 We're going to turn it over to Brayden Murdoch from George Washington, in the case of PICC. Okay, so as was mentioned, my name is Brayden Murdoch, coming from George Washington University, going to present a patient who came in with PICC, punctate intercordopathy. So for the patient, she was a 33-year-old, previously healthy female who came in with this light spot in her central vision that had been going on for two weeks. Initially, she had been seen by an outside provider who would refer her in, and she said that this light spot had persisted with some photophobia and just general eye discomfort, but otherwise, tonight, any pain, swelling, topsy is headaches, floaters, or other visual distortions. So for her, kind of just a timeline for her initial presentation to provider was about a week after the symptoms started. At that point, they did some imaging. Unfortunately, we do not have that imaging at this time, so I'm just going to kind of describe what we looked at from the patient's phone. MAC-OCT was performed showing a PED template of the phobia with some subretinal fluid. Color photos of the left eye also showed some ovoid yellow, hazy region in the same region, as well as on the FA, there were these two hyperfluorescent lesions in the laminar phase of this left eye. So at that time, this macular lesion, kind of unknown etiology, they started Bactrim DS for what they suspected was possibly an infectious cause, and they asked her to come back in a week. So at a week's time, she followed up, had additional imaging. Color photos showed these new punctate lesions in the temporal region from the macula, as well as on the FA. She had many punctate, hyperfluorescent spots, temporal to the macula, which was changed from before, so there was some concern that the Bactrim wasn't working and this might be something else. So she was actually referred here for an evaluation for a possible multifocal coriditis or another white dot syndrome. So when she initially presented to us the past medical history, ocular history, and social history, it was really non-contributory. One exam, really the only finding we had from her visual cutie was that the left was a little bit worse than the right, but she didn't have any correction, so that'll be important later. Otherwise, pressure ocular movements were normal. On the slimpy exam was notable for vitreous cell, rare vitreous cell in the left eye, right eye being normal. Left eye also noted in the macula those same yellowish spots that were noted before by the outside provider. A couple of those in the temporal region from the macula. So we had imaging done at that time and I will preface that by saying that she was actually outside of the network, so we didn't perform all the imaging that we would have liked to because she was paying out of pocket for these imaging studies. But from what we did ascertain, we had FAA, autofluorescence and OCT performed. As we can see here on the left, it's a little bit difficult on the projector there, but there's these punctate lesions kind of spanning temporally to the macula that are kind of limited by the superior and inferior arcades. On the OCT on the right there, we can see, looks like the PED is actually increasing size from what we were able to see from her phone record, as well as we have this sub-RPE accumulation and this overlying heterogeneous hyperreflective substance that's possible SRF, temporal to the macula there with some disruption of the ISOS junction. So OCT is pretty similar to the autofluorescence that we saw before with those punctate lesions in the same distribution. So for her the assessment and plan, so with her presentation and worsening with the backdrop basically not being helped in any regard, the differential was pretty broad. A lot of the posterior uveidities were considered, especially since you didn't have any anterior inflammation or intermediate signs of inflammation. We did also consider like a sarcoidosis or an autoimmune cause to this. At that time with the OCT imaging, the thing we were most concerned about was this PED and CNVM in the left eye. So we thought that this was probably most likely secondary to inflammation, although we did also consider other causes of the CNVM. In her age group myopia would be a common cause, trauma and macular degeneration in an older patient. So those really didn't fit the bill for her. So we decided to proceed with anti-vegeth therapy. So ILA was given in office. Steroids were considered, but we wanted to rule out any infectious cause. And then immunomodulation therapy was also considered if this were to progress or recur in that same eye or spread to the other eye, we would consider it more. She was told the follow-up in a week. And we had etiology work up, which is basically the lab work that we do for common causes of uveitis, including sarcoid, TB, syphilis, toxo, CBC, and CMP just to complete that. So she returned about a week later, a few days later, and her vision was a little bit more distorted than before. After finishing her antibiotic course, otherwise her exam was stable, no imaging was performed at that time. All of her lab work had come back completely normal. So we felt confident at this point to initiate P.O. steroid therapy to see if we could help improve her symptoms. Of note, we were interested in doing an Osrodex implantation, but due to her out-of-network status, cost-prohibited nature of Osrodex we considered, we continued with the P.O. steroid therapy. So we had her come back in a week to look at things, and this is the imaging at that point. So the auto fluorescence is a little bit difficult to tell, but there is some resolution to those punctate lesions. Most starkly, what we can see significant from the OCT is there is a great regression of that edema and flattening of that PED. Unfortunately, at that time her vision was basically the same as it was. So there's probably some residual fibrosis, maybe even some changes there that were affecting her vision. So that was actually the most recently that we saw her. She's a patient currently followed, so we'll be seeing her in a few weeks to kind of evaluate her further. So I wanted to talk about PIC, which I was completely new to the world of uveitis from this rotation, and it's a world that is just completely fascinating to me. So PIC is one of the most rare of the posterior uveidities. It was first described in 1984 in 10 myopic females who were really noted for blurred central vision, photopsia, paracentral scatoma, and this yellow-gray lesion kind of in the same distribution. Incidents is an estimated 1.6 in a million. The data is super sparse as far as how they're actually able to recognize patients with this disease. So it's likely that it's more common than this, but this is what's on the books. As far as pathogenesis, the main thing that's been proposed that this is like an autoimmune response to some polygenic environmental stimulation, be it anything from infection, immunization, to stress. Common clinical presentations is basically what I presented here today, healthy, although our patient was not myopic, Caucasian females in their 30s, with this scatoma blurred vision, and then the other things that are mentioned there, metamorphosis. So the diagnosis is really difficult because it's kind of a diagnosis of exclusion. Imaging is helpful, but it's not going to cinch the diagnosis for us. I'm not gonna really delve into the findings at this time, but I do wanna explain that ICG is actually probably one of the more helpful diagnostic features as this pathology occurs at the RPE junction. So we do see that on ICG as it illuminates the coroid. So that would probably be the most helpful for us in diagnosing this disease, although that wasn't performed at this time. OCT may also help support the diagnosis as well as the treatment and management for a lot of these patients who have CNVM that can be treated and improve visual outcomes. And then of note as well, I can't go on without saying that flio imaging is also being studied. Actually here at the Moran, there was an Arbor presentation by one of the residents I hear, Dr. Gensher, who basically looked at flio imaging to evaluate active lesions versus inactive lesions and possible response to therapy. So I think that's probably gonna be the future. I wanted to present more about the time constraints as such. So treatment, it ranges, and it kind of depends on the patient's presentation. Obviously with our patient being so close to the phobia, we wanted to implement treatment quickly. But in a lot of patients, observation is perfectly fine. Depending on their response to treatment, it may be, like I mentioned, with anti-veg F or immunomodulation and steroid therapy. And there's some mixed literature about what's been done and what's been effective. So I think a lot of more information needs to be had on that and research with that. And then as far as the clinical course, it does, without CNVM, the visual QD and visual response is actually quite good in this disease. I wanted to mention probably the most important thing from this is there's a lot of things that can be similar to PIC in presentation. Things that are really big takeaways from PIC is that there is no vitritis. So it is like this posterior inflammation that doesn't have intermittent or anterior inflammation. It does involve the choreo-retinal layers with these small lesions, which is different from other pathology. And it's strictly limited to the posterior pole. And there is scarring and CNVM versus other diseases like muses, which don't have that. So that is my presentation there. They're my references and special thanks to my preceptor, Dr. Mercer Luchel and Jim Gilman and Glenn Jenkins for their imaging. Thank you.