 So thank you for coming. It's for your benefit. So we'll start off with a case 27-year-old person with unilateral pain, redness, photophobia, and ciliary flush is pictured here. Recurrent episodes of bilateral alternating non-granulums, anterior uveitis, lower back pain. Differential diagnosis, okay? So differential diagnosis of unilateral anterior non-granulums, anterior uveitis. So number one idiopathic, then the HLA-B27-associated spondyloarthropathy, which includes ankylosing spondylitis, reactive arthritis, inflammatory bowel disease, and psoriotic arthritis. Then herpes can do anything, okay? Lens induced, bay-shuts, drug-associated uveitis, always remember drugs as a possible cause of uveitis, TINU and posmishlosmin. High-propane uveitis, as you can see here in a patient with Bay-Shet's disease. So the kind of history that you would want to get in a patient like this is a history of, you know, arthralgias, low back pain, oral and genital ulcers, and many anterior uveitis can give you oral and genital ulcers, not just Bay-Shet's disease, skin lesions, GI and medication use. I think that your labs can be tailored. CBC differential on metabolic profile may or may not be indicated, but certainly, you know, an HLA-B27 in a patient with lower back pain, you know, 80% of patients, you know, 50% of patients supposedly are positive for B27, you know, and a very high percentage of those patients may have an underlying spondyloarthropathy. If you're going to get films, you know, lumbosacral films are not very helpful in terms of anglousing spondylitis, because the action is in the sacroiliac joint, and these days, probably, they get MR, you know, rather than plain films. And then urinary beta-2 microbiome is a actually very good test for screening test for tubular interstitial lymphitis and uveitis syndrome, which is typically non-grain almost anybody knows what these signing findings are? Right, on the right, and that's associated with writers, okay, which is no longer call writers, right, because he was a Nazi, and they're expunging him from the lexicon, along with Wegener, anyway, so yeah, that's right, and of course, Sercenate Balanitis, sorry, it's early. This is a slide, a delayed onset endothelitis. What is the kind of, you know, one of the findings here that might give it away? A patient comes in, it's post-op, he's had, you know, post-op inflammation, give him steroids, it comes back. Any pretty good finding on this pretty good photograph that might help you? So typically, you know, yeah, a capsule plaque, so patients with delayed onset endothelitis, and that includes not only propoenobacteria agnes, which is a common, that city's organisms that you see in that, but also, you know, fungal organisms. The organisms like to hang out in the capsule, in the capsule plaque, okay, so you can actually induce this by sometimes yagging patients, but in terms of treatment, you, the capsule, the capsule needs to be removed, along with intravascular angamycin and vitreous biopsy. So, iris nodules, anybody want to tell me what these nodules are? What about the ones that are near the pupillary margin, what are those called? Kepi. Kepi, you remember that, you know, Kepi with a P and then pupillary margin, and then bisocular nodules are more in the stroma. Okay, this is actually a patient with sarcoidosis. This patient was treated with prednisone and topical corticosteroids, and these nodules went away. Her pedicaridic UBS, these are classic signs that you might see in a patient with her pedicaridic UBS, and the right is a immune ulcer, you know, immune stromal reaction, kind of like an octaromaniac plate, and then on the right is sectoral iris atrophy, okay, board question, true or false, sectoral iris atrophy is Pepinomaniac of Rathus-Holler-Zoster, keratoma UBS. False, why is that? That's right, it was classically taught that, but it's a very useful sign. It's usually due to ischemia of the iris, and it is not necessarily Pepinomaniac. Just clinically, you know, UBI's would diffusely distributed keratic precipitates, herpes, you know, varicella, and then also think about sarcoidosis, Fuchs heterochromic urus, like what, UBI syndrome, and toxoplasmosis. Differential diagnosis of hypertensive UBI is, okay, herpes until proven otherwise, including CMV, okay, because patients, you know, competent patients can develop CMV, UBI, it's uncommon in these parts of the world, but more common in the community. Opossumir-Schlossmann syndrome, Fuchs heterochromic UBI syndrome of sarcoidosis and toxoplasmosis, so that's kind of the differential. Okay, 25-year-old white guy presents his first episode of non-grain almost anti-UBI-itis with unilateral hypoponion, so it's kind of the differential of hypoponion UBI-itis. What laboratory test is the most appropriate? What's the answer to this question? What's that? Well, so a guy's presenting with hypoponion. Do you want to, like, just let him, give him a hall pass? No, probably not. Yeah, I would go with C, right? So, probably the most common cause of hypoponion UBI-itis is HLAB-27, so it's easy, but it can be, you know, bad things, okay, like leukemia and endophthalminus, but the history should help you with that. And every patient with UBI-itis gets a serological test for syphilis. Why wouldn't ANA and rheumatoid factor be appropriate? Well, you would test that maybe in a child with chronic non-grain limits of anti-UBI-itis. It usually doesn't present with a hypoponion UBI-itis. And lupus, you know, usually doesn't produce UBI-itis at all. Okay, so a 35-year-old white guy presents a pain-readed sphotopovian vision, really bad vision in his right eye. He has mutton-fat carotoprosyptase, a microhypfema, and red blood cells in his anterior chamber. Okay, white cells in flair, no posterior sneak-in, intraocular pressure of 50. Okay, what are we thinking about in this patient? Hypertensive UBI-itis. What's the, yeah, so that's probably the first opportunity in your mind. There's a little bit of hyphema. Is that consistent with a herpetic UBI-itis? What happens to the iris? Schemic, right? So you can actually get some hyphema. Okay, so what finding would you expect to see here? Or might you expect to see what would be the absence question? B, yeah. Okay, this is the kind of stuff they ask you on the board. You know, it's not exactly, you know, straightforward, clinically. Okay, in contrast, 12-year-old girl with non-grain limits of anti-UBI-itis, chronic white eye, as you can see here, posterior subcaps are cataract, and, you know, oligarchicular arthritis. What are you thinking about in this eye? JAA, or chronic intra-UBI-itis in kids, which can be exactly like JAA. Okay, so folks can, in adults, it can be this way. Frequently, we'll have just, you know, a very low-grade cell, no posterior subcaps, and high-pressure and cataract. Always think about syphilis sarcoide, TB, herpes, and then immune recovery UBI-itis. So the workup would be a little bit, you know, more extensive. You would want to, in a child that had that, you would want to order an ANA. Okay, that would be useful screening test. Okay, chest x-ray. Okay, so, you know, Dr. Rick's here consulted, you know, over at Primary Children's Hospital with this five-year-old girl with red eyes, but you also have noticed this discriminative rash and, you know, discrimination in the groin, and kind of a cherry-lips. Great, excellent. So, Kawasaki's is pretty unusual, but it's kind of a board-type thing. Stevens Johnson would be maybe a little bit less common in a kid, right, but certainly, you know, a patient who has an exposure or a toxic shock or something like that. So, mucocutaneous lymph node syndrome, usually in kids, you know, less than 10 systemic manifestation, as we've seen here. You know, oral and mucosal erythema, fever, painless asymmetric cervical adenopathy. So the big thing is myocarditis and coronary arthritis, right, that can be life-threatening. Usually, ocular manifestations are pretty minimal, but usually a bilateral conjunctivitis and characteristically spares the limbis, and you see it in the first week. There can be optic disc adema and dilated veins. Okay, moving along. So you guys know who this is, right? This person up on the left, you know? Died this year, last year. Yeah, okay, it's David Bowie, right? So, David Bowie had a chromium, but it was due to trauma when he was young. If you look at his pupils closely, he's got a, you know, he's got a blue, bright eye and a brown, like that. In any case, so iris hetochromia, fuchs hetochromia. I'm dating myself. I don't know. So fuchs is something I like to ask about. It's also called fuchs uviatus syndrome. Okay? So the findings, you know, iris hetochromia, the lighter pyrus color in a brown eye or darker blue, darker iris in blue eyes, because you have the anterior pigment layer is gone. They describe these so-called stellate tachypia. Okay? So they actually look like little stars, and they're distributed usually throughout Bucornia. Cataracts and elevated pressure are very common. And another board question is, patient has, you know, iris hetochromia, and they have high pressure and you do a, you know, parasitesis on the patient, and they have high pyrus. What's happening? They're, that's a so-called amslur sign. Patients with fuchs can have these little iris vessels within the angle, but can believe. You can also see that during cataracts surgery. So it's usually unilateral. Okay? And recently it's been shown, there's been a lot of lures on fuchs, right? It's Ernst Fuchs described this in the 1800s. But I, there's been pretty convincing, you know, molecular data to suggest that rubella is idiopathic genocryness. And the incidence of fuchs has decreased dramatically since people have been immunized. Other associations for non-board questions, okay? So frequently you see these kind of toxo-like scars in the protein. So toxoplasmos is also associated with that. And some of the characteristic findings is the absence of posterior sneakia. Okay, as opposed to the presence of posterior sneakia in, in evasion with chronic low-grade UVIs. There is frequently a chronic low-grade UVIs that does not seem to form posterior sneakia. Okay, so chasing after half-plus or one-plus cell in a patient with fuchs accelerates the cataract by dosing them with steroids. Okay, and enhances their IOP. So that's the one instance in which you might not want to, you know, really be aggressive to that answer you. Okay? The other thing is, the other question that sometimes arises is, as far as cataract surgery is concerned with intraocular lens implantation, it's not, you know, it's not a no-brainer to put a lens in an eye with UVIs, right? So there would be certain kind of indications to do that. But the diagnosis that is associated with the best prognosis for toleration of an intraocular lens is flux therapy for the cyclitis. Okay, so what's, what do you do next for this five-year-old patient with oligarchicular ANA, GIA, associated irdocyclitis, that's unresponsive to topical steroids with methotrexate? Right, I think that's right. So you wouldn't want to just give them unopposed steroids in place of child, especially at risk for systemic steroids, growth refrigeration, consideration. And you want, you know, that they're unresponsive to topical corticosteroids. You might give them systemic corticosteroids if it's severe in both eyes as bridging therapy for methotrexate. So you, the early implementation of steroid sparing therapy in a step-ladder algorithm is, you know, usually an anti-metabolite first. And then if they don't tolerate or don't respond well to an anti-metabolite, which occurs in about 40% of the time, then you move on to usually a biologic. So humera, which has recently been approved, or infliximab would be the next step after that. Okay, so we had this teenager that presents with bilateral anterior cell and flare, vitritus, after bout of fevers, arthritis, increased serum creatinine, and eosinophiliuria, bilateral, 19-year-old female, a little vitritus. What are you thinking about in this patient? Tino. Tino. Yeah, right, exactly. So visceral-alarm migraine associated with toxoplasmosis is a cutaneous diagnosis, right? JAA can be bilateral, but usually not associated with high fevers and isilfinir. TINU is associated with fevers and arthritis, increased serum creatinine. Correct, usually they are, right, and can be actually quite severe. So about 11% of patients, you know, will require, you know, immunomodulation in some of our series. Okay, here's a young woman that presents with floaters, snowbanks, snowballs, with episodic paris thesis. So we're kind of moving along anatomically in the uveitis world, okay, from the front to the to the middle of the eye, so-called intermediate type of uveitis, right? Okay, so intermediate uveitis is not the same as parisplanitis. Okay, intermediate uveitis just designates an anatomic location for inflammation, okay, in the vitrious peripheral retina, in peripheral retina, and usually peripheral vessels, okay, and intermediate uveitis can be associated with systemic disease, as we will see in this moment. When it is not associated with systemic disease, we call it parisplanitis, basically, okay. So you would describe intermediate uveitis if the patient had a diagnosis of sarcoidosis, which is certainly in the differential, intermediate uveitis associated with sarcoidosis, the uveitis, intermediate uveitis associated with multiple sarcoidosis. So characteristically, patients will have peripheral vasculitis, as you can see, obviously, in the color, and then the fluorescent angiogram shows it sometimes more distinctly, particularly with wide-field fluorescent angiography and macrodema, common accompaniments. So, as I mentioned, it can be associated with systemic conditions such as multiple sarcoidosis, sarcoidosis, always considered and all syphilis, of course. Lyme disease, as we were talking about last night, uveitis all the time. We're in our little conference last night. Lyme is actually the most frequent presentation, its most frequent presentation is in intermediate uveitis in patients that have endemic areas. So if a patient comes in, you know, I was hiking and I got this targetoid tick bite here, which we'll see shortly, and that's diagnostic, that skin lesion is diagnostic. And then there are uncommon mimics, okay, or uncommon conditions that can produce each of you, you've got such as a fungal endothelitis, cat scratch disease, toxoplasmosis in a very peripheral lesion. And then non-inflammatory infectious disease such as ocaroschemic syndrome, you know my name, peripheral vasculitis, and inflammation associated with ischemia. So we want to exclude syphilis sarcoid and TB, Lyme sorority, when appropriate. So here it might not be appropriate or without history. And then consider a neurological workup. That's a discussion for, you know, a lecture, okay, but there is an association that you should know about between parsculinitis and the development of multiple sclerosis. It's about a 16% risk, okay, particularly in HLA DR patients in five years. Okay, that does not mean that everybody's going to get multiple sclerosis or that you freak your patients out and tell them that they're going to get multiple sclerosis because that is a clinical diagnosis, right? And the McDonald criteria I think require, you know, separate neurological events separate in time, right? So the issue is do you scan everybody, you know, and I don't do that. Most people don't. It doesn't really make sense to do that because even if you scan them and you find these little things there, many times the neurologists won't treat them. So it's a controversial area. Unless they have something that tips them over. So you will notice in the clinic, patients with intermediate UVS, you know, when we're taking a history, we always ask them about signs and symptoms of MS, okay, parasthesias, bladder, bowel, incontinence, you know, et cetera, optic neuritis, obviously. But when they come in for follow-up, I ask them those questions again just to make sure because, you know, you don't know if they will develop or not, okay? So wide field fluorescing angiography is becoming actually very useful and maybe confounding and confusing in this diagnosis in terms of, you know, how aggressively to treat patients because many patients who are normal will have a little staining and maybe a little leakage in the peripheral retina. And it's difficult to know what to do with that parastomized patients. So from my perspective, the patient is seeing well and has no macrodema and is asymptomatic and has some staining of their peripheral vessels and the periphery, but not, you know, posterior to the equator, I would deserve that. A word about sarcoidosis. It can cause any type of ubeitis, okay? 25% of sarcoidosis, you know, may have ubeitis at some point in time during their course of their disease. The organ's affected pretty much any organ, but in order of frequency, lung, skin, reticular, endothelial, lymph nodes, and eye. You know, the use of ace in life design is a little bit controversial. I think it's useful in patients that have signs of grinding along with the entry of ubeitis and if they're elevated, okay, along with, it kind of puts you in the ballpark, but it's not necessary, okay? Because really the diagnosis of sarcoidosis is based on, you know, biopsy, and if you were the most, as you'll see in a minute, the most useful screen test is the chest x-ray. The other thing that is often overlooked is that sarcoidosis can affect the liver and that not infrequently transaminases will be elevated in patients with sarcoidosis. So it's useful to look at those. Aces confounding in patients that are on ace inhibitors, right? In children, the ace can be physically elevated. A lot of ubeitis specialists will order it, I order it frequently, but I don't place a whole lot of weight in it. Chest x-ray is abnormal in 90% of patients with active disease, okay? There are patients that have signs of sarcoidosis on their on their ophthalmic examination that may have a apparently normal chest x-ray. So your clinical suspicion is still present for sarcoidosis. In those patients ordering a CT chest with thin cuts is actually a sensitive test to pick up disease that may be missed on chest x-ray. That hasn't been completely vetted, but there's good evidence that's the case. So non-cazing granuloma is typical for sarcoidosis, but not, you know, there are other things that can give you a non-cazing granuloma, right? It is useful in patients with sarcoidosis to look for areas other than the one to biopsy to make your diagnosis. So not infrequently, patients will have skin lesions, okay? So lupus pernius is a common finding in patients with sarcoidosis. You can make the diagnosis with a skin biopsy, a little less invasive than doing bronchiol, if you want to revive your directed biopsy on the lymph node. Likewise, the lacrimal gland is a useful place. The conjunctiva can be actually a useful site for biopsy. You know, about 20% of patients, 15% of patients will have the conjunctival nodules, and biopsy in the nodule may be diagnostic, but the blind biopsy of the conjunctiva is not diagnostically useful. So you may get a consultation from the pulmonary or whatever it is that would you do a conjunctival biopsy to exclude the biopsy of sarcoidosis? Look at the patient if they have a nodule, that's fine, but otherwise it's not very useful. So here are, you know, some just pictures of the multitude of findings that you can see in patients with sarcoidosis. Just put this international workshop criteria up that there are categories that have not been completely verified for the diagnosis, definite, presumed, probable, and possible. So definite is biopsy positive, presumed is compatible with bilateral adenopathy. So there are going to be patients that have biopsy that have hyaluridinopathy, that have stage 1 disease, that pulmonary is not going to want to treat, that are doing fine with their pulmonary function test, but they've got UVitis. So the organ system that is driving the inflammation guides treatment. And then probable, that's the kind of more sticky category. So that's where you have no hyaluridinopathy, no biopsy, nothing to biopsy, and then signs and laboratory investigations, and about 60% of the patients will be positive. And then there's the possible. So, you know, the chest physicians, you know, insist that, and I think they're right that, you know, I mean that sarcoidosis is a multi-organ system disease, okay, and that it's difficult to just make the disease just on the eye findings alone, okay. So it requires more than one site. Oh, I'm sorry, just in terms of science, okay, that are useful, okay. So these are these tent, and you can read this paper here, it's actually quite good, okay. These kind of tent like, enterosneakia, that's common in patients with sarcoidosis, higher magnification. You can have these tush, debauch, I'm sorry, my French is horrible, but candle wax drippings, okay, that are exudates around the veins, periflebitis is a very common finding in patients with sarcoidosis, you can see here. Then you can have these accumulations of philometry exudates, otherwise known as snowballs, okay, in the inferior part of the planet. So hence, you know, the differential diagnosis of intermediate UVIs. And then not infrequently and characteristically, these kind of whitish, cordy-retinal spots, particularly in the inferior periphery. What's the diagnosis? I'm coming from New Jersey, I got it, you know, or Long Island. It's Lyme disease, what is the name of this? Erythema migrants. Erythema migrants, right. So in the correct, you know, context, that's diagnostic of Lyme disease. We were talking about this last night about serology and, you know, Western blot, which is necessary for the diagnosis, but this is diagnostic, right? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Huh? Ha? There's something here. You know, tick-borne illness, endemic to Northeast and mid-Atlantic and upper Midwest. So kids are more susceptible to playing in the brush and, I guess, older people. And there are systemic stages, just like there are syphilis, so it's a spirochetal disease, okay? Early, erythema migrans is an early sign, then disseminated, fever meninges, Bell's palsy, which is a very common sign, seventh nerve palsy. It is Lyme disease in endemic areas, sarcoidosis, arrhythmia, it's an arthritis, which are serious, and then persistent, usually neurological disease. So there are many, many manifestations, okay? And it depends on the stage of the disease. So early in the stage of the disease, conjunctivitis is the most common. Intramutate uveitis is probably the most common presentation. You can have a posterior uveitis with vasculitis. Clinical diagnosis is important, along with supportive serology, PCR, with Western blotting. The differential diagnosis in a child is JAA, and then treatment is with IV antibiotics at neurologic doses, just like syphilis. Okay, so the hallmark presenting sign of intermediate uveitis is fibrin in the anterior chamber, posterior sneakia, vitreous cells punched up peripheral coronary artery. All at once? C, right, so it's a disease mostly of the vitreous and peripheral retina, right? In children, you can get an anterior uveitis, but usually not with fibrin. So that's, I think fibrin would be more associated with a B27 associated disease. Sarkoid uveitis is characterized by non-granulose anterior uveitis, chronic rhinolomaceous anterior uveitis, granulomous pan-uveitis. You can do anything, okay? So syphilis is a great masquerader. Sarkoidus is a great masquerader. TB is a great masquerader. 25-year-old white female horse rider from Long Island, you know where this is going. You know, I present this with bilateral intermediate uveitis. So, you know, the clues are in here, right? So from an endemic area, peripheral phlebitis without, you know, snow banks, not that that's necessarily important. In addition, you know, so we're talking about the differential diagnosis of intermediate uveitis from a person using an endemic area for Lyme. So you would want more than Lyme, sorority, and suspicion. That's basically the idea. Okay, so we kind of talked about this entity last night. So this is a patient, actually it was a patient, it was a real patient of mine, that really nice guy that used to do a lot of traveling. I was, you know, worked for the LDS church, was in Nepal, Thailand, Myanmar actually. And presents with, actually this is, you know, five days after his presentation. But he presented to me with the rule out vein inclusion, okay? Rental vein inclusion. You can see that he has areas of retinal whitening, retinal vascularitis, and vitritis, his media is not clear, okay? And some intramental hemorrhage. He has acute retinal processes. So, just a word about the differential diagnosis of multifocal retinitis and vascularitis. And you think about the necrotizing herpetic retinopathy's arm and porn, which is just a variant of that. We were talking about this briefly non-necrotizing herpetic retinopathy. But then C and B toxo, syphilis, sarcoid, TB. So those, the top four entities, okay, are, you know, the major players, okay, and things that you need to exclude. And then when a patient comes in with a retinitis, particularly, you know, at any time, okay, it gets more difficult and more dicey when the patient's immunocompromised, okay, because then you have a broader differential diagnosis. And then the history is very important for risk factors for other things that can cause endocrinitis that is endogenous, such as ibidrugin B as previous surgery, you know, iatrogenic immunosuppression. So the clinical features of ARN, it usually presents two-thirds of the time unilaterally, but can be bilateral, so-called BARN, bilateral, hereinolucrosis. Patients present with acute decrease in vision pain, redness, photophobia, floaters, elevated intraocular pressure, right, herpetic, hypertensive UVIS, dryneolomates, UVIS. And the fallow eye can be involved in one to six weeks or up to 20, it's been described up to 20 years. In the acute phase, you have these multiple yellow-white dots usually in the periphery, as you can see here, okay, they're so-called thumb prints in the periphery that coalesce rapidly, okay, within a matter of days, and progress centripetally to the posterior fold. Okay, so the hallmarks are retinitis, okay, vitritus, sorry, and occlusive vasculitis, okay, usually in orderitis. So those are the diagnostic criteria, clinical diagnostic criteria that have been elaborated by the American U.S. So BARN is a clinical diagnosis, okay. Other things that you can see are optic nerve edema, retinal hemorrhage, corral thickening, and then if you do nothing, it resolves into three months, but, you know, it can resolve like that, okay, without treatment. So widespread necrosis with multiple holes and a very high incidence of fractional retinal detachment. You can usually combine fractional regmatogens, which is very difficult to fix, okay. Optic atrophy is also, I think, an important sequela of this disease that can actually occur even with good treatment, okay, and can adversely affect the visual outcome. These are the diagnostic criteria I mentioned. Retinitis, occlusive vasculitis, and then inflammation, okay. PCR is extremely useful and highly sensitive and specific in confirming the diagnosis, but you don't wait for the result of the PCR in order to initiate therapy, okay. So it's positive in the earlier stages of the disease. Usually varicella and herpes simplex type I, you see older patients that meet in 40 years, and then you can be infected with herpes simplex type II. Usually younger patients. There is a potential for concurrent CNS involvement, particularly with herpes simplex, okay. That's extremely important because that can, you know, kill the patient, all right. And there is any neurological involvement. I would get neurology involved and have the patient admitted to the hospital for intravenous encyclopedia, as opposed to oral encyclopedia with objections as it was just discussed. So the conventional regimens IV acyclovir, you know, 10 milligrams every eight hours or 1,500 milligrams, you know, per meter squared. And then after two weeks or 10 to 14 days of this, transition them to oral antiviral medication, acyclovir or equivalent. Many people will place patients on an aspirin at the time of therapy because to help prevent the occlusive vasculitis, though I'm not sure that does help it. I think it's worthwhile. Do you do that? Yeah. The big problem, one of the big problems is involvement of the cell OI, okay, which can be reduced significantly, you know, in a year by treating the patient with antiviral therapy after you've treated them with high doses of acyclovir. The study was, I think, for three months, you know, I keep patients on it almost indefinitely, particularly if they have a bad outcome. The regimens include, you know, valcyclovir or equivalent. Valgancyclovir is also effective, okay, patients with CMV. And then intravitral therapy with floscarnate or ganscyclovir are both, okay. Typically, and then after the patient has been on antiviral therapy for usually, you know, 12 to 24 hours, these patients usually have a lot of inflammation in their eyes, so I start them on pregnancy. Rental detachment is common. Prophylactic barrier photocoagulation is controversial, though I do perform it. I'm glad that I have done it in many eyes because they had these big areas of detachment that have been prevented from it. And then vitrectomy for the complications. There's been some talk, some studies about using vitrectomy prophylactically. I'm not convinced that that's a good idea. Particularly since they're young, their vitreous is attached, their eyes are hot, it's a complicated surgery. Whether or not you do it prophylactically or therapeutically when they have detachment. The, you know, prognosis is horrible if it's not treated. But it's better and pretty good if they are treated. Although, you know, there is tremendous variation in the literature, I think, in terms of the visual impact. Just for your information, I mean, when a patient comes in and I'm pretty convinced that they have ARN and they're, and they, I don't need to admit them or perform vitreous biopsy. Perform a aqueous tap, usually. And then administer intravigil therapy at the same time. Start them on anti-barrel medication. And steer as the following day. I might treat them with anti-toxoplasmic medication, but if I can't see the lesions, I'm not convinced that they don't have toxoplasmic. So all that is done up front before the AC result of the aqueous PCR is back. Sorry. So this is a 16-year-old African male with this focal area of retinitis, okay? Visions down, they have the tritis, low back pain, shortness of breath, okay? They have a little vascularitis, I think. Maybe you can see that. Here are the lesions themselves. So the differential diagnosis, focal retinitis, you know, an otherwise healthy person is toxoplasmosis. A younger person toxoplasmosis, you know, and then the others here. This patient's laboratories were, we, was very positive for a high IgG of toxoplasmic, okay? So it makes the diagnosis. I think the clinical diagnosis is, toxo is number one in my mind, although I don't see a discrete satellite lesion in that, that patient, and the IgG was certainly suggestive. It's not a confirmatory diagnosis because the prevalence of toxoplasmosis in the population is high, okay? So classical treatment regimen is dariprim or pyrimethamine, sulfadiesin, fulenic acid, and then steroids after the initiation of antimicrobial therapy, if there is significant and we treat for about four to six weeks in an immunocompetent patient, patients that are immunosuppressed may need chronic antimicrobial treatment. This is the evolution of this particular lesion and you can see that they did actually have a coronary scar. So who do you treat, okay? Some small active peripheral lesions may be observed, okay? So if the patient has 20, 30 vision, a small amount of retracin, a tiny little area, you know, peripherally, you might observe that patient, okay? Usually I treat most patients that come in, okay? In order to limit the scar size, treatment is certainly recommended for any lesions affecting the macular, the optic nerve, or large blood vessel, significant vitrititis, and certainly in any patient's immunocompromised, okay? Something that is important to think about in an immunocompromised patient, particularly in AIDS patients, if they are immunosuppressed, then they have a toxoplasma lesion that's classic, okay? They may not have a classic toxoplasma lesion. They may have a lesion that mimics CMB retinitis because of the inter-expression. But if they have toxoplasma, so you need to image in your brain because about 10 to 15% of those patients will have CNS toxin. So the alternative treatment regimens include clinda and sulfidizing together, okay? Trimethoprim, some of them, sulfonylboxylobacterin, twice a day, is actually a good treatment and has not been shown to be inferior to other treatments, although I usually use it in patients that have non-macular threatening lesions. Personally, I usually use the combination of azithromycin with or without pyrimethamine or atovacrone for patients with post-year-old threatening lesion, or intervitual clindamycin and dexamethasone. We were discussing that last night. I mean, frequently patients with toxoplasmosis, you know, they're uninsured. They have bad inflammation in their eye. Their follow-up is going to be uncertain. You know, you want to treat them. And whether or not they're going to be able to afford medications, you are aware of the fact that the makers of the newly acquired owners in Darip and increase the price of that by like 1,000 percent, right? So this is atypical presentation. So here's, you know, the Renee Choi, you know, picture up into the left. That's, you know, everybody would, no one would, you know, mistake that for toxoplasmosis. But it can look like, like the lesion to the right. It's more diffuse, you know? And then you can have actually acquired toxoplasmosis like the guy down the bottom to the left. It acquired macular lesion with no peripheral scar, okay? No previous history. And then here's this brain lesion patient with AIDS. So here are a couple of toxoplasma quiz questions. Most toxoplasmosis is congenital disease, true or false? So false, recent epidemiological studies suggest that the majority of toxoplasmosis is acquired and much of it is acquired postnatal. Okay, acquired disease comes from eating undercooked beef or exposure to cats, true or false? Mostly false, right, okay? So usually not beef, okay? Litter, kitty litter, gain usually. And then contaminated vegetables and water. And I think that probably water is probably the most common, most important. Okay, acquired toxoplasmosis is a clinical diagnosed laboratory testing of supportive pulmonary. Mostly true. Okay, you know, nothing's always true, right? Okay, so it's supportive. It certainly can be supportive in an immunocompromised patient, right? Okay, so mostly true, you know, negative IgG is helpful, okay? So if you have a negative test, you know, it doesn't have a toxoplasmosis, okay? But a positive PCR, you know, is supportive. Say, for example, in the picture that I showed you before, the atypical presentation, just, you know, widespread retinitis. That can be toxoplasmosis in an immunocompromised patient, particularly in an AIDS patient, right? So you can perform PCR of the vitreous fluid or routine serology, which is less helpful that may help you in the diagnosis. Even under the best circumstances, PCR for toxoplasmosis is not that sensitive, right? It's specific, but not that sensitive. What's this? What category is this? Just neuroretinitis, right? So you have, you know, swollen nerve and a partial macular scar, right? What's the most common cause of neuroretinitis? This is a poor question. So, Bartonella, right? So cat scratch disease is caused by Bartonella, Henselier and Bartonella, I think, Quintana, they're like seven different Bartonella species, but those are the two that cause the most disease. You see it mostly in kids. So there is a systemic component, so there is an arithmic papule at the inoculation spike from the cat scratch and a flu-like illness with regional adenopic deaths. Useful information. Ocure disease occurs in about 10% of the patients with either paranoid, ocular, glandular syndrome or neuroretinitis, okay? So the picture that I showed you before of a neuroretinitis, there's also another, there are other variants of neuroretinitis, right? So this isn't a lecture about neuroretinitis per se, just a brief board type of thing, but neuroretinitis, it can also be idiopathic so-called labor-stellate neuroretinitis. It can also be caused by other, a lot of other organisms, including tysoflasmosis syphilis. So you have to, and vascular disease, okay? Hypertension, okay? So there's a broad differential, infections, same thing here. So syphilis, Lyme, TB, Duzin, you know, Herpes, historical aid, and then vascular disease, right? Hypertension, diabetes, AILM, pseudoterm. The thing is that the natural history of cat scratch, associated with Bartonella is good, okay? So most of the patients recover visual through 2025 without treatment. However, there are patients that do poorly, and those patients need to be treated with systemic disease. So some kids will have bad systemic disease or cat scratch disease, and they will be treated with, you know, usually we're fampan, okay? And they don't like to use doxycycline, you know, in kids, right? Okay, so peripapillary scarring punched out mid-peripheral scars and crudely vascularization. No vitreous cells, what is that diagnosis? This is a poor question. C, pose. Okay, accurate histoplasmosis syndrome, right? So presumed accurate histoplasmosis syndrome has these characteristics with no vitritus, okay? If there was vitritus, what would the diagnosis be for the purpose of board examination? Multifocal corditis and panubiasis, okay? This is a patient with burr shot. You can see these creamy type of lesions in the corae, okay? Usually concentrated around the optic nerve. They usually have mild vitritus and pretty good visual purity. The angiogram is more useful in showing the vascolytic component of the disease and optic nerve involvement. The lesions themselves are not usually very highlighted because there's heterogeneity in the lesion and their age. Whereas ICG, as you can see on the right, shows lesions more clearly. So the major differential diagnosis is sarcoidosis. So the absence of hyaluridinopathy is important. In the initial description of burr shot, the absence of a snow bank is also important. HLA829 is associated with 95 to 98% of patients with the diagnosis of burr shot. But 8% of the population is positive for HLA829, okay? So screening patients with HLA829 is not a useful screening test because the positive predictive value of that test would be like 50%. The negative predictive value of a negative HLA829 in a patient that has a picture like that is useful because it's probably not sarcoid. I'd probably not burr shot. It may be something like sarcoid or lymphoma. This is a 31-year-old healthy woman with a history of fever, proto-malase, rash, red eye, decreased vision, history of UTI. Characteristic placoid lesions in the back of the eye. I'm just trying to put stuff up there that they may ask you about before. So this is ampy. Usually, ampy has a little bit of cells in the back of the eye. Some vitreous cell and haze usually occurs in young, otherwise healthy patients. And it's usually a bilateral disease. Just X-rays. Normal lads are usually with normal limits. There's a characteristic angiographic picture of ampy which you can see here with early blockage and late-standing lesions. ICG just shows hypo fluorescence of lesions. Suggesting that the disease is in the coroid or the coriopaplaris. I think that there's been a lot of controversy as to whether where the disease actually is. And OCT, high-resolution OCT, and I think OCT-A suggests that the disease isn't due to the coriopaplaris. Just a word about ampy is that the patients came to know about CNS disease. So if a patient has any signs of CNS disease, they need to be hospitalized. So there's controversy about treatment of ampy. A lot of people will say, oh, it does need to be treated. Their outcome is good. 80% of people have visual acuity better than 2040 or better. There is no evidence to suggest that treatment really alters the outcome, visual outcome. But it does make it go get better faster and I think may limit the amount of scarring that occurs. So when these lesions heal, they heal with hyperpigmentation. It's in the macula. And it can be associated with serous retinal detachment. I think it's reasonable to treat them with serous. So I think anybody with CNS disease needs to be treated. We've answered this question. Birch-eyed retinal coriopathy is associated with, what's the most common cause of visual loss in patients with birch-eyed is macrophagema. Iris nodules and posterior synchia, they don't usually get it. Vitaligo of the eyelid is characteristic of VKH. Cortiline vascularization can be seen with all of these diseases except for which one? A. So JIA is an anterior uveitis. Usually not like that. Serpiginous-like corditis. The key is serpiginous-like corditis. Is what? B. Right, exactly. So it's associated with TB. This is a patient with a multiple corditis due to sympathetic ophthalmia. So, you know, I went to a uveitis specialist the day once and the lecturer was charged with, you know, talking about the difference between VKH and sympathetic ophthalmia and got up and said trauma and walked off the stage. So it's pretty much true. So a history of trauma or surgery, you know, is required for the diagnosis of sympathetic ophthalmia, okay? They frequently have similar findings including vitilogio-poliosis and allophysia. For board purposes, and I mean for board purposes only, okay? The cordocapularis is involved in patients with VKH and not in sympathetic ophthalmia, okay? It probably is involved if given enough time. So this is a patient with exuded retinal detachment, okay? Due to VKH. Here, findings that are typical of patients with VKH include poliosis and vitiligo, okay? And there's another sign called sagura sign. Are you familiar with that? Dr. Choi, what is sagura sign? That's where you get it around a little bit. Right. So perilimbal vitiligo is seen more commonly in Japanese patients. Another board question, right? So the characteristic fluorescein finding in patients with VKH is punctate areas of piper fluorescence which increase in intensity, leak and pool, okay? Causing these neurosensorial apathetic. Are you all seeing that? If left untreated or not treated aggressively early enough, this is what you see in patients with VKH is the sovereign fibrosis scarring. There's no history of acute trauma or surgery. And then three of the following four signs, it's a bilateral disease, okay? It can present asymmetrically, okay? But if you have unilateral exuded retinal detachment, it's not VKH, right? So it's bilateral disease. Posterior UBI is for exuded detachment of sunset glow fundus, which is a later sign of the disease. Neurological signs, tinnitus and stiffness cranial nerve or senus problems, which are more acute signs and cutaneous findings such as alopecia polioces, the lago, which are secretricial or late findings, okay? This is a differential diagnosis of exuded retinal detachment in uveitis, okay? It's actually useful to think about this. So posterior sclerosis is something you may not have to think about initially, okay? Syphilis, central cirrhosis, you have your little fusion syndrome. Sympathetic can perform that sarcoid. Okay? So this is the differential of down and full stenosis. You can see it in sympathetic fatality, but you can also see it in VKH and also see it in sarcoid and TB. This is a hypoping in uveitis, in the patient with Bechette's disease. Okay? Bechette's disease typically causes a vascularitis, which is a cluxus, you can see here with large areas of non-profusion, which is actually very prognostic for the visual prognosis, and chalky white areas of retinitis. Okay? Occur findings, occlusive retinal vascularitis, vascular occlusions, caudable spots, neovascular tissue, patrice hemorrhage. 100% of patients have oral and mucous membrane ulcers, okay? Archea monodotism is classically described in Bechette's disease, although probably an acne-formed follicular rash is more common. Thrombophlebitis, arthritis, large visual occlusion, including DDT, and CNS disease. This is a large, aptus ulcer in patients. Differential diagnosis of oral ulcers, erosyclitis, and arthritis. This is useful, I think. Bechette's reactive arthritis and sarcoid. This is something you probably won't see, but it's a board type of thing. This is a... let's just for sake of discussion, this is a person from Indian subcontinent that presents with this kind of vitreous hemorrhage, and the abascularization of periphery. So it's a so-called ills disease, or adiabatic retinal vasculitis, that is thought to be due to hypersensitivity reactions to work your protein. Okay? So high prevalence in Southeast Asia. In India, men, women, women, high proportion of patients have a positive PPD test, and vitreous hemorrhage and vasculitis are commonly seen. Most patients see be treated, you know, with probably anti-vegeta therapy and laser. And vitreous hemorrhage, you know, decreased vision due to vitreous hemorrhage. This is a patient with multiple vocal corditis. This is a 40-year-old African female immigrant. No fever, chills, weight loss. 15-millimeter PPD. So this patient with tuberculosis. Okay? This is also tuberculosis. Okay? This is also tuberculosis with a tuberculoma. They have the many phases of TB. This is also tuberculosis, or subringinous-like tuberculosis. Okay? So it can produce many different things. Okay? It's usually presumptive diagnosis. Quantipheron gold, just for the purposes of your board examination, quantipheron gold tests latent tuberculosis, not active disease. Okay? And exposure to the chest x-ray can be normal in patients with tuberculosis, uh, uveitis, or ocular TB. So that extra pulmonary sites are important to consider. This can be a really difficult diagnosis to make. And sometimes, you treat the patient empirically with anti-tuberculosis treatment. The, uh, for a patient with established disease, it's usually a four-drug regimen. Okay? With top-of-the-peer-actors depending upon the treatment information. The incidence of TB in the United States is increasing. Okay? In a big way, as is syphilis. The quantipheron gold assay, as we've talked about, is a, uh, uh, screening test, you know, for latent tuberculosis. All of these guys have syphilis. Okay? I just, syphilis is a great imitator. Oh, the church lady has syphilis too. Yes. In my clinic, the church lady came in with, she was referred in with mutes, okay? She had a rash on her palms, okay? And she had these punctate areas, which I'll show you in a minute, uh, uh, uh, uveitis. And I was talking to her and I asked her, is there any possibility, you know, that you could have a sexually transmitted disease that my husband could, and she had syphilis. Okay, so the most common, uh, you know, manifestation of syphilis is a posterior uveitis 50% of the time, but it can produce pretty much anything. There are some characteristic presentations of syphilis that you should know about. One is this, uh, uh, syphilidic posterior plaqueoid corbitin, as you can see right here. So it's this typical kind of area right here, okay? With a blocked leading edge and hyperfluorescent, you know, later. Okay? The other characteristic presentation posteriorly is the patient, the church lady, okay? That had these, uh, superficial retinal precipitates. You can also see a optic nerve, just an optic neuritis, okay? This is a patient that, you know, who has HIV negative and had risk factors, you know, for, uh, HIV that he just presented with, uh, optic nerve involvement. So always consider syphilis in your differential diagnosis. Always think about testing a patient for HIV that has syphilis. They ca- they go together and use both specific and non-specific Japanese testing, okay? So I'm just going to, just the important point with syphilis is that it is a neurological disease, okay? And needs to be treated with, um, intravenous penicillin G, okay? At neurological doses. Not a shot of penicillin in the butt. Okay? This is a lady, uh, so in term, masquerades, uh, and we're almost done. I know we're over time here, okay? But this is later the presented with, um, vitritus non-responsive, um, vitritus and these characteristics of retinal infiltrates. So, intravenous, if she was 60, some 100 years old, intravenous lymphoma was a, uh, very high on her differential diagnosis, okay? And she, um, underwent, she had non-specific white matter changes in her brain. In retrospect, maybe, uh, lymphoma, um, she underwent a vitreous biopsy and, uh, subrenyl aspirate and had poorly differentiated, uh, limited cells, okay? So, always think about lymphoma in your differential diagnosis. So, here you have a 45-year-old person, not your typical age, right? So, it can occur in younger people. With unilateral vitritus, unresponsive to corticosteroids. So, that immediately is a tip-off, okay? If the patient's getting worse with corticosteroids, unresponsive, you know, um, think about a masquerade syndrome, no neurologic symptoms, better yet a vitreous biopsy with monomorphic lymphocytes, but large, nucleated, prominent, and nucleolite-scanning, et cetera. So, M.R. and L.P. are negative, okay? So, this patient has intravenous lymphoma that needs to be treated with individual therapy. So, these are just a couple of, a couple of questions on, uh, that I think you guys probably know. This is an important question, okay? The immunosuppressive medication is most likely to be associated with secondary neoplasia, neoplasia in the long-term use, is what? Cyclo-phosphamine. Cyclo-phosphamine, right? So, cytotoxic medications can be associated with increased malignancy and mortality, okay? Complications of biological therapy, okay, humera and inflix-map include all of these, okay? So, all of these have been described, okay? A lupus-like reaction, lymphoma, infections, and exacerbation of demyelinating disease. Can you mitigate that with methotrexate? Not, pardon me? The drug induced this, can you mitigate that with methotrexate? I'm not, not always, but you give methotrexate in order to reduce the incidence of it, but methotrexate is given more to prevent the formation of anti-chimeric antibody to inflix-map, which will reduce the efficacy of the medication. The last part is on AIDS, okay, and HIV. So, just briefly, the most common opportunity to infection in patients with AIDS is CMV retinitis, okay? You can get syphilis, you can get toxoplasmosis, you can get porn, but the most common is CMV, okay? The advent of heart of anti-retroviral therapy has reduced the incidence of CMV retinitis significantly, okay? Like, by 90%. This is what typical CMV looks like when you post to your post, so-called pizza pie or tomato ketchup retinitis that falls in the reflector layer, usually in the arcades. There's another look to CMV, which you can see in the periphery, okay, so-called granular type of retinitis that the activity is in the leading edge here, and then you can also see a frosted branch type angiitis associated with that. So, heart has, you know, reduced the, you know, the prevalence and the incidence of new CMV retinitis significantly. We're going to Myanmar tomorrow, and we're going to see a lot of, probably less CMV than before, okay? But in the developing world there's still a problem where people don't have access to medication. They're late presenters, and they don't come until they're sick, so they frequently don't come with CMV. And then, you know, so patients, cutaneous, can also be a major problem presenter. So that's all I got for this.