 So, today we'll be talking about a group of diagnosis that nobody in this room wants to have, and outside of the presenters today, probably no one even really wants to deal with treating, and that's the infectious uveidities. So, uveitis due to infectious ideologies accounts for 15 to 20 percent of all cases in the United States. That number is higher worldwide, and at some tertiary referral centers, it's upwards of 30 percent. infectious uveitis can often mimic immune mediated causes of uveitis, and so we have to be intimately aware of these various clinical presentations of certain infections in order to have an appropriate diagnosis and timely management. Dr. Palestine, my mentor at University of Colorado used to have a saying about treating uveitis and that there's infection, there's cancer, and there's everything else. Everything else meaning inflammatory diseases, which is basically treated the same, steroids, immunosuppression, cancer, we have time to figure out, but infection is really the one that's treated entirely differently, and the wrong treatment can actually make it worse, such as steroids. And we know infectious uveitis can affect all different parts of the eye from front to back. This is a case of, we're all familiar with the herpetic dendritic keratitis. This is infectious scleritis due to pseudomonas after a teridium surgery, and this is an individual with recurrent anterior segment inflammation that ended up being diagnosed with a P-acnes infection of the implantable columnar lens requiring removal of the ICL, and of course our notorious posterior infectious uveitis. There are some diagnoses that are particularly urgent in identifying due to having rapid progression and a threat of permanent vision loss, so I'd like to call on a couple of residents if you can think of your top one or two diagnoses that you don't want to miss on call. Okay, good. Anything else? Great. Okay, so this is an ocular emergency. When a patient presents with a hypopoean, of course we don't want to just assume it's HLA-B27 disease. It could be, but the most important diagnosis to rule out is infectious endothemitis, either post-surgical, which is the most common, or endogenous, which can be related to IV drug use or indwelling catheters, et cetera. Typically, a history can differentiate between inflammatory and infectious causes of a hypopoean, but when in doubt, no one will be faulted for performing a TAP and inject. And then acute retinolucrosus or a necrotizing herpetic retinitis. This is typically from VZV or HSV, and as a reminder, this happens in otherwise healthy individuals, albeit with very bad luck. And there's a classic triad of vitritus, occlusive retinal vasculitis, and peripheral necrotizing retinitis. And this progresses very rapidly within days, and treatment consists of high-dose systemic antivirals and often intravitural antivirals. There's a high risk of fellow eye involvement and retinal detachment. And this is why we dilate every patient with UVitis, because we don't want to miss ARN. So if you see someone with anterior segment inflammation and you don't look in the back of the eye, or if you're only looking through an undilated pupil, these lesions can start in the periphery, and so you miss it. And so you think you're just dealing with anterior UVitis and miss this crucial diagnosis. There was a study published in 2016 that reviewed lawsuits related to UVitis in the United States, and the top diagnosis by far associated with litigation was acute retinolucrosus with the average settlement of $750,000. You needed some financial motivation to dilate. Some other common offenders are old friend syphilis, which is known as the great masquerader, since it can present virtually any way it pleases. But a typical case of acute syphilitic posterior placoid coreyretinopathy, we can see this large yellowish lesion in the posterior pole, and it has classic OCT findings with disruption of the ellipsoid zone and these pyramidal shaped RPE deposits, which normalize with treatment, which is 14 days of IV penicillin. Ocular TB, Dr. Shakora will touch on this today. Toxoplasmosis is the classic headlight in the fog, which describes a focal area of retinitis seen through the haze, the fog of vitritus, often next to a pigmented atrophic scar right there. And so toxoplasmosis is a parasite and seroprevalence in certain parts of the world, such as Brazil's upwards of 80%. CMB retinitis, this is the more indolent cousin of acute retinolucrosus, and this happens in immunocompromised patients, historically aids patients, but these days we see it in patients with malignancy or those that are iatrogenically immunosuppressed. Retinella or cat scratch disease is a gram negative bacteria that causes this classic macular star appearance in neuroretinitis, and this is actually believed to be a self-limited disease, but most cases that are vision threatening, we would treat with doxycycline or rifampin and an addition of oral steroids. Fungal endophthalmitis or fungal choreoretinitis can occur in immunocompromised patients, and this is a classic string of pearls finding. And then we have the zebras, more oddball infections of infectious uveitis, toxocoriasis, which causes a peripheral granuloma with a stock to the optic nerve, West Nile virus is characterized by these targetoid lesions that occur in a linear fashion along blood vessels, duzin, which is a diffused unilateral subacute neuroretinitis when we have a nematode wandering around in the subretinal space, leaving a wake of destruction in its path. And then sister cirrhosis, so the next time you think you're having a bad day, at least you don't have the larval form of a tapeworm in your anterior chamber. And then a whole other host of rare infectious diseases that typically occur in tropical climates that can affect the eye, and we won't touch on those today. So how do we know what we're dealing with? Well 90% of the work is done by taking a good history, figuring out where the patient lives, what do they do, what do they eat, taking a review of systems, we ordered blood work, and then of course taking a sample from the eye, so an AC or vitreous tap, we can send it for gram stain culture, viral PCR, toxo PCR, now there's universal PCR, and more recently metagenomic deep sequencing. And rarely do we have to biopsy the sclera or the retina. So we have to maintain a high suspicion for infectious uveitis, if we're treating as inflammatory and the patient's not responding appropriately, we may have to reconsider our initial diagnosis and dig further or biopsy. If a patient presents with new uveitis, always dilate the patient so we don't miss iron, and please never inject steroids into an eye with uveitis if you're unsure of the diagnosis and haven't rolled out infectious causes. So to end, we'll have a quote from our own Dr. Vitale, if you're alive, you're at risk for syphilis. Thank you. Dr. Shakur. Here we go. Hi, everybody. There's the presenter. All right. Now it's time to play the game. Which eyeball is this for the residents? What does this look like? Mandage shrimp. Right. Amazing. Can't believe you guys got this. But so interesting animal. It's only four inches long. It has these modified mandibles that can strike a target at 1500 Newtons. So if it was human size, it would be able to punch through one foot of plate steel. Nonetheless, talking about TB today, nobody makes any money off TB. Here's a 28-year-old Haitian gentleman. He had pain, blurry vision, and his left eye for three months, and he comes in. He has an unidentified retinal object in the right eye, but the left eye is the one that we want to focus on. And you can see lots of vitritis, creamy discoloration of the retina and this little, what looks like a retnochoroidal granuloma in the periphery. As you would do with the unilateral inflammatory disease, often, in a patient who's young and otherwise healthy, we sent a large volume vitreous sample for PCR, which was negative for all comers, including mycobacterial DNA. His PPD, however, was quite positive. His guantepheron gold was positive, and he had a good response to four-drug therapy coming back to about 2040 without the addition of steroids. Here's a 54-year-old lady who was seen by my colleague, Dr. Patel, when he was at Cornell. She was from Mexico. She's diabetic on insulin, very poorly controlled, has hypercholesterolemia, and is on Coumadin for atrial fibrillation. He's had redness for six months, did not improve on prednisone, and referred to a uveitis clinic in 2015. Now, for the residents, when you see this kind of scleritis, when you see these kind of creamy placoid nodules under the conjunctiva, always think about infectious scleritis, particularly if it's unilateral. The guantepheron gold was positive, and it was decided to treat her empirically for tuberculosis or tubercular scleritis. She was started on four-drug therapy for TB, started on prednisone, and variable doses of methotrexate. She was not terribly compliant. Her scleritis continued to progress. Biopsy was done, which is entirely negative. She was on and off TB therapy for a year, and disappeared as often these patients do. Four months later, comes to the ER, hasn't been taking her meds. Still taking her Coumadin, hasn't been taking her insulin, has been throwing up because she's in DKA, and sure enough, she has a perforation of the globe. Bad news is that you can't see out of it any more good news is that we get more pathology. And unfortunately, this eye was inoculated. And interestingly, zeal nielsen stains, acid-fast bacillus staining was negative, but the samples were sent to Dr. Rao back then in Duhini, and real-time PCR revealed tuberculosis. So TB scleritis is particularly bad. Here's a 60-year-old Caucasian lady first seen in 2010 with worsening eye pain and redness. Her workup was negative, including a PPD in quantiferon gold. And she had a poor response to local and systemic steroids. And here it is again, once again, this unusual-looking unilateral scleritis with maybe some features of interstitial keratitis as well. When we checked, her quantiferon gold was positive, her chest extra was normal. ID would still not treat as active extra pulmonary tuberculosis. And that's a whole other issue, convincing people that patients have TB, because you can't, it's hard. This progressive worsening of the scleritis, fortunately, she came in with these little subconjunctival furnace-sealed nodules, which were biopsied and sent for PCR, and sure enough, mycobacterial DNA was identified. So she was started on four-drug therapy, prednisone and celsept, as often these patients need to be. And despite this, the globe perforated 10 months after perforation, presumably because of a delay in diagnosis and a delay in the initiation of treatment. So it's important to treat these quickly, if possible, despite it being a fairly indolent infection. Tuberculosis is a global health problem. In 2013, there were 9 million cases with 1.5 million TB-related deaths worldwide. More in 2011, less in 2015. 1 to 2% of patients with, yeah, animations, 1 to 2% of patients with systemic TB develop ocular disease. And there's a high rate of TB in endemic areas, patients from endemic areas, HIV-positive patients, immigrants, refugees, the elderly and minority populations. And in the non-HIV cohort, the elderly have the highest rate of infection. TB can really present as anything, but you really wouldn't suspect it in a non-granulometous anterior uveitis. You should suspect it in anybody from an endemic area or with certain risk factors. And beyond the uveatic manifestations of the disease, you can see tubercles on the skin of the ilate, corneal, fraternals, conjunctivitis, scleritis, and intersexual keratitis. A classic presentation of coroidal tuberculosis is, in fact, multifocal, sub-prisonous coriditis. It differs from idiopathic inflammatory sub-prisonous coriditis in that it often tends to be multifocal. It is still more common in men than in women, and it is considered to be an inflammatory manifestation of a posibacterial infection. But you do have to treat TB and the inflammation associated with it. It can be bilateral in some cases, although mostly unilateral, and there can be vitritis, which is what differentiates it from idiopathic inflammatory sub-prisonous. Here's a 62-year-old gentleman referred with worsening sub-prisonous after two years of prednisone and immunomodulatory therapy. And this ended up being tubercular coriditis, and the reason for that, what kind of stands out in this particular case is that, yes, there is that kind of helicoid centrifugal migration of this lesion encompassing the macular, but there is this peripheral coriditis that you don't often see with typical sub-prisonous coriditis. Of course, you can see it with relentless black coid, but that's another story. So, according to Dr. Rao, nursing Rao, who used to be at Doheny, and is an expert in the United States on tuberculosis, features suggesting tuberculosis to include endemicity, the multifocality of lesions, unilateral lesions, a vitreous or AC reaction, which you don't typically see with sub-prisonous, and the lesions tend to be macular rather than very papillary, and of course, a response to anti-tubercular therapy. Another feature of this disease is that, in addition to the typical helicoid spread of sub-prisonous retinal coridopathy, you also see these little sub-retinal coroidal granulomas or nodules, rather, which can point you to the diagnosis. So, TB-UVI just has multiple presentations, and there's really no consensus thus far on classic features because there are no classical features. It can affect all the tunics of the eye. And the diagnosis can be made presumptively, even when there is no pulmonary or systemic disease, the majority of ocular TB is actually entirely extra pulmonary. The skin test can be useful. What we perform more commonly over here is the quantiferon gold assay, although an article in Chaston 2011 showed that there's really no superiority of one over the other, except in the BCG vaccinated, which in this room I am, but perhaps not anybody else. 50% of patients with ocular TB have a normal chest X-ray, but 40% have a normal chest CT. You can biopsy the ocular tissue, but PCR and culture is notoriously difficult in this disease. And sometimes you just have to make the diagnosis in response to empiric treatment alone. One person who does see a lot of ocular tuberculosis is Dr. Biswas in southern India, and he reported ocular morbidity in only 1.39% of 1,000 patients with acute pulmonary, active pulmonary and extra pulmonary TB. He mentions that the definitive diagnosis is difficult, acid-fast smears and tissue culture, and even PCR from ocular tissue is very difficult. So when your ID physician asks you if you can take a sample of the vitreous and check for TB by PCR, you have to tell them that the chances of a positive TB test are only about 30 to 40%. And that a negative test does not rule out the disease. Positive test, of course, does rule it in. So here's a 54-year-old gentleman as an illustration of this issue who was noted to have vascular sheathing after cataract surgery in the left eye. His quantiferent gold TB was positive. His vitreous sample was negative for TB by PCR, and his chest extra was unremarkable, so ID decided to treat him only for latent tuberculosis. So he started on isoniazid and prednisone. And this is how his vasculitis looked right after when he was diagnosed after cataract surgery, but after being on steroids for six weeks, he presents with this, this acute granulometous anterior uveitis, meaning that it wasn't latent TB. And sometimes when you have a new unilateral tubercular or suspected tubercular process, you do have to treat with for drug treatment, even if you're not sure whether it's latent or, or, or active extra pulmonary TB. Jim Rosenbaum, one of our colleagues that in Oregon wrote this nice editorial TB, to be or not TB. He has a way with words, sadly. He needed a Bayesian analysis of TB testing in, in uveitis and the positive predictive value in endemic areas is obviously fairly, you know, robust, but in, you know, in affluent Caucasian Portland. The positive predictive value of the test is not, not very high. And his contention was that, yes, I do not test routinely for tuberculosis, unless there are risk factors or if the disease is unilateral or if the disease has features that may be consistent with granulometous disease. He says, does say that it, that it is important to rule out tuberculosis, if you're going to immunosuppress a patient. So the question is, should we be testing all patients with ocular tuberculosis for TB. And, you know, in non syndromic uveitis of, and if you're not going to immunosuppress a patient, non granulometous disease. You probably don't, but in granulometous disease, you certainly do test when there's atypical features. And when a patient comes from an endemic region, it's important test. Do I test all comers for uveitis? No. If somebody comes in with an acute and anterior uveitis that looks like HLAB 27 disease, then no. But if it's a posterior uveitis, and I know I'm going to immunosuppress a patient, and I know I'm going to put the patient on systemic steroids, I tend to. But ocular tuberculosis is really hard to treat. And if you don't test, then you're more likely to have a delay in diagnosis at some point. Therapy is really not very effective in delayed cases with only 40 to 70%, you know, a complete cure. And tuberculosis does have a very high inucleation rate of 30%. So missing the diagnosis is kind of a big deal. So why not just plan to PPD. The largest case series in the United States is only 17 patients, meaning, you know, obviously this is in the post HIV era, or it still exists, but the post and epidemic era. And this is Debbie Goldstein and, and Sergio Patel and Howard Tessler out of UIC at the time. And they report on multiple manifestations of ocular tuberculosis including optic nerve granulomas, posterior lesions and multifocal and sub-pigenoid tuberculosis. And off the 17 patients that they reported on 14 were mycobacterial, three were non-mycobacterial, three patients were white and non-Hispanic. Eight of the 17 patients were actually born within the United States. 12 had a history of possible TB contacts and five had no risk factors at all. Only half had bilateral disease. Four, or half had bilateral disease, you know, contradicting the dogma that it can, it's usually unilateral. Four had scleritis, two had granulometous anterior uveitis, and 11 posterior. Posterior uveitis tended to be bilateral, by and large, all other disease tended to be unilateral. 86% have had at least one positive TB test. Two patients with negative screening had non-tuberculosis mycobacteria. Less than half had positive chest imaging CT scans or chest x-ray. So that does not, you know, positive chest x-ray does not make a diagnosis. A negative chest x-ray doesn't mean you don't have tuberculosis. This tends to be extra pulmonary in nature, more than half. 76 had isolated ocular disease where there was no sign of active pulmonary or extra pulmonary TB elsewhere in the body. Only four patients had evidence of systemic TB. And here's the worst part, the average delay of referral to a uveitis service was almost two years. And in this case, being the majority, being Caucasian actually worked against you, where nobody suspected, you know, a Caucasian gentleman coming in from in the suburbs, having of having tubercular disease. And therefore, they had a far, far longer delay in diagnosis and a delay in referral than patients who you would traditionally think of as having tuberculosis, the HIV positive, elderly nursing home, refugee coming from an endemic region. So those people were actually protected from a delay in diagnosis. A delay in diagnosis was associated with a negative CT of the chest. And once again, I think it's important to realize that this happens to be more likely in an extra pulmonary disease in its entirety. Then not profound vision loss was associated with a delay in diagnosis. Those with profound vision loss had their disease diagnosed an average of 1260 days. An average time to disease control was 137 days after initiation of anti tubercular therapy with or without immunosuppression. Supplemental doses of steroids to control inflammation was not associated with shorter periods until control of the disease. The disease tends to relapse. I always ask my ID colleagues do with the patient on at least six months of for drug therapy if tolerated, and that reduces the rate of relapse in this disease, just as it would in men and GLTB. The relapse rate was a higher relapse rate was associated with the use of supplemental steroids and immunomodulatory therapy. Three eyes were enucleated. These patients tended to be patients with scleritis. So in summary, think about tuberculosis. You don't always have to test for it when it's highly unlikely. The prognosis for my co bacterial ocular disease is not great. Longer therapy is needed than you need for systemic disease and that's something that I often communicate to my public health and infectious disease colleagues. I tend to ask for. And after multiple treatment failures in a number of patients, the ID, my ID colleagues over here do agree usually to put patients on six months of anti tubercular therapy for drug. There's a high risk of relapse that necessitates prolonged for drug treatment and concomitant immunosuppressive regimens may be necessary. Ocular TB is uncommon in the United States. But, and it only accounts for about a half a percent of referrals to tertiary care. However, it does exist and the morbidity is fairly high. It typically occurs without apparently apparent systemic disease, although of course, 1 to 2% of patients with systemic disease can get ocular manifestations. The absence of pulmonary TB should not delay or prevent anti tubercular therapy do not listen to people who say you only need to treat for latent TB because once again this can lead to bad outcomes. And for here, consider the diagnosis of TB even in patients who are not from or who have not been to endemic countries regardless of their race. Caucasians in the US had a significant delay in diagnosis with which correlates with increased morbidity. I'd like to acknowledge Dr. Patel, Dr. Vitaly and the photography departments at these various places. And here is a mantis shrimp, breaking a sea snail with great force. Questions. Yes. Oh, and is associated with a higher rate of relapse. Why, why do you, why do you suggest using use the steroids to decrease the need for, for surgery. steroids are associated with a lower rate of structural complications. So, for example, if you have a patient with pan uveitis comes in with and it has a positive TB test and you know, this patient has TB, you start on anti tubercular therapy, but the reason you start on steroids is to prevent dense vitrides and try to quell that vitrides to decrease the rate of psychotic membrane formation and decrease the formation of epiretinal membranes and fractional retinal detachment. So, yes, it does not influence the, the time to full control, but it does diminish structural complications that can be blinding. Yes, like anterior uveitis with hypopion with like rifabutin treatment for these patients. And how do you kind of differentiate that between like activation or typically you're not using refabutin in in current regimens for tuberculosis you're using your fampin. Fampin does not have the same incidence of anterior uveitis that refabutin does. Yeah, that's a, yes, it can be difficult, especially if you don't have a view to the back. Anybody else? All right. Dr. Karaja is going to present a case. Thank you. Good morning, everyone. Today I'm going to present a challenging case of pilot bilateral pan uveitis that we have recently seen in our clinic. Third to seven years old African-American woman presented with painless blurry vision in both eyes. And at that time from this examination, as we see here in the color pictures showed that severe optic discidema with hemorrhages and engorge and torturous vessels, as well as the elevated appearance of the posterior pole in the right eye. And in the left eye, in addition to the vitreous haze, there wasn't this high premia and edema, as well as multifocal cordial lesions at the peripheral retina. Here we see the fundus autofluorescence images. And on all CT, there was a serious retinal detachment with cystoid macular edema in the right eye. And left eye showed CME and subretinal and subpoval fluid. We also did fluorescent angiography for the patient, which showed severe disc leakage, as well as leakage from the peri vasculature in the right eye. And in the left eye, less severely, but similarly, there was a disc leakage and leakage from the major arcade vessels, macular leakage and leakage from the peripheral capillaries. We also did ICG for the patient at that time, which showed multifocal hypofluorescence lesions in both eyes, which was actually more apparent in the left eye, given the serious retinal detachment of the right eye. And interestingly, normally, we would expect hypofluorescence of the disc, however, in the right eye, there was then hypofluorescence appearance of the disc, given the severely impaired blood retinal barrier. Visually, Q2 was counting fingers in the right eye and 2015 in the left eye. There was no cells but 1 plus fillary in both eyes, along with multiple posterior synechia in both eyes. In the fundus examination, there was on 0.5 vitreous cells and 1.5 vitreous haze in the right eye and 0.5 plus cells and 1 plus vitreous haze in the left eye. And overall, with these findings, the patient had multifocal coriditis and panuviitis, optic discidema, and serious retinal detachment in both eyes. When we look at the background of the patient, she was actually from Central Africa. However, besides that, ocular and medical history was almost completely unremarkable, as well as the review of the systems. And the patient had been treated with topical diphylopredinate and cyclopentalate prior to her presentation to us. So in the differential diagnosis, we considered multifocal coriditis and panuviitis, what Koenage-Hertha syndrome, ocular sarcoidosis, tuberculosis, toxoplasmosis, and toxocaryosis. We did some blood work for the patient, which showed positive ANA and slightly elevated lysozyme levels. However, we couldn't start the patient on any treatment at that time, given the pending quantifuran levels. And unfortunately, the patient was dealing with the social challenges and we couldn't reach the patient to have this workup done. And unfortunately, 10 days later, she presented by herself with severely decreased vision in the right eye. And at that time, there was even worse discidema in the right eye, as well as the white ischemic appearance of the retina and blood hemorrhages all over the retina in the right eye, and with similar findings in the left eye. And OCT also showed serious retinal detachment of the right eye. So we considered combined CRAO and CRVO in the setting of severe discidema in the right eye. Visual acute was unfortunately NLP in the right eye and the other findings were almost similar to the initial presentation. At that time, we forced the patient, actually brought the patient ourselves to the lab for the quantifuran testing, which showed positive quantifuran levels. And we also did chest CT at that time, which showed no evidence for granulomatose disease in her lungs. So with these findings, we diagnosed the patient with presumed ocular tuberculosis and planned to start antitubercular therapy readily and actually admitted the patient by the infectious disease team. And also we planned additional oral prednisone after the initiation of antitubercular therapy. Regarding antitubercular therapy, the patient has been started on rifampin isoniazid by prioresinamide and moxiploxacin instead of a temporal given the ocular toxicity per ID team. And we also continued to topical therapy for the patient. Two weeks after the initiation of antitubercular therapy only, there was unfortunately no view to the retina in the right eye. However, there was some improvement of the discidema in the left eye, which some atrophic appearance of the corridor lesions in the from this examination. OCT also shows some improvement of the CME in the left eye and visual acutus significantly improved the 2025 in the left eye. At that time, we started the patient on oral prednisone 60 milligram daily with slow tapering and also continued to topical therapy on top of the antitubercular treatment. Two weeks later, she showed further improvement of the discidema and corridor lesions even resolution of some of those lesions and there was an almost complete resolution of CME on OCT. Visual acutus further improved the 2020 in the left eye. Unfortunately, at that time, right eye developed 360 MBI and fundus examination showed further improvement of the inflammation in the left eye. We plan to continue same treatment with further tapering of oral prednisone and almost one month later after the initiation of antitubercular therapy and two weeks of oral prednisone with tapering. There was a significant improvement of the discidema in the left eye with resolution of some of those corridor corridor lesions and the atrophic appearance of the remaining ones. And OCT also showed complete resolution of CME in the left eye and B scan at that time showed unfortunately traction retinal detachment in the left right eye. Visual acutus was barely like perception in the right eye, but 2020 in the left eye and we plan to continue the same treatment with further tapering of prednisone for the patient. So in conclusion, high suspicion for infectious uveitis is crucial and it should be first through a lot with the patients with ocular inflammation. And patient history and the background is very helpful for the diagnosis of these patients. And in addition, infiltrative versus inflammatory appearance of the discidema may be also helpful for the differential diagnosis, especially with the patients with severe and aggressive course. Currently, the diagnosis of ocular tuberculosis is presumptive. And there's in recently very nice guideline collaborative ocular tuberculosis study group, define the consensus criteria, especially for the management of ocular tuberculosis. And according to that, in summary, suspicion for ocular tuberculosis in terms of ocular findings, along with the positive quantifuron testing should bear an antitubercular therapy. And after the initiation of ATT, systemic as well as the topical series is helpful for the control of the inflammation, given the immune reaction to the microorganism in the pathophysiology of the disease. Thank you. I just had two questions. One was the moxie being a substitute for a thambutol. So that's something you'll commonly see with TB treatment for ocular specific disease. ID for some reason thinks that we shouldn't be using ethyl butyl in ocular disease. Honestly, in a situation like this, I couldn't care less. I have a follow up question. The, when I think of like serious rd, things that cause it, I guess infectious etiologies is not one thing that comes a high to mind. I guess you can kind of consider this as a combined inflammatory infectious issue that went on with this patient but was there any particular thought process behind that and also why the traction rd developed. Yeah, so to Dr. Warner's question that these are the structural complications that you want to avoid. And this is the utility of using oral steroids over topical. Unfortunately, this patient was, you know, pardon my slang but hosed. At the time we'd seen her she. The disease had not been identified there was definitely a very raging posterior UVA just and she'd been treated with topical steroids for two to three months. So this fractional retinal detachment occurred, possibly as a result of an exodative rd that then developed sub retinal and pre retinal proliferative retinopathy. And by now you can throw as many steroids that is at it as you want and it's not going to resolve because now it's a mechanical issue. And the utility of doing anything surgical to this right eye is limited. I'll be presenting a case that hopefully highlights kind of an interesting case that hopefully highlights kind of the, the diagnostics and the work up and some of the multidisciplinary kind of nature of taking care of different type of patient which is infectious endophthalitis. So to kind of walk through it's this is a 54 year old man who presented with vision loss in the right eye. He essentially described that two days prior to presentation he lost quite a bit of sort of vision in that I associated with some dull aching and redness, but no pain with eye movements flashes float flashing lights. And no symptoms in the other eye. He's otherwise quite healthy. He had PRK in both eyes and notably as far as social history and kind of exposure so he's an actively practicing radiologist he travels quite frequently domestically within the country going to conferences so he had just spent time in Boston, frequently travels to California in the West and so forth, but nothing essentially no obvious new or sort of unusual exposures in that context, including new animals and notably no high risk exposures such as IV drug use. But what he did note and what was quite apparent in talking with him in the emergency department was that he was feeling systemically unwell. So 10 days prior to the presentation he had described this febrile illness with a fever is up to around 102. Arthralgias he had watery diarrhea and he had this ongoing non productive cough with some pleuridic retro sternal chest pain. He was seen as PCP several days prior and was prescribed oral is a thromycin without much change in his symptoms. His wife felt like he just seemed to, you know, more tired and maybe just seemed a little bit kind of more cognitively slowed compared to usual just feeling unwell. So in one exam his left eye was completely normal. His right eye was count fingers at one foot he had normal intracular pressure no relative afferent peopularity effect and he had quite significant amount of intracular inflammation so he had four plus cell with fibrin in his anterior chamber as well as four plus cell with quite a bit of vitreous haze. So this photo is actually a couple days after presentation, showing the right eye which has diffuse central vitreous haze and sort of this vitreous debris beneath the optic nerve, but quite impressively he had this sort of large sub retinal or sort of creamy yellowish elevated lesion, as well as two smaller similar lesion superiorly that we're concerning for for abscess ease. And so the working kind of diagnosis or the working kind of framework for this patient is that he's a previously healthy, I mean, presumably immunocompetent patient, presenting with acute or sub acute endogenous endophthalitis with these multifocal choral abscess ease in the context of a febrile illness. And so then this got gets into kind of then the, the sort of stepwise approach to his work up so he was actually seen and and sent same day from an outside ophthalmologist who had done a tap and inject with the concerned friend ophthalminus as well and he had an injection of vancomycin septazetine and dexamethasone in that eye. And then kind of promptly was kind of underwent a systemic work up, which showed first that he did, you know, consistent with his symptoms had some type of systemic illness going on so he had a mild leukocytosis white kind of 12.5 and a reasonably elevated inflammatory markers with ESR 16 a CRP of 12.8. Other kind of blood testing looking for infectious so blood cultures urine cultures, signs of immunocompromise HIV, looking for other atypical infections like syphilis TB and impossible exposures like Lyme and Bartonella were all sort of sent and ended up coming back negative. So, most notably kind of getting kind of honing in on his symptoms with his febrile illness the kind of first step was getting additional radiographic imaging with a CT chest. Based on his kind of ongoing cough and retro sternal chest pain. So he ended up getting a CT chest without contrast, which described this sort of ill defined mass like collection in the subcranial region in his media stynum with possible foci of calcification and gas and this was done without contrast. Thankfully, our patient also happened to be a radiologist and somehow he had ended up reviewing his scans. I think I might be paraphrasing from what I remember but essentially he and the formal radiologist read recommended rechecking the chest with contrast. A repeat CT with contrast showed this sort of subcranial rim enhancing collection associated again with foci of gas and calcifications there was a similar appearing collection in the right perihyla region. And based on this again there was a high concern for infectious etiology, potentially bacterial or even fungal mycobacterial and less likely a malignancy. Given also, I think, so this was kind of at this point, a concerning source of infection there is also concern that given the patient sort of multifocal abscesses in the eye as well as the report from his wife that is sort of cognition just didn't seem quite normal he ended up undergoing an MRI brain which showed innumerable ring enhancing intracranial lesions also suggestive of multifocal intracranial abscesses less likely consistent with metastatic or neoplastic lesions. So at this point the patient was started empirically on IV antimicrobial so vancomycinamiropenem infectious disease kind of in further investigation with the patient in trying in you know ensuring that this wasn't another sort of non bacterial process. Investigate further endemic fungi. So blastomycosis histoplasma and so forth, particularly in the sitting again of this patient's travel history he also had spent time at Bear Lake in caves around a lot of he said where a lot of bats were present all of this and the testing ended up coming back negative or in the blastomycosis was thought to be sort of a non specific echocardiogram was unremarkable and the aqueous tap ultimately from his eye ended up coming back, essentially with no growth. The next step was to get sample. So the best source was felt to be from the subcranial collection. The patient underwent a nebronchial ultrasound with bronchial alveolar lavage and a needle sampling which ended up growing tissue cultures showed bacteria which is predominantly streptococcus angiosis, as well as Staphylococcus hominus the ladder which was thought to be a permanent. All other testing and for fungal mycobacterial etiologies were negative. But, so this was the culture but notably even the Gramstein showed potentially additional organisms so essentially a poly microbial collection with the streptococcus angiosis which is predominantly thought to be known to be an oral and GI flora. So then at this point the question was how did it get in the subcranial space and this highlighted circle here is the esophagus which is passing through that region. And so the concern was that this patient actually somehow had a leaking or a perforation of his esophagus that may be the source of this infection and seeing it undergoing a contrast esophagram which initially was read as normal but upon further discussion with the radiologists on the case found that he had actually an esophageal diverticulum with a very tiny area of extravasation just in that the mid esophagus just in the area, the subcranial space of the media stynum that was thought to be the source of infection. So this was ultimately thought to be again a susceptible area of a diverticulum and the patient reporting that he potentially had this episode of food impaction while he was feeling unwell and sick with diarrhea and nausea and so forth. The patient then underwent an upper endoscopy to look more carefully at this region, which again showed the diverticulum, but it appeared at this point by the time he had this test that the area had the defect had closed off and there was no more actively leaking contents from the esophagus and they did some further sampling as well. So the final diagnosis in this case was an esophageal diverticulum with perforation and leak that was complicated by a disseminated infection with medial stynal intracranial and crudal absceses. So the patient was ultimately transitioned to IV seftra axon and oral flodril and metronidazole for six weeks, followed by switching that to oral and nasolid and metronidazole for another two months. On serial imaging so six months later and his brain MRI showed resolution of enhancement of all the intracranial lesions and his medial stynal absceses had resolved. If we follow his ocular exam, so this was just several days after presentation with these sort of active looking absceses and significant vitreous haze. This was just about a week or a week and a half later you can see really nice flattening and sort of more atrophic appearance of these cortal absceses the three out in the periphery and improving vitreous haze. And this is the month later, and then this is two months later, I'm showing kind of resolution of the active infection and really nice improvement of the vitritis and this patient with improvement in vision. I think kind of kind of interesting your key points so with endogenous endoplamitis most patients do have an identifiable system identifiable systemic infection, and hence the need for a really careful systemic evaluation, but interestingly, a reasonable portion of patients will have no no systemic symptoms outside of their eyes at presentation so 20%, and over half of them will present first to an ophthalmologist for evaluation, kind of highlighting the importance of recognizing this and and initiating the systemic The cultures from the eye aren't perfect so there's a 50 to 75% rate of culture positivity from the vitreous with endogenous bacterial endoplamitis again, highlighting the need for systemic investigations to figure out a source and an etiology. The most common risk factor in the United States for endogenous bacterial endoplamitis is intravenous drug use but there's many others, immunocompromising conditions and, and, and so forth and then treatment is systemic antimicrobials. Plus remind us introvitrials which is what our patient received and potentially attract to me. And this is just highlighting again the many possible sources the table on the left showing that patients ultimately can be found to have liver abscess to use pneumonia endocarditis sources can come from anywhere and highlighting the need for a thorough systemic evaluation, and so forth. That's everything. Questions. Thanks for presenting this case. Did this patient have any like esophageal motility conditions prior or did he complain of like regurgitation or dysphagia or like anything prior prior to this or during while you're seeing him or not that he was obviously aware of I think it ended up coming out after the diagnosis was made that he had, he would had issues potentially at times with like what felt like food impaction or like but nothing that he sort of had ever had worked up or knew about prior.