 And then this is this fluorescent angiography, so unfortunately our laser is not working, but you can see I put the seconds a little bigger here, so basically beginning goes down to the end. And the thing I wanted to point out here is just the really delayed arm to retina time. So already at 33 seconds, we don't have, you know, most of his arteries filled and you know, we know that the normal arm to retinal time is somewhere around 15 seconds. So very much delayed arm to retina time. And then you can see later on in the fluorescent angiography, he actually has some disc leakage too, which is going to be more relevant. Who's laser is that? Oh, you got it. Awesome. Thank you. That's awesome. Yeah. Thank you. Awesome. Okay. Yeah, so you can see some disc leakage down here at four minutes, 45 seconds. And then just once again for completion's sake, this is fluorescent angiography of the left eye, which appears fairly normal. Switch off. It's just a carotid filling. It's so much retinal edema. Yeah. It kind of looks like there is at 20 seconds, but it's a little bit worse. Yeah, definitely not normal. And then this appears fairly normal. And then of course we did a radiological workup at this time. So we did a CT scan to roll out any sort of traumatic optic neuropathy, any sort of fracture and impinging on the optic nerve. That was completely normal. We did an MRA brain, MRA neck to look for any vessel disease. And those were both within normal limits. And then we also obtained an echo with the bubble study, which was within normal limits. So I actually wanted to go through the MRI and MRI neck and brain because there are some interesting findings there that I wanted to talk about. Unfortunately, Dr. Davidson, kind of our neuro radiologist wasn't able to be here, but he was nice enough to kind of walk me through the different slides about what's important and what's not important. So this first MRA that we see is the arrows are pointing to what we see is the ophthalmic artery. This is the best study, probably some motion artifact, and this was not a dedicated MRA of the orbits specifically, but we can't see a short segment of the ophthalmic artery. Usually we can see a little bit of a longer segment, but for this particular study this would be considered within normal limits. And then this is the MRA of the neck, which of course what we're looking for here is any sort of crotted artery dissection, which we don't see here. And then this is the interesting slide that I wanted to point out. So the diffusion signals asymmetric at the posterior right globe. So you can see right about here we see this diffusion, abnormal diffusion signal, and this isn't usually a location that we can interpret confidently. It's an area that has a lot of artifact on these diffusion images. But when we see, when we look at this ADC map on, I guess, when you're looking up here on the left right here, this is how we confirm a diffusion abnormality. And so basically if you see black over here, that means that it's a fairly real diffusion abnormality. And like I mentioned before, this isn't the best study for it, it was not an orbit study. But in the context of retinal ischemia, which we saw in fluorescence and geography, this is probably real. And the cool thing about it is that if you look at where this diffusion abnormality is, so you really can't see the optic nerve, but it's just temporal to the optic nerve. And what's temporal to the optic nerve? That's going to be the macula where we saw this diffuse retinal whitening. And so just kind of a really interesting radiological finding that I was actually paged about this after the fact that Tending reviewed it. Dr. Stagg, you were raising your hand? Yeah, I was just wondering if you could talk a little bit about the decision to do an MRA. Is that like anyone, have they done it already when you got there, or anyone with a CRAO now? What looks like a CRAO? Do we do an MRA? So we're going to go over the protocol we have here at the University of Utah with this. Was it in response to your findings? Yes. Absolutely. Okay. So moving on here, this is once again his photo, so T2 is one of the best sequences for globomorphology. And this is his T2 that we don't really see any sort of layering, we don't see any retinal detachment, it looks like a fairly normal scan here. And then, so we basically did a pretty extensive work up in terms of working up this ischemic etiology of his retina. And the only thing of note is, as CBC had decreased white blood count at 2.9, his dry-cluster ions were a little elevated at 2.03, HDL was low, ESR 11, nothing to get excited about. Pertinent negatives, I think more so are the fact that his A1C was 5.5, so not diabetic. And then his whole hyperquibular workup was negative. And then of course, his fundus findings really didn't show any evidence of retinopathy secondary to diabetes or hypertension. Okay, so assessment, he's a 56-year-old male who presents to the ER after being struck in the right eye with the corner of a box. He had hand motion at two feet with a right afferent pupillary defect. His imaging was within normal limits for the most part besides those diffusion abnormalities. And his lab workup was significant for elevated trichlyceride level and low HDL. And so he was subsequently diagnosed with a traumatic central retinal artery occlusion. And on his follow-up appointment with Dr. Crum, his visual acuity unfortunately did not improve, it actually got worse, went down to no light perception. His pupils, he did have an afferent pupillary defect, like I mentioned, that was measured by Dr. Crum to be more than 2.7. His disc had a complete 360 degrees of optic nerve pallor. And then his vessels, the arteries looked ghost-like and more, the veins were the only things that we're seeing. We don't have a fundus photograph unfortunately on this follow-up appointment. But we do have a MAC OCT. And I mean, the big difference we can see between the top and the bottom here is this is on presentation. And then below here we see just kind of diffuse retinal thinning, which is pretty common after an ischemic event to the retina. Okay, so let's get into a little bit of discussion regarding this case. So most cases of CRAO, as we commonly see occur in elderly patients, the main causes are vessel disease of the internal crotted artery with embolization of the ocular vessels. To have a central retinal artery in a kid is very, very rare, and it represents only about 8% of all cases of CRAO. And this is mainly due to cardiac disorders, contraception, and hyperquaggulable states if they are to get a central retinal artery occlusion. What's your definition of the elderly and young? I don't want to lay it on me. I've always been young in my mind. I'm not sure what the paper defined as that, but that was not me. And so CRA from trauma is even more rare and is generally associated with hemoglobinopathies or coagulation abnormalities. And we're going to talk about some of those case reports. I mean, they're case reportable because they're so rare. And so the first two case reports I wanted to talk about were done by Sor et al. and Michelson et al., who describes two patients, well, total of three patients who had a sickle cell trait, subsequent ocular trauma, and then developed central retinal artery occlusion. And the interesting thing about these two papers is that they were two separate papers, but they both kind of came up with the same mechanism of what they thought caused the central retinal artery occlusion. And so basically optic nerve edema, you have increased oncotic pressure, which then leads to vascular compression, stasis, and eventual hypoxia. And when you're in this hypoxic state, we've seen that these sickle cell trait patients behave more like the homozygous sickle cell. And so that leads to sickling and subsequent central retinal artery occlusion. For our particular patient, we didn't get the test, the electrophoresis for the sickle cell. He didn't elicit that on history. So sure, he might have it. But unlikely. Why do you say unlikely? Well, I guess... He's from Somalia, right? Yeah, he's from Somalia. I think you have the test. Yeah. Yeah. Yeah. Yeah. And is it as common in Somalia as it is in the African-American population? Yes. Oh, it is. Okay. Yeah. But his CBC was marvelous. Yeah. That doesn't matter for Trey. No. Yeah. It wasn't anemic. Yeah. Yeah. That might be... That's something I wanted to discuss on that last slide is should we screen him for that? You know? Because now he's blind in that eye, so, you know? And then another paper I talked about was central retinal artery occlusion post-retrobulbar block. And so this is an entity that is not surprising if there is a retrobulbar hemorrhage associated with that retrobulbar block. But in these four patients, they did not have a retrobulbar hemorrhage but still experience central retinal artery occlusion or transient central retinal artery occlusion. Now, the different thing about these patients is they had severe hematological or vascular disorders, so they had kind of this predisposition to vascular disease. One patient had severe type 1 diabetes, another patient had sickle cell, two patients had sickle cell retinopathy, and then another patient had carotid artery disease with subsequent ocular ischemic syndrome. And so all these patients, this is a pretty old paper, but all these patients were actually undergoing laser. And so they did retrobulbar block to obtain paralysis of the eye. And so they had several ideas on the mechanism as to how these patients had either this permanent transient or central retinal artery occlusion or permanent central retinal artery occlusion. They said maybe the trauma from the actual injection induces spasm of the central retinal artery. Injection of the central retinal artery behind the globe by the injected anesthetic solution. Less likely. And then maybe with the epinephrine, there was a study that showed that epinephrine does decrease the ocular perfusion pressure by 50%. And then trauma of the injection induces a spasm of the central retinal artery. So they have no idea why this necessarily happened. These were just some ideas that they threw out there. Once again, our patient did not have a retrobulbar injection, but maybe some of these mechanisms related to his central retinal artery occlusion. And then the last one I wanted to talk about, so this study actually looked at five cases of retinal vascular occlusions, not central retinal artery occlusions. So they were terminal vessels kind of in more in the periphery after ocular contusion and otherwise healthy patients. And this was actually a prospective study that looked at all patients suffering from ocular contusions who had significant ocular findings in the posterior segment like commotion, like vitreous hemorrhage. So they basically examined all these patients and they discussed the possible mechanism actually being related to stretching and disruption of the intima of the artery. So the intima of our arteries is probably the, it is the weakest part of the vessel. And in other parts of the body, it's actually known to cause thrombosis. And so they thought that damage to that intima layer exposes the blood to that layer initiating the coagulation cascade. So maybe something, and these patients had no predisposition. So all the patients that had these significant trauma underwent a fluorescence in the angiography and if they did see arterial occlusions, they underwent a full workup for any sort of hyper cragular gold state they had, if they had diabetes, anything like that. So these patients were otherwise healthy. So a couple of questions that remain that I kind of wanted to open the floor up to because I think we are probably going to write this case report up and it'd be interesting to get your own opinion about this is if this truly was a CRAO, why weren't there other physical exam findings kind of like collateral damage? So this gentleman sustained enough trauma to cause essential retinal artery occlusion. Why didn't he have some conjunctival hemorrhage? Why didn't he have a vitreous hemorrhage? Why didn't he have a corneal abrasion like the patients in the last study had? All of those patients had, they had cyclo dialysis, they had lens dislocation, but this guy's eye was perfect besides that posterior segment whitening. Yeah, Dr. Olson. So it's natural on our mind if A happens and B happens that we assume A cause B. I mean that's a very natural thing for people. So obviously lost vision and something happened on this loan, but this strongly suggests that that trauma was probably pretty insignificant. And I can't imagine any trauma enough to cause serious contusion to the artery isn't going to leave some sign of something. So I, you know, I got to go kind of over to Paul saying I'm going to look at something like sickle trait or something else and when you get a significant event, you know people automatically assume that associated with that, you know, is something that happened around that time frame. Sure. Yeah. And it's amazing how people will hone in on that. I'll get them, there's oh no, no, it could be some of the wildest things that they assume this caused this particular event. I mean, the most obvious thing we're seeing out there is, you know, autism and association with vaccination. I mean, there are a couple of kids who ended up with autism and it wasn't obvious until after they got their series of vaccinations and they're still, and it's still out there. And it's been completely debunked. There was that one stupid paper out of England, but people still had that causal relationship. And when I had a chance to study Swedish history for a long period of time, the common event as the days are getting shorter and shorter, mind you, you're talking up where, you know, where you're up near the Arctic Circle, is that the Ferris Virgin in the area, you know, was sacrificed and it worked every year, the day started getting longer after that. So when Christianity came along, they had a hard time eliminating that practice because people were afraid that, you know, if they don't do that, that they're just going to go on a permanent night. Yeah. And so just know that that's just the mindset we have. I strongly suspect that the trauma can't explain it with just zero sign. Yeah, I agree. Yeah, so and then that kind of brings us to this is like, was the trauma just a red herring? And this was just in fact her run of the mill, CRAO. Also, you know, talking with Dr. Chikur about this a little bit, you know, you know, he might have had the CRAO possibly and then the box hitting his eyes kind of like prompted him to pay more attention to that eye covering his other one. And he's like, oh, man, I can't see out of that eye. The box did it. Yeah. Yeah, exactly. It must be the box. So Dr. Sinclair. Okay. Just very quickly. I, I'm trying to analyze a case of my own. I talked with So-Hang Sing-Hae-Rae and Ron Klein about their papers. I said, look, most contusions are not directly on, but often have a torsion of the eye. So could this stretching of the optic nerve cause some sort of sheath abnormalities that could cause this intimal stretching and problems with the endothelium that then clog? But it was interesting on the MRA that you had there that looked like there was some lack of staining of the central retina, of the optic nerve. There was a little bit posterior to that. So I, I agree with Olson here and the fact that he lost consciousness for some time, I think means more a other associated abnormality. I've looked at all of that, but I just, I've looked into this to try to say is there some other kind of abnormality that could be associated with this traumatic, but the fact that he had nothing in the, in the eyeball, even if the eyeball did rotate up enough to put traction on the optic nerve. Yeah. I'm just assumptions. Definitely. Definitely. Yeah. And then my only question too about the CRAO, so he didn't really have a lot of risk factors. You know, if you look at his other eye, he was hypertensive on presentation, little bit of an elevated cholesterol as A1C was great though. Not saying that, you know, people without these risk factors cannot have a CRAO, but just a thought, you know. So I think maybe what we'll do is we'll get a electrophoresis and scan for that, that sickle cell trait. So even though it's extremely rare, all it takes is the, is the right type of bathroma to break off and just happen to hit right at the right time in the right place. Right. Yeah. And all that can happen. Yeah. Rare events still happen. Right. And that's what I tell patients where they have a rare event. I say, you bet. This is something people told you this almost never happens, but you need to understand. I understand. For you, it's 100%. Right. It doesn't matter if it's rare. For you, it happens. Yeah. Exactly. And Brad, I would just add the, I checked, sickle cell is very low, if he's truly from Somalia. He is from Somalia. Yeah. It would be, that's a very low area, but if you're talking about any possibility that you're going to try to publish this, a reviewer's going to hit on that right away. We should do that. Yeah. You have to have that just ruled out because it's in the literature, he's from Africa. Yeah. You wouldn't want to miss that. Sure. Definitely. Okay. And then I think to answer somebody's question, I'm not going to go into this because we're out of time, but there is a pulse protocol on sensual retinal artery occlusions that's very applicable to us because we might be one pulling the trigger on the, calling the stroke code, the stroke team to come in. So really easy to find. I was going to briefly review that, but just for lack of time, I'm going to let you all read that on your own. So thank you. Thank you.