 Okay, so I know a lot of you have places to get, so I'll talk fast, but it basically I'm going to show you two presentations of just kind of a stepwise latter approach to prescribing IMT. Now that we've seen kind of the complexity, and I'm going to show you two cases that are maybe on the most complex side of things that we see in the EVIS Clinic. Both of these are kind of pediatric or at least were originally pediatric cases. I have no financial disclosures. Like I said, two brief cases, basically both anterior and uveitis cases, and I'm going to highlight stepwise treatment algorithms specifically in these clinical settings so you guys get an idea of kind of how we do these things. So the first case is an eight-year-old healthy girl with bilateral idiopathic anterior granulomus uveitis. Workup was unremarkable. Visual acuity was 2025 when we first started seeing her. Pressure was 18 in the right, 33 in the left. She had been on long-term use of maloxicam for joint pain, prednisolone drops, and home atropine for quite a while before she was even referred to our uveitis clinic. When we saw her in clinic, she had capionodules 3 to 4 plus ac cell. We quickly discontinued the maloxicam, started an oral steroid taper to quell her inflammation rather quickly, also stopped and continued home atropine and prednisolone to the anterior chamber inflammation. This is actually a photograph from her clinical exam, there we go, with all these KP's here. You can't even appreciate the cell. So we're talking about a significant amount of inflammation despite pretty frequent use of prednisolone, even maloxicam. So then we, after starting the oral steroid taper, we did an infectious rule out to make sure this was infectious. Like I said, workup was unremarkable. So then we quickly added methotrexate, so then we could taper the steroids. Due to kind of multiple inflammatory bouts over the coming months, she required multiple re-initiations of oral steroid tapers and her vision continued to decline in the right eye despite our best efforts. Most of that was due to cataract development from persistent inflammation and topical steroids. So methotrexate was increased, there were compliance issues kind of scattered throughout this entire clinical encounter and then throughout this she starts developing band care topathy to kind of complicate matters with ongoing inflammation. So then she was started on humira in addition to methotrexate and we eventually got her inflammation controlled for long enough, where we felt at least long enough that we could actually undergo performing a par splint of the tractomy, cataract surgery with the PI, people who are in an academy, and post-herosiniculitis. She, within three months of that kind of complex surgery, she was already 20-40 uncorrected with no inflammation. I'll talk more about our specific perioperative regimen because I think that's important to discuss because these are fairly complex surgeries when we do step into them, but I'll show that at the end. So then the second case was maybe even more complex, maybe not necessarily just from an ocular standpoint, but from a systemic standpoint as well. So this 48-year-old lady had been diagnosed obviously many years prior with JIA and had been followed by Dr. Vitaly for quite some time, but then moved and was kind of lost, at least to us for six years, but had been fallen with an outside ophthalmologist when she was finally referred back to us. Her remarkable medical history was positive for JIA, and she's also HLA B-27 positive. She had had multiple ocular flares even prior to returning to us, and then what was documented in the referral letter back to us, she'd had cataract surgery in both eyes and a retinal detachment repair of the right eye. She was currently on simsio, which is an anti-TNF agent, when she was returned back to ARCARE and then had been on PRET forte four to five times a day in both eyes. Unfortunately, her joints were well controlled on simsio, but obviously her ocular inflammatory component was not under well control. She had previously been stopped when she was under ARCARE on methotrexate. She had had that stopped due to elevated liver enzymes. Remicade and Tosaluzumab had also failed to control joint inflammation, but it worked quite nicely for her ocular inflammation. So we've already gone through multiple agents at this point when she's referred back to us with light perception vision in the right eye, most of that's due to her retinal detachment, then 2100 in the left eye with a positive APD on the right, and then a plasmoid-like reaction with a 2 plus AC cell in the left. Pretty consistent with an HLA B27 flare and a pretty significant one at that. So she needed the full port, full-court press because she was monocular and had significant intraocular inflammation. So she was switched from PRET forte to Durazol. She received an STK at that point and was started on cell sept. And just to kind of highlight what we usually do in adults for cell sept, we started 500 twice a day for two weeks and an increase set to one gram twice a day. We're real fast. For those of us who are sore, what's STK? 17 ounce canalog. Sorry. You know, I'm just going to point out that we're getting to the point where we're using our own individual language and it's part of the, and it's not just us, I mean, in the sciences and other areas. And if you're not in on the lingo, I mean, we all know exactly where that is. I mean, I just hope you're going to be careful on some of these. Yes, the 17 ounce canalog. So basically a periocular steroid injection. Um, she then came back about a month later after that 17 ounce canalog injection pressure was fine. However, returned three months later with recurrent AC inflammation, CME, and subroutinal fluid, which you can see here on this OCT in the left eye was also complaining of significant amount of diarrhea. That was felt to be related to the cell sept. So both cell sept and simsia were stopped because they were not controlling intraocular inflammation. She started on Humira and Imaran, which is an anti metabolite and given an ozardex in the left eye due to this CME and subroutinal fluid. Despite these changes as well as increasing doses over the next several months, she continued to have both ocular and joint flares, despite, like I said, increased dosing. So Humira was eventually changed to another anti TNF agent that we heard about earlier, which did not control her joint disease, but seemed to be doing okay from an ocular standpoint. So that was discontinued and switched for rotuximab. She has been on rotuximab for the last five or six months and seems to be doing relatively well with resolution of CME, subroutinal fluid, and her significant ACM formation. So at least what are some of the pearls that we've heard about this morning that we can kind of glean from? What do we do with IMT? What do we do with EVitis cases? So I think the first and most important thing is to get an appropriate diagnosis so we can treat that. And so that requires both the, you know, full history and examination, and then a differential diagnosis of can't miss diagnoses. And I'll show here on the next slide and I'll mention it now. We always need to, you know, reconsider diagnoses if they're not kind of following what we would expect. And then the big important one before we start IMT, we didn't show anything related to this, but need to make sure we rule out infectious etiologies and I didn't even show that we were ruling that out prior to starting IMT and oral steroids in all these cases. Then we've kind of seen this through all the cases presented today, but anterior inflammation, at least for anterior UVitis, you know, topical steroids to treat the inflammation, then some sort of steroids. So whether that's oral steroids, subtenome kennelar, whether that's just typically topical steroids, any of those agents, if that doesn't work, then usually the next step is anti-metabolites with a steroid bridge, then plus or minus a T cell inhibitor like cyclosporine, then we've heard a lot about biologics this morning. And then something we rarely use, at least at this point, due to side effect profiles or alkylating agents. And that's kind of the stepwise approach we have in a UVitis clinic. Then the other important regard that we didn't kind of nail down that I briefly mentioned earlier was we tried to get at least three months of intraocular inflammation control prior to initiating surgery. Of course, there have been cases that I think my glaucoma colleagues know about that we weren't able to do that prior to needing emergent tubes recently. So there are cases where that's just not possible. Then judicious use of perioperative steroid tapers. I didn't discuss this with the first case, but she basically had one milligram per kilogram per day steroid taper around the actual surgery. And what we normally would do would be two days prior to surgery, and then five days post-stop, we do this one milligram per kilogram, and then every five days tapering that fairly quickly. So what would that look like in adults? So we would start at 60 milligrams for a day, seven total days of that, then we'd quickly go down to 40 for five days, 20 for five days, 10 milligrams for five days, and then stop to help quell the inflammation induced by the actual surgery. And then there are obviously some pitfalls that I've already kind of briefly mentioned. One, ruling out infectious ideologies. The second, undertreating inflammation. So kind of on the opposite sides of both spectrums. So infectious ideologies versus treating or undertreating auto inflammatory conditions. So I say go big or go home. So you really want to hit the inflammation hard early. Otherwise, you're going to see it recur and be back to where you were when you first started. And the other issue is tapering too fast. So you can taper too fast. Of course, on the other side of that, if you taper too slow, then you get, at least from perioperative or from oral steroids, you can get side effects from the oral steroids, which is what we've also heard about. So you're walking a fine line with all these agents. And then I've already mentioned this, but failure to reconsider original diagnoses. If things don't pan out as you would expect them to. And we've seen that recently, even in case yesterday, they were looking at in clinic. So it's something to always be reconsidering diagnoses as you're seeing these patients with complex histories. There's a lot of information. There's a lot of reading out there that you can go to to read further into IMT and doing these things. But I think the big thing is just making sure that you have a diagnosis that you're treating. And then there's a lot of images that have been shown today. But I think the biggest thing that we need to thank everyone for is specifically the patients and their families that have let us take care of their ocular health. And then the rest of the IAS team that lets me take part with their patients and their care of the patients and the imaging staff with all the great images that we've had. So I think, so okay, good. I talked fast enough that I don't think you guys are too late to your clinic, some surgeries and such. So thank you.