 Okay, thank you very much. All right, hello, my name's Christina Lippi, I'm a fourth year medical student from Penn State College of Medicine, located in Hershey, Pennsylvania, which actually happens to be my hometown as well. Has anyone here ever been to Hershey, Pennsylvania? Yeah, okay, good. All right, so for those of you that haven't been to Hershey, Pennsylvania, I just want to let you know that the rumors are true. The street lights are shaped like Hershey kisses. Oh, it's not working, how did you make those? It doesn't, you have to advance with the arrow. Oh, okay. All right, well, like I said. I am using that one. Okay, there we go. So the street lights are shaped like Hershey kisses, both wrapped and unwrapped. The town does smell like chocolate. They're not made of chocolate. The town does smell like chocolate and it really is the sweetest place on earth. So this is the graduating class last year for Penn State College of Medicine. So anyways, you guys should come to Hershey if you haven't already. So my talk today is called bilateral acute angle cloture glaucoma due to oral acetylzolomide. And we'll begin with the case. The 63-year-old female presented to a clinic at Ecuador with chief complaints of dizziness, foggy vision, bilateral ocular pain and nausea. Her history of present illness, she's currently traveling to the Galapagos Islands with stops in Peru, Machu Pichu, and Ecuador. Before she went on her trip, she went to a local travel clinic where the physician there prescribed her oral acetylzolomide for altitude sickness prophylaxis. She was instructed to start taking it three days before her trip, which she has. And then on the seventh day, she started to feel dizzy on this treatment. And within the next couple hours, her vision deteriorated to a white fog and she developed bilateral ocular pain and nausea. So her past medical history is significant for hypothyroidism, hyperlipidemia, and osteopenia. She only, her only ocular history is, she has myopia. Her family history is unknown. Her social history was unknown. And the only medications she was on was syndestatin, synthroid, calcium, femur, and reclast. So they did an exam and they found that her intraocular pressure on the right was 61 and on the left it was 52. Her split-lamping exam showed bilateral oscillary congestion, anterior chamber shallowing, corneal edema, unresponsive pupil, and visual, diffuse visual defects, deficits. So they diagnosed her with bilateral acute angloclosure glaucoma. For treatment, they gave her bilateral laser urodotomies. They also gave her IV mannitol and oral osteodazolamide in order to try to decrease the intraocular pressure. They gave her parent's etymol, which is an analgesic, so try to decrease her pain. They gave her timolol and dozolamide drops to try to decrease the intraocular pressure. They gave her pylocarpene drops in order to try to constrict the pupil and break the acute angloclosure attack. They also gave her penicillin acetate, 1% drops in order to try to decrease the inflammation, and they admitted her to the local hospital. So over the next couple of days, and even after all this treatment, she did not get better. She still had really shallow anterior chamber angles and she also still had really high pressure. So they advised her to come back home for further treatment. So she came back to Hershey, Pennsylvania, where she came to the Penn State Hershey Eye Clinic. And here her intraocular pressure had decreased, the right and the left, it was known to be 10. Her visual acuity was 20, 25 in the right and 20, 20 in the left. Her slant limb exam still showed shallow anterior chambers in both eyes, and her gonoscopy exam showed narrows that were barely open to the regular menstruate. So at Penn State Eye Center, we diagnosed her with sulfonamide-induced bilateral acute angloclosure glaucoma. So for treatment, we told her to discontinue her orocytosolamide and stopped her topical timolol and dozolamide drops. We had her continue on her Prandisolone acetate four times a day. We advised her to avoid ozolamide on all and all other sulfon medications. And then we had her follow-ups weekly and monthly and to see if she returned to her baseline. And on subsequent exams, her visual acuity did come back to baseline. She did develop her normal intraocular pressure and she had deepening of her anterior chamber with wide open angles on gonoscopy. So the patient, yes, sorry. Was she still on endoscopy in this year? No, sorry, we stopped that too. What part of the program did you stop? I'm not quite sure. So I think it was probably stopped at the same time because I'm not quite sure the answer to that because I'm not exactly sure of the timeline of when each of the medications were stopped. I just know that our treatment was to continue her Prandisolone and to stop everything else. So I'm actually not quite sure. I think our thinking was the fact that she wasn't on pylocarbon initially when all this started. So in looking at all her other medications that she's current, she was on, the only thing that really was added was the orocytosolamide. So that's the reason why we kind of thought of it. Okay, so now I'm gonna talk about acute-angle closure glaucoma a little bit. And as you know, it's an ocular emergency. If a patient comes in with acute-angle closure glaucoma, you need to immediately figure out what is the cause of it and how to treat it. Because if you don't, the patient will develop complications and therefore will have things like decreased visual acuity. So acute-angle closure glaucoma can be due to a primary process or a secondary process. So a primary process is like if you had a predisposition to angle closure, which means, for example, you might have pre-existing anatomy that causes shallow angles. It could also be due to a secondary process such as medications, as in this case, emotional stress and dim line. And depending on what's causing the acute-angle closure glaucoma, the treatment differs. So I'm gonna talk about the pathophysiology. So with ocytosolamide induced acute-angle closure glaucoma, what happens is the sole of one of my group is president. And this causes ciliary body edema, uveal fusions and anterior coroial fusions. This then leads to an anterior lateral rotation of the ciliary body, which then causes an anterior displacement of the iris lens diaphragm. And then the displacement of the iris lens diaphragm causes the shallow end of the anterior chamber and therefore angle closure and therefore acute-angle closure glaucoma. But with primary induced acute-angle closure glaucoma, the pathophysiology is different. It starts with pupillary block. And from the pupillary block, then prevents the aqueous humor from flowing between the posterior iris surface and the lens. And this resistance then causes a buildup of aqueous humor causing the bowing of the iris anteriorly and then causes the angle closure, leading to angle closure glaucoma. So the pathophysiologies are different, but the clinical presentation of both of these are very, very similar. So both soft-induced and primary-anchor closure glaucoma, the patient will come in with like red eyes, nausea, and bilateral-ocular pain. On exam, you will see in both cases a bowed iris anteriorly. You'll see a shallow anterior chamber and you'll also see narrow angles on gonoscopy. So basically the physical exam is the same. The only really difference is that the soft-induced acute-angle closure glaucoma is presented bilaterally in both eyes. Well usually in most cases of primary acute-angle closure glaucoma is basically unilateral. So if a patient comes in with acute-angle closure glaucoma into the emergency room, the physician wants to notice if it's bilateral or unilateral and it might give him idea what the etiology is. So overall it's a bilateral presentation that will help the physicians determine that it might be a soft-induced acute-angle closure glaucoma. The bilateral presentation is what's key. So the pathophysiologies are different and also the treatment's different. So in primary acute-angle closure glaucoma, you wanna treat with myotics. So you wanna constrict the people. You can also treat with carbonic and hydrogen inhibitors to decrease the interocular pressure. And you also wanna treat with peripheral aerodonomies in order to create a communication between the anterior and posterior chambers to allow the flow of acute tumor. But with sulfonamide-induced acute-angle closure glaucoma, the treatment's different. The main thing you wanna do is you wanna discontinue the inciting agent. So you wanna stop that. You can also treat with midgeriatics. So the midgeriatics actually causes some silly body, it causes the ciliary body to relax and it also rotates the lens iris diaphragm posteriorly. If you remember when I showed the pathophysiology, the sulfonamide causes the iris lens diaphragm to go anteriorly so the midgeriatics can counteract this and bring it back posteriorly and help break the attack. With sulfonamide-induced acute-angle closure glaucoma, you also don't wanna give myotics. They actually increase ciliary body swelling and worsen the angle closure. So if you remember how we treated this patient, the main thing we do is we stopped the inciting agent. We stopped the acetylamide. And we gave her penicillin to decrease inflammation. We did not give her midgeriatics. We felt like she was on the mend and she was already breaking her attack so we didn't think it was necessary to add another medication. We kinda just wanted to take everything away. So the importance of this case is it shows that acute-angle closure glaucoma can be induced with just a low dose prophylaxis of altitude sickness, a low dose of acetylamide for prophylaxis of altitude sickness, which hadn't been described before so that was a very interesting part of this case. The other thing that this case highlights is it really emphasizes the difference in the pathophysiologies between the primary and sulfa induced acute-angle closure glaucoma, which is really important because if you don't understand why the patient's having acute-angle closure glaucoma, you're not gonna be able to treat them correctly. And if you can't treat the patient correctly, they can have complications from acute-angle closure glaucoma. So these are my references. Anyone have any questions? And to be out here now, I need to invest in the patient. I just wanna see another drug that we're gonna do just to hear me. Well, thank you. Thank you. The last thing I just wanna add is that after I'm done here, I'm actually going to Ghana with Unite for Sight. And I know a lot of people have done international stuff or been to Ghana and stuff like that. So if you have any advice for me, it's my first trip over. So if you have any advice, any stories, or anything you wanna share, tell me out and prepare me. Here's my email. So I'd really appreciate any feedback. Just be really careful about what you need. Okay, that's what I'm told. Okay, I won't keep that in mind. Make sure you get all your prophylaxis and tell them you're perfect. Yes, I have that. They're not perfect. Yeah, so it's serious stuff. I don't mind, I'm gonna send one over and you end up getting it. You should get all that. You're so serious. I don't have the right question. Okay, I won't keep that in mind. I'll just share it. Okay. I've sent a lot of people in and find it. Okay. Listen to what they said. Okay, good. Thank you. Thanks, everybody.