 I think it's eight o'clock, so we'll go ahead and get started. Hi, everyone. My name's Brad Jacobson. I'm one of the PG Y for residents here at Moran. Just as a reminder, if there are any like questions or comments, go ahead and type them in the comment section and then we can address those after each presentation. That way the presenter can go through their entire presentation without being interrupted. So we're going to start off with Catherine who Catherine's one of the PG Y three residents here at Moran. She's from the Bay Area in California and attended medical school in St. Louis. When asked where her ideal vacation is, she answered Southeast Asia for straight food in Antarctica for orca and penguin watching. Couldn't decide on one place. Anyways, Catherine's going to be talking to us about a not so textbook case of GCA. So go ahead and take it away, Catherine. Okay, awesome. Thanks, Brad. So this is a patient that I saw on my last month of consults as a PG Y two. And so I'm just going to go great into the case. So this is an 80 year old woman coming in with one week of painless monocular vision loss in the left eye. And she described her symptoms as about one week ago in on one week ago about on Monday, she started having kind of just generalized blurry vision in that left eye, but then also started seeing some floaters and then eventually saw this kind of dark blob coming over the top of her vision. So it was really interesting and very striking about this patient was her review of systems. So she said about four months ago, she started having my algeas and arthralgias, mostly in her hips and her neck. About three months ago, she started having some shooting left-sided neck pains shooting up to the right side of her face. And notably, she actually went to a sports medicine doctor around this time and was started on a short course of prednisone. And she said that this actually improved her symptoms quite significantly. And after she tapered after steroids, they actually eventually did return, which is actually that right-sided, sorry, the left-sided neck pain shooting up her face. About two months ago, she described a new onset left-sided, throbbing kind of dull, achy five out of 10 left-sided headache. And she also self-volunteered information like scalp tenderness. And she said that it actually hurt her skin to touch or actually comb her hair. And all throughout this time, she was developing more generalized fatigue and weakness. So these are just some quotes that I found really memorable from her and that she again kind of self-volunteered. And she really kind of almost classically described this textbook proximal muscle weakness and jaw claudication. So I just remember her motioning and holding both of her sides of her jaw. She said, yeah, it really hurts on both sides when I chew more than four mouthfuls, which I thought was very memorable in her kind of clinical course. And then just some history. She was otherwise a pretty healthy woman, had a very active lifestyle. She had a history of hypertension that was previously controlled, well-controlled in medications, but now was doing just fine on diet and lifestyle modifications. She did not have any other vascular risk factors, including diabetes. She had cataract surgery in terms of her past ocular history. But otherwise, like I mentioned, it was pretty healthy and a very active woman. On MRI showed chronic micro vascular disease, but with otherwise unremarkable, there was no evidence of stroke. There was also no abnormal appearance of the optic nerve or orbits. And her laboratory results on admission were notable for elevated inflammatory markers. As you can see here with platelets, ESR and CRP. And so on an exam, she had a slightly decreased visual acuity in the left eye associated with the left APD. She also endorsed some superior peripheral deficits on the left eye on bedside, confrontational visual fields. Otherwise her pressure color motility were normal and her anterior segment was normal. Most notable on her dilated fundus exam was kind of the C-shaped kind of edematous fluid cuff nasally, which you can actually see here. And it was quite striking how pale the edema was and kind of coming up on my indirect exam. You can see this was very nicely captured by Dr. Sean Collin as he was taking body call with me during this evening. And then she did actually come from an outside eye care provider who provided this 30-2 Humphrey visual field. And this showed a pretty dense superior arcuate defect in her left eye. And I don't think that we had visual field testing. She didn't come with visual field testing from her right eye. So in summary, we have an 80-year-old lady who's presenting with one week of painless monocular vision loss and pale nerve edema in the left eye in the setting of three or four months of left-sided headache, jaw claudication, scalp tenderness, proximal muscle weakness, and elevated ESR-CRP. So normally I would ask the residents for a differential diagnosis, but in the interest of time and also getting to the salient learning points that I want to discuss today, I'll just go ahead and say that there should be one disease entity that's quickly rising to the top in terms of high suspicion that, of course, is GCA. So a few words about GCA. This is a systemic vasculitis that affects the medium to large vessels in the body. It is almost exclusively a disease of the elderly and tends to affect females more as well as those of Scandinavian descent. Depending on the source worldwide, the incidence is about 15 to 35 per 100,000 persons over the age of 50. Of course, the classic kind of consolation of symptoms, you have headache, jaw claudication, vision loss, scalp tenderness, and also polymylogical rheumatica, which is a kind of a systemic complex of proximal muscle weakness and also girdle muscle weakness associated with fatigue that can also be classically associated with GCA. It can affect the superficial temporal arteries, but it can really, it classically affects the superficial temporal arteries, but can really affect any vessel, any branch of the aorta. And vision loss can be a result of anterior artery ischemic optic neuropathy, or AION, but really it can, GCA can present in other forms of ischemic vasculitis, including symptoms of depopia, eye pain, and can really manifest as anything from cranial neuropathies to a vascular, a retinal vascular occlusion. And so gold standard is a temporal artery biopsy, which we'll kind of get to in a little bit later in our discussion. And then steroids are mainstay of treatment, though a tasselusumab, which is a anti-human interleukin-6 receptor monoclonal antibody. And other steroids bearing agents are coming on the market. And tasselumusumab was most recently improved in 2017. So for our patient, she was admitted for three days of IV cell-imagerable one gram daily to the inpatient neurology service. And then she was discharged on high-dose oral prednisone. And her temporal artery biopsy was planned for the next day. So she showed up to Moran pre-op, and unfortunately she was found to be tachycardic. And incidentally on an EKG, she was found to actually be in AFib with RVR. So we sent her to the ED and she was diagnosed with new onset paroxysmal AFib that was attributed to her initiation of high-dose steroids. So we had deferred her biopsy, of course, at that day and had kind of tentatively planned it for a later that week. So on Wednesday, I was paged by the inpatient cardiology team as an FYI as a consul resident, which if you didn't know is never a good thing. And so they actually told me, unfortunately our patient had presented to the ED with chest pain and had heart attack. And her EKG actually showed ST elevation, so this was a STEMI. She was emergently taken to the cardiac cath lab, which showed 100% LED inclusion and she underwent emergent percutaneous coronary intervention. So this is actually part of her balloon angioplasty that I grabbed from her cardiac cath imaging. This is actually a schematic that is part of her, this is a schematic actually of her vessels that was included in the cardiac cath report. So you can actually see she has a 100% distal LED occlusion, kind of more in the apical region. And the video that I showed is her balloon angioplasty and they were able to get pretty, restore pretty good blood flow just after balloon angioplasty and didn't need to get for more senting. So fortunately our patient recovered well and she was in stable condition and good spirits and she remained in the inpatient unit. But this of course throwed a wrench into our diagnostic and also management plans. So we pretty much were a little bit stuck. She was now on a 48 IV heparin drip on blood thinners and of course in no kind of medical condition to continue a temporal artery biopsy safely. So what were we to do? This was kind of a pretty big challenge. Given her classic presentation, we thought about treating her kind of more or less empirically for GCA without a biopsy. However, getting her off steroids was more or less of a priority now that we were pretty sure it had caused this cardiac event. And also we discussed that without a diagnostic procedure management would be difficult for symptoms recurred or relapsed in the future with inappropriate cessation of treatment or early cessation of treatment. And we had not gotten to the bottom of the etiology during the sensitive time window. So kind of if only there were a safe noninvasive way to help us reach our answer. And I think I hear kind of some of you pondering, but also thinking maybe I hear you guys thinking that maybe we could perform a bedside ultrasound with Dr. Harry while she was inpatient in the CBICU. So of course that's what we did and we were very fortunate to be able to complete that next day in the inpatient unit. So a few words on Doppler ultrasound. So this is a, the classic kind of sign that we look for on a color Doppler ultrasound is the halo sign. And this is inflammatory exudates as well as edema surrounding the vessel wall and into the tunicum media. So this is called the halo sign. It is a hypoechoic rim of vessel wall edema. And then also like I said in inflammatory exudates and you actually see kind of this dark rim around both longitudinal and also cross sectional views of a vessel. It's also non compressive. So does not go away with compression of the vessel. So the benefits of Doppler ultrasound are very apparent. Especially that it can provide immediate real time information. Just kind of at the bedside. It's non-invasive and cost effective. When comparing that to what we think about with temporal artery biopsy, there can be a delay in procedure and logistics, coordinating our time, coordinating patient, patient care coordination. And also sometimes coordinating the cessation of blood thinners and things like that. So that we can do the procedure safely. And also sometimes there can be a diagnostic delay in actually reading the pathology sites themselves. When compared, of course, to the immediate real time information that you can gain from Doppler ultrasound. Complications of the biopsy include facial nerve injury, wound infection and scalp necrosis. And depending on the source, of course, false negative rates very, very widely from 1.8% in the literature to 34% in the literature. And most people is tripping. Skip lesions, lack of temporal artery involvement in the manifestation of the GCA itself, or if there was any response to steroid therapy prior to the biopsy being taken. Of course, Doppler ultrasound does not come with its own caveats. The first is that it's not standardized in terms of the equipment that different groups are using and the acquisition of images as well as the interpretation. And it's also operator dependent. Of course, not everybody has a wonderful Dr. Harry at their disposal at their institution who can kind of not only be the expert in obtaining these images, but also helping us interpret them. And studies that have been conducted so far in the literature with analysis of detection rates of GCA have been pretty small in terms of sample sizes with less than 100 people. And then a systematic systematic review that was recently published in JAMA kind of published in the GCA. And also sensitivities and specificities have also had a wide range so far in these small studies. And we're ranging from 55 to 10, to 100, sorry, 55 to 100% sensitivities in 78 to 100% specificities in the published literature. So for our patient, we performed a Doppler ultrasound at the cardiac ICU. And we also have a wide range so far in these small studies. And we're ranging from 55 to 10, to 100, so far in these small studies. So far in these small studies, we performed a Doppler ultrasound at the cardiac ICU. We also performed a B scan and it showed no emboli detected posterior to the lamina crosa. And she did have a positive halo sign in her bilateral temporal artery. So it was interesting that even though she had, of course, we classically only take a biopsy, we take the side that is the affected side, which was her left side that she was experiencing vision loss. But she actually had a positive halo sign in both sides, which shows that it's not invasive. You can take a very good look at both cross-sectional and longitudinal view of both vessels. And so if you can kind of see with me here, she had this hypoechoic rim or that dark green halo around the vessel. And if it's not obvious enough, I've highlighted it with an actual halo. And so these are a little bit, some more pictures of that hypoechoic rim. This is another cross-sectional view here of her left temporal artery and then a longitudinal view. And then in the latter half of the page, you can see her right temporal artery also had a hypoechoic rim that fluid kind of, that fluid rim of halo of edema indicating inflammatory disease and very convincing for a GCA. So in our patients kind of taking her whole clinical picture, her clinical presentation, her elevated inflammatory markers, the fact that subjectively in terms of her vision, she had improved very much. So with the initiation of high dose steroids and also now with this new information of ultrasound, we were comfortable foregoing a temporal artery biopsy and continuing to treat this as GCA. Rheumatology was consulted and they were on board and they got the patient onto a safe kind of tapering regimen of prednisone. And they've been managing her ever since. They also were able to have her, start in Tosalizumab as a expedited initiation of that steroid sparing therapy. So of course, if you have been to resident research day in recent years, you know that you're familiar with this topic as presented by Dr. Harry and also Dr. Michael Burrow. It was one of our chief residents last year. And I believe that that the resident role of that research project has been taken over by Dr. Abigail Jebaraj. So definitely ask Dr. Harry and Dr. Jebaraj about this project. They are currently recruiting patients for validation and detection of GCA. So a lot of kind of interesting and exciting things to come in terms of validation to use this modality to diagnose GCA while the TA biopsy still remains, of course the gold standard for diagnosis. So I also had a question in terms of our patients, cardiac disease and her heart attack, which of course was very, very striking in terms of her clinical course. So I had talked to her cardiology team and they were fairly certain that the new onset paroxysmal AFib had, of course played a pretty large role in the thrombus that ended up in her coronary arteries. And that was attributed to the high dose of steroids that she was started on. But it was a little bit kind of peculiar because she had only been on steroids for four days at the point that she had presented with AFib and she only really, symptomatically and also documented had one occurrence of this new paroxysmal AFib and that was one day prior to her heart attack. So I had wondered if GCA or maybe vessel while inflammation had played a played a role in her myocardial infarction, talking to her cardiologist, definitely on the differential she in her cardiac catheterization, the angiogram, it did show some vessel wall some mild vessel wall, luminal irregular irregularities. But this is fairly nonspecific though it can be present in a vasculitis. So looking in the literature, aorticitis and inflammation of the aorta and aortic dissection and aneurysms is a is a pretty well documented occurrence in GCA or complication of GCA. However, a coronary arthritis is much less is much less of a is under recognized in terms of a complication that can happen of GCA. So in the literature, I found about maybe four or five case reports, very few where there's actually biopsy proven coronary arthritis from granulomatous inflammation in a patient that had biopsy proven temporal arthritis with vision changes and then subsequently had a myocardial infarction. And again, these were postmortem biopsy proven results for coronary arthritis. And then also also in the literature, there have been several kind of large population studies. This one came out of Canada, where they did show an increased risk of cardiovascular disease in GCA when comparing or when controlling rather for hypertension hyperlipidemia and medications. And this was actually thought to be attributed to the fact that GCA and vascularities can are pro athero thromb, they promote atherosclerosis. They're also have an increased rate of thromboembolism. And then finally, there was a large cohort study that came out of the Annals of Internal Medicine recently. And this was a large population study, think about 3,400 patients. And this came out of the UK primary care database. And they also showed increased risk of cardiovascular disease, including myocardial infarction, stroke, peripheral vascular disease, and associated with GCA. And they noticed that the increased rate of these vascular events actually most commonly occurred one month after diagnosis of GCA. And they attributed this also to complications from steroids in terms of that high dose steroids are also associated with being pro atherosclerotic. And the fact that since a temporal artery biopsy is our gold standard, sometimes cessation of blood binners or things like that can maybe lead to vascular accidents. So a quick slide, of course, on steroids. We know that steroids are not benign. And Dr. Nescher in the junior journal of rheumatology, they published a 15 year study, 15 year survey of 43 patients. They followed after treatment of GCA and 58% of these patients developed at least one major steroid complication in an average follow up of three years. And the majority of these complications were bone fractures and infections, but of course we do know that steroids can cause multitude of things including exacerbation of existing diabetes and hypertension, robotic events, atrial fibrillation like it was in our patient, GI bleeds and other kind of comorbidities or worsening of comorbidities. So for our patient, thankfully she had preservation of vision. She's 2020. This, her first follow up in clinic with us was one week after discharge. So about 10 days after her initial presentation and initiation of treatment. And so her symptoms had almost completely resolved without recurrence. She was on oral prednisone and then also she's still on an prednisone taper rather and continues on Tosilus map and is tolerating these well, relatively well without side effects. Her atrial fibrillation and cardiac health are stable. They're talking to her cardiologist, her type her hypertension right now is the is the biggest challenge while she's still on prednisone. So this is when she was seen in neuro ophthalmology clinic about again 10 days after presentation, one week after discharge, you can see that she just has a touch of edema and fairly and measly, but it does look improved when she first came to us on the initial console presentation. And then also her superior arcuate defect has improved in the left eye as well. So some takeaway points. My intention in presenting this case wasn't so much as an M&M and certainly not to be a comprehensive review of all the facets of GCA, but I just thought it was very striking in terms of when things kind of become more challenging and when we aren't able to perform diagnostic and management, the way that we typically do. So of course, also in this patient, she is kind of the most classic textbook clinical picture of GCA that I have encountered as a resident. And it was very, of course, striking when she self-volunteered all that information in terms of jaw claudication and proximal muscle weakness. So there's some teaching points, especially as a resident that I took away from this case, especially it being a very memorable case in my last month of consults last year. So that of course we know steroids are not benign and we should do also everything in our power to not only facilitate diagnostic testing as soon as possible, but also work with multidisciplinary teams to manage these medications. That would ultrasound of course can aid in diagnosis and not only provide more information, but this was a great patient example of how this can actually really be a helpful diagnostic tool when a temporal artery biopsy is not possible or not safe to perform given the medical considerations. And then of course working with rheumatology is very important in the management of these patients, not only getting them on the appropriate dose of steroids and a safe taper, but also now that we have steroids bearing biologics that we can use at our disposal. And of course just keeping in mind those very rare systemic complications, but things like cardiovascular disease should be kind of in the back of our minds given this patient's outcome and then also working with cardiology or other teams to manage these conditions, especially kind of looking out for them during the one month immediately after diagnosis. So I just wanted to thank Dr. Harry, Dr. Warner and also Dr. Patel and as well as Anna Contino, she's the attending of cardiology. And then also some of my internal medicine friends for helping me locate the LED on coronary artery vascular anatomy for this presentation. So here are my references and I'd probably take any questions. Some things Catherine, I think Dr. Harry, you had a comment, right? Right, so I just kind of jump in here for a second. That was excellent Catherine, very good presentation and discussion. As you read the literature, especially rheumatology literature, there's a lot of variants. Some articles are very strong. Doppler ultrasound is going to take over and obviate the need for temporal artery biopsy. Others are iffy and say, well, it's not that great. You can do it, but you still need a biopsy. So kind of we're going back and forth. I think the study, we're starting with Mike Burrow and Abby's going to help with our goal is to get more numbers just to get higher numbers and get a higher sense of the value of it. So far we're pretty good. I think we've got about 22 patients in the study officially and a couple of others that were unofficial and were 100% so far, but I don't claim that's going to be forever. But unfortunately with COVID, like everything else, the study is kind of on hold. We weren't allowed to proceed until we kind of resolved the COVID situation. So we can still do them. It's not part of the study, but we can still do the biopsy. So like in this case, it's available. If you have a patient that's a problem with the biopsy or logistically or medically, we can still do the Doppler ultrasound. I think personally, if I see a case where it's bilateral, the halo sign, that's pretty strong. If I see that, I think we're really probably as good as a biopsy or better. Also the idea of the skip lesions in biopsies are always an issue. That kind of goes back and forth again. If you get a long section, probably it's not so much, but again, maybe Doppler could help in that sense to identify the part of the artery that doesn't have a halo sign and then guide the biopsy for that. So another role possibly for a Doppler at some point. So anyway, again, just a very good discussion. Thank you, Catherine. Thanks, Dr. Harry. This is Jeff Betty. I have a quick question too, actually. Are there points now where your pre-test probability is such that you're going to treat no matter what, we can forego a biopsy, even in the absence of ultrasound and then second, just indication contraindications for tussilism, ma'am. Yeah, I would say that actually I had a slide that I took out kind of for a time, but let me see if we can pull it up here. But the American College of Rheumatology, actually their diagnostic criteria that was actually developed in the 1990s, it actually has, if you guys can see my screen here, they recommend, they said that three out of five of these diagnostic criteria, so age over 50, nuance that localized headache, and then also a, or like scalp tenderness or temporal artery tenderness and then elevated ESR and then also a positive artery biopsy. If you have three out of five of these diagnostic criteria, that can be up to I think the high 90s in terms of specificity and sensitivity. Though some people, of course, have criticized this and it hasn't really been updated since the 1990s. So I think from rheumatology standpoint, if you have a very convincing clinical picture, even in the absence of the gold standard of diagnostics, you can go ahead and kind of treat as GCA. I think in our practice, we very, as most as possible, as much possible, as much as possible, we pursue diagnostic testing and then tussilizumab actually didn't get a chance to really review in terms of treatment contraindications. If anybody else has any comments, of course, to add, or if Dr. Harry has additions in terms of when to kind of forego, when we feel comfortable foregoing a biopsy. Well, thank you for that, Catherine. I would think in this case, given the presentation, no matter what I had seen on ultrasound or temporal artery biopsy, I can't imagine not going forward in treatment, which again would just be a question of whether, certainly with the biopsy it would be needed. Yeah, I think our concern was how to justify keeping this patient on a really high aggressive dose of prednisone. And we didn't have kind of something to more hang our hat on, especially since she had these cardiac events. And then also working with rheumatology to get her on tussilizumab more quickly. And then just if we had maybe, if we had tapered down her steroids too quickly, and she had a recurrence of disease, just things like that to consider in terms of feeling comfortable enough to go ahead to do that regimen. But I agree with you. It was already very convincing. Another question too is how long on steroids would you negate the biopsy or the ultrasound? So that's always been an issue. They say that you're safe to start steroids and do a biopsy within a few days. That's the kind of this classic teaching, but you know, how long? I saw one patient on it for 14 days. They still had a very positive halo sign. So that's another question to kind of answer this, how long would steroids be if they start affecting the biopsy results or the ultrasound results? Right, exactly. Catherine? Dr. Olson and Dr. Petty asked the question of steroid sparing agents, biologics, other immunosuppressants. You had touched briefly on tussilizumab. Can you clear up or sort of readdress that question of when the rheumatology service is using tussilizumab? Yeah, I actually didn't do that. I didn't really delve into that in terms of time, in terms of my own reading. So I don't have that information that readily available, but I can definitely look and then also. Okay. I mean, I think that just basically the answer for you, Jeff and you, Dr. Olson is that there has been a very large study of tussilizumab, which is a biologic. And it has proven to be a very significant. Um, steroid reducing agent and the rheumatology services basically starting everybody on it immediately. But it is not a steroid alternative. You would not use it in the acute setting instead of loading up with steroids when somebody's losing vision, but they definitely are using it to, to try and get people off steroids or to the lowest possible dose more quickly. And it does seem to be quite safe and effective. That's good. A methotrexate is sometimes also used in terms of a steroid sparing agent. Right. No other steroid sparing agent has been shown to be steroid alternative. Right. So it's not, instead of steroids, it's to try and reduce the dose of steroid. Right. All right. So just for sake of time, I think Dr. Patel had a comment in there as well. So we could read that, but I think we should move on to Mike Murray. Um, who is also a PG Y three here at the Moran ice center. Uh, so Mike was born in Salt Lake, but spent the first five of his life living in keto Ecuador. He went to med school, Baylor and Houston and his dream vacation spot is hiking and scuba diving in New Zealand. Um, Mike will be talking to us about a diabetic with blurry vision. So go ahead, Mike, once you get that screen shared. All right. Can you hear my microphone? Okay. Yeah. You can see my slides. Yeah. Perfect. So I'll be presenting today, uh, case, uh, senior retina clinic. It's a diabetic with blurry vision. Uh, she came in as, uh, with a complaint of blurry vision in both eye. Um, and she described, uh, she's a 45 year old female with past mental history of diabetes. She had NPDR in the right eye, PDR in the left eye on the Friday's ARDS hypertension. And she had been referred three months before for floaters and a shadow in the left eye, uh, from up to. In at Moran and was found to have vascularization elsewhere in the left eye and got PRP, uh, 844 spots with the other specific. And then she represented back to clinic for follow-up visit three months later. And we'll talk a little bit about this patient had a little bit of difficulty with compliance and follow-up and pain for things. So that's why it took so long, but she had continued blurry vision in the left eye and a new blurry spot in her right eye. So she said she had no pain, discomfort or flashes. Uh, she said she'd been using a lot of pseudo-fedrine for congestion the last couple of days prior to the visit. Um, and then just other past medical history things. Her last amnesty was 11.4. She described occasional headaches. Uh, she's often lost the follow-up. As I mentioned before, and she was more of a beast with the VMI in the sixties. History and surgeries were kind of non-contributory. Medication issues on diabetic and hypertension. Medicines occasionally took time. So, um, I was just a family history and the social history. I know smoking or drug use. So in clinic, her visual Q. Do is 20 25 30 at the visit three months prior. I had had a drop in vision from 20 70 at that visit three months before the 2250 pupils, extroactual movements were normal. The IOP was slightly elevated in the right. I'm not sure if exam anterior segment was relatively normal. She'd had Smithers hemorrhage in the right. I let it exam. She had some blurring of the disc margin in the right. And the cup to disc was about 0.2 in both eyes. Uh, there's also a blurring of the disc margin. I know. Acula showed, uh, and for a temporal NVE in the right. Otherwise in the periphery, she had new buds, uh, NVE nasally and dot blood heme in the right eye. And then she had some laser scars and, uh, dot blood hemorrhages in the left eye. And the past DFE from the three months before show this was kind of new changes. This is a fun this photo of both eyes. As you can see, uh, there's blurring of the disc margins more in the left eye. Is the OCT of the macular in the right eye. Uh, it was relatively normal in the left eye. However, uh, there was a, uh, an attraction will detect. So the differential diagnosis in this case, uh, we kind of go through, you know, vascular causes, uh, bilateral spontaneous CRBO, hypertensive optic neuropathy with retinopathy. I'm infectious causes. So she's a neuro retinopathy. H diabetic papillitis. And eventually macular. Uh, her blood pressure was checked. Your internet is really bad. Do you want to move over here? Yes. I just told me my internet was really bad. So I'm going to come over here. We got a mobile presentation. Yeah, that'd be great. And only as I'm walking, my internet is still not up at my house. Uh, so thank you for hurricane force wins in utsa. The. Joke that snowed yesterday. We had a hurricane force wins. So the locusts are coming next week. So beware. Um, okay. Her blood pressure was checked in clinic and it was elevated. Oh, Brad, could you grab two papers that are in there? Thanks. Uh, her blood pressure was checked in clinic was highly elevated. She was sent to the ER for further management. In the ER, she had labs, a CBC, a troponin were normal. Her CNP showed glucose that was elevated three 30. Uh, her UA had some glucose and yeast in it. And then her BNP was elevated. Uh, she had an MRI brain without contrast. It didn't show any concerning intracranial findings. And then her chest x-ray did show mild pulmonary edema. Uh, her echocardiogram and EKG were normal though. Oh, she was admitted for two days. Uh, diagnosed with high. It's thought to be exacerbated by her pseudo-federing use. It was quite copious actually over the last couple of days. And then also submit non-compliance with her envelope, a pain and her. High. So she had her blood pressure lowered with libato all, uh, and it was, uh, Also determined that she should get some LASIK diuresis for her mild heart failure. And then she was scheduled for fall up with ophthalmology two weeks later. Then at that fall up visit, uh, her vision was then 21 25 in the right eye and count fingers in the left eye. And if you recall her vision had been like 20 30 in the right eye and 20, you know, she was like 21 25 in the left eye. So still decreasing vision. And she's found to have new onset, Macula Dima, uh, and the right eye continued Papaladema. And then she had that persistent traction retinal detachment of the, uh, to dealing needs surgery. And she also needed more PRP in both eyes, but the patient was really reluctant because she had issues that. You know, happened temporarily to her after her PRP in the left eye. This is the fondest photo again, um, the blurring of the disc margins and that appearance of. Dima is greater, especially in that left eye. Um, you know, the vessel is definitely obscured there. And, uh, she still has that heme emanating from the disc and hemorrhages kind of throughout the retina. This is the right eye. As you recall before it had been normal. Now she has a new Macula Dima. She has a new Macula Dima. She has a new Macula Dima. And some intra retinal on both sub retinal fluid. A left eye continued to have this kind of tractional, a prancing of attachment and worse into Dima. This was an OCT of her retinal nerve fiber layer. Uh, as you can see, uh, worse in the left than the right eye, but both very thick end, especially on those, uh, graphs that you can see below. So at this point, um, I've asked an injections, um, in consultation with the neuro ophthalmology team, it was thought to delay retinal surgery for this tractional retinal detachment in the left eye until the optic nerve Dima, uh, was resolved because, uh, pressures can fluctuate during surgery and worries about that. Uh, uh, integrity of the left optic nerve. So, uh, the patient was started on dimox 500 BID and decided, uh, the course was to get an LP to measure opening pressure. And Macula Dima did not improve, um, in five days after that and then followed up in five days. So the patient followed up five days. This is three weeks total after that admission for the high. And the vision was still poor, but it had improved slightly from that. I could have Dima had slightly improved. Um, all right. So this is, uh, just an F a, uh, as you can see, there's leakage, uh, emanating from the optic nerve in both eyes. Um, but there was no vessel staining, uh, a non-profusion, uh, suggestive of like a CRVO picture. And finally, uh, just to kind of jump to the, uh, diagnosis, a lumbar puncture showed an opening pressure of 29 centimeters of water. And otherwise, uh, she had normal CSF studies. So, uh, the next visit was with neuro ophthalmology. Uh, this was one month after the admission. Um, and they confirmed, uh, the patient kind of didn't have many symptoms of elevated intracranial pressure, uh, dyplopia, transient visual obscurations, or pulse, tell tinnitus, but she did endorse a little bit more of a headache history. Oh, that was kind of daily mild headaches. And then I contrasted headed imaging was ordered as you recall in the ED, it was a non-contrasted MRI. And then an AA, CC, ESR, CRP Inc. It were ordered and the increased the dimox to 1,000 milligrams. Okay. So then this was the, uh, visual field that was taken. As you can see, kind of a global depression in both eyes, a little bit more patchy, uh, but with definite, you know, blind spot enlargement in that right eye. Um, and then, you know, kind of a superior RQ it, um, partial inferior. Uh, in the next visit with retina, um, this is two months after the admission vision was, you know, markedly improved 2030 in the right eye, 2060 in the left eye, uh, macular edema was resolved in the right eye and was just mild in the left eye. And then interestingly, the, uh, this tractional retinal detachment of the map. Um, so no plans were made for surgery. Um, but we did treat the macular DMI in the left eye. And the patient did actually agree to additional PRP in the left eye. Uh, so cumulative total was about 2000. This is just showing the resolution of that macular DMI in the right eye. And then in the left eye, uh, you know, that reduction of that traction. Then finally, four months after admission. Um, the patient had been lost to follow up. Uh, the patient actually contracted COVID-19. Uh, but still a relatively good vision. Uh, increased macular DMI in the left eye. That was kind of expected. Uh, she was supposed to follow up a little bit sooner. And then finally the, uh, you know, CT, uh, being a ground didn't show any signs of any signs of thrombosis. Uh, the sleep study was still pending and she hadn't received those lap plan was just to continue treating, uh, the right eye with a vast in, um, to prevent recurrence of this PDR, uh, hemorrhage and then to continue diamox 1500 BID per neuropath. So, uh, discussion a little bit about IIH. So mechanics, um, basically the optic nerve sheath, uh, is continuous to the subarachnoid space. And so increased pressure, uh, from that, back to that space gets transmitted through, uh, to the optic nerve. And then there's a gradient difference between the anterior end of the optic nerve and the intravenous. Welling, uh, the retinol gangling cells, occurs and then the common signs and symptoms that we got this transient visual obscurations and diplopia, uh, due to cradle nerve six, uh, dysfunction. And then signs on, uh, image or empty cell, uh, transfer sinus stenosis. Um, the incidence is, uh, one in 100,000, but it actually jumps to about 20 and 100,000. If they're, uh, women who are obese. And as you recall this, uh, patient had to be in my of 63. Actors. Eight in women. Secondary increased, uh, intracranial pressure is an interesting topic. Uh, we're trying to kind of purge out of the literature that this is the actually idiopath. Oh, tetracycline, vitamin A, OCPs, lithium, SLE, hypothyroid, OSA, would not be, uh, technically idiopathic intracranial hypertension. Um, just want to talk a little bit about the modified dandy criteria. Um, so the above picture is Walter Edward dandy. It's interesting. He was born in 1897. He was the son of a railroad engineer, but became the father of pediatric neurosurgery. Um, dandy Walker malformations, a bunch of different things that he's famous for. He described, uh, four criteria. That eventually were codified in the 1980s by a Dr. Smith. And then our very own doctor degree, um, added the criteria listed on here, number three and number six. Um, and so this is kind of the criteria that we use to diagnose IH. Um, there is about the production of CSF versus the drainage of fluid. Um, some people think that, you know, in excess of CSF production or an increased volume of blood or brain tissue cause an overproduction issue. Um, there's also, um, there is about the obstruction of the venous plexus draining, um, which can cause problems. Um, absorbing through those arachnoid granulations. And then this kind of, uh, wicked feedback. Any case, diamox works to inhibit the carbonic and hydrous and the chloride plexus and reduces a CSF production. Um, just to shift gears a little bit because, uh, we had kind of thought that this, uh, edema and decrease in vision, uh, could be due to Mac of the DMA. Oh, looking into that a little bit. Um, and in a recent study, uh, 76 eyes that got treated about 14 eyes still had worse in visual acuity at three months. So, uh, worse in visual acuity at a month or a week after is quite common. Um, and, uh, um, um, um, um, um, um, um, um, um, um, um, um, um, um, and, uh, they did have, you know, macular edema that was, uh, substantially thickened and they also had sub foveal serious detachments and about 69. So that's, you know, 10% of these eyes. So it's not uncommon. And, uh, not unusual to see after PRP. Other hand, um, in a recent study of 55 patients that had papillodema, five patients. Um, so a little bit less than 10% have, I don't see, um, a rise from the parapabular region, um, from my age specifically. Um, so usually, and I was looking up the, from the parapabular region, um, from my age specifically, um, so usually, and I was looking up the analysis. There's this tissue. Um, it's called the嫌emiter. Mediatric northern tissue of cunt. And that's glial tissue that kind of has a ring around the optic nerve and creates type of fluid from the optic nerve into the retina. and then you have some continuity between this subfoldial region and the optic nerve. Often, this is why, and this is a table from that study, the fluorescein angiogram doesn't show leakage into the macula from the vascular, or instead of vascular leakage. Okay, just a little bit about, you know, hyperreflectives kind of subretinal spaces on OCT. I know we're getting a little short of time here, but there was a study by Savini, 12 eyes who had various types of optic dystidema, and they talked about how their theory was that in addition to leakage of fluid, extensive swelling of the optic nerve can actually elevate and create kind of a tractional separation between sensory retina and RPE, and this might have been actually what was going on in the left eye of our patient. This is not heavily reported, but it certainly makes sense to have some traction and kind of vitro macular traction due to elevation of that optic nerve. Just in the interest of time, other entities that I looked at that can cause both optic nerve edema and immaculate infection, diabetic papillopathy. This was reported a little bit more in patients who have a quick reduction in their sugar, which could have happened to her in the hospital, but we're kind of looking at initial presentation for her. Something that that diabetic papillopathy is actually from with NAON because of it's kind of a reversible ischemia of the pre-laminone nerve tissue, but honestly we don't understand it very well. And then obviously hypertensive retinopathy and subrenal fluid from NAON. One interesting study that I found found about 10% of patients, eight out of those 76 patients that did have evidence of sub-phovial fluid in NAON and their FA should stay in the optic disc but didn't have accumulation of fluid around the macular. So it was truly thought to be from the nerve. Just a couple of take-home learning points. Thinking about horses versus zebras, we're thinking about bilateral CRVO, which is rare and associated with cancers and stuff like that. Their horses, IAH in this case, may have been a little bit more likely versus a zebra. The other importance of checking patients' vitals in ophthalmology clinic, it was a good catch to check that her pressure was actually 220 over 100 and though that didn't end up being her final diagnosis, it certainly was not healthy for her. And then getting a multidisciplinary approach involving her ophthalmology is definitely important, especially in these complicated patients. And then finally, intervention is not always the answer. Classically, you would want to repair a tractional retinal detachment at least within a month and do it kind of quickly. But delaying surgery was obviously the right choice here. And with proper treatment for papillodema, the macular edema and that traction is all done on its own. These are my references. Big thanks to Dr. Wong, Dr. C, and I'm happy to take any questions. Stop staring at my screen here. Great presentation, Mike. Are you guys able to hear me? Can anyone hear me? I can hear your audio clearly. Oh, okay. Yeah. Thank you. So I just wanted to clarify, you know, one point here, which is that when she developed the macular edema, it was two weeks after she developed the optic merivadema. So I didn't treat it with a vasten because I did not think it was diabetic macular edema, usually diabetic macular edema. I don't think developed that quickly. So I expected that with controlling the optic merivadema, that macular edema would improve. And that was the case. Sorry about that. We got some feedback from you. Thank you, Elaine, for the clarification. Let's see. I think Dr. Warner wanted to be unmuted for a comment real quick. Well, she has a lot of medical problems, right? And so I was wondering what you were thinking about, you know, her hypertension causing the disc edema. Some people with very bad hypertension can have elevated intracranial pressure. Most do not. And the other question was about her congestive heart failure. I don't know how detailed the look into that was, but obviously right heart failure can also lead to quite intractable elevated intracranial pressure. You know, we all remember back in medical school looking for jugular venous distension as a sign of congestive heart failure, but those jugular veins are coming from somewhere. Yeah, I think it's definitely something that first I'll take the hypertension question that for her, obviously she wasn't controlling her hypertension, but I think what made us think less that it might be the root cause was that once she had it well controlled, the nerve edema persisted in those visits afterwards. As for playing a role in the etiology, you know, of why her feedback loop got started, et cetera, could definitely be playing a role. I think also her BMI is here. And then for the CHF, her echocardiogram in the ED showed that she had mild, I think it was right and left heart dysfunction because she did have some kind of pulmonary edema that was backing up, but I think they thought it was left heart causing right heart. And once they diarhesed her mildly, that got better. And then I think Dr. Hartnett would like to be unmuted potentially. Ethan, did we get Dr. Hartnett unmuted? Okay, Dr. Hartnett. Yeah, thank you. Very interesting case. Thank you, Mike. Nice presentation. So it, you know, in retrospect, I agree, there wasn't a lot of vitriol macular traction in that left eye. It's not always easy to see that, you know, at the at the first step when it's so complex. But one of the things to think about when doing PRP is to limit the number of spots per session, especially in those eyes that not only have PDR, but have signs of extremely severe, non-proliptic diabetic retinopathy, which I think are signs that can be also similar to inflammation that you see would see on a fluorescent where you might have staining vessels, but those would be like venous beading or Irma or lots of hemorrhages. And the reason for limiting it is the same way when we think about the crunch phenomenon in giving a vast in that when you do a lot of PRP, you may be reducing the angiogenic drive a lot, but you're also probably increasing inflammation as well. So just something not necessarily related to this case, but just I think can be helpful. No, I think that's definitely it was at, you know, the top of our minds differential wise, because she had had that PRP in the months before. So I think it's definitely a good point. All right. Thanks everyone for comments. I think Megan always wants us to remind the CME link is in the chat if everyone needs it. And I'll kind of mute myself if anyone has other things to say or Ethan, if you need to tell us anything, let me know. Mike, I think there was one more comment by Dr. Huang. If hypertension or CHF caused her nerve edema, wouldn't it have improved with control of hypertension or CHF? Yeah, I think that's what we were talking about how the interplay between those sort of got resolved because the ED helped us resolve her, you know, hypertension and CSF day or Easter controlled her hypertension and then she had persistent nerve edema. But I think it's definitely something that is common and we can always think about. All right, I think that's it. Go ahead and wrap up. Thank you for everyone for joining and thanks to Catherine and Mike for your presentations.