 So it looks like it's eight o'clock, so we'll go ahead and get started. For those of you who I haven't met, my name's Russell Swan, I'm one of the PGY-2s. I've been on our introducing our two Grand Rounds present tutors today. So first up is gonna be Lori Myers. She is a 14-met student that's joining us from Indiana. She went to undergrad at Indiana University. So she's one of my, as she coined it, one of my big tenemies in Nebraska. She's enjoyed her time here at Utah. She's worked with Dr. Crumb and Dr. Petty. And she's looking forward to her Grand Rounds presentation enormously, so without further ado, I'll let you go. Okay, good morning, everybody. Like Russell said, I'm gonna take my shoes off. Like Russell said, my name's Lori, and I am from Indiana. And I've had a great month here, and so in the true spirit of July in Utah, I'd like to talk about open globes. Just to give you an outline of what I'm gonna talk about, I'll present two cases. I'll give you the data up until post-op day four, and then at this time I'll pause to discuss something very rare, very elusive, very dangerous, and highly feared in ophthalmology. If you're sitting there hoping that I'm gonna talk about Bigfoot, you're wrong. He is elusive. Second guess might be this guy, but no, you're wrong again. I'm actually gonna talk about sympathetic ophthalmia. I'll go through it, and I'll end with prevention, and that'll bring us back to our two cases where I can go through the pros and cons of each treatment option and the outcomes. So case one is a 63-year-old male. He presented with trauma to his right eye after falling and hitting his face on a countertop. Unfortunately, he also has a past ocular history of keratoconus and a status post-bilateral PKPs in the 1980s. He also has a medical history of hypertension, hyperlipidemia, coronary artery disease, and an MI. So this is what he looked like when he presented to the Moran. Dr. Bell saw him. He had a right open globe. He had effectively extruded his vitreous, his lens, and part of his iris out through his pupil, and he had a right lower lid lack. To quote a famous ophthalmologist, "'We were literally looking through a hole "'at the slit lamp directly at the retina.' "'Then he vows salvage, "'and whatever was left came out "'with a large supercoeroidal hemorrhage.' And this is what it looked like, sorry if you had jelly this morning. But fortunately, Dr. Bell and Dr. Kinnerd were able to successfully close his lesion, and he was watertight at the end of the procedure. He was placed on standard post-operative medications, and we saw him post op day one. His pain was a six to seven out of 10. He was NLP in the right eye, but acuity was 20, 70 in the left. Pressures were 18 and 13. He had a right APD. His motions were full. On slit lamp, he had chemosis and subconch heme. His PKP was still in place though, and all 16 sutures were there, and his Psydel was negative. His AC was shallow and formed, and the iris was mostly absent, and then he had extensive supercoeroidal hemorrhage. I couldn't find the B scan to show you, but he had some diffuse intraocular debris. On day two, he complained of a headache, a seven out of 10, but he didn't have any pain in the actual eye. At this time, he began to endorse the depression and was NLP still. His pressures had increased to 24, and his Psydel was still negative. His AC was still formed, but he had this persistent coeroidal hemorrhage that was beginning to push up into his anterior chamber. So Dr. Kenner placed him on Bremonidine and referred him to low vision. We saw him one more time in post op day four. His pain had decreased to a four. He was still NLP. Thankfully, his vision and his left eye was improving, but he didn't have an AC in the right anymore. It was just basically blood showing up on the back of his graft. So here I'll pause and I'll switch over to our other case. This was a 33 year old male, and he presented after a firework injury. Happy Fourth of July. I don't have pre-op photos, but he did have a 12 o'clock to six o'clock corneal scleral limbal area laceration that was successfully repaired. Unfortunately, he had a posteriorly extending laceration that was unable to be completely closed. Again, standard post op medications. We saw him in Plastics Clinic on day four, and he had pain with movement of the right eye. His pain was a three. He was NLP in 2020 in the left, and he was also depressed. He had such severe lididema that he was having a mechanical ptosis. He also had chemosis and subconge hemorrhage, and his AC was just disorganized and filled with blood product. So again, I'll pause. Just to review, we have two gentlemen with trauma to their globe. They underwent high quality repair, the best that the surgeons could do here at the Moran. And then they're faced with this decision to either observe that eye to eviscerate or to enucleate, and part of the reason we have to talk about this is for sympathetic ophthalmia. So what is it? It's a rare bilateral diffuse granulomatous non-necrotizing uveitis, and it's developed after surgical or accidental trauma to the exciting or inciting eye, you can call it either one. It's thought to be T-cell mediated, and it doesn't show a predilection towards any particular age, sex, or race. But it does seem to have a genetic predisposition. At this time, the most common attributable cause is ophthalmologists. So everyone sitting in the room might be responsible one day for this, but it's especially with vitreo-retinal surgery. The etiology is not exactly known, however, one of the more common theories is a cell mediated response to retinal photoreceptor antigens. You'll hear more about this S-antigen that when induced into models, it shows a uveo-retinitis. You also might hear of melanin being the cause, and when it's used to induce uveitis in animal models, you'll see inflammation in more of a spatially correct area, so the iraciliary body in the chloride. However, when you look at patients with sympathetic ophthalmia, they don't all have anti-S-antigen antibodies, so that's not a perfect explanation either. My favorite theory, just because I find it the most interesting, is this lymphatic drainage theory. So in an intact eye, intraocular antigens go straight to the bloodstream and to the spleen. However, if you damage the eye and expose uveal antigens to the conjunctival drainage system, it's routed through regional nodes, and you can have kind of a possible pathologic response there. And then lastly, there's this adjuvant theory that there might be an additional infectious component that causes a local upregulation of inflammation, but no specific bacteria or virus has been consistently isolated. So I like to think about what the patient's gonna ask me. They're gonna say, doc, chances of getting this. You can tell them, one in 3.3 million. It was previously thought to be more common, but as the epidemiology's changing, we're seeing less military-related trauma to the eye, and we're seeing an increase in intraocular surgery. So this is a number that's probably gonna continue to change and be debatable. And also it's important to note that non-penetrating injury can cause sympathetic ophthalmia, such as YAG or proton beam radiation. When will it show up? So you can tell them anywhere from a week to 66 years, and that probably won't be a satisfactory answer. I like 90% within one year a little better. What should you be looking for? The patients can look for photophobia. They can look for near-vision changes, and they might just show up with a red eye as well. More importantly, what should we look for as ophthalmologists? Your anterior exam, they might have an increase in pressure or a decrease in pressure, depending on if they have a trabeculitis or their ciliary body is shut down. They can also have kind of a fat-looking iris from the lymphocytes infiltrating, and then later in the disease, kind of more of a chronic severe finding will be posterior synechii or mutant fat KPs. On the posterior exam, early in the disease, they'll show up with optic disswelling or an exudative retinal detachment, and then kind of the board's buzz phrase thing they talk about in the posterior exam are these Daelin-Fuchs nodules, and these are just gonna look like, you can see the little arrows, they're gonna look like little yellow-white clusters located sub-RPE or even sub-neuro-sensory retina. If you're interested in histology, what happens is it starts out with RPE hyperplasia, and then you'll have macrophages moving into the area and kind of an epithelioid type cell, and then later in the disease process, you get these lymphocytes down low, so you can see the purple vandal lymphocytes and then the blue arrows are pointing to macrophages. They can vary very late in the disease course, even rupture. So if you do it FA on these patients, you might see areas early in the phase of hyperfluorescence and hypofluorescence. The hyperfluorescent areas are from vessel leak from local inflammation, and then the hypofluorescent areas should correlate with the Daeland-Fuchs nodules. So I was interested, because I hear this guy's name a lot, who is Ernest Fuchs. He's actually an Austrian ophthalmologist known for these pathologies and many more. He made significant contributions to sympathetic ophthalmia, and he also wrote a textbook that was known as the Bible of Ophthalmology for over 50 years. He would fit in quite well here at Utah. He was an avid mountaineer and an international teacher, and I read a story where he went to Scandinavia to teach and he brought back what they were calling snowshoes at the time, and he effectively introduced skiing to Austria, so he's an interesting guy, very handsome. Make sure you include on your differential, TB, sarcoid, syphilis, and fungi. You also wanna think about inophthalmitis, lens-associated uveitis, and definitely, definitely VKH syndrome. Treatment will be systemic steroids for at least three months, and then you can taper them down. If you have a patient that won't tolerate systemics, you can try steroids bearing medications like methotrexate or cyclosporine. You can also try intravitrile medication, or steroids, excuse me. For the anterior uveitis, you can do cycloplegics or migreatic agents, and then for recurrences in the CME that will inevitably develop, you can give periocular steroids. So these patients are gonna be in your office for a long time, and they're gonna be there frequently. They can have loss of vision and tycis ball by if left untreated. However, with prompt aggressive therapy, 60% will return to 2040. Unfortunately, 25% may still become legally blind in the sympathizing eye. Other complications are neobascularization. You can have optic atrophy, cataracts, glaucoma, CME, and rarely you can have extraocular symptoms like hearing loss and vitiligo, which makes sympathetic ophthalmia even harder to distinguish from VKH. So back to prevention. Number one, and this isn't debated at all, is you need to properly close that initial penetrating injury. And number two, which is a little more debatable, is whether to have surgery or to observe these patients, and that brings us back to this decision tree. So the pros of observation are that the majority of eyes, if you leave them, will not require a nucleation just for pain. You'll also have a better cosmetic result. You can send them to an ocularist and they can fit them with a scleral shell and they'll have great motility. And there's this psychological benefit that often I think people forget is that the patient will get to keep their own eye. Another important thing to think about is visual acuity in the exciting eye may actually end up better than visual acuity in the sympathizing eye. Cons, of course, are you still have your risk of sympathetic ophthalmia, you could have continued pain, and you could have a tisical eye. If you decide to enucleate them, you do reduce the risk of sympathetic ophthalmia, and you may improve pain. However, you're gonna put your patient under general anesthesia, they can have damage from the litter attractors, they can have complications from the orbital implant, such as migration, they can pop out, they can cause pain or erosion over the implant. Invisceration, you'll have less disruption over the orbital anatomy, you'll have good end prosthetic motility, good cosmesis, it's less invasive, you can use a MAC, and you may have lower rates of migration or extrusion of the implant. Cons are you can miss uveal contents, and you can still have implant complications. So the trend right now when it comes to surgery is to eviscerate over a nucleic. Theoretically, evisceration could cause sympathetic ophthalmia. However, two different studies have shown that that's very rare, and in the last decade, they've only seen two cases of it. So your patient's probably gonna ask you, what if my vision returns? You can tell them two studies where patients were NLP prior to primary closure showed that about 70% of patients remain NLP. And I think the follow up on these studies was pretty good. It was definitely months, maybe even years, I can't remember. Something associated with a poor post-operative outcome is a zone three injury, which for those unfamiliar, zone three is more than five millimeters outside of the limbus, so that red area. So back to our cases, we have our 63 year old male. He's very likely to remain NLP. He had good closure of his defect. Something I didn't mention in the ED presented, he had low O2 saturation, he does have a history of coronary artery disease, and he does have difficulty with induction, so we need to consider that when thinking about anesthesia. His pain does appear to be improving, it went from a six to a seven down to a four. And when I saw him the first time, his wife was crying, he was very distraught, even at the thought of referral for abisceration. So that's also something to consider as just your patient's psychological status. So after consultation with Dr. Crumb, he decided not to have surgery. Patient two, he had zone three trauma. Remember that posteriorly extending laceration that we couldn't close. And he's at high risk for infection and remaining NLP. So after talking with Dr. Crumb and the team, he agreed to proceed with enaggliation. That happened 10 days after his initial injury. He underwent the surgery successfully, had a 22 millimeter implant, and his muscles were attached anteriorly. So here's a picture of him post-op. Here's a zoomed in version. He's having trouble opening that eye, but he still has a lot of swelling causing atosis. And when we help him, you can see that he has the conformer in place and he's doing quite well. And here's a video. So this is just to show you his motility. And this is even with enaggliation. We're telling him to look right, look left, look up and look down. And then he'll do that again. Okay, just some take home points. Surgical prevention of sympathetic ophthalmia is still very controversial and it should be regardless of what you'd prefer as a provider, it should be a careful discussion with your patient. Remember to consider factors other than the risk of sympathetic ophthalmia, like risk of anesthesia, the quality of the initial repair, pain, cosmesis, the psychology of an ophthalmia, and even the referral to a plastic surgeon for an anophthalmic discussion. And also lastly, have a high suspicion for sympathetic ophthalmia in patients that show up with bilateral UVitis after ocular trauma, ocular surgery, and even after non-penetrating ocular injury. These are my sources. There was a really good review article published recently this year. If you're interested, I can let you know about it. And then I'd like to thank Dr. Olson and the Moran. I've had a great month. Everyone's been very nice to me when I get lost or need into the locker room. Drs. Krum and Petty were my mentors. Drs. Adesha and Kinnerd, Dr. Bell, Dr. Swan and definitely Alicia. And here's the picture of me when I went to, I got crazy and got up at 4 a.m. and drove to Moab in one day. But it was worth it. And then just a little fact, I like to just draw, so here I am trying to draw the arch. So at that time, or at this time, I'll take questions. I believe so, yes. One week to 66 years, it can show up, but then they recommend a nucleation within 10 days. So there's it. I'm glad to see you're ready. I'm not. I'm not. Why am I? There are papers from the 70s where after trauma, it is 0.2 to 0.5%. But after surgery, it's 0.02%. That's the best data I could find. I didn't see any data specific to supercordial hemorrhage, no. Yes. For trauma, it was 0.2 to 0.5%. Yes, this is so very rare, right? And Dr. Petty did refer patient number one to Dr. Ward. So, yeah. Oh, actually both of them. Okay, great. Thank you.