exciting things that represent where he really has been out there on the cutting edge doing some amazing stuff. So we're extremely proud of Ike and I'm very pleased that we can have him here. So we've got an exciting day. We've got some nervous residents that are going to get a chance to give their presentations. And we always appreciate that. And I think with that, Bob, I turn it over to you, don't I? OK, the next two patients are both patients from my practice. And I'll be presenting the first one. And then David Phillips will present the second one. Those of you that have had a chance to, hopefully all of you, had a chance to see the patients upstairs. So I'll go through these quickly so we can save our time for the discussion. An 88-year-old female presented to me for a glaucoma evaluation with the main complaint that she just couldn't tolerate any drops at all. She had had a history of numerous IOP spikes in the past, but really couldn't tolerate anything except for maybe some Brynza. She had a past ocular history of pseudo-exfoliation. She had anatomic narrow angles and received an LPI in both eyes back in 2004. She had FACO in both eyes successfully and again had several episodes of very high IOP spikes. Nothing significant on past medical history other than she's just on Brynza. That's the only drop that she could really tolerate left eye. Nothing remarkable on social history or review of systems. But her left eye was not correctable to 2020 blurry vision. On presentation, 2040 vision in the right, 2200. And particularly of note here is that she had well-controlled IOPs when I first saw her of 14 in both eyes. Normal cornea thick is actually thicker corneas than average. And her gonia was quite narrow, particularly in the right eye. I had a very difficult time seeing any trabecular mesh work although she appeared to be fairly deep centrally. In the left eye with indentation, I could see maybe just a little strip of the TM there with some mild pigmentation. The remainder for exam was notable for patent PIs in both eyes, pseudofakie in both eyes. And she had really minimal cupping. OCT was normal both eyes. Everything was in the normal range. And her visual field showed some very minimal scattered changes in both eyes, but relatively preserved visual field. So this is her clinical course. And just to draw your attention to the IOP, the left eye spiked in April of last year. And then earlier this year in February, the right eye spiked. And we've been unable to control her with anything other than Cymbrensa SLT wasn't an option, nor could she tolerate any other drops that we had available. So this is her clinical course. She had an anterior trectomy, goniosynicalisis, and a gap procedure in the left eye. And what I noted during surgery was by the time I made my first incision with the paracentesis, there was constant posterior pressure. It was very difficult to maintain the chamber. So the anterior trectomy in the left eye was actually unplanned. I went ahead and did an anterior trectomy, I had drive a trectomy through parisplania just to get enough chamber deepening, and then I proceeded with the goniosynicalisis and gap procedure. In March of this year, she underwent the same thing, but because I knew what had happened in the left eye, I went ahead and did a trectomy right from the beginning, and she underwent the same procedure, goniosynicalisis and a gap procedure. Her current pressures are 19 in the right eye and 12 in the left eye, and she's currently on no drops. But what I'm noticing on clinical exam, and those of you that had a chance this year, is that her AC continues to shallow, and the angles are getting more and more narrow, and the dilemma I have is, do I need to do anything preemptively before she completely zips up her angles? So now I'm gonna just show you some PenaCAM photos. I didn't have any other ability to image her angles because I saw her primarily in the community clinics, but this is a PenaCAM from the right eye in February. It looks remarkably shallow, but you'll see in contrast to the most recent PenaCAM photos, how she's much more shallow. This was a left eye in February, quite deeper. This is the eye that had the first gap procedure in goniosynicalisis. And then again, now in May, we're closer to this time, we can see that the right eye is really significantly shallowing, and the left eye as well. And then this is just kind of a montage. The top photos are the earlier PenaCAM photos from February, and now we can see in May on the bottom half are the two PenaCAM photos showing the significantly shallow anterior chambers in both eyes. So for discussion, some of the things that I wanted to bring up today were, why is her AC shallowing? Why does it continue to shallow despite the procedures that she's had? And why is this patient's IOP relatively well controlled despite what appears to be progressively narrowing angles? And is there such a thing as benign malignant glaucoma? This is oxymoron, but something for discussion. So I can bring you up. Well, thanks Craig. This is, I think you summarized it very well. And I think, as I think you've indicated already, I think this is really a picture of malignant glaucoma. She seems to have susceptibility, seems to have a pre-existing history of angle closure and narrow angles. I don't know what her biometry was, or axial length to be. You're trying to look at her. Okay, I'm guessing she's talking to her. When I talked to her, she says she was into bifocals and she was 30. So likely she's a hyper-op short eye. Post-operative at least had been myopic. She's been able to see without glasses. So her eye was likely sitting forward, as you indicated there. I think that right now, as we sit here and examine her here, she is zipped up. She's got PAS pretty well all the way around. She's got a shallowing chamber and this is consistent with malignant glaucoma. The treatment for malignant glaucoma, in our experience and many others, is to create a unicameral eye. It's not to do with dractomy, but it's to create a unicameral eye, which can be done anteriorly, can be done by laser, basically by making a larger dractomy by lasering through the zonules in the capsular bag and then trying to hit the anterior hyaloid and having immediate deepening of the chamber, as well as surgical, which can be done with a cutter anteriorly or through the parcellina. And that will be the definitive treatment that whether this patient needs it or not is another question. If we did do it for this patient, though, that wouldn't be enough because this patient now has, of course, 360 degrees PAS. So at the same time of doing that, irrital zonule hyalodectomy, as one would call it, it would be important to do a gonosynchialisis at the same time. So we're going to do a gonoscopy, releasing the synechia and allowing for free access of aqueous. You know, her pressure, it's quite interesting when I go closer. We see patients who have what appears to be 360 degrees a positional or even a synechial closure, sometimes with normal pressures. And why is that? Well, this patient is 88. This patient is not secreting as a normal patient would, or sorry, I shouldn't say normal, as a younger patient would. There is, of course, the UV start-outflow mechanism pathway that still is still typically intact, even though the story of body space is not visible. And those may be some of the reasons. There's probably some of her angle that's still functional in important areas that may be still accounting for her IOP to be controlled, although she's pretty labialous now, it's like, and that's probably one reason for that as well. I don't think there's anything as benign. I think it's controlled within glaucoma. She has not been on cycloplegics, has she? Okay, so that's one thing that may be considered, I mean, I know she doesn't tolerate aqueous suppression, but that's typically the combination of treatment. One can do that. We find it's very hard to get people off cycloplegics. Although the surgical treatment may appear to be aggressive, I think it's generally well tolerated than in a controlled fashion. The challenge for her, she's 88, her pressures are relatively okay on her current IOP. She says she's seeing okay, although she's depending on her glasses for things that she's used to, and her fields are normal. And that's, I think, probably the conundrum that we find herself in. But invariably, and it's hard to know, life expectancy here, I think she's gonna get continual problems. And eventually her IOP will get further out of control. Her disease will be hard to treat now with her chambers shallowing even further and her nerve is more at risk. She's also potentially at risk for vascular events as well if her IOP shoots up. And so I think I would have a good conversation with her about the next step, which I think would be to do a combined irrital zonule hyalodectomy using a surgical approach and agonicyclicis. And why surgical? Because laser is not gonna resolve the PAS and may infect her over as far as worsening of her problems. That's what I would say in my immediate point would be, we published about three, four years ago a series of about 25 patients after routine fecal, after routine fecal that develop malignant glaucoma. And for the residents in the room, please read the Harry Quigley, Jackson Memorial Lecture, Academy Lecture, but maybe seven, eight years ago. And the reason why we don't call this is it was misdirection, because that's a misnomer, malignant glaucoma is the correct term, which is a constellation of cordial expansion, loss of vitreous conductivity due to compression forces from the coroid. And an eye that's susceptible, meaning a small lens iris channel, because of the small nature of the middle segment in these small eyes. But I think that's I think what would need to be done here. And again, interesting in our case series, every single one of the 25 patients were all female. And there's a lot of discussion about angle closure and gender and coroidal vascular permeability. We're also gonna publish this series of patients that we found as a seasonal variation as well, as far as the presentation of living glaucoma. It's a lot we don't quite understand with this, but certainly in this patient here, I think if this patient was a lot younger, for me it'd be hands down, get in there. At this point I can see the argument to maybe treat a recycled page. I see how she does, maybe watch her IPs for a while, but I think she's gonna run into trouble as we go along here. That'd be my thoughts. I don't know what the rest of the group thinks, but very interesting case. Why do you think there's such a female performance? What's the reason? Well, I mean, historically, of course, there's been obviously discussion about gender and vascular permeability, immunological differences as well between genders as well. I think that those things play a role. It doesn't seem to be a biometric reason between male and female eyes. Some of these patients are younger as well, hormonal differences as well. So another difference that I don't quite fully, I think, appreciate or understand yet. But that's something I know. We know angle closure is more common in females and it seems to carry over with magnetic glaucoma. So post-faco, anybody post-faco, and even an eye that's, a couple of the pearls I will mention, magnetic glaucoma doesn't always present with a pressure of 50 with a flat AC. You can have subtle magnetic glaucoma. The angles can be still relatively open, slightly narrow with a pressure that's slightly elevated or even normal, but a lens-eyes diaphragm that's moved forward. Anybody who ends up being myopic after surgery, especially in a small life, it's gotta be a number one differential. Is there actual displacement of the lens? Ruling a capsule block syndrome and other issues as well. So I think that's an important concept. And a magnetic glaucoma after faco is not necessarily uncommon, especially in susceptible eyes. So I can tell you that a lot of people floating around are like this. I imagine in a case like this, it's about a 60-year-old patient and has been going on for a long time. Very hard to treat now because of the synechia and the elevated pressure. So it's a great case to present. So thanks for sharing that. Hopefully a good discussion. Do you think in your series where there are a lot of patients with Tuorax, I mean, is this, how do you... Yeah, so Suorax is good. When I first heard the story, I thought maybe does she have Luzonules? So that's a good question about differential. Does she have Luzonules? Is the IOL pushed forward actually because of Luzonules? We've seen that, of course, happen. Does patients have a large somerings ring? Rarely that can happen. We can see a big somerings, push everything forward and cause progressive angle closure with somerings proliferation. She has surgery recently though in March, so I think it was recently, right? So, and I saw a bit of somerings through the aridectomy, but doesn't seem to be large. In our series, we didn't have enough to really look at and see whether there was a correlation between that. I think that, I don't know if that's the primary issue with her. Prior to surgery, of course, as we all know, circulation can often convert to angle closure. So, and typically because of, again, the lens shifting forward. So going to ask to be very important, please, please, please do go on your all as much as you can, because I know it's a bit of a lost art and for the residents in the room, you know, carry that go on your lens in your pocket just like you carry a 90 and a 20. So it's a support tool in our inventory. Thank you. Morning, everybody. David Phillips and one of the glaucoma fellows. Got another case here to present. She was here earlier for everybody to kind of get a view of. So initially she was referred for poor vision following YAG, late in 20, 20, 15, was seen by our cornea service with a pressure of 43 in early 2016. She was initially referred for decreased vision in that right eye to the cornea service. And she was promptly referred to Dr. Chai after starting convigana, Latina post. The vision did improve after starting that. So the vision was kind of just a steamy cornea from an elevated pressure. Past ocular history includes a macular hole in the kind of an eye of non-interest today with the track me for that and subsequent cataract surgery OU by an outside provider and then a YAG in both eyes. The right eye having kind of a bout of inflammation treated with Durazol and subsequent kind of pressure issues and non-improved vision. Past medical history, COPD requiring O2, history of GERD, pulmonary nodule in 2013 on CT that resolved by 2014. Social history, kind of an ominous sign when a glaucoma specialist is going through all of this but really nothing of interest except being a former smoker. Positive change kind of, this is kind of retrospectively going back since about 2014, 2015 of eye color change in the right eye, but everything else was kind of non-significant. Initial exam with Dr. Chia demonstrated 2020, a little eccentric in the left, probably from that previous macular hole, pressures were controlled, GONEO was performed a little deeper on the right. No NVA or NVI was noted. Some people irregularity on the right was noted prior to dilation. Talked with Dr. Chia about her, she just had kind of these multiple iris nevi that were fairly insignificant in nature at that time. And this would have been the initial exam in early 2016, PCIOL with an open capsule. So the IOP was doing great. Thought we'd leave her on the Luthana Prost, stop the COM again, and see her back in four weeks and kind of stage her with a field. That was her initial field. So we got that field, and after stopping the COM began, her pressure bumped up. We restarted the COM began, and pressure came down. We wanted to repeat that field since that was her first field she ever taken, just to kind of confirm things. Follow-up visit, the field was confirmed to be that severe, which I'll demonstrate here in just a second. IOP was 17. Closer GONEO now, thought there was a fine vessel superior, some kind of trace fine pigmented cell in that right eye, some lacy iris, NV mild heterochromia with the unaffected blue iris being lighter than the involved right earity. There's that field, which just basically confirmed we've already kind of discussed this, so I'll save discussion for the end. So kind of putting it all together, we thought unilateral advance back home in the setting of heterochromia, lacy, NVI, and mild inflammation. With the retrospective scope, you would, and thus the presumptive diagnosis of Fuchs heterochromic erycyclicitis, looking back there was probably a lack of the typical crippless iris that you normally see with Fuchs, and Fuchs typically presents at a slightly younger age. So hindsight being 2020, that might be a knock against that, but continue the present drop regimen and follow closely at this time, since her pressure was responsive. Vision remained good, pressure remained down at the visit in August, then November, she spiked up to 23, discussed risk benefits of a teraclylectomy with myomycin. Decision was made to proceed, working on the presumptive diagnosis of Fuchs. Operation in early January, which I participated in really uneventful, except for some mild bleeding upon entry of the AC with the dynecaratome, which resolved on its own. We kind of attributed this to, the not uncommon lacy vessel leakage that you can see when decompressing an AC in Fuchs. Did well postoperatively, as you can see there, had to cut one suture. And then at that point, you know, these nevi started to kind of just morph and become enlarged and kind of develop prominent in, neo over the nevi themselves, and that prompted referral with UVM to Dr. Schor and Dr. Harry. And we're very fortunate here to have Dr. Harry. It's not the tool, it's the craftsman. He's an amazing craftsman as far as giving us some amazing images on ultrasound. So it's a true blessing. But again, you can see these lesions. And I'll go through, these are the photos that Schor obtained, or that we obtained prior to sending to Dr. Schor to quote the, I guess, late Jim Comey. These are mildly nauseating. Go neo photos here, obviously very concerning. Kind of multi-nodularity, some crippless features here with high PAS. So we'll cut to the chase, then we'll get to the discussion. So at this point, you know, it's looking back, you know, Fuchs was our working diagnosis, but at this point, Iris Melanoma has galloped to the front of the list versus a metastasis, Dr. Schor and Dr. Harry kind of got together and they thought these masses were pretty solid and robust, so they were, you know, with it hurt previous history of a pulmonary nodule, previous smoking history that a met was probably their leading thought. And he thought that the chronic anterior UBI since secondary glaucoma were all secondary to the above. Plano is an oncology referral here at the U, based some baseline labs to rule around in kind of inflammatory process, basically a pan scan with a scan of the brain as well, all to basically make sure this wasn't a met. If it's not a met, then let's get some tissue. And all that turned up negative, we did get some tissue with a AC biopsy, iris biopsy and vitreous biopsy with iris repair as you could see, you know, on exam today. The Dr. Manlis, you know, basically confirmed the diagnosis of a spindle cell melanoma, the iris and ciliary body being involved, vitreous psychology although had policy of cells did demonstrate the presence of two malignant cells. We discussed with Dr. Park, we discussed with our UBI's fellow, discussed with Dr. Shields. And we've also sought the opinion of Dr. Wynward here locally, but, you know, and we've kind of discussed that, but at this point, you know, further management thoughts, you know, kind of where to go from here and put your input. Yeah, yeah, give us an easy solution for this. Well, it's a tough case and I think it's again, this is the purpose of having these rounds, right, to be able to learn from our experiences. I think, you know, the retrospect of course is obviously easy to look back and say, you know, this is probably what happened. The differential of course and the patient, she's, how old was she again? She's 60 something? 68? 68, so I mean, you know, she is certainly a little old to, you know, to present as a fuchs, you know, Isindroma being the list of differential course as well. You know, an entry statement is Genesis again, but, you know, it really doesn't fit the profile. And so I think, you know, retrospectively, the course, I mean, melanoma is higher up in list. I've had to do a number of these cases over the years, managed differently. I guess fast forwarding, of course, and, you know, the challenge, of course, is we've got a trap now and the patient's got, you know, melanoma, which is something we typically try to avoid. So, yeah, pose lots of challenge. What to do with the trap? And then what to do for her primary lesion issue? She's 20-25 right now and she's pretty happy with her vision. Talking to her, I mean, this is kind of an acquired issue. She says she's had baby blue eyes for many, many years and recently has developed these changes. So it certainly fits in with the time course with melanoma. And she, and I asked her, did she have previous eye care providers following up? You know, someone had been seeing her, did anyone comment about Anivas or spots on her iris? And she wasn't sure, but that would be interesting to kind of look at that as well. You know, putting us at the trap issue, we've had good success doing either a partial or totally heredectomy with plaque therapy if there's already body involvement, which often there is some. And, you know, with our service in Toronto, we've had some good success with that. We often will combine this with a prosthesis later on. She's got an intact capsular bag. She has had a yag though, unfortunately, so it makes it hard to use the bag, but that's something that one could consider. You know, nucleation obviously has got to be up on the list in these scenarios, and I'd be curious what the oncology folks feel. And by the way, just to put a plug in, we just checked out the recent survey. Carol Shields and I just published a review on surgical management and radiomanagement of iris melanoma, reviews of protein bomb beam therapy, radioplac therapy and surgical therapy. But the trap part does concern me as far as the risk of dissemination. I think that, in my mind, I think about a shutdown of the trap with a complete iridectomy and a plaque, but I think that, I don't know, I think she's kind of, you know, on the edge of thinking about nucleation here, unfortunately, you know, I think just with the positive findings and the trap, you know, in these cases, I do defer to my oncology colleagues. I'm happy to deal with this surgically, but from the oncology side, I would defer to the experts in the area. Yeah, up case. What's the outcome with doing a complete iridectomy and plaque therapy? I mean, is she gonna have reasonable vision? Absolutely, absolutely. I expect her to have very good vision. Maybe some CME risk. Of course, the visual functional things and the, you know, the photophobia and other issues are gonna be potentially present, although that is variable. But, you know, we'll put together our series at some point. We've got about maybe six, seven patients like this. Most of them I have had, though, have been a partial iridectomy, for example, or just only plaque therapy, you know, but this is a total iris and I don't know. I think that's gonna be, you know, a question. So Alan and I have, certainly over the years, you have done a fair number of these, and I always felt, though, that once it's into the angle one, it looks to me like this is into the angle. The UBM showed that it's everybody involved, yeah. Well, you've got an angle, obviously, your iridectomy is to get that part, and if it's 360, is that possible for a patient? So that's the question, to what extent is it? Yeah, exactly. If it's 360, like... If it's vocalized, and I don't know if you can do that, and Alan, we've had a couple of cases we've shared in which we've done, you know, an irritable cycloctomy and had a good result. Yeah, I think that, you're obviously right, Randy. I mean, I think... But when it's 360... If it's 360, and I don't know what, I don't know if the UBM showed, I got the impression... So it's more than two o'clock hours, that's what my impression was. So you could plaque that, and then deal with the iris. So that's one... You're absolutely right, Randy. If it's like a ring melanoma, or a complete 360, then you're not gonna be able to get success with that. And by the way, plaque therapy often helps with IAP reduction as well, we've found. When the pressures are up, where we do... We typically treat cyclo-diode with these, right? If the pressures are up before plaque therapy, we'll cyclo-diode these patients, if we need to before the surgery, before they're plaque. But I still wonder whether this patient needs to have their nucleation. I still wonder about that here. She's got a parent that has a father who died from pancreatic cancer. Her mother has breast cancer with meds. She's a smoker as well. She's got some risk factors, all that history part. Talk about history, guys. History is so important, right, with all these things. Do you think a nucleation is gonna get cells that spread through the tread? Or are you talking about the xeneration? Oh, I think xeneration might be a bit much here, I think. But I do worry. I do worry, but I think that's a pretty big step to go forward to. It's a big step, by the way, in the hand. Once it spreads, it's a bad situation. Yeah, it is, it is, it's a hard one to grapple with. I don't know if I go so far as seeing a xeneration for a theoretical concern. It'd be very aggressive. Even when I'm wondering whether nucleation could be, I'm waving between that. But again, I would defer to my oncology experts to me if I saw that. I mean, a nucleation with carefully taking all of that anterior congeal to go beyond. So, the obvious distinguish between nucleation and xeneration, nowadays we have, we do this along with melanomas, so I'm trying to preserve as much tissue as possible with your nucleation, nucleation plus, which is, as you say, we can preserve the congeal type of anterior orbit. And then there is a medial and advanced xeneration, which is a complete, I think a total xeneration will be over 38 for sure. But we also do frozen sections during the nucleation, so we can take samples from the bunch of fiber, you get the eyeball, but at that time you dissolve that. And if the cells are okay, we preserve the lining. And so, once the decision is made, if the eye has to go, then we find the cells. Well, and I'm wondering whether that would be an interesting thought to do a biopsy there. I'm not aware of any case reports, though, and it's hard to prove, I guess, of a trap done with the systemic dissemination and link back to the trap. I'm not aware of that, but it's theoretical. Secondly, when we think about aqueous flow through a trap, where does aqueous flow? Well, it flows through the congeal type, it flows through the microsys, through the tear film, it flows through lymphatics, lymphatics are important, and it flows through the episcopal veins, aqueous veins. So, I think probably, time the management here is gonna be important to try to address this soon, but I think, I think even doing a nucleation is still gonna be long-term risks here in this patient, so. Thanks for sharing.