 All right, so welcome everybody. Very happy to see you all here. We have a real treat today here. So we've had four amazing medical students join us at the Marinite Center, just really bright and talented folks and just kind of genuine people. They're coming all from all over the country and we have kind of a lineup here that's pretty awesome. So we have the first student, Marshal Henry, who's joining us from the University Utah School of Medicine hometown kid coming in from BYU and his undergrad as well. He is a case today titled the case of a chronic scleral buccal infection. So really excited to hear that and I'll have you come up, Marshal. Good morning, everyone. Please continue to enjoy your burritos as we get started. This is a case of 25 years scleral buccal infection, which Dr. Shakur and I worked on together. So grateful for him for his help. I wanted to just first start off by pointing out some of the highlights of this rotation. It's been world-class, very grateful. Thank the residents, faculty, fellows for welcoming me into the clinics and ORs in their time. But they spent teaching me special thanks to Dr. Fuller for all of his efforts into preparing me for interviews and things upcoming. And Dr. Shakur as well for helping me with this case. I wanted to thank Gino. He got me front row tickets to a hip hop dance battle during this rotation, which was incredible. So thank you, Gino. And I also wanted to thank Dr. Jardine and Chandler for their coordination and help during the rotation. Also wanted to just give a quick shout out to my family as kind of a get to know me as well. This is my daughter, Millie May, who I think looks like a fortune teller in these hats, which is so cute. And my wife and I at our hip hop dance battle, which was awesome. And then our dog, Nash, who looks properly annoyed by my little girl. So that's me. But getting into the case, the patient was a 67 year old female with the history of retinal detachment of her left eye 25 years ago. And it was repaired via a scleral buckle surgery. Shortly after her surgery, she developed recurring episodes of swelling, pain, redness of the left eye. She was seen by various ophthalmologists during the 25 years in between when her surgery was and when she presented to us. The episodes were treated with antibiotics, steroids, or some combination of both. And they often rapidly resolved after treatment. When the patient was referred to Dr. Laura Rochelle in November of 2021, she wasn't experiencing a flare at the time, but the report from the referring provider said that she had scleritis, myositis, and pain with eye movements. And she'd had a previous lab workout for some of her symptoms, which included HLA-B27, and that was positive. Here, we have an external photograph. This was five years prior to her presentation to the Moran, but it's showing a left, lower, and upper lid edema and redness relative to the right eye. And again, this was five years prior to her presentation to us. Her past ocular history is significant for a retinal detachment in the left eye, status post-thero-buckle repair. She had a wet, age-related macular degeneration in her right eye, status post-multiple of asthen treatments. She had dry AMD in the left eye, an epiretinal membrane in the left eye, history of cataract surgery with lens repatiment in the left eye, and then a cataract in the right eye. Her past medical history was significant for HLA-B27 positivity as well as rosacea and pleomorphic adenoma of her salivary glands, status post-resection with lymph node dissection in 2014. Her medications, she took some daily vitamins, used prednisolone eye drops occasionally when she'd have these flare-ups, as well as metronidazole gel when she had rosacea flares. Her ocular exam at the time that she presented to Dr. LaRochelle was the following. She had a visual acuity of 2050 in the right eye and 2040 in the left eye. Her pressure in the right eye was 19 and 18 in the left. Her slit lamp exam showed 1 plus NS and trace PSC in the right eye, and the fundus exam showed myopic peripapillary atrophy as well as nasal lattice and inferior scarring. Her left eye had a posterior chamber IOL and the fundus exam showed myopic peripapillary atrophy symmetrical to the other eye with peripheral scarring and a buckle that was with good height. So continued history after her presentation to Dr. LaRochelle in November of 2021, she continued to have multiple mild episodes of eye swelling and eye pain. She would be treated with a short course of oral steroids and her symptoms would rapidly resolve rather quickly. She returned to triage a few months after her initial presentation to Dr. LaRochelle and had a severe flare of eye swelling which I'll show you in the next slide and redness. Because of her symptoms, Dr. Harry performed an ultrasound which showed some inflammation surrounding her buckle. Strangely, immediately after the ultrasound, she developed increasing IOP to the 30s and she needed eyedrops for lowering of her intraocular pressure. Due to her symptoms and evidence of inflammation on ultrasound, we ordered a CT scan with non-contrast and I'll show those slides in just a bit. So here's an external photograph similar to the one that she'd had five years prior showing significant swelling and redness of her eyelids. This was when the patient presented to triage and had an ultrasound with Dr. Harry. This is the ultrasound performed by Dr. Harry and we've highlighted the orbital inflammation that we see on ultrasound here. And this is the CT scan of the orbits, non-contrast and you can see enhancement. Y'all see my cursor? No, but in the left eye, there's enhancement around the sclerobuckle which Dr. Shakur assured me is not the usual appearance of a sclerobuckle on a CT scan. And here's just another slide showing that enhancement around the buckle. Ultimately, because of continued episodes of inflammation and evidence of orbital inflammation on imaging, the patient was taken to surgery for removal of her sclerobuckle. The surgery was without complications and the sclerobuckle at the time of surgery was not exposed, which will be important as we talk about sclerobuckle infections. And we sent the sclerobuckle for cultures which grew staff capitis. And I wanted to ask Dr. Shakur a question at this point. Dr. Shakur, if you suspect that a sclerobuckle is infected, you have to wait any amount of time before you remove the buckle to allow the retina to heal or you just immediately take the buckle, thanks. So you just, yeah, so for those who are on Zoom, Dr. Shakur was saying the optimum time to remove the sclerobuckle is about six months after surgery. Unless there's signs of infection then you would just immediately remove the buckle because you can have complications like a scleral abscess. And the risk of retinal detachment is much smaller than the risk of infection. So is that correct, Dr. Shakur, or anything else? Oh, sorry, orbital abscess, thanks. Her post-op care was a continued course of antibiotics and steroids. And at four months follow-up, the patient was symptom-free. She had no signs of uveitis or orbital inflammation. And I wanted to touch on sclerobuckle infections briefly. So they're a relatively rare complication of sclerobuckle surgery. The incidence that I found was about 0.2%. Interestingly, they have decreased over time as we've changed our materials. So from what I read, it was typical that you would use a scleral sponge as like a type of buckle, but now we're using silicone bands and the incidence of infection has decreased because of that. And then the etiology is typically exposure of the sclerobuckle following surgery leads to seeding of the implant with bacteria. Some of the symptoms of a sclerobuckle infection, what I found is that the most common symptoms are pain and redness of the eye, but you can have swelling, watering, foreign body sensation, or diminished visual acuity in some cases. The success rate of sclerobuckle surgery is between 85 to 90% in the treatment of retinal detachment from my sources. However, there are some intraoperative and postoperative complications of the surgery. You can have scleral perforation from scleral passes, hemorrhage, endoplamitis, scleral abscess, brittle detachments, altered refractive error from the shape change of the eye due to the buckle. And then what we talked about today, late periocular infections and implant extrusion. So I wanted to touch as well on some of the unusual findings and the take home points of this case. I think number one, the fact that this woman had a 25 year infection is fairly unusual and not something that I've ever seen before. So I thought that that was an interesting finding as well as the fact that the implant wasn't exposed. From a study that I read of about 130 infections, 85% of them, the buckles exposed. So that's kind of the predominant thought is how they're, of how these infections begin is the buckles exposed and bacteria seeds the buckle. If they're not exposed, it's thought that bacteria at the time of surgery actually seeds the buckle and leads to the infection. So it's possible that this woman had bacteria and had an infection basically from a few days post-op to 25 years when we removed the buckle. Her HLA-B27 positivity, Dr. Shakur and I thought was a red herring in this case. I thought it was somewhat confusing that she had evidence of orbital inflammation in this history of HLA-B27 positivity with seven to 11% positivity in her population. And as well, we talked about the length of the infection. The last thing I would mention is sclerobuckle infection is almost exclusively managed with removal of the implant. I did find one case where they presented a case where they treated it with just with oral and IV antibiotics, which I thought was unusual, but all the other ones I found, it was surgical removal of the implant. Thank you. Any questions? Maybe not. So the question is, did you find any evidence of bacterial colonization of non-clinically infected buckles? From the study that I read, it was all patients with clinically significant infections. So I didn't find any. I don't know if Dr. Shakur has any thoughts on that. Buckles that are not extruded or infected are not removed. It's part of the known, whether there is a need for bacterial colonization. So you had a partner from that question. Yeah, Dr. Wong. So Dr. Shakur said the study that we're referring to was all patients with clinically significant infections. So they had signs of infection symptoms, but they're patients who don't have a clinically significant infection, the buckles don't get removed. It would be hard to find evidence of that. Thank you. Yeah, Marshall. So we have Courtney Goodman here next, coming in from the University of Miami-Miller School of Medicine, with Baskin Palmer Ophthalmology Department. She did her undergrad at Duke University and she has a fabulous presentation for us today, titled The Art Through the Lens of Ophthalmology. Please come up, Courtney. Hi, my name is Courtney Goodman and I'm a fourth year medical student from the University of Miami-Miller School of Medicine. And today I'm really grateful to be given the opportunity and from the encouragement of Moran faculty to present a topic that's been very dear to me. I'm a visual artist and at my medical school, I was part of a medical humanities pathway and I pursued a capstone project focusing, exploring the relationship between art and ophthalmology and I'm excited to present that to you today. And much of my influence comes from the insight of Dr. Michael Marmore. So let's get started. Okay, so these are my objectives. So first, let's start with an obstacle illusion. So these are mock bands and you can see from these different gradations of the bars that it almost looks like each individual bar isn't completely uniform. As you approach an edge, it almost looks like there's a darkening towards the edge from the darker bar and a lightening towards the edge from a lighter bar. However, when we separate these individual bars, you can see that each bar is actually uniformly colored. And so an explanation of why the eye is so attracted and even enhances these edges is rooted in the organization of our retina. These millions of photoreceptors, each are broken down into units that interact with each ganglion cell, which sends through the optic nerve into the primary visual cortex. And these photoreceptors are organized into retinal receptive fields so that they are either excitatory or inhibitory. If you take a look at this diagram and we shine a light and you'll notice that if you look at the receptive field, such as the one corresponding to the letter D, you'll notice that when it's partially illuminated that there's an even greater excitatory response when the receptive field has an edge, whereas the one that's all entirely illuminated, it doesn't have as excitatory as a response. So this explains why our eyes are so attracted and even enhance edges. If we look at this cave painting that was made 30,000 years ago, you could see that these mock bands emphasize edges. And you can see that for example, this picture of a rhino stands out from the background, even though it's mostly colored through the rock of the cave. Salvador Dali was also, you had expert use of the mock band and you could see from the different areas of the painting that the edges almost seem like they're illuminating and the mountains in the distance seem to be distinct from the background because of these emphasis at the edges. Georgia O'Keeffe also used these edges to make flower petals stand out in her paintings. And I recently had the opportunity to visit the Navajo Nation and visit Antelope Canyon. And I noticed that mock bands could even be found in nature's artwork, as you could see at these little highlighted edges or I highlights these edges through the use of mock bands. And of course I have to bring my own artwork into the presentation. So this is one of my paintings and you could see how our eye just naturally emphasizes the edges so that the edges are a little bit darker, a little bit lighter at each junction. And so now I'm gonna briefly touch on optical illusions and there's a modern movement of op art. And this is a drawing made by Bridget Riley in the 1960s. And you could see that it's almost as if our eye is a little bit unstable when looking at this. It seems to have a shimmering quality. And there's been studies that have looked at a gaze mobility when looking at optical illusions. And there seems to be a correlation that is rooted in the fact that on our retinas when you have a stimulus, it quickly fades and a micro movement is needed in order to refresh the image on the retina. And so this is in the form of micro saccades and ocular drift that seems to emphasize the shimmering effect of these optical illusions. And it's not just modern art that includes these interesting optical illusions. Even Native American nations have used optical illusions such as the Navajo Nation in their rug making. And you could see that these closely spaced lines and the micro movements of our eyes even enhance the shimmering quality of these rugs. And now I'm gonna move on to a topic of color. You can see that our eyes are also quite bothered by these differences in color. And it's because these colors are equal luminant. And you can see if we change it to black and white, they lack an inherent contrast between them. They are of similar brightness. If we look at Andy Warhol's Marilyn Monroe's, you can see that some of these Marilyn Monroe's are a little more comfortable to the eye than others. If you fixate on the top left Marilyn Monroe, for example, it almost looks like the head lacks form. And this is because when we use our trick of turning it to black and white, it's because that those colors lack contrast. So if we think back to art class, the opposite sides of a color wheel are complementary colors. And complementary colors have a risk of being equal luminant if we allow them to. For example, red and green are inherent opposites and are opposing colors. And you can see that they can be similarly luminant, which can pose a problem for our eyes and the discomfort that they feel if they are juxtaposed. And this phenomenon, of course, is deeply rooted in our retinas with our different cones of red, green and blue and the inherent receptive fields. It is impossible to perceive a combination of red and green due to these opponent circuitries. So Vincent Van Gogh, he used complementary colors, but it seems comfortable to our eye. Here's a juxtaposition of blue and orange. And you could see that when we use our trick that the contrast, there is contrast to this image. However, if you had brightly orange hair, this would probably seem more uncomfortable to the eyes since they have more equal luminance. Here's a successful use of complementary colors that have different contrasts. And you could see that when we use our trick of flipping the black and white that even though there's blues and oranges, the different luminances make this painting make more sense. Similarly, this is a painting that might not make sense in real life as these are very different colors onto a human portrait. However, they make sense when we look at the different luminances and the contrast that they create. And I thought in this painting, it was quite interesting that there was quite a use of equal luminant colors of blue and orange near her neck. And I think that this served to draw the eye more to her face. And of course, I have to bring my own paintings. So I tried to juxtapose or use color to shade. And when using the trick of turning to black and white, it maintained the contrast of the image so it feels more comfortable to the eye. Claude Monet, he intentionally used equal luminance in his painting. You could see that the orange almost seems like it's shimmering on the water, the sun. And when we flip it to black and white, it fades. And there's been studies that looked at this exact painting impression sunrise. When they had subjects fixate right on the boat, there was a phenomenon known as choxlar fading in which the sun transiently disappeared. And it's because it lacks contrast. However, with a micro-secade, the sun reappeared. And now I'm going to touch on our last topic, pointillism, which has an interesting phenomenon in the visual processing. And you might remember pointillism from the movie Ferris Bueller's Day Off and how Cameron was very fixated on this painting. And the phenomenon of pointillism is deeply rooted in our retinas as well. And it is due to our receptive fields are able to distinguish that there are differences in the actual points of pointillism, the dots. However, the larger receptive fields that detect color actually detect a blending of the color of these dots. So let's take a look at an example by Henry Edmund Cross. So the background, interestingly, juxtaposes complementary colors, blue and orange, which you think would cause confusion in this image. However, when you combine complementary colors, it actually creates a dull blending because they can't be combined in our natural perception. So it gives the perception of a dull background. Similarly, here's another painting by Maximilian Loos. And you could see that the use of blue and orange points that make a dull background. And here's one of my own drawings of an OCT image. And you could see the use of pointillism that even though these are complementary colors, appear dull to our eye through the blending. So in summary, I've discussed several fundamentals of visual processing and how they relate to our perception of artwork. And of course, this is not to downplay the role of culture or experience when perceiving artwork. And so probably one of the most important fundamental rules of artwork is contrast as our retinas are very drawn to the edge based on the physiology of the retina. And optical illusions equal luminant colors perceive shimmer and instability likely through the involvement of microsaids, saccades that constantly refresh the image. Juxtaposing complementary colors that use different luminances creates a stable image with striking colors. And finally, pointillism is a technique that showcases how our different sizes of receptive fields can allow us to perceive visually distinct dots but with blended colors. These are my references. And I just want to say thank you so much. This has been an amazing month. And I've worked with wonderful faculty at Moran. And I couldn't be more grateful. Here's my many hikes and some drawings at top of the mountains. And thank you so much. Any questions? We can bring up the next slide, Joe. You mind helping me out? I can't job again, Courtney. We have here Carrie McKinnis-Smith coming in from the Mayo Clinic, Alex School of Medicine. She did her undergraduate at Carroll College. And the title of her presentation today is Quantity and Duration of Explosion to General Anesthesia for Pediatric Patients with Retinal Blastoma. I'm hard to follow, Courtney. I wish I had some creative artwork of my own to showcase, but no such luck. I'm Carrie. I'm a fourth-year med student from Mayo. And I'm going to present a topic, a research study that I've been working on with Dr. Rama Subramanian. She's an ocular oncologist, a PEDS ocular oncologist at Phoenix Children. She used to be at the Moran, so some of you may know her. We've been looking at the quantity and duration of exposure to general anesthesia for pediatric patients with retinal blastoma. We just recently had this published in APA, so that's pretty exciting, you know, next week, I think. I don't have any disclosures. So a little bit of background. In 2016, the FDA came out with an advisory that said, repeated and linked the use of general anesthesia or sedation drugs. And young kiddos, so they were talking about children under the age of three, may affect the development of children's brains. This was a really controversial statement. It sparked a lot of discussion, not only on behalf of patients and their families, but also by anesthesia societies and surgical societies. There weren't any studies really at the time of that advisory, like prospective studies that had looked into this. So at that time, the gas trial and the Panda study started, those are two like large scale prospective studies looking at this exact topic. They're now five to 10 years out and they've both published preliminary findings that have said, you know, single short exposures to general anesthesia probably don't have any long-term, or I guess five to 10 years out, any neurodevelopmental effects. But there's been some studies also since then that have showed that repetitive and length the use of anesthesia does increase the risk of learning disorder and ADHD development in these young kiddos. So as you know, retinoblastoma is interesting because it deals almost exclusively with this patient population, right? It's almost always diagnosed in kids under the age of five and it requires a really thorough assessment, not only for treatment, but also for diagnosis, you know, MRIs, exams, all this stuff that may be a little bit more straightforward in the adult population, often requires general anesthesia in young kids. The treatment has evolved a lot of the last couple of years and decades. Now, to kind of break it down, simply we focused on the main treatments of intravenous chemotherapy, so IVC, which is the systemic option, intra arterial chemotherapy, which is injecting chemo into the ophthalmic artery, IAC, and then a nucleation. And then obviously you can pair some of these options with like adjuvant therapies like TTT or cryo or laser, that sort of thing. And then active surveillance, it's interesting because it not only occurs while the patient's undergoing treatment, but also after they enter remission, right? So the length, the frequency, how long this is required is dependent not only on like the clinical factors, but also on the patient's age, their maturity, how long they may require anesthesia for a good thorough assessment. So the objectives of our study, they were really threefold. First was just to quantify the duration of anesthesia for the most common procedures that these kids are undergoing. Second was to determine the number and duration of anesthesia per kiddo, undergoing diagnosis and treatment. And then third was to stratify these exposures according to clinical factors. So overall, we just wanted to say how much anesthesia are these kids going for, going through in their retinoblastoma journey because that hadn't been done before. To do this, we did a chart review of 43 patients with retinoblastoma treated at PCH. This is actually a pretty good sample size for retinoblastoma just because of its rarity. We excluded any child who got any of their retinoblastoma care outside of PCH. So like Dr. Rama still gets quite a few of her patients who follow her from Utah and Louisville, kind of around the country, but we excluded anyone who had like MRIs done outside of Phoenix Children's, that sort of thing, because we wanted to encompass all of their retinoblastoma care. And then we excluded any child who was lost to followup. Here's the data we collected. And then we calculated the amount of anesthesia. So every time a patient underwent any procedure, a number related to the retinoblastoma, we counted that procedure. And then we counted the anesthesia time by looking at the anesthesia op-note and the anesthesia start time to anesthesia stop time. So we excluded induction and emergence times. This is just a general overview of our demographics, our clinical characteristics. We had 43 patients, 28 of whom had unilateral disease, 15 who had bilateral disease, pretty similar male, female breakdown. And then the age of diagnosis over 96% of our patients were diagnosed under the age of four, which is pretty in line with previous estimates. And the average follow-up timeframe for all of our patients was right around 36 months. So that was the time from diagnosis to their last ophthalmology exam before our chart review. This table starts breaking down the procedures by the anesthesia times by the most common procedures that we encountered. The six most common are listed up here. You can see that EUA is by far and away the most common procedure. There are 356 procedures done on the 43 patients. Average is out to about nine procedures per patient. Nine EUA is per patient over the average three, plus or minus three year follow-up. And each EUA lasted on average 45 minutes. The longest procedure by far was intra arterial chemotherapy. This is interesting because it's gonna have a lot of inner institutional differences. We have pretty much one interventional radiologist who does our IAC. So it's hard to kind of minimize the operator bias that comes in there. But each IAC at our institution lasted 275 minutes per episode, but obviously not all kids are getting IAC as a treatment. This slide breaks down the anesthesia exposure by laterality. So you can see we had 28 patients with unilateral disease, 15 with bilateral disease. It's important to see that the follow-up times are about the same for the two groups. That's there on the bottom, the 36 month follow-up timeframe for the two groups. What I want you to see is how much more anesthesia the kiddos with bilateral disease are undergoing, which makes sense. We can talk about that at the end, but that's pretty straightforward. The kids with bilateral disease were undergoing more anesthesia in terms of both number, 26 exposures and duration about 1,700 minutes overall compared to 400 minutes. For the next couple of slides, I'm going to break it down by ICRB tumor grade, which is the international classification of retinoblastoma. It goes from A through E. It's the breakdown, the grading system or one of them of retinoblastoma and the treatment type. Like I mentioned, we use IAC and Charteral chemo, IVC, the systemic intravenous chemo and then a nucleation as the primary treatment options. But it's important to know the ICRB grade and treatment type obviously have a lot of interplay, right? Because the tumor grade is going to dictate a lot of what treatment is recommended for the patients. So you can see that none of the patients with ICRB grade B, which is on the more mild end were recommended in nucleation, for example, or even systemic chemo. They all under ICRB grade C. And then for the patients with ICRB grade E, which is the severe disease, none of them underwent IAC. They all either were nucleated or at least had systemic chemo. So it's important to note that these two interplay a lot. So it's hard to do like the invariant analysis. We didn't break that down. This slide is just looking at patients with unilateral disease. So only the 28 patients with unilateral disease. And it's breaking it down by ICRB tumor grade. So it's interesting to see that those with more mild disease, so the grades B and C, were exposed to the most anesthesia, right? So they had 20 exposures compared to six and 4.5 for the ones with more severe disease. And then they were also exposed to the most anesthesia in terms of duration. They had almost 2400 minutes compared to 312 and 397. I'll talk a little bit about why we think this is. And then lastly, if we break it down by primary treatment options. So again, IAC and charterial chemotherapy intravenous chemo and nucleation. And then these can be paired with focal therapies. What we wanna see here is that a nucleation is associated with the least anesthesia. So three exposures median and 290 minutes of exposure for the kiddos who are nucleated. And then intra-arterial chemo therapies by far and away associated with the highest amount of anesthesia. So 18 and a half exposures for 2100 minutes of anesthesia time. So over similar follow up times, those with bilateral disease are exposed to much more anesthesia than those with unilateral disease. This makes sense, right? They have higher tumor burden. They're more likely to have germline mutations so they have more recurrence. And they're more likely to be directed towards like the vision-sparing therapies because you're not gonna recommend bilateral and nucleation. So they're gonna, more likely gonna have IAC or IVC which is associated with more anesthesia. And then second as patients with, for unilateral disease, patients with more severe disease were actually exposed to less anesthesia than those with more mild disease. Which may seem counterintuitive at first, but it makes sense because patients with severe disease are often directed straight to a nucleation which again is associated with less anesthesia compared with, for example, intra-arterial chemotherapy which often is employed for the patients with a little bit less, you know, the ICRB grades B and C disease. So take home points from the study. The treatment of retinoblastoma requires prolonged and repeated exposure to general anesthesia. That was really the goal of this first part of our study was just figuring out how much anesthesia these kiddos are exposed to. The next studies need to, we wanna stratify the exposures by the time since diagnosis which we didn't do with this study. So breaking it down into how much exposure is required for a diagnosis, how much is required for treatment and then how much is required for post-remission follow-up. And then second, we're working on a study right now to determine the potential effects of these anesthesia exposures. So we figured out, you know, this is how much anesthesia these kids are exposed to but why does that matter? Does it matter? Are there effects and what are these effects? So we're working on like a, we're pairing up with neuropsych that we're coming up with a survey right now that surveys the parents of these 43 kids to not only look at, you know, does the kid have an IEP in place? Do they have a diagnosed learning disorder? And then also looking at quality of life for the families, the parents, how the amount of anesthesia, the number of exposures, how that may be a burden for patients and their families and how that can affect our decision-making going forward. Here's my references and I'll open it up for some questions. Yeah. All of these exposures, is there anything that Aparna's managing differently based on this information or does the known risk of cancer and requirements of treatment just outweigh any potential, you know, outside of the anesthesia? Right. I think that's... And sorry. Oh, the mic's on, you're good. So I think that's kind of a multi-faceted question. We talked about that, you know, what can I do before the next time and how, before I know if this is even causing any effects. You know, Dr. Rama said, what can I do now that I know that these kids aren't going so much anesthesia? I think part of what she's saying is trying to pair up some of her procedures. So rather than inducing a kid for anesthesia for an MRI and then the next week for an EUA and then the next week. So she's trying to like pair up more of them and maybe do them all at one go and go from EUA straight down to MRI, which can help minimize some of the quantity of exposures and duration of exposures. And then I think the other part is just track is that should be done in the first part. You know, sometimes the kids are inducted for anesthesia and then we sit there for 20 minutes waiting for, you know, just logistics of the operating room to go. So I think some of that is just minimizing unnecessary anesthesia time. But other than that, it's just something to bring up in conversation with parents. You know, this is still what I recommend and I see as an option, but it is associated with anesthesia. You know, it's not a reason to jump to a nucleation because it's associated with police anesthesia, by any means, but it's just another aspect of the conversation. Yeah, for both of those examples, there's some real cost savings as well on just minimizing, you know, combining procedures, minimizing anesthesia time. That could be an important driver in changing your finger as well. That's pretty amazing to see the average amount of time for a court to be placed in an hour. That's just crazy. Yeah, and we figured, I mean, even with the UA, it's because like, each at the UA on average, I mean, I've only been in a handful. I'm sure many of you have been in any more than I have, but it seems like a lot of them to me seem like 15, 20 minutes. So by the time you're new, some of the surgeon walks in and scrubs in. And then some of them are obviously paired with local therapy. So by the time you feel a little razor, a little cry out, that's up and on average it's 45 minutes, so that's up with each patient's 39 minutes. Awesome job. Again, awesome job, Carrie. So we have last but not least, Janine Yang, who's absolutely a superstar. So she did her medical school at Drexel University College of Medicine. I did undergrad there as well. And then because she's so awesome, she did a research fellowship at Mass Eye and Ear with the Harvard Department of Meta, or Department of Ophthalmology. Her title today is A Curious Case of Chemosis. Thank you for the kind introduction, Mark. I hope this presentation is as amazing as he makes me out to be. And thank you to everyone who stayed for the end because I know it's quite a marathon to stick around for the end of Grand Rounds. But my Grand Rounds is titled A Curious Case of Chemosis. So our patient is a 75-year-old male, one month progressive, redness, tearing and swelling, difficulty moving his eye and decreased vision in the left eye. Of note, he did see an optometrist about two weeks prior to the ED who did prescribe steroid drops without much improvement. And on review of systems, he was noted to not have any trauma, fever, headache, nausea, vomiting, neck pain, or stiffness. For his past medical history, surgical and ocular history, it was insignificant other than hypertension and hypercholesterolemia. And his initial labs on admission were within normal limits. So for his exam, his vision in the left eye was 2,200. If pupils were equal, round and reactive to light bilaterally, he did have increased intraocular pressure in the left eye at 31 and globally restricted extraocular movements in that left eye. Continuing the exam findings on the left eye, he did have proptosis, ptosis, injection, hemosis, and contractile prolapse. And for the dilated fundus exam, he did note bilateral torturous vessels as well as some corridors in the left eye. So as I say, a picture is worth a thousand words. So this next image is a little shocking. This is clinical photos taken at his initial ED admission. You can see there is quite significant chemoses and proptosis. So for the differential diagnoses, things that we consider would be intracranial neoplasm, any sort of increased intracranial pressure. It could also potentially be some sort of infectious or inflammatory cellulitis of the eye. Vascular etiologies are also very possible and there are a wide variety, all listed here below. Lastly, less likely is adiopathic intracranial hypertension, or it could also be some form of atypical thyroid eye disease. So on further questioning, the patient does recall that the optometry system first did order a head CT and the patient says it showed a broken blood vessel behind the eye. Next, a CTA head and neck were ordered and the patient was started on IOP lowering drops as well as erythromycin ointment. So this is the CTA head and orbit. You can see here that this is a CTA, so it is contrast enhancing all of the arterial systems. You can see this is the orbits and there is some proptosis and enlargement swelling of the left eye. Furthermore, you can see the other two foci of hyperintensities, which are the internal carotids in both views and beside the left internal carotid, there are actually two areas of hyperintensity with more softer edges dimmer in intensity and these are actually correlating to the leakage of contrast from the left internal carotid into the surrounding area. So in furrow temporally is the leakage within the cavernous sinus and then you can see super nasally is actually leakage into the supraphthalmic vein. So now knowing these new imaging findings, we can now go back to our differential diagnosis list and the one that best fits this clinical picture and imaging is the carotid cavernous fistula and specifically in this patient, it was a type B left-sided carotid cavernous fistula. So what is a carotid cavernous fistula? It is one type of abnormal vascular connection between the carotid and cavernous sinus systems and it is generally known to be caused by traumatic injury, usually from some sort of head injury. It can also be caused by surgical intervention or adrenal necrosis, but it can also be spontaneous in 30% of cases and the risk factors are atherosclerosis, hypertension and any sort of vascular disease. The symptoms that it produces is due to the congestion of the venous drainage of the orbit and this is due to most usually disappear in a fear of stomach vein of failing to drain into the cavernous sinus and so the actual symptoms does vary based on the type of fistula in direct. It is the most prominent and acute with the classic trite of chemosis, pulsatola eczepalmos and oculibury. However, it is important to note there are indirect carotid cavernous fistulas which have a more variable presentation and more subacute presentation and here are some other ophthalmic symptoms that you can see on presentation as well. Just a brief review of anatomy. So the cavernous sinus does have very high value real estate because of the contents including the internal carotid artery as well as a lot of cranial nerves and you can see in the bottom image that the drainage system of the orbit is from the superior ophthalmic and fear ophthalmic veins in the central vein of the retina into the cavernous sinus. Just to illustrate the different types of fistulas better you can see a graphical representation as well as a table. So type A is the direct form which is a direct connection between the internal carotid artery and the cavernous sinus which explains why it is so acute it is a very high flow system and types B through D are indirect and they are due to dural branches of the internal, external or both branches of the carotid artery, excuse me. So for the management, initial diagnosis does require some diagnostic testing and imaging and usually CT or MRI is recommended as a first line because of its noninvasive nature and it can usually detect the location in the presence of the fistula although a DSA or digital subtraction and geography is required before any sort of intervention and generally for intervention if a patient is asymptomatic, you can just observe but if there are any symptoms the patient does require emergent transvenous coil embolization. So in our patient after this diagnosis was discovered the IOP lowering drops were discontinued the patient was admitted for emergent coil embolization of the superior ophthalmic vein and he was discharged on erythromycin ointment and followed up in aquaplastics clinic with Dr. Marks and here are some clinical photos five days after his procedure you can see there is significant improvement in the chemosis and proptosis of his left eye. His visual acuity was improved from 2200 to 2040 and he did have a covering mobility of his left eye although he did still have some restriction and extra ocular movements and some dyplopia. So some general take home points a crowded cavernous fistula is an abnormal AB fistula usually after trauma but up to 30% of cases are spontaneous. The classic chart of chemosis post-altoxophthalmos and ocular brewery are usually expected but not always present especially if it is in a spontaneous case when indirect low flow case and diagnosis does require a high index of suspicion usually a diagnostic testing with CTA or MRA are warranted however a DSA is gold standard imaging required before any sort of surgical intervention for symptomatic cases. So here are my references and special thanks to Dr. Marks for his contributions and guidance in his presentation as well as in his aquaplastics clinic. I wanna thank all of the faculty and residents for an amazing month and I'm open to any questions.