Lecture: General Approach to Uveitis Patients

DR MOORTHY: Good morning, everyone. I hope you can hear me well. My name is Dr. Ramana Moorthy. I’m actually a uveitis and retina specialist in Indianapolis, Indiana, in the United States, I’ve been in practice for about 12 years, and today we will be talking about the general approach to the uveitis patient. I’m gonna begin my talk here. And I realize many of you are probably joining me at the end of a very busy day. So please forgive me if I go too fast. I’ll try to not go too fast. And I will try to take questions and answer some of your questions that I received previously. And also, as much as I can, towards the end of the talk. This is a very basic, fundamental talk about uveitis. And I thought it would be good, judging from the questions, also, that I got, so that we can discuss this. So uveitis, or ocular inflammatory diseases, also, for the uveitis specialists, includes things like orbital inflammatory diseases, scleritis, scleral keratitis, peripheral ulcerative keratitis, things that are difficult to manage in a general or comprehensive ophthalmology setting, but require the expertise of someone who is an ocular immunologist. I have no specific financial disclosures here to tell you about. What is the purpose of the uveitis evaluation? Why do we… So when a patient presents to us with ocular inflammation, we really need to kind of assess the current situation, to determine if the disease is acute, that is, the patient had red, painful, photophobic eye and had inflammation in the anterior chamber, or is it recurrent? They’ve had many episodes before, and it’s separated by more than three months between episodes off of therapy, and is recurrent, or is it chronic disease, where the patient may have a white, quiet eye, but present with very severe inflammation in the anterior chamber? That is a hallmark of chronic disease. Or they may present with floaters, or gradual progressive vision loss. This is important because of prognostication. Acute and/or recurrent diseases generally can be managed and may have a self-limited course, and can be treated aggressively with corticosteroids. Whereas chronic disease requires much more than corticosteroid therapy. In infectious cases, it’s important for us to put them on the appropriate antimicrobial medications. Finding the etiology and leading into that is very important. So when I think of uveitis, I try to separate it broadly in my mind into two categories. Infectious and non-infectious. And let me answer one of the questions already. Two or three people asked me: What are the common causes of uveitis? It depends on where you live. If you’re in the developing world, in places such as in Southeast Asia, sometimes in portions of the African subcontinent, in certain parts of Central and South America, infectious etiologies are by far the most common causes of uveitis. Things like toxoplasmosis, tuberculosis, leptospirosis, syphilis, HIV associated infectious conditions, cytomegalovirus retinitis — these are very important causes of inflammatory disease. And missing the cause of inflammation, treating it erroneously with corticosteroids, systemic or local injections of steroids, if it’s infectious, can doom the eye to blindness. So that’s why it’s important for us to know whether it’s infectious or non-infectious. So identifying also the disease-related complications is another reason why we evaluate the patient. And then we try to find the best therapy. So if it’s infectious uveitis, we put the patients on antimicrobial agents. And then we can add corticosteroids after they’re on appropriate antimicrobial coverage to control the host’s immune response. Whereas if it’s a non-infectious uveitis, we can start with corticosteroids and probably proceed with immunosuppressive therapy in the chronic disease states that are very difficult to treat, if they’re not responding to steroids. History taking is everything. I often will get consultations from providers where I don’t have access to the history that you may have taken. You know, if you don’t take a thorough history in uveitis patients, you’ll be doomed to be ever lost in the fog of uveitis ignorance. I hate to put it that way, but it’s true. Whenever I have taken a poor history, I find myself groping in the dark as to what the cause of the uveitis may be. It is very time-consuming to take an adequate history, but without this history taking ability, we really can’t treat patients with uveitis appropriately. It’s very time-consuming, and teasing out relevant and contextual inflammation that is important for you in making the diagnosis from the noise — because as you though, patients tell us lots of things that are completely irrelevant to their management. And I think that’s the art that comes from practicing for a long time, and repeatedly practicing. So we want the particulars. Hey, how long have you had this problem? How long has this been going on? Has it occurred before? What are the things that caused it? What did you do when this occurred? Were you hit in the eye before you had the uveitis? Well, it’s traumatic uveitis, then. Or was there something else, was there another event? Were you ill? Were you running fevers? Were you having night sweats, chills, and weight loss for the last three months and had a cough that’s been productive? That’s TB. What are the other non-ocular — do you have a skin rash? Evidence of oral aphthous ulcers? Evidence of a chronic cough, sputum production, hemoptysis, weight loss, fevers, not feeling well, feeling run down, chronic abdominal pain, change in your bowels, a history of Crohn’s disease, ulcerative colitis, bloody diarrhea? Problems with chronic inflammatory changes in your hands or your wrists or toes or feet, or other joints? Do you have chronic low back pain that gets better with movement? All of these kinds of things can be helpful. Do you have cats at home? Cat bites? Have you been out in the bush drinking unfiltered water? Have you been in places where you have black flies and you’ve been bitten by black flies, or waded through rivers, exposing you potentially to things like onchocerciasis, have you had treatments in the past for ocular inflammatory disease? And systemic disease. Do you have high blood pressure, heart disease, other things you’re taking medications for? And asking about past ocular history. Have you had previous surgery in your eye, previous non-ocular surgery, et cetera? These can also be very helpful, in terms of helping you diagnose. So when you do the review of systems, the skin is very important. The person on the left here that you see with a classic dermatomal rash of healing kind of eschars that you see from vesicles that are crusted over, from zoster, and involvement of V1, and mild ocular — herpetic zoster keratitis in his cornea. And you can see that this is a person that you want to follow very carefully. Here in the top middle, you’ll see a patient that’s got granuloma annulare, associated with systemic sarcoidosis. And similarly, on the top right, you see a patient who has lupus pernio, a characteristic feature of sarcoidosis. Another person on the bottom right, erythema nodosum, which is non-specific for sarcoid, but evidence of hilar adenopathy and involvement of other glandular enlargement, such as her parotid gland. And here you see a patient with poliosis and vitiligo on the center bottom who had chronic Vogt-Hirata syndrome. This is a patient with Behcet’s disease. This is a characteristic finding. Patients who have Behcet’s have evidence of aphthous ulcerations like this. Or patients who have pulmonary symptoms such as fatigue, dyspnea, cough, fevers, et cetera, that may indicate systemic sarcoidosis. This is a patient who has massive glandular involvement and multiple organ system involvement from sarcoid. Do they have gastrointestinal systems such as abdominal pain, chronic diarrhea, bouts of tenesmus. This is a mystery diagnosis I’ll discuss later. But this patient had hepatic enlargement, retroperitoneal nodes around the aorta that were enlarged, and had this biopsy of the jejunum that we’ll talk about a little bit here. So also the genitourinary system, recurrent urinary tract infections, hematuria, musculoskeletal symptoms we’ll talk about, zoonotic or arthropod exposure, such as cats or insects, and travel history. This is important for those who live in parts of the world that I don’t. I live in the luxury of all the things we have in the United States, with all the resources that we have, and many of you, I understand, are in places where the resources may be sparse. I know many of you, from all the consultations that I do, you all do a wonderful job. I think it’s very difficult to do some of the things that you do with your resources, but you take great care of your patients. So that’s really important for me to keep in mind. And sometimes I may ask things of you, when you send me consultations, about: Why is this data missing? And I’ll come to that in a moment. But I think it’s something that I need to keep in mind too, when I’m asking you what else did the patient have. But many times, it’s the history. And any of us could take the history. All of us have face-to-face time to see the patient and talk to them. And you don’t get just one chance. You can go back and ask patients, if you see something on the exam and you think of something, ask. I always think of this as an evolutionary thing. Once you finish the history and the review of systems, you can go on and have done some of the non-ophthalmic exam, like the cutaneous exam or looking at the joints, et cetera, and you can kind of go on to examination of the eye. The uveitis specialist is a master of the ophthalmic and systemic examination both. You have to know everything about the ophthalmic examination and really feel comfortable about it. For me, this means not a torch light exam. You can’t judge chronic inflammation in a child by looking at them with a pen light or a torch light. It’s not going to give you adequate information. That’s like… Closing your eyes and trying to look at the skin. It’s not going to help you. You definitely need more data. You need to look at the periocular skin in a well lit room. Look at ocular motility. Do confrontational visual fields, examine the pupils for APD or light near dissociation. This is often forgotten. And then look at the conjunctiva. Look at the eyelids. Do they have lupus pernio rash like I showed earlier? Herpes zoster lesions? Look if there are granulomas that can help confirm the diagnosis of sarcoidosis or other disease. There may be Kaposi’s sarcoma lesions in a patient who may have AIDS, which can clinch your diagnosis. Look for previous stromal scars, previous herpetic disease, active herpetic disease. If KPs are mainly on the inferior third of the cornea and Arlt’s triangle, it can tell you it’s a certain type of uveitis compared to diffuse KPs, which can indicate herpetic disease. Look at the AC, flare and cell, with the highest intensity illumination. The conjunctiva, cornea, anterior chamber, all these parts of the examination require you to have a slit lamp. A slit lamp biomicroscopic evaluation of the anterior chamber is of utmost importance in the evaluation of the uveitis patient. If you don’t have a slit lamp, it’s going to really hinder you, because you will not be able to tell how much cell and flare is there in the anterior chamber. You have generally — I will follow the guidelines of the standardization of uveitis nomenclature. If you Google SUN criteria in Google Scholar, you’ll find the appropriate journal articles that will actually show you what the criteria are, and how we grade cells. It’s a very involved topic. But it can help you standardize with what the rest of the… What other uveitis specialists are doing around the world. This was a worldwide kind of uveitis nomenclature criteria. And look at the iris, for transillumination defects. Loss of crypts, presence of rubeosis, presence of iris nodules on the iris margin. Called the Koeppe’s nodules, or on the stroma, Bussaca’s nodules. You can look at the lens for PSC or inflammatory membranes. Presence of posterior synechiae. You also need to do gonioscopy, which is often forgotten, but it’s particularly important if a patient has low or high intraocular pressures in uveitis. Especially in high pressures, you want to look at the angle and look for signs of peripheral anterior synechiae, signs of angle vessels that may indicate Fuchs, signs of neovascularization of the iris and the angle. This is very important to evaluate the uveitis patient. So in a broad category, remember that acute cases of uveitis — anterior uveitis in particular — will present with limbal injection. Fine tiny KPs in the lower third of the cornea. And fairly severe anterior chamber reactions that may vary from mild, one plus to two plus cells, or about 10 to 20 cells per high powered field in a 2 millimeter beam on highest intensity, to hypopyon, too numerous to count cells, and they’ve formed a layer of pus like you see here on the left. The intraocular pressure is often low. There may be acute posterior synechiae and anterior synechiae formation that can be broken with mydriatic agents. In chronic disease, you may find there’s no injection, the eye may look white and quiet, but there may be rip roaring inflammation in the anterior chamber, large keratic precipitates, and the patient may have large or severe anterior chamber reaction, but often will have more flare in proportion to cells, indicating chronicity. Posterior synechiae may be present and peripheral anterior synechiae are often present. Intraocular pressure may be high, especially if the patient is not well managed or has been on chronic steroids for a long period of time. So that can also be a tell tale sign of some chronic disease. There are a few acute uveitic conditions that cause high intraocular pressures. The most important are herpetic diseases that you need to keep in mind, followed by toxoplasmosis, followed by a condition such as syphilis. So high intraocular pressures, especially in unilateral cases of inflammation in the anterior segment or even the posterior segment, that may indicate infectious conditions such as herpes simplex or varicella zoster virus. And then potentially toxoplasmosis and syphilis. Then we dilate the pupil. Every uveitis patient has to have a dilated examination. Again, if you don’t do that, it’s like closing your eyes. It’s like the old story of the men closing — three guys closing their eyes and trying to feel an elephant and try to put their thoughts together. You’re not gonna have a complete story unless you do that. So you have to look at — once the pupil is dilated, and hopefully it will dilate — you need to look and assess the vitreous for cells and haze. Differentiate that from the haze caused by a cataract or corneal haze. And then look at the cells themselves. Are they pigmented? Are they white blood cells? And you’ll be able to tell. Are they red blood cells? You should be able to tell looking again… Using a slit lamp. It’s very important under the microscope to look at that. To evaluate the patient. And then look at the retina. Beginning with the optic nerve. Then assessing the vessels. The optic nerve — you want to look for cupping or disc edema to indicate if sometimes that may be present in acute inflammatory processes. And you want to look at the retinal vessels. Is there vascular sheathing? Presence of retinal hemorrhages, indicating vascular occlusion? Presence of peripheral retinitis? In the macula, are there complications of diseases that involve other parts of the eye? Cystoid macular edema, choroidal neovascularization, of the disc or elsewhere? These are complications of diseases that occur in other parts of the uveal tract. So if somebody has, for example, only anterior chamber cells, and nothing in the vitreous, but has cystoid macular edema, that means they have anterior uveitis complicated by cystoid macular edema. However, if they have vitreous cells, nothing in the anterior chamber, pars plana snowbanking, and has optic disc edema, then they have optic papillitis, secondary to their intermediate uveitis. They have intermediate uveitis. They don’t have panuveitis. This is important, because it’s important for prognostication, therapy, et cetera. So again, looking at the peripheral retina is important to make sure that you do not have any signs of retinal tears, retinal detachments, tractional retinal detachments, complex retinal detachments, which can plague different forms of uveitis, particularly infectious uveitis. And then again, don’t forget the other parts of the body. Because the eye can’t exist alone. You know, if it was the case — the eyes could be dropped off and you can evaluate them and the patient could pick them up and stick them back in their head when you’re done with them. That’s not appropriate. Right? They’re stuck to the rest of the body and the brain. So you have to evaluate the rest of the body. Because what’s happening in the eye may be many times just a harbinger of what’s happening in the rest of the body. That’s where uveitis becomes particularly important, because it can be life saving. Not just sight saving. To make the right diagnosis and treat the patient appropriately. So look at the skin, the mucosa, the joints, the things that are readily available. You know? To you. We’re not asking you to do gynecologic examinations at the table. That’s not appropriate. We’re asking you to look at things that are very obvious. And I’ll show you some pictures of that. So after you do all this stuff, and put your information together, you know, you’re still not sure what the diagnosis is. You can kind of — in your mind — think of patterns of disease. You know? So if you see somebody who has a unilateral focal retinochoroiditis, with white lesion in the retina, with a lot of vitreous haze and cells, you think of toxoplasmosis. If you see somebody that has corneal scars and iris atrophy and elevated intraocular pressure with diffuse KPs and anterior chamber inflammation, that’s herpetic disease. Until proven otherwise. If there’s a patient who had previous cataract surgery, presents with unusual capsular opacities, vitritis, and pain, that’s late onset endophthalmitis. It’s fairly uncommon, but can be caused by fungi or bacteria. If someone has a necrotic granuloma in the posterior pole with pus that’s collected between the posterior hyaloid and the retina, that’s aspergillosis. A classic presentation for that type of disease. If you have four patterns of frosted branch periangiitis, brush fire, granular or pizza pie retinitis, that’s CMV retinitis in a patient with AIDS. And if someone has peripheral or macular granuloma and evidence of fibrous bands that extend from the disc to the periphery, that’s toxocariasis. These are patterns of disease you may want to recognize. Here are some patterns of disease in the skin that you may not want to miss. A vesicular or dermatomal rash here. That’s zoster on the top. The image on the middle is a patient who has a palmar rash. It’s a macular rash. With some desquamation. This patient likely has syphilis. He has the same thing in the other hand. This rash has live spirochetes. So be careful when you are touching the patient or shaking their hand. Because those spirochetes can be transferred. And here is a patient who has erythema chronicum migrans, this rash related to tick bite from Lyme disease. Lyme borreliosis occurs in certain parts of the world, and certain regions of the United States. Here’s a pattern you don’t want to miss. Three days after cataract surgery, the patient has pain and vision loss and presents with this. This is an endophthalmitis. You don’t need to do the uveitis work-up. What you need to do is take the patient to surgery, do a vitreous tap, and inject intravitreal antibiotics in the patient and send for vitreous and aqueous cultures. Do aqueous tap as well. This can be done sometimes in the office. But if it’s more severe, it may require pars plana vitrectomy. Here’s vitritis, in a patient with severe vitritis. If you see something like this, and you have vitreous haze, you need to look carefully. There’s lots of vitreous snowballs here. This patient had toxoplasmosis, peripheral toxoplasma granuloma that activated, with significant retinochoroiditis, with a pigmented scar. This is a patient that has pseudohypopyon. Not really hypopyon. Received preservative-free triamcinolone, and many of the particles have fallen into the anterior chamber here. That can be sometimes confused for an infectious hypopyon. Here is a patient with toxoplasmosis. You can see the whitish retinochoroiditis. This is primarily a retinitis that extends into the choroid. You can see retinal hemorrhages. And if you lock very closely in the magnified image, you can see vasculitis, the perivascular sheathing of inflammation along the retinal arteries and venules that occur adjacent to the lesion. Very characteristic of toxo. But this is in a ten-year-old boy that presented with acquired toxoplasmosis. Here is a patient from Dr. Goldstein’s image with very advanced tubercular panuveitis. He has a large choroidal granuloma here inferotemporally in the macula and multiple other granuloma in the posterior pole. And has evidence of even vascular involvement. Sorry. I keep flipping back and forth here. I’m sorry. Vascular involvement with sheathing of the retinal vessels. Here’s a patient that has tuberculous serpiginoid choroiditis. TB in particular regions is a very common cause of uveitis. Here’s a patient with Bartonella infection from cat scratch disease. This patient developed a severe neuroretinitis. Ocular Bartonellosis — the most common manifestation is focal choroiditis. If a patient has a focal choroid lesion like what I showed you earlier from toxoplasma, Bartonellosis should be checked. Here’s a patient that has AIDS and cytomegalovirus retinitis. Or the patient may be immunocompromised from iatrogenic causes like cancer chemotherapy, et cetera. Here’s a patient who has acute retinal necrosis syndrome or necrotizing herpetic retinitis from zoster. And he’s immunocompetent. So this is very, very — all of these patterns are important to recognize. You can also use imaging, and many of you have access to very fancy imaging technologies. Sometimes I don’t even have access to some of this stuff. High definition OCT is very important to assess the macula for macular edema. Presence of choroidal neovascularization, and also enhanced depth imaging nowadays is very useful to quantitate the presence of choroidal inflammation to determine how effective your therapy is. Is the choroidal inflammation going down? Is the choroidal thickness decreasing as an indication of a response to therapy? And the fluorescein angiogram, especially ultrawide field angiography, can be very characteristic and helpful looking at the extent of uveitis. Sometimes the uveitis may look like it’s mainly in the anterior segment with mild vitreous inflammation. Most of the inflammation anteriorly. But when you do the angiogram, you may see signs of peripheral venous leakage indicating a more intermediate uveitis. That changes how you treat the patient. Choroidal inflammatory diseases can be evaluated with ICG angiography. That can be very helpful. And the B scan or ultrasound can be useful for medial opacity, and some of you have access to ultrasound biomicroscopy, that can help you evaluate the anterior chamber as well, to evaluate other causes of inflammation in the eye. Such as intraocular lens malpositions, presence of tumors of the iris or ciliary body, or even granulomatous inflammatory diseases in those areas that are hard to evaluate otherwise. So once you have all of this data that I was alluding to earlier, summarize what the patient has, in a one line statement. So, for example, you saw somebody with a hypopyon. Well, this patient you may say is a 27-year-old male with a hypopyon uveitis in the right eye. With metacarpal phalangeal joint redness, patchy psoriatic skin rash over extensor surfaces. This patient is probably HLA-B27 positive, it’s likely the patient has psoriasis or psoriatic arthritis. And they’re linked together. And he has hypopyon uveitis. You can refer them to a rheumatologist and manage their uveitis with frequent steroid drops and mydriatics, and often that will be adequate to take care of the patient. Sometimes you have to use corticosteroids. But in this situation, what blood test would you order? That’s the next question I’m going to get to. You can be very focused in how you order blood testing. Many of us rely on blood tests, thinking that it will make up for our deficiency in our examination, or in our history taking. It won’t. Because unless you look for the etiology as a problem focused approach, you’re not going to find it by a scorched earth approach of doing every lab test known to man. It’s expensive, not helpful, certainly doesn’t help the patient, and may give you test results that you don’t know what to do with. So laboratory testing is only supportive of your presumptive diagnosis. It’s not a substitute for good history and examination. You can never go wrong in evaluating uveitis patients or testing for the basics. Around the world, syphilis and TB still are important causes. And you can tailor that additional testing to what diseases may be more common, or that you’re seeing more commonly in your practice. For example, there may be a contaminated water source in the community that’s resulting in toxoplasmosis cases. So you may see a whole slew of cases of toxoplasmosis, back to back, that’s occurring because of unfortunate access to contaminated drinking water supply. That’s been documented in many parts of the world. So syphilis, TB, and sarcoid are three things that I always test for in the United States. But again, remember that in your part of the world, it may be a different set of diseases. And again, let me go back to saying that infectious conditions that cause uveitis are far more common in the developing world than non-infectious uveitis. And remember also that the uveitis work-up evolves with the disease course, and you get more than one chance for many of these conditions. You may not find it initially with your thorough evaluation. So examine the rest of the body. Ask questions. Go back and reevaluate the patient. And if you see something different on the examination and the clinical course is not following what you think it should follow, then you need to look again. And evaluate again and rethink the problem. So this is an evolution of findings. Also, don’t order tests. That won’t help. If you have somebody who has anterior uveitis, I see many patients ordering antinuclear antibody and rheumatoid factor. Lupus, which is associated with elevated antinuclear antibody levels, and rheumatoid factor, which is associated with rheumatoid arthritis, typically cause scleritis. They may cause in very advanced disease retinal vasculitis. But they rarely if ever cause anterior uveitis. So it’s very important not to necessarily order those tests. The only exception to that rule would be a child who presents with chronic ocular inflammation in both eyes, with a white quiet eye with posterior synechiae and a lot of cells in the anterior chamber. And they may have joint pain. Those patients may have juvenile idiopathic arthritis, for which antinuclear antibody and rheumatoid factor checking would be important. Because you can categorize the form of juvenile idiopathic arthritis that they have. And treatment will be based on which group they fall into. And the pediatric rheumatologist would be involved in the management of that patient. There’s other things. For example, the HLA-A29. We know this is associated with birdshot retinochoroiditis. If someone has a hypopyon anterior uveitis and a normal retinal examination, they don’t have birdshot. There’s no point in ordering HLA-A29. Because 5 to 8% of the population is going to be positive for HLA-A29. The positivity and association and that hypopyon anterior uveitis — they’re not associated. They’re not related. But if somebody has birdshot-like lesions with creamy lesions in the choroid, hundreds of choroidal lesions, and in the posterior pole, cystoid macular edema, mild vitritis, then it’s appropriate to check an HLA-A29 to confirm the diagnosis of birdshot retinochoroiditis. There’s invasive laboratory testing that can be done in the office, or in the operating room, that can be helpful these days. Particularly for infectious uveitis, obtaining anterior chamber tap, if you have the facilities, obtaining PCR studies, looking for evidence of DNA fingerprinting, if you will, the presence of mainly viral causes of anterior uveitis and/or posterior uveitis and toxoplasmosis can be done by taking a small sample of aqueous fluid. Usually 0.1 CC is enough to run 3 or 4 PCR tests. If you have something — mainly vitreous involvement with vitritis and you don’t know what’s going on, often a vitreoretinal surgeon will be asked to perform a pars plana vitrectomy if we’re worried about the possible of lymphoma, if we’re worried about the possible of other infections we haven’t identified, when someone has rapidly progressing vision loss in both eyes, we don’t know what’s going on and can’t get it controlled, we’ll often perform vitrectomy or a retinal choroidal biopsy, which requires very advanced vitrectomy techniques. So the diagnoses that you don’t want to miss and mistreat are primarily the infectious uveitic conditions, and occasionally neoplastic conditions. So what are the things you don’t want to miss? The most important things you don’t want to miss are necrotizing herpetic retinitis, treating patients — not dilating patients who have anterior chamber inflammation and high intraocular pressures, and looking at the fundus is a cardinal mistake that I see many times that results in misdiagnosis and mistreatment of patients who have this condition. And the results of vision loss are devastating in this disease. Because it’s rapidly progressive. You don’t want to miss the diagnosis of syphilis or tuberculous uveitis. That’s very important. And again, helpful things are going to be what you find in the systemic evaluation and the non-ocular examination as well. So you don’t want to miss systemic vasculitic syndromes. If you have somebody who presents with a really bad case of scleritis, you don’t want to miss checking an antinucleophilic antibody on them, a cartilaginous inflammation with relapsing polychondritis or skin rashes. You don’t want to miss a paraneoplastic syndrome associated with sub-RPE and subretinal infiltration of neoplastic cells. There are other things like non-neoplastic masquerade syndromes, chronic retinal detachments, hereditary retinal dystrophies, that can masquerade as uveitis, but they’re not uveitis at all. And occasionally you can see patients with advanced cancer. That can have paraneoplastic conditions related to cancer that look like uveitis, but they’re not. The uveitis is actually caused by the cancer. What do you do for treatment? Well, treat infectious uveitis with antibiotics first. Steroids work best and most effectively starting at high doses and tapering in general when you’re dealing with non-infectious uveitis. And remember, in infectious uveitis, if you treat them with steroids, without antibiotics, appropriate antibiotics, you’re going to make the uveitis much worse. Sometimes irreparably worse and blind the patient, if you give high doses of steroids in a patient who has herpetic retinitis, for example. Chronic disease requires chronic therapy. Tell the patient: You don’t treat diabetes with one shot of insulin and say you’re cured. If you have disease of eye inflammation for a year, two years, three years, it’s not going to go away in a week with treatment. It’s going to be there forever. The eye is an immunologically privileged place, and chronic inflammation, unfortunately, is very difficult to get rid of. If the etiology is unknown or unsure, always treat and cover the worst possible condition it can be, and fine tune based on diagnostic testing results and clinical response to therapy. It’s very important. Sounds really fundamental, but it’s often mistaken when we’re kind of confused about what to do in a patient who is in front of us, and we’re really concerned about their ocular condition. What not to do. You don’t want to blind the patient by treating the patient blindly. Remember that statement. Don’t blind a uveitis patient by treating the patient blindly. That means you didn’t do a dilated examination. But yet you say anterior chamber inflammation. You saw high intraocular pressures. But you gave the patient a periocular steroid injection. That patient may have herpetic disease and may have retinitis, and you would have made the herpetic retinitis completely go crazy, and within a week, they’ll be totally blind. I’ve seen that happen in my practice. Where people have just… It was not done. And that’s not something you want to do. So be very careful. And if you don’t know if the uveitis is infectious or not, do not give intravitreal regional or systemic steroids, unless you are sure the uveitis is non-infectious. Unless you’re sure that you ruled out the infectious causes. And topical steroids can be used almost always in a patient with uveitis with impunity, except if you have somebody who has epithelial defects from untreated infectious keratitis. So a corneal ulcer or herpetic disease — you don’t want to put those patients on topical steroids. But if the corneal epithelium is intact, in general, you can use topical steroids in the treatment of uveitis. Whether it’s infectious or not, generally, with relative impunity. Let’s go to the first question of the day. Now that I’ve blabbed my head off for you guys. How do you make a definitive diagnosis on this patient? You see this patient — I’m showing you on the top right a gonioscopic image in the angle. The angle shows complete obliteration of the angle structures by presence of diffuse peripheral anterior synechiae. The conjunctiva here shows… Oops. Excuse me. Shows nodules here. And then you see this very prominent and characteristic pattern in the fundus. Anybody know what is the definitive diagnosis? Let’s see what you guys chose. So here the diagnosis — there are many possible answers. But the definitive answer… What is this? This is sarcoidosis. This is sarcoid panuveitis in a patient. That is called — the top right image is called a Berlin’s nodule. That is a nodule, granuloma, of the peripheral iris in the angle. Very characteristic of sarcoid. These are sarcoid granulomas in the conjunctiva in the lower left. And then… In the lower right, you’ll see images of the classic cache de bougie inflammation, with excrescences along the retinal blood vessels. This is a very characteristic finding of sarcoidosis. And the definitive diagnosis of sarcoid is tissue biopsy. What is the easiest biopsy that you can do? Look at the conjunctiva. There are granulomas there. So you can take a snip biopsy, send it to the pathologist, and have them rule out presence of intraocular foreign bodies, acid fast bacilli and fungi, and have them do those stains to rule those things out. And you’ll see a granulomatous inflammation without significant caseation that is characteristic of sarcoid granuloma. There may be epithelial cells, palisading lymphocytes, but you won’t see a necrotic core suggestive of caseation that you would in TB. So this is how you would make the definitive diagnosis. Chest x-ray may show signs of hilar adenopathy, angiotensin converting enzyme level has low specificity. Only about 55% to 60% specificity or sensitivity for sarcoidosis. Unless it’s extremely high. And aqueous paracentesis will probably not be helpful, because that may only show mixed inflammatory cells under… Under the microscope. And a PCR evaluation for viruses would be negative. So again, knowing what you know about sarcoid can help you. But the definitive diagnosis requires you to have this. So this is the conjunctival biopsy results. Excuse me. I don’t know why it’s going backwards. So you can see here… This palisading lymphocytes and the large giant cells, epithelioid cells without caseation, suggestive of sarcoidosis. Next question. What serologic test would be diagnostic on this patient? He has a palmar rash in both hands and then he has a very characteristic lesion in the central retina of the left eye. This is called a placoid chorioretinitis. What would you do in this patient to treat them? You can cure this person. Let’s see what you guys thought. I want to see if you were paying attention. Because I showed the picture previously. 42% of you got the right answer. So again… I would not order antinuclear antibody or rheumatoid factor. Why? Does this patient have lupus? No. I didn’t tell you much about this patient. But this is a pattern recognition question. The patient has a macular rash with desquamation in both hands and he has a placoid chorioretinitis. This patient has syphilis. And the syphilis diagnosis is made most accurately using an antitreponemal antibody test. Treponemal specific test. So ordering a VDRL on a patient who has syphilis will not help you unless the patient has recent exposure as primary syphilis. A VDRL can be transiently positive and then become negative very rapidly. Whereas antibodies against the treponemes, such as the fluorescent treponemal antigen or antitreponemal IgG, will remain positive for the life of the patient. Now, a positive IgG indicates previous exposure and presence of postprimary syphilis. This is very important. Because in presence of uveitis, when we see uveitis in syphilis, it’s almost always postprimary syphilis. So that’s why the treponemal testing is very important. This should be treated as neurosyphilis. With IV penicillin — high doses of IV penicillin G for two weeks. For 14 days. Okay? And so this is a very, very important characteristic pattern recognition thing you shouldn’t miss. And syphilis is common worldwide. We see it a lot in the United States. In metropolitan centers. Here’s a fluorescent treponemal antibody test. You can see the corkscrewed fluorescent antibodies that are staining the spirochetes on the dark field here. Very characteristic and beautiful example of a fluorescent treponemal antibody test. Very useful test in evaluation of uveitis. Here’s the next question. What lab test would be diagnostic in this patient? This little boy was six years old. He has very characteristic changes on the chest x-ray with presence of adenopathy and large mediastinal whitening. Paratracheal enlarged lymph nodes, evidence of elevated hemidiaphragm on the right side, and also you can see that the patient has in the CT scan, in this coronal image, that he has a very large paraaortic and paravena cava large lymphadenopathy. This patient also has on your torch light exam evidence of posterior synechiae, 360. They live in India. So what is the most useful test that is going to tell you what the diagnosis is in this case? If you had to order lab tests? Let’s say that the conjunctiva did not reveal any granulomas. Any lesions. The eyes are white and quiet. Where they’re from can be very helpful in making the diagnosis. Do we have the results? Good. Most of you got the PPD skin test. That’s right. This patient is a young child with tuberculosis. They got treated with antituberculous therapy. But look at his skin test result. You can see this is a skin test that was placed, and you can see it’s already been a few days, but there’s still a very firm, significant reaction in the skin test. This patient had ocular tuberculosis with significant pulmonary disease and got treatment and really had a spectacularly successful course. This is a very important example of how you can save the life of a patient. So this patient presents with ear pain. And eye pain. The auricular cartilage is very tender and inflamed. She’s been bothered by this for a few weeks and noticed in the last couple of weeks that the eye has become very painful. She can’t sleep. So what is the condition and what would be the appropriate test that would help you make the diagnosis? Let’s see if you were paying attention. Because I mentioned this earlier. Yes. Very good. Okay. I’m very pleased at your answer. This is excellent. So getting the antineutrophil cytoplasmic antibody? Why? Because this patient likely has relapsing polychondritis, and required cytotoxic immunotherapy and Rituxan treatments along with systemic immunosuppression. This is a very characteristic finding. I’ve seen this presentation in my practice at least a dozen times. So it is something not to be missed. You can get other testing. I would not fault anybody for checking the other tests. But the key test, the most important test, would be the antineutrophil cytoplasmic antibody. Lupus can cause scleritis, but would probably not cause the relapsing — the chondritis. It can be tested as well in this particular situation, since the patient has scleritis. So this is one situation where antinuclear antibody is okay. All of these would be potentially in the panel of tests. But the number B — letter B — the antineutrophil cytoplasmic antibody, both the antimyeloperoxidase and the (inaudible) are the two that you look for. Very good. Here’s another example of a patient with necrotizing scleritis and relapsing polychondritis. You can see the epithelial defect. It’s still active scleritis and active necrosis. Once the epithelium heals in these cases, the necrosis usually stops. Isn’t that interesting? That’s a good way to follow your response to therapy in these cases. Look at the epithelium over the conjunctiva and cornea. This case has a small irregular hypopyon present, steamy cornea, plasmoid aqueous, giving a hazy view, and on the back he has a pink based white top rash that’s very characteristic. What would be useful in this test that would make the diagnosis? Let’s see if you’re paying attention. So this is not an infectious case. It’s likely an autoimmune condition. Let’s see if you guys got it right. This is a patient who has psoriasis. Okay? Has very bad psoriasis. In fact, his psoriasis was on his face, and he tried to commit suicide. Because he was so disgusted with the appearance of the psoriasis. And he presented also with severe vision loss, related to this very severe uveitis. This patient has HLA-B27 positive anterior uveitis. HLA-B27 is the most common cause of non-infectious hypopyon anterior uveitis. If you see a hypopyon, HLA-B27 may be positive. Especially if the patient has other manifestations of B27 associated disease. Other things you could check in this patient include an antitreponemal IgG or FTA. Those are the two tests I would get on this patient. Syphilis, because of the uveitis. Not because of the skin rash. Sending them to a dermatologist for a dermatology punch biopsy will be definitive for the diagnosis. But I don’t think you even need to do that. Because it’s so characteristic. A29 is useless. It would not be a helpful test. B51 would not be helpful. This is not a Behcet’s associated rash. And antinuclear antibody is really not a useful test in this situation. Because lupus doesn’t cause anterior uveitis. Let me go now and spend a few minutes, as I have — I know I’m getting close to 8:00. And I appreciate your patience. And listening to the talk. And I will present to you some cases. That were presented to me. And how I kind of tried to figure out what they had. So many of these turn out to be infectious. Some are not. And let’s see if I can go through a few cases. And I will try to go fast. I’m sorry. I just want to try to tell you… This is mainly to… Not wow you with my ability to diagnose something. I stumbled on to some of these diagnoses. So please do not think that I am that smart. I was very lucky and very fortunate in these cases. And I have many, many cases where I don’t have an identifiable cause of inflammation. So let me go back, before I start the cases, and let me tell you again. Remember, that in the developing world, infectious uveitis still is more common than non-infectious uveitis, as to the etiology of the inflammation. Number one. Number two, chronic disease requires chronic therapy. Number three, infectious uveitis should be treated with antimicrobials first. And then steroids can be added later to control the host immune response. Always dilate. Number four. Always dilate a patient who has uveitis to look at the posterior segment, to get more clues and to determine a pattern recognition to make sure that you’re not missing anything in the back of the eye. And number four, look at the other parts of the body. Not just the eye. Okay? To help you in the evaluation of the uveitis patient. The skin, the joints, the mouth, the mucosa. All of those things are very helpful. And then… Remember that the slit lamp is very important for you to be able to assess how much cell, how much flare, how much vitreous cells, what is the exact fundus appearance, and ancillary testing can be helpful as well. Once you put all of that ancillary testing together, then you can come up with a very tailored approach to doing labs, and tailored laboratory evaluation is very important. You don’t want to bankrupt the patient with testing. Or bankrupt your system with tests that are unnecessary. And get tests that… Getting tests that you don’t know what to do with — you have to own the tests that you have. Dr. Lim from Australia once said this in a talk. And I appreciate it. When you order that test, you own it. It’s yours. You have to explain it to the patient and yourself. If you shrug your shoulders… I don’t know what that means… You probably shouldn’t have ordered the test. Case one. 27-year-old male with floaters in both eyes and shortness of breath. Weight loss of 30 pounds over 6 months. Lives in a trailer, very poor, several cats at home. Very poor, impoverished conditions. Vision is 20/50 in both eyes. No one at home to take care of him. He’s a little bit developmentally delayed. So his cornea shows granulomatous KPs in inferior third of the cornea in both eyes, 3+ cells and flare in the anterior chamber, 3+ vitreous cells in both eyes, cystoid macular edema in both eyes, and this is the fundus appearance you see. Hazy view. Small choroidal lesions here, vitreous haze, a little bit of disc edema, there may be even some perivascular changes. You can see in the right image towards the bottom, below the disc, small white spots, which are choroidal lesions. Here’s the fluorescein. This is very helpful. You can see multiple areas of small choroidal lesions that stain in the later phase of the angiogram. This is a 9 minute frame. And you see characteristic findings. Later I found out — white deposits on the surface, these are preretinal deposits on the surface of the retina and the periphery. Strange. What is that? Well, you know, we did some evaluation because of other symptoms. All of his tests, the FTA was negative, quantiferon TB was negative, angiotensin converting enzyme level was 59, high normal. His Bartonella, because he has cats, negative. So it was not cat. But the CT of the chest was positive. And his dyspnea was evaluated. He was found to have severe pulmonary hypertension. And look at that. He has contrast CT — shows a lot of enlarged peritracheal, mediastinal lymph nodes, retrocrural lymph nodes as well, and these were biopsy — this massively enlarged main pulmonary artery was present as well. Pulmonary artery aneurysms are characteristic of Behcet’s disease. But he has no oral aphthous ulcers, no signs of necrotizing vasculitis. But this very severe multifocal choroidal inflammatory process. So what are we gonna do? Maybe we should biopsy these nodes. Look at the abdomen. The abdomen also shows significantly enlarged liver. And he has nodes adjacent to the aorta. And he has significantly enlarged periaortic lymph node. And other retroperitoneal lymph nodes as well. This is pretty impressive. The biopsy was done and showed granulomatous inflammation. They said… This is sarcoid. Let’s put him on steroids. As he was on steroids, his inflammation worsened. As he was tapered. Initially got better and then he got worse. Then he started getting fevers. He didn’t feel well. What is it? Infection? Non-infectious? We didn’t know. There were many specialists involved in his care. What do you think we should do? I said… What is that stuff in the vitreous? I don’t know what that is. He’s got a lot of floaters. He has symptoms. Let’s do a vitrectomy. Let’s see what the vitreous shows. And we were able to aspirate some of that preretinal white material. And I had excellent pathologists that were able to look at it. They actually found lymphocytes, enlarged macrophages, that contained PAS positive material, and I had them do a PCR. Qualitative PCR. Which was… So… Whipple’s disease. We found this was indeed Tropheryma whipplei. Very rare cause of uveitis. But he had jejunal biopsy. Because he had gastrointestinal symptoms. These are the intracellular PAS positive macrophages present in the intestinal villi, in the substantia propria. You can see very characteristic findings. This is diagnostic of Whipple’s disease. The patient was treated with rifampin. For six months, along with Bactrim. And became inflammation free, off of all medications, he’s been doing well for the last decade. I’ve been seeing him for ten years. Very interesting case. Right? So we didn’t know. We treated it with steroids. It got worse. This is one of those situations where thankfully we didn’t kill the patient. We found out… As soon as he had fevers, stop the steroids. Get biopsy, do other things, look for other causes, put our heads back together. So you get more than one chance, but you have to be careful. Sometimes the second chance, the eye is blind, because you’ve gone down a path you can’t reverse. You have to be careful about it. This is kind of a fun case. Here’s a 12-year-old boy, presents with photopsias, temporal scotoma in the left eye, vision only slightly blurred in left eye. Medical history otherwise normal, doesn’t take any medications or anything. So vision is down slightly in the left eye, a few cells in the vitreous, and here’s his fundus examination. Right eye was normal. Left eye has mild disc swelling and a very characteristic appearance to the macula. This granularity to the macula. This is a pattern recognition question. He has these funny little faint white spots. And let’s do… An ICG angiogram. I think autofluorescence image would have been even better. I don’t have it. I didn’t have — this was an older case. I didn’t have the autofluorescence camera in that practice. In that office. But look at these hypocyanescent lesions on the ICG. Hundreds of these lesions that are present. But the vision is very good in this patient. The OCT would have been very characteristic too. Shown ellipsoid dome disruption with small focal excrescences, in the ellipsoid zone. This is a very characteristic finding. All of these changes. Especially the macular pigmentary changes. Characteristic of multiple evanescent white dot syndrome. This patient within two weeks — his symptoms resolved and all of those white spots went away. There was no recurrence. So this is a very young patient. Unusual. Who had multiple evanescent white dot syndrome. Non-infectious — we don’t know what the cause is. But these are an unusual condition. So here is a patient. This is a more difficult case. This might be something you might see. Here is a 67-year-old man who presents with a 6 month history of painless, progressive vision loss in each eye. And the past medical history is negative. He has never been hospitalized. But his vision loss is profound. He’s on no medications. Has no cells in the anterior chamber, but 3+ vitreous cells in both eyes, sheets and clumps. Vision is hand motion in the right eye and 20/100 in the left eye. He’s been treated with oral steroids prior to presentation. And this is what he had. Massive retinal and subretinal lesion extending from the optic disc into the posterior pole. With retinal hemorrhages, intraretinal, as well as subretinal involvement. And dense vitritis in the right eye, and in the left eye, moderate vitritis and haze and subtle punctate lesions you can see in the left eye on fluorescein, and in the right eye, this massive lesion with retinovascular involvement, intraretinal involvement. What do you do here? This patient has already lost vision in one eye. And is on his way to have a similar course in the other eye. This is a very serious problem. In this situation, tissue is the issue. And tissue — if tissue is the issue, you go to the source. Where you find the problem. So we did a vitrectomy on this patient. Here is the vitreous biopsy. We actually did a retinal choroidal biopsy on the patient as well. Because of this large mass of retinal lesions. We didn’t know — and the cytopathologist immediately came back and said this is large nuclei, prominent nucleoli, scant cytoplasm, large nuclear reaction — we see in the choroid and retinal destruction, similar cells. Large nucleus, prominent nucleoli, scant cytoplasm. This is a very malignant B cell lymphoma or primary CNS lymphoma. Here you see the immunoperoxidase staining consistent with lymphoma. So this patient has primary CNS lymphoma. He had fortunately no intracranial involvement at the time, amazingly. But he developed then later, despite very aggressive chemotherapy, he lived for three years, lost vision in the right eye, but in the left eye, maintained decent vision until his death as a result of CNS disease. He was treated very aggressively with systemic chemotherapy. And recovered quite a bit of functionality. But unfortunately succumbed ultimately to the disease. So this is a disease where you can save the life of a patient, prolong their life, by making the right diagnosis. Next case. 65-year-old African American woman presents with sudden severe painless vision loss and floaters in the right eye. History of hypertension. Review of systems is significant for non-productive cough for a year. Weight loss of more than 15 pounds in six months that was unintentional. Vision was hand motion in the right and 20/40 in the left. She had cells in both eyes in the anterior chamber, and she had more cells in the vitreous, in the right eye than the left eye. And the right eye had very massive lesion in the central retina, with exudative detachment in the macula, white large lesion centrally. And she had no poliosis, vitiligo, hearing loss, or tenesmus. Fluorescein angiogram performed. You can see the multifocal process, with leaking and pooling in late phases of the angiogram and disc staining. PPD was negative but angiotensin converting enzyme level was high, along with chest radiograph that revealed bilateral hilar adenopathy. TB can be made with a PPD skin test, but the diagnosis of sarcoid can only be made by biopsy. It revealed non-caseating granuloma, no mycobacteria, no signs of fungi. This was characteristic of sarcoid. The patient was treated with mycophenolate, required tube shunts, and the left eye unfortunately was lost to glaucoma. This is the subretinal process after the treatment of glaucoma. Here’s the other eye. You can see the advanced glaucoma in the left eye. But… You can see she has more cupping in the left eye. But this is after many years of treatment. So that patient had sarcoid. Again, non-infectious. Treated with immunosuppressive medications and steroids. Next one is a 39-year-old male with two week history of blurred vision in the left eye. No past ocular history, no medical history. Lesion is 20/25 in the right, 20/400 in the left. Flare and cells in both eyes, but no KP, no synechiae, rare cells in the vitreous in right eye, 1+ cells in the left eye. Here’s what his autofluorescence image looks like. You can see this funny lesion — I showed you this earlier. Here’s the placoid chorioretinitis. This is syphilis. You know that. When you look at his skin rash, here is the OCT. Of this acute lesion. You can see the disruption of the — diffuse disruption of the ellipsoid zone with treatment that completely returns. And the patient’s vision improves. So you have historical details. And you find out that he has… He is MSM, monogamous, has a male partner, and no arthritis. He is HIV negative. He knows he’s been tested for HIV. We did an FDA test on him, VDRL, HIV serology, and the sarcoid-syphilis-TB work-up as well that revealed that he was FTA positive, VDRL was negative, all the other tests are negative. He was treated with intravenous penicillin for two weeks and recovered completely. And the partner was also evaluated and treated. Next case is a 69-year-old… This will be the last case, and we’ll take a few questions and I’ll close up here. 69-year-old white female with painless subacute vision loss over one week in both eyes. Metamorphopsia and a few floaters but no photopsias. The symptoms tell you this is probably something happening in the back of the eye. Even though it’s acute. She has floaters, metamorphopsia, that’s all retinal or vitreous symptoms. You’re gonna look more into the back of the eye. So she had dyspnea, weight loss, and arthralgias. Interesting. Vision is 20/60 in both eyes. Vitreous cells, as I said. And there’s a little bit of disc edema and a serous retinal detachment in the posterior pole in each eye. There’s fluid in the macula in each eye, and vitreous cells. There’s no peripheral choroidal lesions or vasculitis. You can’t see this. I’m sorry. This image never projected well. But… The inferior part of the macula is out of focus, because there’s fluid in the macula. You can see that there’s loss of the choroidal orange. That’s fluid in the macula. The other eye too — there’s a smaller puddle of subretinal fluid in the inferior paracentral macula. Here is the fluorescein. Starry sky pattern. Look at like Vogt-Koyanagi-Harada syndrome. But she doesn’t have hearing loss or any cutaneous findings, she’s not had any headaches or ringing of the ears, et cetera. That kind of thing going on. Hearing loss. She has no signs of poliosis, vitiligo, that sort of thing going on. Very mild inflammation. Here’s the other obtuse, starry sky pattern. But she’s got this dyspnea, funny cough and weight loss. Something is going on systemically. So we did a work-up. And why did I get an antinuclear antibody in this patient? I didn’t get it because I suspected initially… I got it because she met some of the systemic criteria that suggested lupus. She had… We obtained a chest x-ray, which I didn’t… That showed bilateral pleural effusions. And the antinuclear antibody, serologically, was highly positive. And the antinuclear antibody, the pleural fluid, was highly positive. So even though lupus choroiditis is very rare, this patient did not have nephritis from lupus. But this patient had lupus. Very unusual presentation for lupus. Why am I showing you these weird cases? Well, even though I told you that you don’t have to — in selected cases, if the systemic history or your findings on a chest x-ray and other things warrant you to look harder, sometimes we go back and get the test that we would avoid in the typical management of a patient who has uveitis. This patient had posterior uveitis. Weird presentation of multifocal choroiditis with inflammatory changes and was older. And those — and she had the evidence of pleural effusions and chest x-ray findings that suggested… Hey. There is something going on here that’s systemic. That we need to look for. So that’s why we obtained the antinuclear antibody. But again… I would not obtain an antinuclear antibody or rheumatoid factor on evaluation of a patient who had anterior uveitis, for example. So this is a very interesting case. And this patient met more than five criteria for the diagnosis of systemic lupus erythematosus. And she had done well on low dose Plaquenil and ultimately was taken off Plaquenil. Also was maintained on Imuran for a long time. I’m gonna stop there. I think we’ve run out of time. I want to see if I can answer a few of the questions. So let me just see… If I can answer them in the order that they were sent. The first question is: Does uveitis usually have a rapid onset after tick bite in cases of Lyme disease? No. Often the patient may have… So Lyme is Borreliosis — it’s like other borrelial diseases. It presents with skin and arthralgia first. The uveitis is later. Full disclosure — I have looked for Lyme uveitis in my practice, in my region of the country, for 30 years. I have never found one case of what I would say is Lyme uveitis. I know it exists, it has been reported. But it’s low frequency, low yield. You’re more likely to have a false positive for Lyme disease testing than you would have a true positive in my part of the world. It’s a series of tests that are obtained for Lyme uveitis. It’s a battery of antibodies. Antibodies to various antigens in Lyme. You have to have a panel of ten or so, and you have to have four to five of them positive to make the diagnosis. If a patient has four recurrences of toxo in two years, would you suggest prophylaxis? Yes. Usually with Bactrim. Sulfamethoxazole, trimethoprim is what I use. Second, how does ultrasound help me diagnose eye disease? It’s because of blood vessels? Well, ultrasound is useful for the evaluation of the choroid. The thickening of the choroid. And so it’s useful in the management of choroidal inflammatory diseases, perhaps. Or scleritis. So posterior scleritis in particular. And I think that it is useful when you have medial opacities. What test would you send to check for sarcoid? The definitive test is probably a chest x-ray and a biopsy of a conjunctival or mediastinal lesion if the chest x-ray findings are positive. Chest CT can be done if the chest x-ray findings suggest the presence of sarcoid with mediastinal or hilar adenopathy or parenchymal changes in the lungs. If you have no conjunctival nodules, a blind conjunctival biopsy is not useful. You should have a directed biopsy, just like directed blood tests. So it’s very, very important for you to do a directed biopsy. So if you have lymph nodes and nothing on the conjunctiva, a pulmonologist would have to help you to do a transbronchial or transmediastinal biopsy. In the case of anterior uveitis, when I need to do sampling of aqueous or the vitreous, by which procedure can I do that? Aqueous paracentesis — I prep the patient with topical tetracaine. And use topical Betadine to sterilize the eye for five minutes, use a sterile lid speculum and gloves and sterile 30-gauge needle and syringe that’s primed and gently take out very carefully following the needle — temporal limbus approach. And have the patient laying down flat. Sometimes people do it in the slit lamp. There are actually kits that are available. The eye centers in Singapore have developed these, through Dr. Soon-Phaik Chee. She has developed a small apparatus to do it at the slit lamp. I usually sterilize with topical Betadine to prevent endophthalmitis. TB syringe, 30 gauge needle, and aspirate the aqueous. I’ll be careful to go over the angle in patients who are phakic and under the intraocular lens for patients who have pseudophakic. Is triamcinolone effective for birdshot choroidopathy in Third World countries? Yes, but it’s for acute treatments, if you will. It’s not a great way to long-term maintain patients with birdshot. It’s a lifelong disease. Lifelong treatment with immunosuppression is often required for patients who have birdshot. It’s one of those conditions where long-term immunosuppression can slow the disease process and can maintain vision. Lactating mothers and pregnant women with uveitis can be treated with oral corticosteroids. I think that it’s always… If they have severe disease — and topical steroids of course are fine. Steroids can be used throughout pregnancy. Whenever a patient is on steroids during pregnancy, they should be seeing their obstetrician. And often a high risk obstetrics person may need to be involved. There are certain immunosuppressive medicines such as azathioprine and biologics such as Humira can be safe to use in pregnancy. This is important to keep in mind in the treatment of those folks. Patients of child bearing age — very difficult to treat chronic non-infectious uveitis. Because those patients cannot often be placed on the typical immunosuppressants like CellCept or methotrexate, which are contraindicated in patients who plan to have children, who are pregnant, lactating, et cetera. How long do you give azithromycin for patients with toxoplasmosis? 250 milligrams, BID. What would we expect to see in TB uveitis? That would be a two-hour talk on TB uveitis. There are many great uveitis specialists I know, who I have tremendous respect for. Like Dr. Rathinam in India, who can give a much better talk than I can. Put it can present as anterior segment, intermediate segment, posterior segment, and panuveitis. All of the above. And it is usually granulomatous in nature, progressive without appropriate treatment, can respond to steroids alone, but that is a very, very serious problem, if you treat the patients with steroids alone and they have TB. If they have pulmonary TB that’s active and ongoing ocular TB, the pulmonary disease can become disseminated and miliary, and you can kill them. It’s important to treat them with antituberculous therapy and add corticosteroids. Corticosteroids are necessary for the treatment of TB, but only with ongoing and appropriate antituberculous therapy. How long do you treat anterior uveitis? Well, if it’s acute, most episodes last from 8 to 16 weeks. You need to treat them with a slow taper of topical steroids, and mydriatic agents should be used as well. If the patient has disease that lasts longer than 12 weeks or you’re not able to taper them off to lower doses of steroids gradually and the inflammation does not quiet, the patient has chronic disease by definition. And chronic disease requires chronic therapy, and that may require ongoing use of topical steroids at low doses, long-term. Along with mydriatics long-term, and the patient may require immunosuppressive therapy. Can we give steroids in hypopyon? If it’s caused by infection, no. Initially you have to treat them with antimicrobials first. If the hypopyon is due to endophthalmitis, you have to treat the endophthalmitis with antimicrobial intravitreal injections of antibiotics, vitreous tap, aqueous tap, cultures, and give topical cultures frequently and topical antibiotics frequently and treat that way. If it’s a sterile hypopyon and previous history of autoimmune disease, you can give steroids. If you don’t know, treat with topical steroids and then proceed based on the situation. Fuchs uveitis — I would not treat it with topical medications. It increases the risk of glaucoma, which they’re at high risk of anyway. It’s caused by previous rubella virus exposure. And you can see as the cytomegalovirus — may also be an underlying cause of Fuchs-like syndrome. These patients do not necessarily require any specific steroid therapy. If they have classic heterochromia. And findings… They’re at high risk, 50% will develop glaucoma. 50% will develop cataracts. So they’re managed as if a normal patient with cataracts. So you don’t need to necessarily do anything. Can you give empiric antibiotics like azithromycin and steroids while waiting for reports? Depends on what you think it is. If it’s a viral retinitis, azithromycin is not gonna help you. If you think it’s a necrotizing retinitis going on, I would put them on antivirals. That’s the worst thing that could be. No steroids. Add the steroids later, after you’ve started the antivirals, while waiting for results. I hope this is helpful. These are all great questions. Wonderful to see you all and I hope you have a wonderful rest of the week. Thank you for your attention and have a great weekend.