 All right. Good morning. Good morning, everyone. Welcome to our first sub specialty grand rounds of the year. We're very pleased to have our neuro ophthalmology department here presenting to us. Just as a reminder, for those who are relatively new to the department, we do sub specialty grand rounds. Each division is responsible for one day each year. And this is really an opportunity for your division to get in front of the faculty, update us on what's new, if there's new procedures, new staff, new medications, new surgical procedures that we should be aware of as faculty. This is a great opportunity for you to update us all on those. And then really a great opportunity to showcase some of the interesting cases that are coming your way and utilize your fellows to help us learn. And so with that, I'll turn things over to our neuro ophthalmology division. Thank you. Thank you for the kind introduction. We're just going to go ahead and get started. Our first presentation is a clinical presentation from Riley Philbin, who is our pediatric neurology resident rotator. I'm sure that all of you, many of you have worked with her and she was awesome. Thank you for the videos from the screen. Cool. I don't need them. Hi, my name is Riley Philbin and I'm a child neurology PG by three. And I'm going to talk to you guys today about an ocular movement disorder case that I admitted while on service with PCH neurology at primary children's and then was able to see during follow up in Dr. Bagunta's pediatric neural neuro ophthalmology clinic. So this is a previously healthy six year old who presented with difficulty moving her eyes for the past two weeks. Two weeks ago, the right eye began appearing isotropic followed by one week later, the left eye appearing isotropic. There had been recent suspicion for a GI illness with vomiting and sore throat prior to symptom onset with no other major changes. The patient began bumping into objects frequently, having more difficulty navigating the stairs was growing has a tete amulet. There were no reported falls or concerns for head trauma during this time. But her mother also noted new slurring of her words and avoidance of eating social history was significant for a recent move from Hawaii. In the primary position her eyes were notable for isotopia bilaterally left greater than right after an examination revealed 2030 vision visual acuity in the right eye with 2025 in the left eye with normal color vision bilaterally and no RAPD present The front examination revealed equal pupils with risk reactions minus five adduction deficits bilaterally minus two adduction deficits bilaterally intermittent vertical nystagmus will motility on up gaze and down gaze Intermittently able to briefly adduct each eye with significant effort and the ability to adduct on convergence with the oculosephalic reflex being absent neurologic exam was otherwise notable for Possible dysarthria but preserved deep tendon reflexes stereo acuity was zero for three and animals and zero three for circles. Now I'm going to play some videos and this was once the patient was admitted. This wasn't her first presentation. The one eye at a time good all the way up and it has sound too. So in the first vision video, you can see that the right eye has full super reduction and in production with minus five adduction and minus three adduction. Little bit there. Good job. Okay, switch eyes for me. And then on the left eye, you can see are also full with super production in production with a minus five adduction deficit and minus three adduction deficit go down towards your toe. Way down. Good job. Now we're going to do right and left. I know that's the hard one. Good. Good job. Okay, she's very cute. Now the last thing uncover your both eyes. And then this next video. Good. One night at a time. Good. All the way up. Good job. Yeah. There we go. This next video just highlights the component of her vertical nystagmus and up gaze. Good. Go all the way up again for me. Good job CC. Good job. And then this last video highlights her overcoming her adduction deficits with convergence with some significant effort towards the end here. Good. Perfect. And I go all the way. Okay, so initial exam was concerning for possible bilateral accommodative spasms and she was discharged with very close outpatient follow up. Exam three days later in clinic grew increasingly concerning for bilateral horizontal gaze palsies and she was subsequently directed admitted to the PCH hospitalist service with neurology and ophthalmology consulting. At this point, her differential was most concerning for a demyelinating lesion either something acute like a post infectious syndrome or the initial presentation of a more chronic condition. A brain tumor that particular localization most concerning for diffuse midline glioma are formerly known as the infamous DIPG some sort of active ongoing CNS infection as well as nutritional difference deficiencies such as B12 or folate deficiency. On admission MRIs of the neuro access were obtained with pertinent findings noted within the brainstem as you can see in these pre and post contrast images. So this demonstrated confluent T2 flare hyper intensity and enhancement within the peri aqueductal region dorsal midbrain dorsal pons and dorsal medulla extending to the region of the OBEX with a geographically separate lesion highlighted by the arrow. At the right ventral cervical medullary junction this involved the facial colliculi and abducens nuclei bilaterally and the presence of the geographically separate lesion suggested that this may be more representative of a post infectious or inflammatory demyelinating process neoplasm at this point was considered less likely but not entirely excluded. And then this is just the axial views of the same lesion right through here and right through here and on the other one you can see with these arrows this kind of more extensive lesion at this point as well as this separate satellite lesion at the junction. Perfect. Thank you. There we go. Perfect. And of course now it's gone on the screen. So thorough autoimmune inflammatory and infectious workups were initiated following MRI with pertinent findings outlined in red including positive aqua porn for and glial fibrillary acidic protein antibodies as well as a strong lung cancer. The rest of her workup was overwhelmingly negative with the workup results that were available at the time neurology and ophthalmology both felt comfortable treating this as a post infectious process with a five day course of high dose methyl prednisone. Unfortunately there were minimal improvements in her speech and eye movements during this time. She then underwent a two day course of IVIG. With rapid return to baseline of speech and significant improvement in her eye movement abilities. She was discharged on 60 megs per gig or 60 megs per day of prednisone with a taper with further considerations for IVIG treatments if her progress plateaued. And then she was discharged on 60 megs per gig or 60 megs per day of prednisone with a taper with further considerations for IVIG treatments if her progress plateaued. So final diagnosis still to be determined or hopefully maybe probably not her aqua porn for and you've had titers were very low and likely represent Paul false positives. These same antibodies were also tested for separately on her erupt demyelinating disease panel and were negative on that panel. Pete's autoimmune neurology was unable to send any repeat testing on her CSF studies as it was rejected by Mayo Clinic for add on due to degradation of the sample in storage. This patient was last seen August 10th and Dr. Vaguntas Pete's neuro ophthalmology clinic with improvement in her bilateral horizontal gaze palsies disarthria and isotropia and is now wearing glasses and isotropia. Unfortunately, the family had to cancel their first Pete's autoimmune follow up appointment, but this has been rescheduled for today, September 20th with Dr. Lou. So hoping to be able to attend that this afternoon and see how she's doing. So this slide serves as a brief anatomy overview for anyone like me who doesn't know what to do. But bilateral horizontal gaze palsy is a rare presentation caused by bilateral interruption of the medial medial longitudinal fasciculus, abducens nuclei, or paramedian pontine reticular formation, or a combination of the three. This lesion, the lesion in this slide serves as a brief anatomy overview for anyone like me who doesn't have all of these memorized, but bilateral horizontal gaze palsy is a rare presentation caused by bilateral interruption of the medial medial longitudinal fasciculus, abducens nuclei or paramedian pontine reticular formation, or a combination of the three. This lesion, the lesion in this patient appears close in proximity to the abducens nuclei and to the PPRF containing the excitatory birth cells for horizontal gaze. Bilateral involvement of projections from the PPRF or the abducens nuclei would be able to explain her horizontal gaze palsy. The key difference, kind of theoretically, in differentiating between these lesions lies in assessment of the oculospallic reflex. In the most simplified version of this arc, angular rotation of the head causes endolymph in the horizontal semicircular canals to rotate opposite to the direction of the head, causing activation of the ipsilateral vestibular nucleus with inhibition of the contralateral vestibular nucleus, causing the doll's eye reflex that we've come to know. Both vestibular nuclei then activate or inhibit both abducens nuclei, which send signals to the corresponding ipsilateral lateral rectus and contralateral oculomotor nucleus through the MLF. The abducens nuclei are imperative in this reflex arc, and the absence of the oculosophallic reflex in this patient would theoretically localize this lesion to the bilateral abducens nuclei. The oculosophallic reflex is often preserved in an isolated PPRF lesion due to a direct connection from the contralateral medial vestibular nucleus directly to the abducens nucleus, which can bypass the PPRF entirely. So while there's not a whole lot of literature of pediatric horizontal gaze palsies, I did want to briefly highlight this case of an 86-year-old male with left internal capsule stroke who could not initiate horizontal saccades to the right with preserved oculosophallic reflex consistent with super nuclear right horizontal gaze palsy. Anatomically the frontal eye fields are located between the premotor and prefrontal cortex and crucial for super nuclear control of horizontal conjugate gaze. Descending frontal eye field fibers project to the PPRF in the brainstem, and lesions of this circuit at the PPRF abducens nucleus and or the MLF can produce various horizontal ocular deficits. The majority of stroke cases with conjugate gaze deviation are seen with cortical lesions affecting the frontal eye fields, as opposed to this case which demonstrated disruption of frontal eye field fibers in the anterior limb of the internal capsule. The intact oculosophallic reflex and rapid resolution of this gaze palsy in this case is more consistent clinically with frontal eye field super nuclear lesion compared with a pontine lesion. Neuroimaging did not end up identifying any sort of pontine lesion in this patient that would otherwise have explained his deficits. This case just further highlights the anatomic localization of these various pathways as they exhibit control over components of horizontal gaze. So once bilateral horizontal gaze palsies have been identified, there's a wide differential to consider. It is most important to note that the likely etiologies differ significantly depending on the age of the patient. In adults, bilateral horizontal gaze palsies are highly concerning for multiple sclerosis, and cerebrovascular accidents represent the most common unilateral cause of horizontal gaze palsies, together with MS accounting for more than 50% of cases. In pediatric patients, post infectious etiologies are thought to be the most common presentation of horizontal gaze palsies followed by brain tumors. Other etiologies considered in pediatrics that would less commonly present in adults include cure email formations, nutritional deficiencies and metabolic conditions. There's also concern that this may represent an initial presentation of a more chronic demyelinating lesion in this patient, particularly since repeat antibody testing could not be performed. So one last note I wanted to touch on is why did it look like this patient had accommodative spasm in her initial visit to the ED? So it turns out that this phenomenon has been reported during attempted ABduction in patients with horizontal gaze palsies. These paradoxical movements are theorized to be part of a near reflex substitution in which meiosis and myopic shift in refraction accompany the convergence movements. This has been well described in a pediatric patient with right-sided facial colliculus syndrome due to a pontine AV malformation, which manifested as near reflex substitution and convergence spasm on attempted rightward gaze. The authors proposed that the lesions of the version system, which are located in the ponds, would result in overactivity of the virgin system located in the midbrain, and this clinically may present as accommodative spasm. The mechanism of this rare ocular movement disorder is still not clearly understood, and there's ongoing debate regarding whether this is secondary to a peripheral infranuclear mechanism or a central super nuclear mechanism. But regardless, this article was helpful in explaining why her depresentation very did closely resemble bilateral accommodative spasm. In conclusion, bilateral horizontal gaze palsies in pediatric patients are rare, but the differential is broad, particularly within Peds. Involvements of cranial nerves, other cranial nerves can help guide level of concern for the localized lesion versus a more systemic process. And like in our patient, we may not confidently identify the ultimate cause of onset. While we hope this represents a one-time event most consistent with acute disseminated encephalomyelitis, she may end up having some sort of relapsing, demyelinating condition that will need to be followed more closely over time. For now, follow-up will be most pertinent to monitor eye position and response to treatment, while in the long term the patient will need to be followed to evaluate for any new neurologic symptoms. And that's the end. Those are some sources. Yep. They did the MRI at the subsequent when she was direct admitted. So yes, she really did not get a scan of the first visit. So we were called initially at our easy ED visit and her exam wasn't quite as profound as it was the next day. Her lethargy and her poor speech and all of that. But yeah, probably should have gotten that scan the first time around. I can also comment on that because I actually was the one who saw her in the ED when she first presented. It was a really tough exam. I see a lot of kids in a lot of different stages of life in the ER. And when we first saw her, she was old enough. She couldn't read the eye chart to do like the near chart to do numbers. So she didn't know numbers. We were doing visual acuity with the tumbling ease. I tried even having her do the color plates to kind of boost her ability in the exam. And so I wasn't really sure if she was just like super shy. She was in the ER. She just had this huge move. And it was really hard to get her to participate. Now looking back, it's very obvious that those were symptoms of what was going on. And so I reached out to the neuro ophthalmology service and was like, I'm actually not sure. And we elected for prompt follow up. So I'm going to have to get it down first. Sorry, what was the question? Dr. Long. Oh, sorry, did did she have those abduction deficits when she was first seen? She did. And and now, I mean, looking at those videos, right? It looks really obvious when she's in the ED, but she was almost so flat. I was like, if she's just like not and then given how she participated with like visual acuity exam, confrontation, visual field testing. I was just like, is this girl just like, is there actually something wrong? Or she's just like not participating in the exam. And so I was, I was really unsure what was going on. Yeah, I mean, I think there's a good learning there with the new abduction deficit. I mean, I am baffled as to how she didn't get a scan in the ED. Even if you are convinced of accommodative spasm. I mean, we could have dilated her to and see what that did with the with the with the accommodative spasm, but often a lack of information from the patient to means that we need to dig a little deeper. No, easier said than done. I know, but yeah, interesting. How is she now? Is she still isotropic? Is she still over a month ago? How come we're patching there? The answer was yes. She's still eat. She was still isotropic, but that was a month ago. She was closing one eye a lot because because of our isotropia. So we're patching the contralateral. I did encourage her to use it. Interesting. Okay. Do you have any thoughts? Do you have any thoughts, Bob? Bob just took a giant bite of food. So of course he got called on. Okay. Dr. Katz's presentation is is the main the main show here. And so we're going to I'm just going to breeze through this because his presentation is downloading. I just wanted to briefly mention a an addition to our temporal arthritis protocol. Which should shortly be on pulse. As you know, we have a current temporal arthritis protocol. You can search under GENSA arthritis or temporal arthritis. As you know, this is a condition of inflammation of the medium sized blood vessels, which mostly affects the older population. And the constitutional symptoms are somewhat nonspecific, often associated with polymyalgia rematica. I wanted to mention a scenario in which a 65 year old woman with a diagnosis of fibromyalgia, presents with a new headache, but specifically not jaw claudication. She has no visual symptoms. Her said rate is just a titch elevated. Her C reactive protein is two platelets at 240, which is normal. Her primary care physician who just went to a CME program on temporal arthritis calls for an urgent temporal artery biopsy and started steroids immediately. So one of the things that you can do is you can go to Dr. Ings. Really amazing normal gram online where you can calculate that the risk of GCA in this scenario is about 8%. So not super high, but not zero. Dr. Harry is out of town. And so what are you going to do? You're going to call the surgeon and get a stat temporal artery biopsy? Well, I want to ask you to consider adding this to your regimen for this type of situation, especially vessel wall imaging is a high resolution MRI technique where you use gadolinium to enhance the wall of large and medium size blood vessels. And there's a protocol available through our radiology department and Scott McNally is the point person and can be phoned, paged, called at any moment, day or night. Just mentioning the literature. There was a study in 2017 prospectively of lots of patients, many of whom had biopsies, some of which were positive. That's actually a pretty high positive rate on biopsies. But the MRI was abnormal in 60 patients. And my favorite statistical useful thing is the positive and negative predictive value, the negative predictive value. So a normal MRI of the blood vessel wall predicted normal temporal artery biopsy in 98% and a positive predictive value of 48%. So not super specific, but quite sensitive. And there was a second study out of Germany, which is extremely granular in comparing radiology and skip lesions and all that kind of stuff. But it's similar type of results. And so both studies showed a loss of sensitivity after about five you five days of corticosteroid use. So you do have less than five days of steroids to get this done. Temporary biopsy, you have several weeks probably temporal artery ultrasound, according to Dr. Harry, you can lose a positive in a day. So we ask you to add that to your regimen. It's not necessarily inexpensive. It's not necessarily easy to get, but it can save people a temporal artery biopsy. It can also make a diagnosis in a patient in whom a biopsy may be contraindicated because of medical issues or gadolinium sensitivity can sometimes be an issue. We had a really great patient for this, but she was truly allergic to gadolinium, so couldn't get this test. So she I believe ended up with a negative temporal artery biopsy. So I just wanted to put in a plug there and the updated protocol should be on pulse. Thank you. Brad, I think is next. Oh, Kathleen, I think is next. I don't know how to do this. So. What's new. Press the right button. Yeah, thank you. Well, I, I want to bring up three things that you should know about idiopathic intercranial hypertension in 2023. Our treatment goal to start with is really to prevent visual loss and we have a great protocol for fulminant progressive visual loss with papillodema and you should all be aware of that. And we all know that we do medical therapy first for patients with IIH, but if their vision progresses, we do a surgical procedure. And I'm going to talk about a new procedure that's gaining traction. The second thing is we want to reduce the headache because we've really found that headache is what drives the visual quality of life. So as your headache worsens, your visual quality of life also worsens. So we want to improve vision and we want to improve the quality of life. That means we have to take care of the headache. So the first new thing is that IIH is now being considered probably a metabolic disease that abdominal adiposity can affect venous pressure and then venous pressure can increase the intercranial pressure. And we're finding out that there's an increase in insulin resistance in women who have IIH compared to BMI and age match controls and there are also inflammatory markers. And this brings up a new treatment that is being proposed for IIH in addition to lowering the intercranial pressure. And that's a glucagon like peptide or a GLP1 agonist. This is in the news. I'm sure you've heard about it. But this is a gut neuropeptide secreted in the small intestines and it's been used for diabetes and weight loss. And it does a couple of things. One is that it inhibits glucagon release and lowers the blood glucose. And then it signals the hypothalamus to say, hey, I'm full and I don't want to eat anymore. Plus it causes nausea. And the other thing about this is these receptors is they are in the chloride plexus. And in laboratory animals it was found to reduce the intercranial pressure. And this drug is in the news. It's being touted to improve diabetic retinopathy, glaucoma, you name it. But for IIH this is what we're looking at right now. You're going to hear different names for this drug. Exenotide also goes by biata. And then semi-glutide is wegovi, wejovi, and ozimpic for diabetes. And it's the same drug, but it's got a different trade name depending on what it's treating. And it does lower the weight by 15%. It has been studied in IIH. In Birmingham, England they inserted little sensors to follow the intercranial pressure. In 16 patients who were enrolled, it was a prospective trial. They all had this pressure reading at two and a half hours, 24 hours, and 12 weeks. And this drug did lower the pressure at all of those time points. And then there was an open label trial of 39 patients. 13 had received the GLP1 receptor agonist. And 26 had usual care. Weight loss was definitely increased with the GLP1 group. There was no difference in the visual outcome at six months. The headache, it did improve a little bit more with the GLP1. And the big side effect was nausea. The second study for weight loss is the bariatric surgery trial that just came out. This was a trial that randomized 66 women with BMIs over 35 to a weight watchers program or a bariatric surgery. And it did lower the intercranial pressure. And the RU&Y procedure was the best procedure for weight loss. And they lost a lot of weight. Their quality of life did improve. Their headaches did not improve. And remember that weight loss surgery and weight loss alone is not going to fix the vision right away. So we still have to follow the vision very carefully. So there were no deaths, but there was one bariatric surgery complication of obstruction. Okay, the other new thing that I want to touch about is venous sinus stenting. We have known for many, many years that as the venous pressure goes up, the intercranial pressure goes up as well. And you can see this graph from 1934 where the CSF pressure rises as the venous pressure rises. And this brings up the fact that as our venous pressure rises, you can get venous outflow obstruction because the vein will reduce itself. And then you get venous hypertension. You get decrease in CSF absorption. Then you get increased intercranial pressure. And then you get more stenosis. And many times in our patients with IIH, we see this venous sinus stenosis, either unilateral or bilateral. So the new kid on the block for treatment of IIH is venous sinus stenting. And the indications are usually when you have a big large arachnoid granulation, as you can see, I think my arrow is working or maybe not. But anyway, you see the big arrow there at the arachnoid granulation. And also the septi are also present. And you can stent across these. Here's a stent going through the septum. The indications are it has to have greater than eight millimeters of mercury, pressure gradient across the stenosis. And the pressure really has to be elevated at 220 or 2020 millimeters of mercury. And these people have to be on clopidrogel and aspirin. So there can't be any contraindication to that. And it has been used for severe disabling headaches associated with intercranial hypertension, focal neurologic deficits, rampant papillodema, and visual changes. There was this large metadata meta-analysis that came out on 49 studies, 250 patients. And you can see that the pressure improved in almost all of them. The transient visual obscurations also improved, pulsatile tinnitus improved, headache resolved in 37% improved in 41%. But of all the parameters that again was the least likely to resolve. Papillodema did resolve in 41% and improved in 38%. But there are complications. And the main one is thrombosis. There's been subdural hematomas, intracerebral hematomas, cerebral edema, stent migration, and even death. So if you're going to look at all of our procedures, you can see that in this review, it was a wonderful review that looked at all of them. You know, nursery fenestration really is very helpful for papillodema. But the other procedures do treat at the stents, the shunts. Visual fields improve in all. Most of them have some headache improvement. Maybe the optic nursery fenestration is the least. And then you can see that all procedures have complications and shunts. The problem is about half of these can fail. And so we kind of shy away from shunting. So in conclusion, IIH is most likely a metabolic disorder. Definitely more work needs to be done. I think it behooves all of us to know about the GLP1 agonist about weight loss. We don't really know what the effect is going to be for headache or visual loss. Weight loss surgery is a treatment for weight loss, but not for visual loss. And stenting may play a role in treatment of some patients that don't respond to medical therapy or some of our other even surgical therapies. That is all. Do you have any questions? Yes. How long does it take to see the results of the stenting? So from the papillodema to go away? Well, the pressure will go back to normal almost immediately after the stent. And as you know, papillodema is very variable from person to person what actually happens. But the pressure will lower almost immediately after the stent. And then the papillodema usually gets better within a few weeks. But 30% is the female preponderance. So the question is about women and metabolic disorder and the female preponderance. Well, we do know that obesity, diabetes and this metabolic syndrome is more frequent and women all by itself. People with IIH are more prone to, let's say, polycystic ovarian disease. And so there are these metabolic and endocrine abnormalities that are being thought to be more prevalent in women than in men. You know, the answer is definitely not out there. But you know, we have a lot of obese men and we don't see that much IIH. It's got to be the hormones. So apparently there's going to be a fire drill at any minute. So it is a drill and we're not supposed to evacuate. So I do some medical legal consulting as a side hustle. And it's actually very interesting. I learn a lot about how doctors think, how lawyers think, and also really see some interesting medical things go wrong from which one can learn. And so I got permission from a plaintiff who had sued her ophthalmologist because they missed the diagnosis of the tuatary tumor. I got her permission to present her case here just for an example of like what not to do as an eye doctor and also kind of get a little insight into how the medical legal system works. These are my financial disclosures. They're not relevant to today's presentation. I was inspired by this article by Noble David in 2006 where he also did some legal consulting and he presented six cases in the Journal of Neuroothemology where ophthalmologists had been successfully sued for missing the diagnosis of pituitary apoplexy. For those of you that didn't read the presentation that I sent by email, this is a 55-year-old patient with two weeks of decreased vision and one day of headaches. On examination, she's got hand motions, vision, and atherm pupillary defect and a pale nerve and one eye. She's diagnosed with ischemic optic neuropathy, told to come back in six weeks. At six weeks, her exam was unchanged. The eye doctor told her to get it evaluated for sleep apnea because she didn't have high blood pressure diabetes or high cholesterol. At 12 weeks, she went and she was supposed to come back in three months, but instead she came back in 12 weeks. No, anyway, she came back early. Now she's got 2,200 vision in her previously unaffected eye. To make a long story short, she went to the emergency room, had an MRI scan which showed a pituitary tumor that was resected, and then she ended up being no-light perception in the one eye and 20-30 in her previously unaffected eye with a dense temporal defect. She was left with just a nasal crescent of vision in one eye, and she ended up suing her the vitreo-retinal surgeon who misdiagnosed her with ischemic optic neuropathy. I was going to ask Dr. Kennedy if the retina doctor deviated from the standard of care, but he's in the OR at the VA. Oh, brilliant. Do you have a microphone? I do, so I can answer for Brandon. I was thinking about this question earlier this morning and I found it a little difficult because we get such good neuro-ophthalmology training here at the program, and so I'm not sure of that skews how I see this, but I personally feel like he might have deviated from the standard of care. There were two big points that stood out to me, and this actually goes to my own question, I think number three, is that when we all learn in general medicine, even through neurology, that if you have a headache with any of these red flag other things, like this patient was over 50, I don't know if it's her first one, but then it was also, it could have been a new headache, but really it had visual symptoms and exam findings along with it. Usually when that happens, it's like a straight way to get imaging right away. And so I think that's a first point, but the other thing that struck me too was that he sent the patient back to the optometrist and there was more vision loss. And that was also another huge red flag that we should be investigating more instead of just chalking this up to a new, or like a refractive error. And so for me, yes, I think he did deviate from standard of care. Okay, yeah. No, I agree with you. And I think this case was settled. It didn't actually go to trial, but I think the defense attorneys were also convinced that maybe their client had deviated from the standard of care. So the question is, did the retina specialist order a sedrate in a CRP? He did not. And you know, I don't know, the patient's 55 years old, her risk of giant slarditis is pretty low. That wouldn't be the first thing on my mind, but he didn't order any tests actually that I know of. Dr. Sauer is going to tell us if the optometrist who originally saw the patient deviated from the standard of care. Maybe, yeah, no. So I think one thing that the optometrist realized is that he didn't know what was going on and that he needed to refer the patient to somebody else who might be able to figure it out. But in terms of did he deviate from the standard of care, I think yes as well, because we all know that to get into retinal specialist, it takes some time. And this patient, as Tony mentioned, obviously had some red flags and needed to be examined and seen a lot sooner. And I think the correct way for the optometrist to refer this patient would have been to the emergency room right away because there was an optic nerve, a pale optic nerve with Audi Dima and that warrants imaging, especially in the setting of vision loss and the new headache. He should have sent the patient not to retinal specialist that can't see them for six weeks, but to the emergency room to get imaging and be seen the same day. Yeah, so I think Dr. Sauer brings up a good point and that is that everything in medicine is kind of black and white. You're pregnant, you're not pregnant, you're alive, you're dead, you're sick, you're well. But everything in the legal system is gray. Nothing is black and white in the legal system. And so this is a gray area because the standard of care for an optometrist is different from the standard of care for an ophthalmologist. And so as an ophthalmologist, I actually can't testify to the standard of care for an optometrist. You actually have to get an expert witness who's an optometrist to express that opinion. But I actually think the optometrist did the right thing. They knew that they didn't know what was wrong with the patient and so they referred them on. I mean, they should have referred them to an optometrist, but at least they knew that they didn't know what the diagnosis was and needed some help. Whereas I think the retina specialist also didn't recognize that they didn't know what was wrong and didn't recognize that they needed to ask for help. Dr. Etheridge, was the ischemic optic neuropathy diagnosis reasonable under the circumstances? Is Tyler here? Okay, so I will answer for him. So I'd say the sine qua none, that means like that with which out one, it doesn't exist. For ischemic optic neuropathy is a swollen nerve. So if you see a pale optic nerve, you cannot make the diagnosis of ischemic optic neuropathy. Now, you could be right that that was what actually happened, but you actually have to have seen a swollen optic nerve in order to make this diagnosis. And the swelling should resolve within about six weeks or so. So I think that the retina, I really fault the retina specialist. Again, you can't assume that just because ischemic optic neuropathy seems like the most likely thing in a 55 year old with no risk factors, then you can't make that diagnosis. Okay, so Dr. DeSautel's was going to talk about posterior ischemic optic neuropathy and its prevalence compared to a compressive optic neuropathy. Yeah, so the short answer to this is no, posterior ischemic optic neuropathy is not more common than a compressive optic neuropathy. There's not a lot of incidence data out there about this for ischemic optic neuropathy on the aggregate comprising both anterior and posterior ischemic optic neuropathy is the overall rate, you know, you're looking at something on the order of like two to 10 per hundred thousand in the US population. But series that have looked at posterior versus anterior ischemic optic neuropathy within ION as I've been seated about only 4% of ION cases are actually P-I-O-N. So the incidence is probably somewhere closer to 0.08 to 0.4 per hundred thousand. So it's certainly much, much less common and compressive optic neuropathy has a rate of about one to two per hundred thousand. Thanks for looking up the epidemiology. But yeah, I think you're absolutely right. Posterior ischemic optic neuropathy is extremely rare and it's actually a diagnosis of exclusion. And so one would never want to make that diagnosis without first chasing down the other more common ideologies like a compressive optic neuropathy. Thanks. We do have a chat question. If the patient is seen in a delayed time frame after the referral and the optometrist didn't specify the time frame is the liability of both parties. I'd say that's another gray area. I'd say, again, as an optometrist, they might not have realized that this is an urgent situation. If the patient then comes to you and there's been a big delay between the time that you see the patient and the time that the optometrist specified, as long as you do the right thing, you're not going to be liable because this is not actually your patient until they appear in your clinic. And so I would say that in that case, the ophthalmologist is probably not liable if they do the right thing after the first visit, not after the third visit. And the optometrist may or may not be liable. Again, that's going to be a gray area. Dr. McCurry was going to talk about whether or not the vitriol retinal specialist should have been expected to diagnose a compressive optic neuropathy, because I mean, like a pituitary tumor, that's not part of being a vitriol retinal specialist. That's diagnosed by other specialties. And I just couldn't, like I actually read that, and this was an actual thing that was written by another ophthalmologist in a report that they filed for the defense. And I was just, that really got my blood boiling because I think that we're doctors first, ophthalmologists second, and specialists third. And as an ophthalmologist, you should, even if you're specialized in vitriol retinal surgery or cornea or glaucoma or pediatrics, you should be able to hear this story, see this patient, and know that they either need to be referred to another specialist, which is fine. You don't have to make the diagnosis yourself or you need to work the patient up. You can't just assign them a diagnosis and let it go. Okay. Dr. Muhammad was going to talk about what missing piece of information caused the defendant to miss the correct diagnosis. Wait a little bit. But in terms of missing piece of information, I feel like in this case, an optic neuropathy of uncertainty in biology, in addition to neurological symptoms including headache, you know, pretends additional workup, particularly brain imaging. So just with those two kind of exam findings and in history, I think it's pretty obvious in our case that that patient should have received a scan or at the very least, sub-stratiality referral to neurophthalmology. Yeah. So this again was a sense that I read in a letter filed by an ophthalmologist in the defense of the vitriol retinal specialist that said that because the patient did not report vision loss in her left eye at the initial presentation, that that was their fault. And because she was a poor historian, that that's what caused the retina specialist to miss the diagnosis. And to me, that's victim blaming, you know, like I'm not even sure that the patient, I mean, the patient probably did have some vision loss in her left eye at the initial appointment, but she was aware of it. Her visual acuity was normal. So to say that the patient is a poor historian and make that as an excuse for somebody missing the diagnosis is inexcusable. No, that's a question for one of the residents. Dr. Polsky was going to opine on whether or not pituitary tumors are slow growing and if the patient had had surgery after the initial presentation, it would have been the same. This is another argument made by the defense. Yeah, I guess a couple things. So it's true that generally most pituitary adenomas are slow growing. Some of the things I read were around like one to three millimeters per year, which first of all, I mean, if someone has a large pituitary tumor that's abutting the optic chiasm, then very minor changes can potentially cause devastating visual changes. The other thing is to not to bring up visual fields again, but if a baseline visual field had been obtained, then they could have objectively, potentially objectively shown if there was any change over time, but they didn't do that. So there's no way for them to show that there was no progression. The other thing is, that's kind of crazy to me about this argument is that they went from hand motion vision to no light perception in the right eye, and they went from, I think it was like 2030 in the left eye to 2200. And so there was objective changes in the visual acuity, which can be explained by what was ultimately found, the pituitary tumor. So I think this argument is not great. Yeah, no, I agree with you. And this is a little bit more gray area, because Dr. Polsky is absolutely right. These tumors are very slow growing, but the fact that the patient had vision at her initial presentation had vision loss of only two weeks and had this new headache tells me that she probably bled into the tumor. And when you bleed into a pituitary tumor, that's pituitary apoplexy, you have rapid expansion of the tumor. And if you deal with it right away, if you decompress it right away, you can save the vision. And if you don't decompress it, then as Dr. Polsky said, even that little additional compression of the chiasm in the optic nerves can lead to irreversible vision loss. That's hard to say. Actually, I'm going to actually push that question off. Dr. Kirsten was asking, because the nerve was pale at the initial presentation, isn't that proof that her prognosis was poor? I'm going to push that off to one of the residents, because that's another question we've got coming up in the time we have left. Dr. Wilkinson, currently rotating on neuro-othemology, what ophthalmic testing at the initial visit would have best predicted the potential for visual recovery, which directly addresses Dr. Kirsten's question. So an OCT... Sorry, saved by the bell. So an OCT-RNFO would have been really helpful in this situation. Excellent. Because thinning of the optic nerve head would have been predictive of worse visual outcomes. Yeah, so that's actually... that there's some literature on this. A retinal nerve fiber layer scan at the initial visit would have best predicted her visual recovery. And I think Dr. Kirsten's right. With a pale nerve, your prognosis for recovery in that eyes might be guarded. It's another gray area, because none of these tests were done. But I think the prognosis for the other eye, which as far as we know was uninvolved at the initial presentation, was much, much better. And so I think we could have preserved vision in her left eye if action had been taken at the initial visit and not delayed by 18 weeks. And then Dr. Wertz was going to address my question. What do we do when we encounter patients who are poor historians? I'm over here on the side. But I think there are kind of two things that come to mind. And one is that you... if you have reason to believe that this patient might be a poor historian, you have to expand your differential and you have to rely more heavily on your exam. So I think in terms of... there are a lot of things you can do in terms of doing more extensive chart review, get more of a sense of what's this patient history, what risk factors do they have. And even just expanding your differential can make you think about things that maybe their history might not tell you. But again, if you're relying on your exam, if you're saying, okay, I'm going to take the objective data that I'm getting from my exam, then... and using that to drive your differential and any potential testing or workup that you might get. And that means that you might do a more extensive workup than you would do for another patient. But that's kind of your job as the physician is to figure out what workup do I need to be not just anchor on one diagnosis, but to convince myself that I'm not missing something else. What are the... the can't-miss things that I need to be ruling out? What are the more serious things? And then kind of as a side note, you know, it's impossible to say whether this was truly part of this particular encounter, but I think anytime you start to think to yourself or consider the possibility that the patient in front of you is a poor historian, you also kind of have to think to yourself, why do I think they're a poor historian? Just because I think sometimes it's easy, you know, if we as physicians often have some unconscious biases as well that might cause us to not take patients seriously or not believe them, or to maybe not consider the things that they're telling us as seriously maybe as we should because of something else that we're thinking about, either we're anchoring on a diagnosis or there's some other factor. And so I think that, you know, before you assume that somebody is a poor historian, you have to be considering that as well. Yeah, I think you're exactly right. I think your point, the thing that I would take away from what you just said, Dr. Wirtz, is when we all encounter patients who are poor historians and in that case we can't rely on the history, we have to go the extra mile with our exam and testing. And so if you want to go down the road of saying that this patient was a poor historian, then you need to go the extra mile as the examining physician and do additional testing, go the extra mile to really figure out what's wrong with the patient because you can't rely on the history. It's not an excuse for not getting the right diagnosis. And in this case, a visual field, absolutely, I'm sure that if the vitriol retinal specialist had done a visual field at the first visit, there would have been a small temporal defect in the left eye and they probably would have tumbled to the right diagnosis and gotten an MRI scan. One neuro ophthalmologist has commented to me that visual fields are the most underutilized test in ophthalmology and I think I agree. That was certainly the case in here. Okay. We have one other chat question. I'd make a case for a visual field whenever there is something funny about the history or exam. That's absolutely true. I agree with that 100%. Visual field tests should always be your go-to when there's unexplained vision loss. That should be your knee-jerk reaction. Dr. Warner has a comment. I just want to add that sometimes the reason why a patient is a poor historian is because they could be afraid of what the diagnosis might be and they want to minimize things and brush things off perhaps even more than the clinician and because they're afraid that they've got a brain tumor, they don't want to mention that word. If they do, they need a scan. Brad, can I ask you something? Yes. It's hard. You should already scan it but before the deal is completed, how would something like this have been worked out and figured out? Dr. Kersen's question is how would you... How would you work this up if you couldn't get a CT scan or an MRI? Let's say you were working in an under-resourced country where that wasn't readily available in the next building over like it is here. I think you can still do skull x-rays just about anywhere. Sure. Yeah, you might see an enlarged cell atersica on a skull x-ray. You could do endocrine testing. If you were suspicious of a pituitary tumor, you could do endocrine testing. You could certainly do a visual field. I think visual fields were around before the Beatles. Even confrontation fields. I'm sorry. A red ball. We're doing fields with a red ball. Yeah, you definitely have to be a little bit more resourceful and when you don't have an MRI scanner in the next building. So I'm sorry we're out of time. Dr. Patil and Dr. Sanchez won't be able to get to the questions that I had sent you. I apologize because it's 9 o'clock. I am red. Circling back to your comments for the end on the timing of the consultation. The highest dollar amount suits in ophthalmology now relate to retinopathy prematurity. And ophthalmologists have been held accountable both for failing to get the patient in in a timely manner. So the time, they've looked at it from the time that it was scheduled, not when you met the patient. And so that you are responsible for that. And the other issue is that ophthalmologists have been found accountable for failing to recognize that the patient didn't show, failing to track the patient down and successfully get them in. In all these circumstances involving bad outcomes with everlasting light, long visual impairment. So be careful with that and make sure your staff is aware of what they're doing because some of these are a bit gray areas. And unfortunately the courts have come down leaning on the ophthalmologist in that circumstance. It's a dangerous world out there. Darn right. Okay. And with that thought, have a great Wednesday. Cheery day, right? Have a delightful day and career.