 All right, everyone. Good morning. It's a couple minutes after eight, so we're going to get started here. Our first presentation will be from a visiting medical student, Joe Arminia. He's visiting from the State University of New York, Buffalo. His topic is going to be ocular manifestations of sarcoidosis. Something that we may not all know about Joe is that he's really excited about being here in Utah because he is a fly fisherman. Although he hasn't had a chance to get out and go fishing yet. And so his favorite type of fishing is a fish for, you know, trout as a fly fisherman, although the largest fish he's ever caught was a bass, not a trout. For those of you who don't know me, I'm Joe Arminia. I'll be talking today about the ocular manifestations of sarcoidosis. So we had a patient last week in the neuro-ophthalmology clinic. It was a 33-year-old white female who was recently diagnosed with sarcoidosis and presented to the neuro-ophthalmology clinic for evaluation of her visual complaints. So in March, she began developing numbness in her lower abdomen, which then spread into her left arm and most of her trunk and also into her right thigh. In April, she developed a Bell's palsy on the right side of her face along with some hearing loss on the right side of their face. The Bell's palsy eventually resolved in three to four weeks. But towards the end of May, she developed the second Bell's palsy on the left side. At this point, it was discussed with her that sarcoidosis was part of the thinking of what could be causing the problem. At the same time as the left-sided Bell's palsy, she developed the left-sided hearing loss as well. And also noticed some vertigo that was directional based on where she looked. And she had increasing headaches and numbness in her face remained after the Bell's palsy resolved. So when we saw her, the Bell's palsy was completely resolved on both sides of her face, but she still described some numbness. So the labs that she had run, she had an ANA, which was negative. Her diabetes workup was negative. Epstein-Barvirus antigen showed possible primary infection that was repeated a few weeks later, and it was back to normal. Her B12 angiotensin-converting enzymes were within normal limits. So I'll talk a bit more about angiotensin-converting enzyme as a test for sarcoidosis. It being negative doesn't really mean a whole lot, but that's just one of the things we sometimes test for. I'm looking for it. So on imaging, she had an MRI of her brain, her thoracic and cervical spine. Those were all normal, no signs of demyelinating diseases or any masses. Chest X-ray was her only really significant imaging. It showed bilateral hyalur, adenopathy, along with mediastinal adenopathy. And she went on to have a mediastinal biopsy, which was positive for non-caseating granuloma. And this didn't stain for any fungi or bacteria. So her ophthalmologic complaints is she had a recent onset of both photophobia and floaters. She had nuance at double vision, which was worse at night than as the day went on. She had ocelopsia when attempting to focus, and this was particularly bothersome driving, and she actually had to stop driving due to it. She would become vertiginous upon right-sided gaze, and she had blurring in both of her eyes, worse on the right than the left. And she had occasional demyelination, but she wasn't realizing at home. But on exam, when she looked up, both with the neurologist who she saw before us and also again with our exam, she described demyel sensations. So her visual acuity was pretty good in both eyes. She was corrected to 2025 and 2020. Color and stereo vision was intact. She had a small right epipulmonary defect, and her fields were full of confrontation and also home for visual fields. Corneal sensation was intact. She did have nystagmus and left-wards gaze, and she still had some minor hearing loss on our exam on both sides, and she still had some facial numbness. So she had a small esophore in all directions. Her intraocular pressure was risen bilaterally, and on slip-lamp exam, we saw a small carotid precipitate in both eyes along with cell in both the interior chambers and the vitreous. On fundoscopy, we saw both edema and hyperemia of the nerves with some snowballs in the right eye. There was no vasculitis observed, but there was some fullness of the left inferior arcade. The groiniascope exam showed some adhesions in the E.I. indicative of trabeculitis, and this was on both sides, and this part is what explained her increase in intraocular pressure. This is her right disc. You can see it has some swelling circumferentially. There's no real abscuration of the vessels yet, and this is her left disc taken at the same time, also rather swollen. So circuitosis is a chronic inflammatory disease which is made up of non-Casey and ingranulomas, and that's how you make the pathologic diagnosis. The etiology is unknown. It's been linked potentially with certain strains of mycobacterium, but that really hasn't been nailed down. Some studies have shown PCR evidence of DNA from the mycobacteria. Other studies have refuted that, so there really is no known cause right now. Presentation can vary widely. Up to 5% of patients will be completely asymptomatic and will just be found on a chest X-ray for some other reason. About 45% of patients will present with constitutional symptoms, and anywhere around 50% of patients will present with cough, hemophysis, or dyspnea and exertion, and even more than that will have some sort of X-ray findings. And the most common organs involved, there are lungs, skin, eye, and lymph nodes, and some sort of eye problem is involved in 25% to 60% of patients. So the diagnosis for sarcoid, there really is no set diagnostic criteria at this point. Pathology is key. There are some other non-specific tests that you can run, one of them being the angiotensin converting enzyme, but it's not sensitive or specific. It can be seen in tuberculosis, leprosy, and also in diabetes mellitus. That level can be arisen. And even if it's negative, it doesn't necessarily mean it doesn't have sarcoidosis, as we saw with our patient. She went on to have the medistinoscopy, which is positive for sarcoid. Directed biopsy, the other thing you can do is look for calcium levels, because non-casin and granuloma tend to secrete 125 D3, which can lead to increased calcium, both in the blood and in the urine. Directed biopsy is better than blind. However, in up to 30% of patients without conjunctival involvement, conjunctival biopsy can be positive. So there may be some utilization of conjunctival biopsy, even in patients without eye involvement, because it's less invasive than a trans-bronchial biopsy. And in patients that have conjunctival environment, that yield goes up to 60%. So manifestations that you can see in the eye are widespread. You can have anything from involvement of the muscles, involvement of the lacrimal tissue to uveitis or even coreo-retinitis. There are no specific extra-ocular manifestations to look for that would indicate to you to look in the eye. It's just probably something that every patient with sarcoidosis should have an eye evaluation because they could be asymptomatic and have a really bad inflammatory problem going on. There also isn't any correlation between the check-stex-ray grading. So, you know, stage one is just bilateral hyalur, adenopathy. Stage two is bilateral hyalur, adenopathy along with some interstitial changes in the lung. And stage three is just interstitial changes. There's no correlation between those stages and if a patient is more prone to have ocular sarcoidosis. So the first part I'll talk about is a kind of extra orbital manifestations. The lacrimal gland and the conjunctiva are the most often involved outside of the orbit. And you can see up in that picture that the lacrimal gland there is, you know, swollen and it has sarcoid. I don't have a picture of conjunctiva involvement or muscle involvement, but you can also have a myositis that kind of mimics the grave's muscle involvement. And it's important that you don't just, you know, because a patient has sarcoidosis and then you also notice proptosis or some other muscle problem, it's important that you reel out thyroid because autoimmune thyroiditis can go hand in hand with sarcoidosis. So a patient could have both of these. So if you see muscle involvement, it's still good to rule out thyroid disease. And cornea is rarely involved primarily but it can be involved secondarily after a really bad uveitis. You can see below some band degeneration in cornea that's been exposed to intraocular inflammation. So classically anterior uveitis has been associated with sarcoidosis and the reason that anterior uveitis has been more associated than a posterior intermediate uveitis is because the older literature has been more of African American, African American female population and that population when they develop sarcoidosis tend to have anterior uveitis. Caucasian women tend to have posterior or intermediate uveitis. So it's based on what your patient, your patient's African American Caucasian, you need to be worried about different things. So you can have two different presentations of anterior uveitis. You can either have acute irradiocyclitis or a chronic granulomitis uveitis. And that's based on if it's just a regular, if the patient just has regular sarcoidosis or if they have the low frins. And low frins is a syndrome made up of erythema de dosum, fevers, bilateral, hyalur, and phenenopathy. And they often, and that's actually associated with better prognosis. And they often have this acute syndrome. And you can see the copay nodules along the interior of the iris here. And then you can see the carotid precipitates down here in the bottom image. And you can also see involvement in trabecular mesh work, which can be associated with increased interaction of pressure, which we saw with our patient. So intermediate uveitis is inflammation of the vitreous, the pars plana, or the peripheral retina. And you can see snow banking with it, although it's more often you're going to see just snowball infiltrates, which we see down here. And there was some snowballs observed with our patient. Nothing as dramatic as this, but there were a couple. And you can see the snow banking up here, which is less common. Snowballs are characteristic of sarcoidosis, although they're not specific. And this intermediate uveitis can proceed a more posterior pathology. So posterior involvement, you can have periflebitis and pervenous exudates are the most common things you're going to see. But you can also have chorital involvement, which is more frequent in the elderly Caucasian female population. You can get a corioretinitis in that population group. You can also have hemorrhagic retinopathy, branch and central vein and artery occlusions, and you can have capillary non-perfusion. You can also see posterior segment granulomas. So here's some pictures of posterior involvement. Up on the left, you can see some retinal vasculitis. Here we can see some corioretinitis. These punch-out lesions are classic for that. Down here, you can see some capillary non-perfusion. And on the bottom over here, you can see a posterior segment granuloma. So the treatment, the mainstay treatment is corticosteroids. And if it's just eye involvement and it's not that severe, you can go with topical corticosteroids and that would be preferred. However, if it's a very severe eye of manifestations, like an optic neuritis or other posterior, or other severe posterior uveitis, it's important to use systemic corticosteroids. And the idea is to give a high dose at first, do a really slow taper, try to induce remission or a cohesin period, and then keep them on a low dose for a while. You can also use low-dose methotrexate in resistant disease or in disease that you're really worried about the patient losing their vision. Cyclopolegias can be used to prevent synechiae. Neovascularization can also respond occasionally to non-steroidal anal inflammatory. So any surgery that you want to do with a patient, you should wait until they're in their cohesin stage or until they're in remission. And most patients will do well with after cataract surgery unless they have damage to the nerve or the retina and cystic macular edema, or cystoid macular edema, or if they had some glaucomatis changes. But in general, the patients do pretty well after cataract surgery. And occasionally, neovascularization will require laser therapy. If they have persistent neo or if they have it due to a bad ischemic retina, they may not respond to just non-steroidals. So in our patient, due to her optic nerve involvement and her increased intraocular pressure, it was opted to go with aggressive treatment. And she was begun on a three-day IV cell medrall, and now she's on a prednisone, 60 milligrams PO daily, which will be tapered off slowly. She also started on methotrexate, 7.5 milligrams, and that can be increased if needed. So these are my references, and if anybody has any questions. I think it was like 50 to 70 percent. Yes, I think that, you know, it's not, you know, it's really the pathology that you have. You need to get a pathological diagnosis to really make the diagnosis. I'm not sure what the exact number of false positives was, but it was high enough where, you know, the pathology is really what you need to make a 100 percent diagnosis of psychidosis. I did not see that, no.