||Andrew G. Lee, MD, Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, TX; Professor of Ophthalmology, Weill Cornell Medicine; Cyrus Daruwalla, Baylor College of Medicine Class of 2023
||So today we're going to be talking about Amaurosis Fugax. Amaurosis Fugax means fleeting blindness. It's kind of a weird word because it's a combination of both Latin and Greek. Fleeting blindness. And so I prefer the term transient monocular vision loss when it's Amaurosis Fugax in one eye, and you could say transient bilateral vision loss if it's two eyes. And so when we're dealing with transient monocular vision loss or transient bilateral vision loss, we're really talking about two circulations that could be involved if the Amaurosis Fugax is due to a transient ischemic attack - a TIA. And so when we have Amaurosis Fugax, a transient vision loss,we'd like to make sure it's not a TIA because the TIA could become a stroke real easily, and so this is actually an emergency and we should work it up as a stroke in evolution. However, transient monocular vision loss can occur from other non-TIA related things. So the duration of the transient vision loss is super important because most ischemic events are seconds to minutes. So for things that last hours to days, those aren't really Amaurosis Fugax, because if you really had a transient vision loss from a lack of blood flow from your carotid to the central retinal arteries for three days, well that's not going to be transient anymore. So the retina has a limited capacity to recover from ischemia, and so if it's three days long or three months long, that's not transient, even if it gets better, that's way more likely the optic neuritis that recovered. So the duration is important and we'd like to have it be seconds to minutes if it's ischemia. Once you start getting to hours at a time, it's extremely unlikely that an ischemic event that lasts more than two hours is going to be reversible in the eye. Same thing with the duration for the bilateral. However in the transient monocular vision loss from TIA, carotid disease on the ipsilateral side is the most likely cause, and if it's transient and bilateral, then we're going to be thinking about the vertebral basilar system and not the carotid system. Obviously either could be cardiogenic, could come from your heart, and those cardiogenic etiologies are usually a trial fibrillation in older patients, but it could be valvular disease, bacterial endocarditis, arrhythmias of different types, and tumors in your heart like atrial myxoma. So they are going to have to have an echo carotid Doppler. And everybody with a TIA from an Amaurosis Fugax is going to have an MRI because we're looking for silent ischemia and that's going to be seen on DWI, which in another video we covered diffusion-weighted imaging and how that could be ischemia, hyper acute ischemia, causing restricted diffusion. So we're really going to be working up Amaurosis Fugax of seconds to minutes at a time as if it's a TIA, looking at the carotid if its unilateral, vertebral basilar, and the heart, doing an MRI scan. Some of these patients are going to need a hypercoagulable state workup, but really you're going to be deferring all of that to the stroke team and let them handle it. The best-case scenario is if it matches the prototype. So the prototype for ischemia normally respects the vertical or horizontal meridians. So if it's a curtain coming down from the top; altitudinal onset,that's a very good symptom that it's TIA, because the blood supply of the optic nerve or the retina is top half and bottom half. Or if the curtain comes in from the side, that suggests it's hemianopic. Inpatients who have homonymous hemianopia sometimes say it's in only in one eye, even though what they meant to say was one side, so you can't be fooled by the one eye, two eye thing based on the history alone. So if they say it's a curtain, it lasts minutes at a time, and it goes away in seconds to minutes, we really should be thinking about TIA. The last thing I'll leave you with is another symptom that is highly sensitive and specific for carotid disease which is if it's retinal claudication. And so you've heard about jaw claudication - if you use your jaw, it hurts, that's the sign of ischemia and giant cell in your jaw. Retinal claudication is the same, but instead of pain, what they get is they lose their vision from lighting condition chain. So if they see a bright light, then they don't have time to recover, and that is a retinal ischemia sign. The light induces a claudication event. So altitudinal onset or disappearance minutes at a time and duration or retinal claudication, those are the symptoms in the Dutch Amaurosis Fugax study that it might be a TIA from ipsilateral hemodynamically significant carotid disease. And then lastly, you should be thinking about a sed rate and a CRP as well as workup inconsideration for giant cell in every Amaurosis Fugax in an elderly patient.