 residency. So, Chrissy Chapman came to us by way of Cornell. We've had a collaboration for the past three years with Cornell and Tanzania. And this last week, we took a large branch of the team there and had an incredibly successful trip. So, those of you that remember Frank from Tanzania, he's got kind of the junior Afro amazing doc. He was there and this is his hospital where he's the only ophthalmologist. And really over the next five to ten years, we'll be collaborating academically with the program to build a training program. Chrissy's former program director and chairman were there and spoke highly of her. So, maybe I'll just record this with my iPhone and send it to the person. And then following that, we'll have Victor Wang who's a neurologist. Hi, good morning. My name is Chrissy Chapman. I'm one of the Glaucoma Fellows this year. I'm going to talk about one of my favorite medications, but also one of the most dangerous. So, steroids and glaucoma. So, I thought I'd go through a couple of pieces of patients that I saw this year that really affected the way that I think about steroids. First, being an ancient little male that two years ago presented to us outside ophthalmologists with eye redness and irritation was giving prednisomone BID to use in the left eye. Kind of disappeared to follow up until he presented to us with left-sided pain, headache, redness, and blurry vision. He was on his mission in England when this happened. And at that time, he had a medical history submitted for asthma. I'll read all and add there. And he came to us with a vision down in the left eye to 2060 that stood in the dialing of people with a 2 plus APD and a pressure of 54. We also found out at that time that he had been using prednisomone BID for the past two years since being prescribed it for his pinwhekula. So, until his segment was submitted for, he did have a pinwhekula, but I was very injected. There were no other manifestations of secondary glaucoma, notaries, and puberty spindles. He was completely open on goninoscopy. And posterior segmentia was really remarkable for asymmetric cupping with a 0.9 cup to the right showing the left eye. Fundus photos don't exactly give it justice to how deeply excavated this cup was. Again, photos. And the OCT, again, for how advanced the squalcoma was, is only demonstrating a thinning in two closures. But the visual field really tells a whole story in this left eye, where he's left with a remaining central field in the left eye that had been treated with steroids. Second case is quite a different patient. This is a 77-year-old African-American male who came to us about a month and a half after his complicated cataract surgery. He had posterior capsule rupture with sulcus lines in place with a lot of post-op inflammation. He had no glaucoma and was put on Durazol to treat the high inflammation and came to us with blurry vision, feeling like there's vaseline in the eye. In this case, he did have an ocular history of glaucoma treated with travitin in both eyes, and when we saw him, he had been taken off Durazol and taken off his travitin in that eye and was otherwise un-combed again in Cosol. His visual acuity in that left affected eye was 2060, pinhole into 2040, mostly secondary to large areas of primosus from the capsule, and high AC inflammation. And his intracular pressure, while all those drops, was 26. Again, he did have sulcus lids in that eye and still had residual churplasty in itself, flare, and open angloma and also in the posterior second exam, demonstrated bilateral and symmetric These photos in our CTR and fall with the left eye already demonstrating a little bit more progression. The last case, again, very different profile, 42-year-old white female with parisplanitis, who had been treated with systemic steroids and most recently topical steroids, and a sub-tenome injection of kinologue for CME. Five months after the kinologue injection, her IOP was still elevated to the 50s, even though she was on maximum medical therapy. This patient was difficult because in her course with parisplanitis, she didn't tolerate any kind of systemic immunosuppression or steroids and really was hesitant to take anything like diamox or methicillin. Again, she had parisplanitis and was on maximum topical therapy and was not tolerating and not willing to take diamox or methicillin. Her visual acuity was 2020, but her pressure was 50 despite all the topical therapy. Again, her angle was open and her cup-to-disc. Initially, what she was seeing with feminist photos, cup-to-disc was symmetric with 0.2 cup-to-disc ratio, and it definitely demonstrated progression over the last four months with elevated AFP. Again, her photos from the beginning, healthy run, and so these three cases demonstrating an atrogenic glaucoma, a young male, a 77-year-old patient, second case being a 77-year-old patient with no glaucoma, active inflammation, and the third being a patient with a long-term depot of steroids. So indications for steroid use, and the ECSC recommends using for active information, to prevent inflammation, or reduce inflammation in the forehead or retina, they advise to start high and aim low, not to tight trade up on steroids, rather start with the appropriate dose to quench any kind of information and then to prevent the pain. The pathophysiology is steroid use glaucoma. It's thought to be remodulation of the level of trapecular mesh work at the level of the angle. On a genetic level, some of the myosinol, which is also associated with dream-out opening of glaucoma, is thought to be up-regulated. Some studies have even demonstrated there's a mechanical aspect where parts of kinologue or parts of the individual injection can actually come in and clog the spectroglyphic. Within steroid glaucoma, it's about a third, a third, a third, a third, a third of mild responders less than six millimeters more curie, which is still could be 20% increase for that patient. A third of that to moderate responders and a third patients can actually increase more than 15 millimeters more curie. So presentation is very rarely less than two weeks, which is why we often bring patients back at a two-week interval to check for IOP. And usually, pressure can reduce, go back to baseline about a week or so after a steroid is applied. So there's some certain patient-dependent risk factors. How do you know glaucoma, able recession glaucoma, or family history even of glaucoma, are all known risk factors for people that might be high steroid responders. Myopia, diabetes, and connective tissue disorders are also associated, as well as children under six might be at higher risk of being strong steroid responders. Steroid-dependent risk factors include the type of steroid, the dose steroid, and the duration of use. So, example, being the first case where the region I've been using steroids for two years consecutively. Drug delivery has really, we have a lot of options besides topical. There are a lot of longer-term topical side, different types of formulations can alter permeability. For board's reasons, penicillin acetate is the best criminal presentation. Again, it's why it might be one of our more popular topicals. Again, some examples of the topicals of use, some being suspended formulations, which might, some patients might have difficulty using or might have a different response if they're not shaken or used appropriately. So, kind of a summary of potencies. Hydrocortisone is kind of the baseline, which things are compared against, but some of the lower potency medications include Vexol. But medium include the penicillin acetate which we use frequently and look critical, which has a nice profile in regards to its steroid response as well, with Vexol being one of our stronger medications. So, just as high risk, your risk kind of equals to reward. Steroids with higher potency also have higher elevating potential. Some good drops to kind of remember ethanol, that's all low-mix and L-rex are all great drops that have a lower risk of elevating high-rex. So, T-none's injections, such as our patient in the third case, have also been used as depots in different formulations and most somewhat recently been used for dropless cataract surgery in a postoperative steroid course as well. So, T-none, again, is a different kind of dosing, whether 20 milligrams or the smaller four milligram dose used in America, still has an elevation of IOP. About 40% of patients will markedly go, patients having a higher baseline IOP are at a higher risk of having elevation of IOP afterwards. And even though we think of sub-T-none's maybe not as invasive or low-standing, 2% of patients in this study that I reviewed required surgery to control their pressure. The spore trial is a well-known trial that used steroids in this manner, and patients we know that it helped with visual recovery, but also had higher rates of cataracts and higher rates of IOP From the study, IOP was elevated to report a 65% depending on the dose, and risk factors included younger age and higher baseline IOP. So, again, it is dosing as well. The Alginx implant has become more popular, and it's also brought more patients to our glaucoma service. And the last for about three months, I mean, the effects can even go into six months with elevation of pressure. And we'll talk about how to manage this. The Redister is also something that's been used to control long-term chronic intracular inflammation. It can last up to three years. Within this three-year period, which it works, 33% of patients end up having pressure over 30, which usually involves the treatment of glaucoma specialists. All this being said, the topicals, the systemic steroids can also have a major impact in IOP, not just oral, but also something like phlonies, where it's a topical intranesal that have been dealt to IOP. So there have been some thoughts about how to prevent or how to predict she might be a steroid responder before doing intravitral or any kind of more lasting steroids. Some physicians advocate doing a four-week trial of topical steroids to see if the patient is a steroid responder. And also, like most of you mentioned before, checking the IOP after two weeks of initiation of steroid is a good way to keep on top of it to see if the patient might be a steroid responder. So going back to our case, it's the first week of the actrogenic, the second week with still active inflammation, and for the long-term impact, we can kind of go through what their risk factors were and what we did for the treatment. So some of the treatments would be to stop the steroid. In the case of our second patient with active inflammation, the new alternative, we're about to switch this to INSAT or any other kind of immune-modulating if the effect is more systemic. Topical, it was the presence. SLT and ALT have been found to have a limited role. I think they may be tried, but they're not overrun in these cases. Filtrations surgery teams have all been used for the use directly electing, and two have been equal. And also, decision of any or a new role of any kind of the implant as well. So in the first case of our patient with adrogenic glaucoma, and this young guy at 19-years-old who had market cupping, and the response was due to an active steroid use. We thought it's stopping the steroid, we could stop the effect. So we don't really want to put hardware, and he was so young for a long time, so we went and ended up having to turn it to regularity. So in this case, this is a modified version, the GAP procedure, which is with the transimmumination. We've been doing this procedure where you create a goniatomy clasp here with an endear blade, create a little bit of space, and instead of using the transimmumination, you can use a 5-0 proline, which we'll show in a few seconds, which is blended with caudary to create somewhat of a mushroom cap that can be led around. So this really decreases the amount of equipment needed to be used for this procedure, and can make it a little bit more accessible. So the goal of this is also to treat where certain adduce glaucoma is really hitting. So this is the powder used to blend the proline to supply more liquid. You can see it creates kind of a mushroom-like cap. So I remember that the proline has fed through the trapeculomesh work and brought out to really work at the level of the trapeculomesh work, which is where the steroid glaucoma is really active at that level. So I'm in second case with a gentleman with active information due to high-potency steroid after carot surgery. We stopped the steroids, switched them to an NSAID, and put them on diamox. He ended up getting a trapeculectomy. And in our third patient with active CME, they've been treated with subtenance canal. She also ended up getting a trapeculectomy, and she's done really, really well. Something interesting about these patients with depots of steroids in the eye, when they're treated with trapeculectomy or with tubes, they often do really well because all of the intraocular inflammation, the things that we're combating to help with scarring are being treated already with the steroid. So that's one question to really kind of look into is whether or not to remove the steroid depot at the time of the filtration surgery, or whether or not to leave it to continue to treat intraocular inflammation. So case updates. The first young boy is now after the GAP procedure. Pressure 12 now off-drops, including steroids. And in second patient, vision still limited to the pheromosis, but pressure is now well controlled after the trapeculectomy. Off-all drops in the third. She can continue to have steroid treatment locally and avoid any systemic treatment for the CME while keeping her pressure. Some summary points. Just to start high in low, identify risk factors for possible steroid responders. She's serious carefully and be aware of that systemic bias. Thank you for everyone that helped with the care of these patients. A comment about dropless cataract surgery. It's been a big thing at most of our meetings. And David Chang likes to point out that in that in his experience, the patients that have the biggest spikes of dropless cataract surgery are in my opinion. So start to move in that direction. One of your slides that I'm sort of at the long have both a high potential and low potential for increase in intracrepressure. So is that after you might agree with this. So should be low.