 Hello, I'm Tina Burton. I'm in a resident in the neurology program and just finished a neuro ophthalmology rotation About a couple weeks ago So I'm going to just talk about a case that we had In clinic there, and it was a case of optic neuropathy in a gentleman with atrial fibrillation So I'll be going over the case all of the ancillary testing that we did the differential diagnosis Treatment and then some conclusions and discussion about the optic neuropathy so This was a gentleman who is 58 years old about a month prior to coming to us He had had sort of this clouding a vision he described it in his right eye as feeling like His lens in his glasses where it was just cloudy and he kept like he would want to wipe it and then he had sudden right eye vision loss and then Late and also developed a retro orbital headache But initially his first symptoms were painless he has a history of hypertension hyperlipidemia obstructive sleep apnea and Was recently diagnosed with atrial fibrillation about six months prior during a just a routine workup for a sinus surgery. He was started on Ami-odorone and riboroxaban at that time for stroke prophylaxis So for his visual complaints he went to his ophthalmologist about him two weeks prior to seeing us he had again the mild clouding of vision in his right eye and the right-sided pain and Vision more acute vision loss that had worsened and When he was seen by the ophthalmologist, he had an inferior nasal visual field Deficit and he was also seeing stars in the right side of his vision Not in the left eye and he noticed a green hue around everything in the dark and on his Funduscopic examination he had some dyskidema at that time So recent medical history we talked a little bit about that Other medications. He's on is levothyroxine Ibuprofen by Torin a meprosal fish oil and a multibitamin family history significant for hypertension hyperlipidemia diabetes and heart disease and He occasionally smokes a cigar maybe once or twice a month and then has two to three alcoholic beverages a week on examination his he was hypertensive despite being on Therapy for that His blood pressure was 134 over 70 his acuity in the right eye was 2025 in the left eye was 2040 with corrective lenses on his pupils were equal and reactive, but he did have a Right APD 0.6 log his visual fields He continued to have that nasal and inferior arcuate defect And then his left side was completely normal his motility was full his color Vision was full in both eyes, and he just had a little bit of trouble with his stereopsis in circles His anterior segments were clear and quiet, and he had a little bit of a cornea Verticalata in his in both eyes and then his interocular pressure was normal at 18 on funduscopic examination He had altitudinal Optic disc edema, and he also did have some hemorrhage and then also a very small cup to disc ratio of 0.1 in the right eye the affected eye, and then in the left eye he had Small small on the small side With a cup to disc ratio of 0.2 his flicker fusion was normal, and then his labs were Significant for a normal ESR and CRP lipid panel Was ordered and he said he was currently on a statin and that it was his lipids were controlled with that and an A1C was also ordered because of his family history of diabetes and his body habitus So we did Humphrey visual fields on him and this just shows that nasal and inferior arcuate defect So the key features of his Presentation were that initially his vision loss was painless. He did develop that headache a little later on but He had unilateral Vision lot vision problems, but he also had small cup to disc ratios bilaterally He had normal inflammatory markers, and we'll talk about why that's significant in a minute and No trauma to the area. No utahs type phenomenon He had a normal neurological examination Otherwise and his risk factors were hyperlipidemia hypertension and obstructive sleep apnea as far as we knew at this point in time And he also had recently started amiodarone. It's about six months prior so the differential on him was for an optic neuropathy and you'll see here highlighted that his was more rapid and onset and the most Compelling Reason would be a toxic or a schemic optic neuropathy given his set of symptoms So I'll talk a little bit about amiodarone amiodarone induced optic neuropathy So Which is what we determined this gentleman had He has an Naion actually so his onset was within this window of four to twelve months of Initiation of amiodarone therapy his was six months Pathophysiology, so it's not entirely known however, they do find that on dissection of all of the intraocular tissues including the optic nerve that they do have some infiltration of Deposits and then also They don't know whether there's actually the amiodarone is a direct toxic effect That causes the vision loss or whether it's just increases the It's something that sort of tips someone over the edge that has risk factors for developing Naion So some people call this a variant of any Naion with slow resolution of the optic disc edema other people in papers have discussed that Like I said, there was this independent risk factor For Naion and initially and then you add amiodarone on Then it develops and then another Pathophysiology that was addressed was there was a paper where they said that in fact Naion Was not attributed to amiodarone therapy as far as they were concerned that they felt that typically these these folks have risk factors for Naion independent of amiodarone and that it's just sort of an incidental finding on physical or on the history So if we look at our patient and we try to tease out whether this is what they would call an amiodarone optic neuropathy or whether this is Naion and he sort of falls a little bit into both categories So his onset was within 12 months. He's male So those are the things that are sort of predominantly found in the amiodarone induced optic neuropathy But then his other issues are that he has a small cup-to-disc ratio Obviously the one it's point one in his affected eye, but he did have a small cup-to-disc ratio bilaterally Which would one would think would preclude him to this and both eyes And then systemic manifolds festations of the amiodarone. He was not having any having any sort of other systemic Sequoia of starting that therapy we did not do a tap on him that sometimes you can find that the ICP is raised in amiodarone induced optic neuropathy and They also noticed that noted that the resolution of the discadema is often much more prolonged in optic neuropathy So our treatment for this gentleman was to first of all stop the amiodarone, which was we think either the inciting Reason or like like I said in the discussion some people would argue that he may have developed an AI and NAI on independently and Then we screened for additional risk factors so that a 1c we know he has hyperlipidemia But we wanted to see if his lipids were actually being treated properly and then you also also had hypertension Even in the examination room And so we wanted we spoke to him about making sure that he was dosing his medications in the morning rather than the evening to try to Reduce the risk of nocturnal hypotensive Episodes that could cause this as well And also to get a good handle on his blood pressure We did recommend that he could try some brumonti Which has been shown to be somewhat helpful in some people but no significant difference in randomized controlled trials But the side effect profile is so low that We thought it was worth trying Other things that have been studied oral steroids Plus or minus whether those are helpful at all optic nerve decompression there was a big trial on that and it was found to be actually detrimental and then anti-vegF injected intra Vitriol is also a therapy. That's questionably helpful But we did not suggest any of those latter three because Some of them are actually detrimental so so conclusions are that Amiodarone just always think of someone who comes into your office with atrial fibrillation Or on amiodarone therapy that to ask about amiodarone therapy because it does put someone at risk for developing NAI on or a toxic neuropathy And then to also remember that in trying to tease out whether it is NAI on or the amiodarone optic neuropathy Just some of the major things that they found Just looking back on chart review Males are typically more affected. It can be bilateral and unilateral You can have an elevated ICP And then you can also look for systemic drug side effects that would sort of tip you off to the fact that It's affecting the patient in multiple Organ systems so and then also to look at the Period of recovery once you identify the problem and assist in treatment of it The optic discadema should resolve within one to eight months But in a true NAI on that can resolve a lot faster And then also to just remind yourself and your patients that even though they stop the amiodarone therapy It doesn't necessarily mean that you're going to Stop the disease progression It obviously can help but the about 10% of your patients will continue to worsen even after stopping therapy Part of this is due to the fact that amiodarone has such a long half-life And sticks around for quite a while even though they've stopped the therapy So and then just remember to screen for other risk factors. So That's about it any questions It's fine to just What I would do is just contact our cardiologist and let them know that you're stopping that medication Have them get seen right away and decide what other Rhythm or rate controlling drugs they would prefer to put them on Yeah, we did not do an MRI his neurological examination was so benign Otherwise that we felt that it was not indicated at that time. All right, thanks Our next presenter today is one of our rotating medical students Ashley burn Heisel and she's gonna discuss with us neuronal regeneration