 Okay, I'm Stuart Walther. I've met a couple of you with my time here, but we'll talk about a pretty common thing we see in practice of all of you, C and B retinitis, but this patient that I'm going to talk about in particular is a little more interesting because in this age when a lot of patients are taking their anti-gredge viral medications, we don't see quite as advanced pathologies or presentations. Normally we can sort of hold this disease a day, if you will. So we'll start off a long time here in the beginning back in June of 2009 when this gentleman was hospitalized for disseminated histoplasmosis and he had a positive CMV PCR. However, you'll see this trend with the patient, but he reports no decrease in visual acuity. But the general medicine doctor follows a good idea to have him referred over to us to take a look at him. And then when the initial exam was done, the point I'm going to look at the most is we got an alternational status and it made it pretty difficult to evaluate, at least, technically, what he's telling us. The visual acuity then receives 2100, 2070. It was difficult, unreliable. The rest of his exam was fairly normal. And then we could see these pigmentary changes, atrophicative changes. It's retinal whitening. Look in the superior temporal region. His left eye was normal. So while he was still hospitalized, he got two injections of a Fosconet and he was began on an induction dose of valcyte. During the hospitalization, he improved his he's actually having seizures for the list of blood vessels. His clinical condition improved and when he was discharged, he didn't start to follow with us about a week. So when we first saw him, way by then, he's, what do you expect? He has some blurry vision. We have his history of injections. He was, at this point in time, at least taking pretty much all the medications he should be taking for having HIV. So he was on a retroviral, anti-retroviral therapy. He was taking a bunch of antibiotics for prophylaxis. His visual acuity, you know, is a lot better now. I don't know if this is because some of it was the ability to obtain correct answers when he was hospitalized, or if this is actual proof of the injections. The rest of what we see is just a pretty normal, except for he has these, we've got to have this deficit in front of his LOD. This little lamp, he has a tracel, anterior interest, and no other abnormal findings. So here's our picture we got from that day. Is that really dark in there? Okay, well at least we can see there's some whitening up here. Probably a lot of lesion. There's a some, you can see this like necrotic retina back here and this sort of scar. Yeah, it's really dark. Hopefully some of the pictures look a little better. But if we could see this at all, his left eye is still pretty normal. So here's a little more of a close-up shot. But this is still, it's still an active eye, and he's gonna receive another injection. This is sort of a mystery picture, I guess. Okay, so he's got a lot of clinical visits now. He comes back. His vision was stable in a one-week follow-up, and he did not receive an injection. Then 10 days later, he's very blurry, no improvement. He's saying he has some floaters, and he's actually reporting some pain, which is a pretty rare finding for CMV or anitis. But we can see, at least here, he does have a decrease in visual acuity, and we'll look at these photos in a second, but he would have gone on another injection to try to pull back. This disease is a little dark, but so we can see that this area on the previous photo was actually a little more, there was a little more of this white scar tissue or an active lesion. And this photo, I think the next photo, we have a closer shot of this. It's the borders a little bit more defined. It's a little bit sharper edge. He's looking like he's improving a little bit still. We did see that decrease in vision, so it's concerning. Right, so here's our close-up shot. We can see the white lesion here, the white enema retina, some necrotic retina, and then there's no hemorrhages in this one, which in the second photo I showed you, there was originally. And OCT, so we can only see the color part on here. He's got a lot of swallowing, this is really thick right here in the macula, and he's got some cystic changes in here. But he's still got sort of a normal curvature of the macula, so considering the amount of swallowing he's got going on, his visual acuity is okay. So we continue to follow him. His visual acuity improves here. If it's another steroid, are we considering a steroid shot because of this, the deem we saw, but with the HIV, and he had a really low CD4 count, you're concerned about giving someone steroids. So then we check the CD4 count. Patient's supposed to come back in a couple more days. He does. We see that he's got a pretty drastic improvement in his vision here. And then, you know, CD4 counts a little low to be injecting steroids, but his eye is starting to look pretty quiet. Looks like the medication and everything are actually doing pretty good at controlling this. I apologize again for how dark these pictures are being, but compared to the last close-up picture we saw in this area, you can see that there's even less patent of areas here. It's more of like sort of some consolidated pigmentary changes and why Legion-Made is just scar tissue formation now, which is sort of what you find in an inactive form of C of E. And then, as we can see in the bottom after this, our patient instead of deciding to follow up, he just sort of disappeared. So in the interlude between him showing back up in clinic, we'll talk a little about C of E. For our basic science fulfillment, we'll talk it instead. It's a double-stranded DNA virus in the herpes family. It replicates in lots of cells in the body, particularly fibroblasts and FDO cells and macrophages. And it's, you know, after the first act of infection remains late in our body, like all herpes viruses, but mostly T cells and macrophages on the bone marrow. I didn't say interesting disease in that when you're an adolescent, only about 14, 20% of the people have it. And as we move on into our adulthood, between 50 and 85% of us have by the age of 40, it's transmitted by pretty much any fluid coming out of our bodies. And it can cause a really broad spectrum of diseases. Something we always remember is the neonatal problems if you have an active C of E infection in a mother. So we can get some octagonal problems there with the corioretinitis, sensual neural hair loss, really bad disease there as well. Then what we normally hear about now is with immunocompromised patients where it causes anything from pneumonia to encephalitis to colitis. In our particular situation, we're going to talk about the retinitis. So it's the most commonly, it's the most common cause of a viral necrotizing retinitis and get immunocompromised patients, HIV patients. If it's untreated, it's going to progress to visual loss and blindness. And if you're seeing this, it's almost a sign of their immune status. If it's an active lesion, their CD4 count is almost always less than 50. And before the advent of our current retroviral therapy, there was sort of a telltale sign that this was the end of your course with HIV AIDS. You're going to like to take about six weeks after diagnosis. So the important part for the people who are doing our triage clinic right now and as those younger students and residents is the symptoms. These people, a lot of times you're just going to have maybe some scatoma or a decrease in vision. Most commonly one eye as opposed to both. And pain and photophobia are very common. So the fact that he was having some pain as I was a little bit abnormal, but that did decrease. And often this infection is just asymptomatic and you know, someone's receiving good care that he's finding to be found before there is a visual impairment. So in the physical exam, it's like everything we do. It's important to do a full exam, not just focus on the retina because you might find signs that lead you towards other diagnosis like lymphoma or Kaposi's. So what you're going to see is hopefully a quiet eye. In the cornea, you can find some stelae, keratidic precipitates. Also, there's rare times that you'll see a UVitis with this. And then we'll talk, you know, just sort of about the different forms of different appearances. So this indolent form, the slowest form, is this granular opacities, saline regions, and occasional hemorrhages. And I think that's sort of what we were seeing in the about the third photo after you've been receiving some treatment where there was these granular changes, but it wasn't this is full on the formative disease like we'll see later. And then this formative form, we have a great way of remembering it. It's a cheese pizza type appearance, the retina. You get these large areas of the chronic retina and white fluffy infiltrates scattered with hemorrhages around the vasculature. And it's important to think that this is something that can progress very rapidly, so I always want to follow it quickly. And after if you successfully treat this, your resolution, you're going to look for just as a RPHV in Pigmateric Plumping. So let's sort of look at a couple of these. Well, as further it goes to this stage of this. So like I said, there's the active regions, which is hemorrhagic, large areas of hemorrhage, background, white and retina. Then there's a brush fire variant, which if you, I guess you've seen maybe if you watch the California wildfires on something in news, it makes it a little easier to visualize, but you'll see a like a yellow white margin that's moving from the periphery normally towards the center. Behind it is a sort of burnt-out atrophic retina. And then the granular form, which is these small white legions with pigment changes in the caudal stage, right, as the end result. So the zones of involvement are important for thinking about how threatening this is. So if it's in zone one, which is 1,500 micrometers from the disc, or about 3,000 micrometers from a fovea, this is something that's immediately visually threatening. We definitely want to start treating this patient, you know, with a very close supervision. And then zone two and three, zone two is from the border zone one, out to the equator basically. It's not immediately visual threatening. And then zone three is from this sort of imaginary circle, connecting the ampoule of vortex veins to the aura. So this is sort of all the semantics classification of what it is. So here we have our actual pictures. These are a little bit a little bit easier to see. But here's sort of the edge of this brush fire with active diseases moving. And behind it you can see there's the sort of burnt-out atrophic retina. The hemorrhagic one, I think it takes a little bit of imagination to see the cheese pizza, but you see these large white active legions and then the hemorrhages all interspersed along the blood vessel. And then the granular appearance Yeah, you can see there's some fine little granular-looking changes here and some pigment clumping. The white active areas are sort of scarred down. So we're looking at a differential of this. First off, you know, if you have CMB retinitis, you always have to think about the underlying causes like HIV, AIDS, patient leukemia, lymphoma. If you're out on drugs or something causing a plasticemia or any other immunosuppressive chemotherapy is also in there. But then there's other sort of spectrum diseases that could mimic this. So acute retinal lacrosis, which is also caused by herpes family viruses. You can just have an HIV. The syphilis can look sort of similar as well as toxo, histo, tuberculosis, and progressive autoretinal lacrosis. So to work up the patient fully, we're going to make sure we look at his C4 count, do a CMB, PCR. And then, you know, this is sort of a newer idea, but if you have someone who has an abnormal looking disease or you're struggling to figure it out, take a vitreous sample and PCR that as well, which has a really high sensitivity for diagnosis. And then you just want to do some other baseline exams. The BU and gradient monitor for potential changes in the kidney function when you're treating a disease. And then it's toxo. Your test reciprocal is to be thorough at least in ruling out some of our other causes. And in rare cases, you can get a vitreitis, which obscures the views in the back of the retina, which in case the ultrasound would be helpful, as well as you can order a chest x-ray and looking for a concomitant PCP. So our goal is to stop the precious disease. It's only been a little bit of a debate as the discontinuation of treatment of it, but basically, whenever we see a CMU retinitis, the preferred method of treatment these days is an induction dose of a valsite, twice daily for three weeks. And then you can bring it down to a maintenance dose of only $9,000 once daily. And side effects of this, it does cause issues for, you know, blood cell production. So you can get a thrombocytopenia or a neutropenia. So with the advent of a nupagin, we can continue treatment, while at least avoiding some complications, having a low-neutrical count. But the main treatment now that's really changing things is using these intramaterial injections, which allows us to get a high-dose drug to sort of ride the center of the action. But the downfall is less for a short period. So there's also intramaterial implants, which have a long-term effect. So our patient after a year manages to come back to us. His vision is now 2600 in his right eye, and we're seeing some changes in his left eye as well, 2030. And when they do the visual field, we can see he's got a field defect here, an inferior left eye on both sides, and he has a almost complete hemisphere loss of vision there. And his pressure is a little elevated in his left eye. So he's sort of scared to think what might be back there. In fact, when we take a look, this is a very large act of lesion. There's a lot of scarring. There's an act of sort of fluffy lesion here. I can see this, but it looks like there might be some traction back here. But it's sort of inclusive right now. And then on the closer view of this lesion is what we see over here. It's an awful also make it out. You can see the fluffy lesion. There's this scar ring. And then in his left eye, what was a great eye. You can at least know that this is a very blurry picture, which is believed to have vitreitis. And then we can see more of the periphery. He has an active lesion here, necrotic retina, and more nasally he actually had some hemorrhage as well. So we restarted him on therapy like we talked about in our methods treating this. He received OU injections at Foscarnet. We started on a vial site. It was a start to pretty much fall up the next day in clinic, fall up week in clinic. And we started to see visual improvement. And then we managed to get records of where this guy's been for the last year. So the whole reason this has happened is we imagine as he's been off his meds. And when he stopped his meds, he was hospitalized. In another case, the Pistoplast, most of his meningitis, they had CMV colitis. But at least currently he's falling off his ID doctor and reporting to clinic. So the important point to take away from this at least is that most patients of CMV or anitis presents unilaterally. But as they managed to avoid their treatment or mistreatments, they have a 50% risk of developing disease and the contralateral eye within six months. But this has pretty much been reduced a lot in our time period by antiretroviral treatment and heart. Something else to look for in these patients is that there's potential for retinal attachment in up to a third of these patients. And you have an increased chance of RD when you have a large portion of the retina involved. So in the right eye of this patient where a large, large portion of the retina is involved, he's at a high risk for RD, at least in the especially the areas of necrosis. And then another sort of newer area is that you can have a uveitis as a reaction to these patients when their immune system recovers. So this guy when he's now re-initiating his retroviral therapy and he's going to have a rise in the CD4 count, he can actually have a flare of a uveitis from some of these viral infected cells that can lead to other complications like cataracts, glaucoma, and get epidural membranes. And you can even have visual loss from this most commonly with a crystal immaculate edema. So it's a pretty broad overview of CMV retinitis and maybe it was at least reminded some of us of some key points with my references. Any questions? And then this is sort of, you know, there's a lot of rambling in all our presentations, but this is the sort of take home point I found that might be helpful for us as younger students or around calm and sort of pull apart some of these different diseases. So with CMV you can see that pain is pretty rare. If the patient has a history of being immunocompromised that might sort of lead you towards that diagnosis as opposed to ARN where you're going to have significant pain as well if you saw like more of a hazy picture. And then you can see more of a sharply demarcated lesion. Or a toxa where it's sort of confident in any of these categories, but the important part here would be that you're not going to see a retinal hemorrhage. You know, this typical headlight and fog appearance. So if you can remember one thing, at least for us younger guys, I think that's something to sort of put in your mind for the rest of the day. I didn't see much of all that. There's a lot of forms of CMV and a lot of different presentations. Like there's the frosted branch, I know it's in textbooks and papers, but it seemed to be a very pretty low occurrence. So I don't want to say this is an inclusive talk. I really keep myself sad about it.