 We are honored to hear from Dr. Craig Chaya, Austin Nakatsuka, and Wade Stoddard. I do just want to note that glaucoma has always been particularly what we'll call them shining stars in their work, that they've always been able to deliver some really important updates that have helped us all stay up to date on the ever-changing field in glaucoma. With that, we'll go ahead and turn it over to the team. Okay, great. I will begin. This is Craig Chaya. Good morning to everyone, and I'm going to provide you just with a quick Moran glaucoma service update, some things that have changed, and obviously some upcoming things that you can look forward to that we can provide on the glaucoma service. I have no financial disclosures. The first thing I'd like to do is bring your attention to something special that has occurred in room one of the operating room. This is the perspective from the assistance scope, and as you can see, looking over the patient's bed, in the corner there is a special photo on the wall. This has been in the works for several months. I'd like to thank the OR committee, particularly Lillian, as well as Angela Burningham for making this happen, and we'd like to aptly name this Crandall's Corner. Alan passed away almost five months ago, and our hearts are still very heavy, and we remember him so much of the impact that he had on our training program as well as many of our lives. So now in this corner, you can see Alan is literally looking over our shoulders, like he always did from his office or whether he was in the operating room. So we asked it, as you operate in room one, pay your respects to Alan, or come by and just pay a special visit to remember Alan. He was a true giant in our field, and we are truly honored that this room now is dedicated in his legacy. Introduction, this is our Glaucoma service line. It's directed by Norm Zabriski, and it includes myself, Susan Chortkoff, Rachel Simpson, Brian Stagg, Barbara Roscoe, and Austin Nakatsuka and Wade Stoddard. I want to give special recognition to Austin and Wade this year. They've been absolutely tremendous in the wake of Alan's death and have been able to really bolster our service and to provide seamless care for our patients. We provide a full spectrum of care from birth till death for comprehensive glaucoma care. Of note, our pediatric glaucoma service is exclusively managed with our PEEDS service, a co-managed service. As far as diagnostics, there's nothing new to mention except for those of you that may be familiar with this new parameter on the OCT. Many of you may find it frustrating when you have a patient with significant peripapular atrophy or a tilted disc or a very myopic nerve. One parameter that you can now measure is the OCT-BMOMRW, which stands for Brooks Membrane Opening Mean Rim Width. This is a new parameter that may be helpful for those patients where it's difficult to obtain good RNA-FEL photos. In addition, we have OCT-A that's available only here at JMEC, and we also continue to have corneal hysteresis available at our mid-value location currently. Other diagnostics include UBMB scan by Dr. Roger Harry, as well as electrophysiology by Dr. Don Creel. I do want to mention that one thing that we can look forward to in upgrades. This was all set back by COVID, but in the future our visual field machines will be able to perform the strategies of 24-2 CETA faster, which should decrease time for testing, as well as the 24-2 CETA faster, which is also improved upon in the 24-2 protocol by adding more points to the central field. This is almost doing a combination of 24-2 plus 10-2. As far as diagnostics, we continue to have sleep apnea consultation through our sleep service, as well as 24 blood pressure monitoring through the EKG lab here at the University Hospital. One new thing that we are just starting preliminary program in is eye care home tenometry. We currently have two devices that are available, and we have some current research projects that are being led by Dr. Barbara Roscoe, as well as Ariane 11. As far as medical care, we continue to provide a full spectrum of array of options in terms of medical therapies that are available to patients. One new thing that I'd like to draw your attention to is a new medication that we now have available. This is Dorista. Dorista is a bematoprost drug eluding pellet that is placed intracamally, that lasts for approximately four months. In the studies, there were some patients, though, up to 25% of patients who had an effect after one pellet injection for up to two years, and up to 40% of patients who had a response past four months up to about a year. This is something new that we've been doing in our community clinics as well as at Moran, but be aware of that. If you're doing a diagnostic exam on patients that have had a Dorista implant, you may notice a pellet in the inferior angle. As far as surgical care, we now have the newest iteration of the eye stent, the eye stent inject W. We continue to provide the hydrus abic, and we also continue to have the omni cocktail blade as well as the GATT procedure. The zen gel stent is our minimally invasive bypass procedure, and we continue to perform terbeculectomy, all forms of glaucoma drainage devices as well as cyclophotocoolagulation. As far as research, we have a number of studies that are ongoing. First, Dr. Roscoe is leading our suit exfoliation studies. Dr. Brian Stagg is leading a decision support tool study as part of his major work, and we have some ongoing clinical studies in both outcome surveys. Pete's glaucoma. We also have a new head-mounted perimeter that is a free-standing head-mounted perimeter in partnership with the Japanese company. It will be studying along, doing a head-to-head comparison with Humphrey Visual Field. We also have a study wrapping up led by Dr. Vakunta on pulse-dialed laser and the effect on patients who have a Sturge-Webber syndrome. Okay, and that concludes our glaucoma service update. Once again, a reminder, if you need to get a hold of our service line, the easiest, fastest ways to page our glaucoma follow-on call, you can also ask any OSS to schedule with any of our providers in Epinran or our community clinics. For those of you that may have interest in outside referrals, this applies not only to the glaucoma service line, but applies to any service line. If you need to have a patient from an outside physician that needs to be referred into the Moran for Specialty Care, these are two people that you want to jot down. They're in our email system, Jackie Martin as well as Cheryl Christensen. Both of them have served as OSS's in our community clinics and have now been delegated to running our physician referral line for outside referrals coming in. Thank you very much, and I'll now turn it over to our fellows to present our cases for today. Thanks, Dr. Shaya. I'm going to go ahead and share my screen. Alrighty, so hopefully my screen is sharing. So I'm Austin Nakatsuka, previously the cornea fellow here, and now the one of the current glaucoma fellows. And my presentation today is called Angle Closure Glaucoma, What to Do When All Else Fails. And essentially, I'll be sharing two cases that presented with interesting and unique management dilemmas, and we'll share how we navigated through those, and these are both Angle Closure Glaucoma cases. No financial disclosures. So, case one. So this is, hello? We can hear you now. Okay, somebody muted me for some reason. This is a 63-year-old female who presented with a red painful eye vision loss and mid-dilated pupil and a pressure of 50. Reportedly occurred upon waking about 2.30 in the morning. She was initially referred from an outside provider when she came in, and her pressure was reportedly about 60s on initial presentation with the outside provider. In terms of her history, it was only notable for a recent UTI for which she was on macrobid, in terms of antibiotic, in terms of treating it. Otherwise, no previous surgical history or family history of glaucoma. This was important to, it's important to look at, especially in these Angle Closure situations, a very thorough med history, because as many of us know, certain medications such as Topomax and other sulfonamide derivatives can precipitate in Angle Closure Glaucoma, and sometimes even a bilateral Angle Closure Glaucoma. And we've actually had a couple of cases of Topomax induced bilateral Angle Closure Glaucoma recently of which I've had to deal with, but this is not the case for this patient. So upon review of her history, her outside provider, which actually was earlier in the morning of prior presentation, I'm sorry, a day before, had tried doing a PI times two, had done maximal drops and diamox as well, and reportedly her ILP never went below 46. And as, and again, upon presentation, her pressure was 50s. The PI was questionably patent, and she was already on max drops and had already taken diamox. And so at Moran, the residents have a protocol to deal with the Angle Closure Glaucoma, and it usually involves medical therapy first with maximum with drops, diamox, and then if that does not work, then usually they page the glaucoma fellow, and we consider doing PIs and or AC taps. And that was essentially what happened. The patient initially had a PI done by the resident and then fellow came in and checked and did some additional PI to make sure that it was patent. Multiple AC taps are also done, but it was noted that the pressure kept rising to the 30s and 40s, even when the pressure had been dropped down to in the single digits, and it would rise to the 30s and 40s, about 30 to 40 minutes after these AC taps. So a couple questions people might have. So why were so many PIs done? First off, in these acute Angle Closure situations, the cornea can get very edematous and thickened, and the view can become very difficult. And so in terms of actually performing the PI, it can be very difficult. And then also making sure that the PI is patented, it makes it makes it very difficult as well. So sometimes these have to be done multiple times to make sure that the laser actually gets through the iris. In terms of the AC taps, there's a couple of reasons for this. So classic thinking is that, you know, why do an AC tap when the AC is going to fill within, as the residents may know, it should fill within about 100 minutes for a normal person, completely fill within at least 80 to 100 minutes. But with AC aqueous suppressants on board, that can theoretically increase the amount of time for the AC to fill. Secondly, by lower acutely lowering the pressure in these situations, sometimes it's thought that the canal can actually open, things can open up, and spontaneous flow can actually occur. And then finally, by lowering the pressure, sometimes that will reduce the amount of corneal edema, which actually itself prevents absorption of these drops. So that was attempted, but did not, did not work. And so I'm sorry, these are not the greatest pictures, but these are pictures of the eye. This was actually after the PI had been done for the fourth time, and it was now definitely patent. As you can see here, you can see a pretty cloudy cornea and a mid-dilated iris, that is the shallow chamber. And it's important also to note that the patient was also faking, which also happened, incidentally, have a very large turidium as well. And so just very quickly, laser PI is basically a method to create another channel for aqueous to be released and access the trabecular mesh working canal directly, once a pupillary block mechanism has been has prevented that from occurring by closing up the channel to the axis of the aqueous directly to the trabecular mesh. So in terms of her core, she was then admitted for IV diamox with the thought that perhaps her absorption orally was not enough. Her pressures were still high. She was actually given manitol as well. And the mechanism of manitol is through osmotic osmosis, drawing fluid out of the vitreous space. And her pressure was still in the low 40s after that as well. So that wasn't successful. And so then we moved on to the next plan. So instead of just doing a laser peripheral aerodotomy, which has already been done, we then moved on to an aerodoplasty, which basically involves the argon laser contracting the iris and pulling peripheral iris stroma away from the angle. And this is a just a quick video of how that occurs. Let me just go ahead here. And so essentially, this is basically just applying a large spot size of the argon laser with low power and lower duration to contract the iris instead of actually trying to pulse through it and pull it away from the peripheral, from the periphery. And so this had some effect. The ILP actually went down to the low 30s for about a day or two, and then rose again to the 40s after that. But it did actually help to clear up the cornea a little bit. And so we also tried adding on rocklutan in addition to her four-drop therapy. And essentially, rocklutan is ropressa and metanoprost. And for those who don't know, ropressa is essentially a rokinase inhibitor that is thought to is another class of medications that increases outflow and decreases episcopal venous pressure and can sometimes help to lower pressure in those refractory to medical treatment otherwise. However, we've been finding it's been very poorly tolerated. And so often we use it in very unique circumstances. And this isn't, I'm sorry, this is not her actual nerve, but her nerve actually looked very similar to this. I realize it's a left eye. But upon examination of her nerve, we noted some optic disc swelling and some disc hemorrhages as well. And this is after being able to get a good view of her retina. And as you can see here, she has quite a bit of swelling on her OCT. And so what is going on here? Does she have a CRVO? Does she have an NAION? And so most likely we think that this was the cause of her optic disc swelling and hemorrhages. And so this is something I wasn't actually aware about, Dr. Zabrowski pointed out, ocular decompression retinopathy. So essentially this is a retinopathy that occurs with hemorrhaging after an acute lowering of pressure. And so it's actually classically occurs after trabeculectomies, where you lower pressures from the 40s acutely down to single digits. And the mechanism is thought to be either due to vitreous displacement that can cause shearing of the capillaries, kind of similar to a PVD, or actually change in the forward displacement of the lamina crebrosa, which causes decreased axoplasmic flow and essentially causes some transient ischemia, kind of similar to the mechanism of CRVO. And so this is something that can occur by lowering the pressure acutely. And it's generally self limited, but it can have some long lasting effects. And so this is a B scan that was done by Dr. Harry. And here, basically you can see some anterior rotation of the ciliary body and the lens iris diaphragm is is anteriorly displaced. And you could see here as well that the angle is essentially closed, a very narrow. And so what's the next step? Well, essentially this patient really needed FACO, she needed her lens taken out. And so we ended up doing a combined FACO with an Ahmed tube as well, just because we were unclear. She had a difficult presentation, and we just wanted to make sure that her pressure was adequately controlled. And so we added the tube as well. And this was done about a week from presentation, you might ask, why did we wait even that long? Well, in these cases, it can be very difficult in terms of the view because of the amount of corneal edema that can occur, and as well as getting some sort of calculations for a lens. And so what we were trying to do is wait for kind of a window of opportunity for us to kind of get in there and get the lens in and put the tube in. And essentially, we're able to do that. Actually, the aeritoplasty did help with that. And so we kind of got in there and put a lens in them too. And this is just her biometry. Just kind of wanted to point out some things. Her axial length was a little shorter than normal, but not that much shorter. Her AC depth was small, and her lens thickness was on the high borderline high side, which all of those things would be consistent with putting someone at risk for angle closure. And she's also hyperopic in both sides. And so in terms of her course, we've been following her post tube for about three months or so. And her pressure has been in the high teens to low 20s, hasn't really dropped too much lower than that. And that's on two to three drops, glaucoma drops, and with her steroid tapered down. Her best corrected visual cue is 2040, and ocular surface does have a little role in that. But her optic disc edema has notably resolved. But we don't know how much damage has been done to her retina in terms of the post, the decompression retinopathy, but at least her edema has resolved and the hemorrhages have gone away. And then we finally eventually got some form of a visual field. And this is a stem five, which is why it looks like this. But actually, surprisingly, she's surprisingly doesn't have all that many visual field deficits so far as we can tell. So hopefully she does not have significant permanent damage or visual field and nerve that will cause her functional loss because of our actions. Case two. So this was a different case. This is a 49 year old female was referred from outside provider for narrow angles, but she actually initially presented to that provider for a basic evaluation. But she had noticed that her vision had been worsening over the past year, especially peripheral vision. And her pressures in that I were around the 30s. And the other I were actually in the low teens. And she was on she had no significant past medical history at all. She had slightly thick packies, she was noted to be narrow in both eyes. And she had she was faking as well. But if you notice, she had a very asymmetric cup of dysracial. And she was also hyperopic. But here you can see in this patient's case, her fields were much different and worse than the other patient. She had already had quite a bit of visual field loss already in that. And that's the right eye. And the left eye was doing okay. And quite a bit of anatomic loss of her optic nerve as well. And so she was started on drops, initially, to see if that would do anything because this is obviously much more of a chronic process in her case. And at a five day follow up, her pressure had not really budged much. And so because of this, initially, it was considered to do an lp, lp, excuse me, lpi to help her out. But it was determined that for her, she would actually need FACO for the predominant reason of opening up that angle in terms of this chronic process. And so she ended up having a FACO done with viscogonial siniculitis, which is basically a fancy way of saying that a viscoelastic was injected into her angle to help open up the angle. And sometimes what we do is we take the cannula and use that to gently lice the peripheral sinicula to help open up that angle on that channel. She had a pretty high powered lens placed for a planal target, and that becomes relevant later. And sometimes we also combine these with ice debt or some other mixed procedures as well to just further help further help their pressures post op. In this case, because her angle was significantly open, following the interop, this was deferred. And post op day one, her lens was noted to be fairly anterior, pressure was a little bit better, but she was still pretty narrow. And so on post op day three, we did a quick MRX because her visual acuity was pretty poor, and it was noted that she had a pretty large myopic shift. And remember, we had aim for a planal target. And so her angle still appeared not narrow and her IOL was noted to be fairly anterior than what would be normal. And so what exactly is happening now is this a continued process of her angle closure, or is this something kind of new and different? And so we think that what was occurring was essentially a form of aqueous misdirection. And so Dr. Tarhan gave a very extensive presentation on this last year. So I'm not going to go into detail, but essentially this is a, this is also known as malignant glaucoma. And it's a process where the lens iris diaphragm moves anteriorly. Usually there's a high pressure. And classically, it actually occurs post some form of incisional surgery for acute closed angle glaucoma. But what happens, what's thought to happen is the aqueous instead of being directed forward into the canal like it should, it is directed posteriorly into the and lock elated into the sequestered into the vitreous cavity or hydrates the vitreous itself. And so there are multiple ways to try to address this situation of aqueous misdirection. Oh, and I'm sorry, I also want to mention that aqueous misdirection is a diagnosis of exclusion. Essentially, you need to rule out other causes of angle closure, such as corrode attachments or hemorrhage, or some form of posterior or secondary reason to cause the iris or lens to move forward. And so there's various ways to deal with aqueous misdirection. And so one of the ways is to actually rupture the hyeloid with the Yag laser. And you can do this actually through an LPI. And so this is kind of known as a irritable zonule hyeloid rupture. And so this was attempted with very minimal improvement. However, the pressure remained pretty high as well. And so surgical treatment was basically was done. And so essentially in this case, a complete paris plane of vitrectomy was done, and then a posterior amethyst was placed as well just to make sure that there was flow. Now, there are other ways surgically as well to address this. You can do an anterior approach with the irritable zonule hyeloidotomy, which was shown in Dr. Hahn's presentation. I'm not going to show that again, but usually definitively for these types of very resistant aqueous misdirection, the full paris plane of vitrectomy needs to be done. And so she's actually been doing very well and has had prophylactic LPI in the other eye. And so I want to give time for questions and discussion, but I just really quickly just want you to be aware of two landmark angle closure trials that I should know about. So this is essentially the ego trial which looked at whether or not I'm doing a clear lens extraction primarily for primary angle closure glaucoma versus doing traditional treatment, which is LPI medical treatment was more effective. And basically there was a lower pressure in the clear lens extraction group. And there was also a there's more cost effect effectiveness and greater they found a greater health status score with using a systemic survey questionnaire. And then it's also important to know about this trial, which is the it's called the ZAP trial, but it's basically a trial that looked at doing laser peripheral iridotomy for preventing prophylactically for angle closure glaucoma suspects. And so essentially they had 889 participants and they did LPI in one eye and the other why I was untreated. Overall, the number of events of angle closure in these suspects was very low. And it did show that prophylactic PI did have some benefit. But because the incidence was so low, the at least the study authors indicated that they did not recommend that prophylactic PI for angle closure suspects. So main points basically management of angle closure glaucoma can be very challenging, be aware of this condition called ocular deep compression retinopathy in other situations as well and be aware of aqueous misdirection and as well. Okay, I would like to open it up and also open it up to Dr. Zabrisky as well if he'd like to make any comments. Someone can unmute Dr. Zabrisky. You should be able to unmute itself. Yeah, thank you. That was a great presentation Austin. I know we're about out of time, but I just want to make a couple of comments, although Austin covered it great. The point of showing these two cases is just, I mean, all of us we've dealt with angle closure and in the middle of the night. And most of them respond to PI and medical treatment and we move on. But these were unique in a couple of ways. The first one was unique in that it just didn't, it just responded poorly to everything. But just an important point, when you look at studies that are talking about taking the lenses out in acute angle closure, most all of the studies, the most important ones, they do surgery in the setting of what they call medically aborted primary angle closure glaucoma. So these studies are not done going into red hot eyes like this lady had. And so you really do try everything conceivable to try to medically break the glaucoma attack before doing any surgery. If you have to go into one of these eyes hot, that is a real issue and fraught with difficulty. So we do try everything we can to break it. And she just was very difficult. But like Austin said, finally, after working with her and doing all of these things, we did literally kind of get a clear window, meaning the cornea kind of cleared enough that we felt like we could get some surgery done and which we did. And then she had a really difficult course. But I think overall is doing all things considered is doing really pretty well. And I think her nerve is fine. And like Austin said, we might be having some effects from that decompression retinopathy. But but I think she slowly is continuing to do better and better. But again, you just try everything you can to medically abort. And then the second case is interesting, because it's a very different picture. This is chronic. She already has a huge visual field defect. So, you know, you're wanting to get pressures down in her case, and you have a clear cornea. So your surgical options are open. We tried, you know, cataract surgery first did goniocinical lysis or angle just opened up wide open. So we felt like maybe we'd make some progress. And we did. I mean, lowered her pressure quite a bit, but still not enough. And so we ended up having to do more. And just a quick little note, when you do have a tractomy in these patients, you do have to do what I call a posterior PI. And that's the critical portion is to, you know, do a PI from the back, which means you're doing a zonular lysis as well as the peripheral oedectomy. And that's what really breaks the cycle. But then the final thing is when you're operating on these patients with these narrow angles and small eyes, you will get refractive surprises. And it's not even in the setting when there's not misdirection, which this lady had, but even in non misdirected patients that they have small eyes and they have these narrow angles, you're going to get some myopic surprises where the lens just stays forward. And I've had it stay forward even after going in and doing a retractomy and a posterior PI. So that's something that I would just caution you to warn your patients about in this setting that there can be eyes that come out myopic. Just because that's the nature of where their lens rise, it just has that a forward displacement of the IOL, which is a little bit hard to predict going into surgery. So just those couple of points. And thanks, Austin, and I appreciate it. It was a great presentation. We'll move on to Dr. Stoddard now. Hi, everybody. I'm Wade Stoddard. Just got my screen shared here. All right. I'm going to be presenting on a case of a pediatric traumatic hyphaema that repled multiple times and try to leave a little bit of time for discussion because I think Dr. Stoddard would like to pull the room on their experiences afterwards. So on January 24th, Dr. Stoddard received a call from an outside provider about a kid, seven years old boy, he was hitting that with a Nerf gun bullet, I think shot by his father and accidentally hit him in the right eye resulted in an eight ball hyphaema. When he presented to the outside doctor, I believe he was LP, he's actually LP through the whole course that I'm going to present. And his IOP was in the 40s. And the doc on the outside had taken him for a pretty prompt AC washout, but had encountered either two tenacious of a clot or rebleeding and was unable to wash it out sufficiently. And the IOP remained elevated. So he was referred to the Moran. So he came on the 24th and we got him into PCH pretty promptly for another washout. And I'll just go to the video here. So this video starts up part way through the procedure. But at the beginning of the procedure, the entire AC was this dense material that you see me tugging on with the retractor there. It was like the whole AC was just filled with silly putty. And we actually you can see there's a 2.2 or 2.4 millimeter incision there. We actually required FACO in order to get the majority of the clot out. And oh, thank you. It had to be mechanically dissected with MST4 sex out of the angle and off the iris with a lot of care. I felt like it was so tenacious that I was going to cause an iridodialysis or something while I was pulling on it. But basically pull off chunks of it and feed it to the FACO tip. And we ended up injecting TPA about four times during this procedure to let it sit for five minutes and loosen things up and then take some more out and repeat and repeat. And we're in there for a long time. And we ended up with this stuff superiorly that we couldn't quite get out. This is pretty much what it looked like at the end of the case. The rest of the case is us looking at the angle and sewing things up. He had some recession. The video quality of the angle is not very good here. But it looked like there wasn't a lot of clot left in the angle. He wasn't bleeding at this time on the table. So we were pretty hopeful that maybe this would be it. And so that's how we left him after that first procedure. So this was his second AC wash out. And we elected at that time not to do an aqueous drainage device because it looked like we had, you know, de-clogged his angle and we're pretty hopeful that it would still have some function. Post-up day one, his IOP was back up to 49. He was LP again and had a seven millimeter layered hyphaema with a lot of that fibrinous material still there. And we were questioning, you know, did he re-bleed from TPA? How much of this is fresh first old? And Dr. Stagg elected to take him back for a Ahmed implant and another wash out, which was done the day after that, which was the 26th. He also was just very injected. All of his vessels, presumably from having his pressure high for a while were just very large bore and it was a very bloody, difficult tube to place. His AC was washed out again just by flushing and a lot of the blood was still loose and came out. And at the end of the procedure, everything was successful. The tube was in the AC. It didn't look like he was bleeding much on the table again. This is his B scan from after that procedure. You can see that he's nice and deep and has some clot materials still superiorly. Post-up day one from the Ahmed valve, his IOP was 30 and he had bled again and was still LP. So he's continued on the standard medical therapy. And at this time, Dr. Stagg was considering that there might be something else going on. So he had consulted hematology and had sent for PTA, PTT, INR, and CDC just as screening. And it was all normal except for a slightly elevated APTT. And hematology wasn't concerned about something particularly severe, but they did agree to try a five-day course of amino-coproic acid oral. So he's given two grams, Q4 hours while awake for five days. And then he was scheduled to see hematology. I don't believe he's had the formal consult with hematology yet. But there was some concern based on his history that maybe he had some easy bruising and that he might have some kind of dyscrasia or diastasis. So post-up week one after his Ahmed valve, his IOP was 16, but he still had 100% hyphema. And at this time, he was starting to look bloodstained. So because of the staining, even though the pressure was 16, it seemed to be getting worse. So he was taken for another washout. So this was his fourth washout. And the view was very, very difficult. So I wasn't there, but Dr. Staggs said he could really only see through the peripheral cornea. And so did as much of a washout as he felt like he could safely do. And this is the UBM before that procedure, showing a lot of fibrinous material as well as some looser bleeding around it in the AC. This is that post-up week one. You can see the brownish blood staining here, getting pretty opaque. And a few days after that, we can see that the clot is getting a little bit smaller, though there's so a lot of material there. And here's an angled slit lamp view of the blood staining, which looks to be involving a good amount of thickness in the cornea. And then on his ultrasound, this was on the 18th, so just a few days ago, he was still a LP, but the clot is much smaller, but he does have this kind of diffusely thickened coroid that thought to be related to hypotony. His IOP had finally come down into the single digits. So just a couple notes before we open up for discussion on intracameral TPA. So TPA's tissue plasminogen activator it converts plasminogen to plasmin, and the plasmin goes on to cleave fibrin products. So the thought is that if you use it in particularly tenacious hyphemas, that it can help clear it up faster. The downside might be that if you have fibrin occluding broken or fragile vessels that by dissolving that fibrin, you obviously might get more bleeding. There's not a lot of data out there. They're all case reports and very small case series. It only fills up about 25 search results on PubMed. So there's not really known what rates of re-bleeding there are, but there are some series where people think it really helps hyphemas go away faster. Typically in adults, in the literature, you'll see dosages intracameral of TPA anywhere from three micrograms up to one of my attendings in residency, like to use 30 micrograms. Dr. Chia will use 25 micrograms in adults. And then in pediatrics, Dr. Chia will use 12 and a half micrograms. There's really not standard dosing guidelines for this out there. And then as far as amino-coproic acid goes, amino-coproic acid is a lysine derivative. It blocks several enzymes that are related to plasma, and basically it helps you plot better. And it seems to have a pretty good safety profile. It's not like giving this to kiddos or giving them a DVT or anything. It does have an orphan drug designation for recurrent hyphaema after some case reports that came out in the late 80s and early 90s in an animal model that suggested that it could reduce the rate of recurrent hyphaemas. But again, this is not something that's particularly standardized. And the dosing for amicars is by weight. So I wanted to open up to discussion. Maybe Dr. Stag wants to come in and clarify what some of his questions might be, but has anyone else seen cases of such tenacious re-bleeding in the absence of known neovascularization or a tumor or JXG, something that would explain it? Like in this case, just after trauma. The other question in this case is, why did he get such bad blood staining if his pressure came down? And so quickly, and if the cornea service has any comments on that, and any other tips or tricks that any of the more experienced glaucoma physicians have with TPA or amicar? Yes, Wade. Thank you. That was a great summary of the case. So yeah, I thought this case was interesting and stressful to me because so he presented the day of the injury to the outside doctor and had just a couple millimeter hyphaema from a Nerf gun injury. And we see that so much. And then outside doctor had him fall up a few days later and the eye was filled with blood with the pressure high. So a re-bleed and we see that sometimes is pretty rare, but then he kept re-bleeding. He ended up with a total of four AC washouts. And so that kind of kind of Wade's first question there. Do I mean, we see so many hyphemes, especially like in triage and everything, we see so many hyphemes. We don't very often see one re-bleed, but then we're kept re-bleeding like that. I was just wondering if anyone wants to talk about any experience they've had with a case similar to that. See if I can see everyone. Well, I'll just make a quick comment. I have not thankfully ever had a patient with this type of tenacious re-bleeding, but it has always made me wonder why, why the recommendations for falling up on hyphemes are so aggressive, right? Depending on where you look, you could find daily follow up for 10 days, which, you know, is just so out of proportion for what we routinely see. So I think these are the cases that essentially precipitate those type of significant recommendations. The other thing here is we don't have a lot of African Americans in our patient population. And that's certainly something that in other parts of the world where you do have sickle cell, I think they certainly see a lot more of this more severe disease. Great. Thanks, Jeff. Yeah, I think that's a great point because, yeah, I mean, resident and then after residency, I've seen so many of those small hyphemes and you're like seeing these kids every day and having them lay down and stuff. And just for how many we see and how few poor outcomes there are, I think you're right is when you see something like this that's really, really, really hard, you know. And then, so the other thing, and I was hoping someone from cornea, we've got, Austin here has got a foot in both worlds, which is nice. But I wasn't expecting bloodstaining because we had the pressure under control. And he didn't have blood in there for that many days. And the pressure was under control. And it kind of went against what the classic teaching, you know, about the risk for bloodstaining and over what time course you'd expect that, depending on the high pressure. So I don't know if anyone from cornea have thoughts about that. Austin, I think that's you. Yeah, so I was just going to say, I probably shouldn't be the one to speak for the rest of them. But actually, myself and Dr. Zabriski just had a conversation. We're having a conversation about this. And typically he has found and, you know, I mean, he's dealt with quite a bit of hyphemous as well and high pressure situations. And typically he's found that usually there has to be some form of high pressure for there to be true cornea staining, cornea bloodstaining that would necessitate a transplant. And that can occur over the course of a couple of weeks. I mean, in this case, it seemed to be pretty early. So that's and I know about this case as well. And it's very unfortunate. But without that high pressure, sort of forcing those cells into the kind of the endothelial endothelium of the cornea, typically that that doesn't frequently occur. And the blood can be in there for a while without truly staining the cornea permanently. Brian. Yeah, yeah, this this norm. So, you know, first off, I just want to say this case is in my experience, this is as bad as it gets, you know, and it's just truly a combination of just some unfortunate events. I mean, to have this eye rebleed so profusely, so many times is just really, really unusual. I don't know that I've ever seen one quite like that, you know, you're talking about, you know, four or so major rebleads in the anterior segment, but and then the blood staining again, I agree with you, you know, I know back in the day, the Will's manual used to break down like has this kind of this recipe practically of, you know, if the pressure is this, you can you have to vacuum your blood after x many days and stuff like that and the higher the pressure, the shorter the time, but certainly we wouldn't expect blood staining like this to occur at the pressures that you have. But it just it's just one of those things to show that, you know, things happen sometimes and that you don't expect. I've had a couple of kids, you know, interestingly, as I'm trying to think of the blood staining episodes that I've dealt with, they were both the ones I can think of are both in kids and and the blood staining was terrible, but they both had really high pressure and and by the time the patient got to us, actually, the staining had already as had already occurred and and you know, I went in and had the exact same experience you did took out the clot, but there was just it was completely bloodstained and the only thing you could see was just in the far periphery. But those both had been associated with you know, outside high pressures that were really significant for about a five to seven days time as I remember. But you know, I think you do I think you did everything right and everything you could it's just that this is a really tough scenario, it just it just really is. Yeah, thank you for talking to me through it as as it was happening to I was talking to both Norm and Craig several times getting advice and thoughts because, like I said, it was a stressful case for me. But so Brian Zog is here raising his hand. Do you want to talk, Brian, or are you able to? Yeah, sorry, it was not letting me unmute there for a second. So Craig brought up a point in the chat about whether or not we can use OCT to kind of figure out the depth of the bloodstaining and it might be useful to have that. It might give us some information there. It can be kind of tricky to to tell for sure on anterior segment OCT, but sometimes you can see it there. But I completely agree with all the comments that have been said here that this is just an unexpected sort of result of his hyphema, but also, you know, with the amount of amount of times that he reblood and then you have to kind of question one thing too is like during the washouts, are you potentially pushing blood kind of into the cornea too with the pressure of the washout? I don't I don't know that I know much literature like when you're doing a washout, how how could that could affect sort of bloodstaining to to try to think, okay, what what potentially could have precipitated the bloodstaining if we were managing the pressure in this situation as well as we could. It definitely even thinking through that it still is an unexpected outcome. So so now we're kind of stuck with a bloodstain cornea with a pressure that's under control. And my my recommendation essentially would be to just give this time to clear and just sort of see what happens. It'll it'll start in that peripheral cornea and then kind of clear centrally if it if it is going to clear on its own. But if not, we'll just have to kind of assess try to figure out the depth of it and decide on what kind of a transplant he might need to sort of optimize his vision. He's seven. Is that right, Brian? Yes. Okay. Yeah, so I think just what what's his treatment actually sorry Brian he's eight. He just his birthday was last week. He was in clinic for his birthday. I brought the text in and we all sang happy birthday to him like Robin. So what what's his ongoing sort of treatment now like what is he on medication wise? So right now I've got him on you know I don't have it off the top of my head but I've got him on steroids antibiotic and I think I've I think I've got him off all pressure drops at this point. Okay. So so my recommendation would be to treat him with kind of long term steroids. You're not going to really worry about a cataract from the steroids in him. He's going to get a cataract from other other issues. So I wouldn't worry much about that side effect of the steroid in the kid. And then obviously managing his pressure to make sure he doesn't have a steroid response. I think you'll have that well under control. And so this the steroid could potentially sort of help with that blood staining. I'm not aware of any other treatment out there. I'll try to look into it for you and see if there's anything else that could potentially try to at least reverse it somewhat. But but like we mentioned in a conversation that we had last week I'm happy to see him and kind of help follow kind of his course to figure out the best next treatment for him. Thank you. Yeah. He scheduled to see you. And who was going to say something? Oh, I was just going to say Dr. Zog just correct me if I'm wrong, but especially I mean with a view like this, like the one that Wade has up on here, you know, a endothelial caretoplasty would probably be very difficult if not completely impossible. And I so in this patient's case, I if it doesn't change, are we think we're thinking more of a full penetrating caretoplasty for this patient? I that's what I would have thought. Yeah, for sure that the hope is that over time, you'll get some clearing. And you don't you don't need an amazing view for a desec, but you do need a view. And in this case, you're not going to have one. So right. So that that for sure is something that we'll have to just see how much clearing will happen over the course of time. And maybe that anterior segment OCT can help us sort of understand that and following up the chemistry and just kind of those those surrogate markers to try to figure it out. So yeah, the OCT is a great thought. He's coming to clinic on Friday. So I'll do that. So one other thought that I had was so his eye has been through a lot, you know, four washouts we talked about and then just the rebleeds and the inflammation. I was wondering if that may have contributed to the blood staining, if there was some breakdown of the endothelium or end with decrease endothelial function or something that maybe let made it more prone to blood staining than otherwise it would have been. And then one other thought one other thing just that I'm worried about now, because that's what we block home a doctor's do is we worry. So his his pressure has was holding like good like in the teens, but it started to go down. And even Dr. Dr. Harry was a little worried about some thickened choroid maybe from hypotiny, his pressure is probably in the single digits now. It's hard to get a good aplenated measurement with his age. But I don't know. I mean, I think the valve was working. I think the valve was keeping the pressure. I don't think there was like accessory leakage. So I've wondered if maybe the clots healed and he's got a big cyclo dialysis cleft that's making the pressure go like putting them at risk for hypotiny, which will be another problem to deal with. So yeah, to me, that's kind of the disaster scenario, right, is that you you end up with kind of the the hypotiny of the eye and that that usually will lead to the demise of the eye if you can't get that pressure up. So so you have potentially having to tie off that tube or or something else to kind of keep that pressure into a in a healthy range is for sure something to to be thoughtful of for sure. Yeah, I wonder if Norm or Craig, do you have any thoughts about that? Like if he's going hypotenuse, I almost worried that tying off the tube wouldn't help because it was maintaining okay. Like and but I can't see if I don't know. Do you have any thoughts about that like management of hypotiny? If he gets that going forward? Well, yeah, I would just say that if he does, I mean, if he does go low, and you've got a tube in place and you've really got low pressure, I think you're obligated to tie the tube off and and then just see what happens. You know, you're right though that if it's a hypotenuse process due to either cyclical analysis cleft or just the ciliary body infarction and kind of, you know, malfunction, which certainly can happen in any of these kind of acute high pressure type cases. You know, I've seen that many times, unfortunately, over the years where you go through an acute like an acute angle closure or an NDG or whatever it might be and and, you know, basically the thought is you've just either infarcted or damaged the ciliary body to the point that that you, you know, end up with low pressure. You know, we can talk a long time about that because that happens. But in this particular patient, if the pressure does go low, then I think I think you have to tie off the tube just to see if that makes a difference. And it might not, but I think you have to do it. I don't know that I would do it now. It's pressure eight. Now I don't know that I'd do it a pressure of eight. But if it starts to just continually go down, then I think I think you'd have to do that. Nice. Yeah. Brian, this is Craig. I would agree that you should tie off the tube if he becomes hypotenuse or if there's evidence of caroidal thickening and hypoteny. One thing that may be helpful too, if he's, I know the pupils almost blown already, but trying to rotate the ciliary body back with chronic cycloplasia may help to seal off some of those clefs if there are any clefs. Nice. Yeah, I forgot to mention that I do have him on cyclopentylate right now. Yeah, you might, it's just a small thing, but you know, if you're really worried about it, you might consider putting him on atropine if you can, like low dose or something. I think atropine in this setting for that particular problem is definitely better than cyclopentylate. Yeah, good thought. I had him on cyclopentylate earlier, but I think, and it's just kind of carried over, but I think I'll switch him to atropine. Yeah, I probably would. Griffin's got something here, and then we're probably running out of time, but Griffin says, it seems like this corneal bloodstaining occurred in Spive, doctor said doing everything right. I wonder if it represents a more dramatic initial injury than originally appreciated. And that could be the case. So the outside doctor who did the initial washout said it was just, there was just active blood flowing while he was doing the washout, and he kind of just stopped and put glue on the eye because he couldn't, like it just kept bleeding and bleeding and bleeding. So I think it was a bad injury to start off with. So, but great. Thank you. I don't know, Craig, do you want to see any closing comments and then? No, just to want to recognize Dan Clegg, our pharmacy team here is amazing. We've been trying to get Amacar in our protocol, and Dan was kind enough to make sure that we could procure the oral Amacar version so that we could start that on this child. Initially, we thought there might be a topical version that we could compound, but there is no commercially available prep of Amacar yet. So we recommend if you have any refractory or difficult hyphenic cases to consider working with Dan and the pharmacy team to administer oral Amacar. Yeah, it does. I mean, it does remind me of how things have changed in terms of just management of these hyphemes. Back when I was a resident, man, we would just be so much more aggressive about putting anybody in the hospital and patching them and Amacar and all that. We should just do that routinely, and it's not done that much anymore, but it's kind of, I don't know, sometimes these really bad cases can happen. So it's like Jeff was pointing out, it kind of makes you rethink some of that old stuff sometimes, especially when you see a case like this. But again, I think everything correct was done. It's just, the initial trauma was very severe. I think that's obvious. Great. Thank you all. So I believe that concludes our grand rounds for a coma, and thank you all for attending.