 Okay, so our next presentation is from Zan Lee and he's going to talk to us about an important distinction when somebody comes in with a vision loss. Is it optic nerve or retina? Hello. All right. Thank you. My name is Zan. I'm a fourth year medical student from the University of Nevada School of Medicine. And I'll be talking about differentiating retinopathy and not taking retinopathy in acute persistent vision loss. So that's just a picture of our Reno campus. We're pretty fortunate to be able to learn in this newly built campus recently. Anyway, so hopefully today after the talk, everyone will be able to identify anatomic etiology and common causes of acute persistent visual loss, as well as identify common clinical features of retinal as well as optic nerve related APVL and finally to be able to differentiate the two. So in terms of our case present, my case presentation is a 33 year old right handed man who presented with central visual disturbances right eye, which for the previous three weeks, it was notable he was hospitalized for severe tonsillitis as well as abdominal pain about six weeks prior to the event. Three weeks later, he developed an onset of vision loss described as a perfect round circle, essentially in the right eye and surrounded by white halos. He also knows a decreased color perception and dimmer vision when comparing his two eyes, right has more loss than left. And he also knows there were some pain pressure associated with the onset as well as nausea, vomiting, all wish that had resolved by the time of the visit. Some additional history. He has a past ocular history of granular corneal granular dystrophy in itself, as well as father and paternal grandfather. And two weeks ago, he had a Humphrey Dunn, which saw the secoscentral scatoma in his right eye only. And a recent brain MRI imaging was shown no abnormalities. And it was only remarkable on the view system for recent stress. Physical exam was for the most part pretty unremarkable. He did have 2080 in his right eye with no improvement on pinhole and near was J10. Whereas left eye did have improvement on pinhole and near was J3. He had no APD and right eye was bright so dark from 7 to 4 and left 6.5 to 3.5. And pressure was normal as well as your ocular movements and confrontational fields. Objective decrease in red saturation, he described it as a burgid in color when looking at the cap that we often use to see whether there's some vision loss. Sillam was pretty unremarkable, except for the obvious corneal granular dystrophy. And dilated fundal exam showed slight to the lange attack to vasculature but otherwise healthy on the right side and left was unremarkable except for a burgdmeister papilla. Macula and bald eyes were difficult to visualize but appear grossly normal. And everything else in terms of stereopsis and color vision testing was normal as well. Amzor showed a central round area and metamorphopsia was surrounding the scintillations. So this is his fundal pictures which is kind of obscure because of his corneal disease but you can see that in his left eye he has this burgdmeister papilla but in the right side for the most part it's pretty normal. There's possibly some central clearing depigmentation in his macula and then there's some slight hypervenoma at the optic nerve a little bit of burning. On that day his Humphrey actually showed a central scatoma which has changed from previous seco-central and OCT of the macula showed normal phobia of contour and both eyes but there was this mild ISOS junction irregularity in the ellipsoid region. And here's the cut of where it is and so here's your RPE and then there's some obscuration of the ISOS junction which is likely causing these visual symptoms for him. So general approach to when a patient presents with the cue vision loss is you have to, you're going to get the history but the main diagnosis starts with determining where the anatomic location is located. You want to figure out whether it's monocular or binocular vision. With monocular vision typically that's going to limit your locations to the globe and the optic nerve. Whereas when it's binocular it indicates the vision is at or posterior to the chiasm. And as a general rule as the lesions go more posterior neurologically they become more congruent and macular sparing lesions like this typically indicates that the vascular vent was in the occipital region. Because of that vascular supply to the macula, to the occipital region that's supplying the macula. And for the general clinical approach you want to do your basic history. You want to ask about the associated pain, associated with atopsia or any nuance of floaters. How acute it was sometimes patients they might accidentally close one eye one day and discover that they have vision loss and they think that's a sudden thing. And one of the most important things in terms of review of systems is to rule out giant cell arthritis or temporal arthritis because you want to possibly say the other eye. And then past medical you would definitely get neurological history because any history of tingling or the like might suggest some sort of MS related issue and then past ocular family history. And then you want to consider the patients comorbidities such as hypertension, diabetes, as well as any hematology abnormalities. And this is just a quick table that I found which I'm not going to really talk about any of the media problems that causes this APVL but I will be speaking about these. And mainly you're going to, the initial clinical presentation is going to give you which way you're going to, which road you're going to go down in terms of which test to order. And then your tests such as a fundal exam, OCT as well as a visual field are going to really give you the diagnosis. And then physical exam like I said visual acuity a patient might have a good visual acuity but they might have poor computational field. So it's definitely important to check basically a system actually go through the entire physical examination and definitely look for APVs that have for in people area defects. In terms of optic nerve disease, there are three classic signs, visual field defect, decreased color vision as well as our APV. These, when these three are present, chances are it's probably a sign of optic neuropathy. So the optic nerve itself may or may not be changed on fundal exam because it could be retrovobar and it could be something that's occurring that's not at the level of the retina that you're visualizing. So this is NAION, some of the most common causes of sudden blindness in patients over 50. And I just want to show like a difference between a normal disc and what it's typically considered as a disc at risk. And this one you can see the cup right there and then here there's essentially no cup. And the theory behind that is there's such a tightly packed nerve fibers that is going through the lamina corbrosa that they're at increased risk for ischemic events. And then this is NAION which is non-arteric ischemic optic neuropathy which is typically in older 65-75 age range versus AION which is much older otherwise can be considered as temporal arthritis. It's pretty different in terms of the presentation. Here you see hyperlumia as well as some hemorrhages around the area whereas here with the AION it's a very pallid optic nerve swelling which is pretty easy to be able to differentiate these two. And then one of the notes I want to make is that in optic neuropathitis which typically is a more slower onset, not really a sudden onset of visual loss, is that they both can present with this pale optic nerve and this is where your history is going to really help you and you also really want to get that, the review system with the constitutional symptoms of AION. And then as for RENNA, the really major common cause is going to be your vascular occlusions, RENNA detachment and acute macular apathy and that's a normal frontose picture. And here, so this is a central RENNA RRE occlusion. It presents with that classic cherry red spot but then you can also have macular sparing secondary to the serial RENNA RREs or you may or may not, and then you often see this box carrying the RENNA vessels as well. And then BRAO, typically more infiltrational ischemia and if you're lucky you might be able to see an embolus and the BRAOs are typically more common from embolus whereas the central RENNA RRE occlusions are more from severe paratostomalsis. And here is that the RENNA venous occlusions, pretty difficult to miss this one because it's often described as blood and thunder shell and it's just a lot of hemorrhaging on all four quadrants whereas similar to BRAO, the BRAO is sectorial as well. And again on the FAA you can see that filtration of the veins. For retinal detachment patients are going to typically come in with symptoms of autopsia as well as new onset floaters very similar to PVD, posterior vitro detachment. Really the only way to definitely diagnose this is using indirect abdominal skill to visualize a peripheral RENNA and if you can't do that due to some sort of media problem you can always do a B scan of the RENNA, of the globe and here you can see that retinal detachment right here which will help you with the diagnosis. And then acute maculopathy was something that I kind of struggled with. I didn't really, it was difficult to understand but it's a various ideology that basically anything that acute affects it, macula, acutely can cause this. Typically you can have neuroretinitis, central serous retinopathy as well as significant macular edema and choroidal neurovascularization. Common symptoms are metamorphopsia and still recovery to light and for the most part physical exam is actually going to be pretty subtle not a lot of science. The main monodiagnosis is going to rely on your OCT and your fluorescent angiograph. And these are just some of the ones I mentioned. In terms, this is a CSR. You can see this classic smoke sacking on FAA and it's time to progress. And all of these typically occur in younger patients and they may be associated with pain but they may not. Here's neuroretinitis. It's classically associated with Bartonella infections. And you can see at first it's not really that much changing and then at two months there's that classic macular star pattern. And then for this is the acute macular neuroretinopathy, very rare disease. I couldn't find a lot, mostly just case reports. And you can see it's pretty much, there's not really that much going on in terms of, in terms of the fun this photograph. But for our differential diagnosis for our patient it was something along this spectrum because he had that sigo-central initial sputoma and then it kind of went into a central which kind of tells you that somewhere in the papillomacular bundle was involved and possibly with the optic nerve as well. Any questions? It was really fast over a lot of material. Right, that's why it was kind of, in terms of the history and the physical exam finding it was kind of difficult to distinguish because he has that, he had kind of some flashing and also some pain associated and typically with your ischemic events within the optic nerve they're going to be painless. And then with the mac, but he said he had some pain. And then besides that he also had the decreased, he didn't have an APD which is kind of led us towards away from the optic nerve. And that's why we're basically the imaging itself comes in and you have to be able to recognize these patterns of pathologies to be able to really accurately diagnose the problem, the disease. The red dissaturation from basically what I read is, it's likely because from the slide of his OCT because it's closer to this phobia where you have a high concentration of color that could be causing it. And also there was some previous inflammation of the optic nerve itself with some hyperemia and telangiotactic changes. So it really seems like it was more of a neuro red 90s picture where it started off as like some sort of inflammation at the optic nerve and kind of went over it to the macula. Yes, no, I actually looked through the records and he was supposed to follow up and I saw a lot of the schedule appointments got canceled. Yes. When you were talking about differentiating, alterating is being a couple of very much different, but you didn't mind. And I would also like to mention I'd like to thank Dr. Warner for recommending this topic for me and for allowing me to do this presentation. Yeah, well, I actually read it. If it was something along the lines of neuro red 90s, because I forgot to mention, he actually had a normal auto fluorescence as well. And his previous course in the angio was normal as well. There's no leakage at the macula. And I don't know if it was done prior, whether it might show a leakage at the optic nerve head. But basically, the multifocal ERG, I saw a lot of articles that said basically it's really still difficult to tell even with it because there's going to be, I wasn't quite sure with the whole process involved, but it had a very low sensitivity towards the graphics in terms of that. In these terms, the other thing is just that the acute macular neural retinopathy, to me, when from my side, is much more rare. They subsequently said on SDOCT that