Case Review: Uveitic Ocular Hypertension and Glaucoma

Speaker 1 (00:20): Welcome to Pupil Pod, where we use clinical cases to guide discussions on board review topics. I'm your host, Ogul Uner, and my guest today is Dr. Eric Rivera Grana. Dr. Rivera Grana is a board certified glaucoma and uveitis specialist at Instituto Oftalmologico in Ponce, Puerto Rico. And I'm so excited to have him on the podcast today. Dr. Rivera Grana, thank you again for joining me.

Speaker 2 (00:43): Thank you so much for having me, Dr. Uner. It's a real pleasure being here and talking about this very important topic.

Speaker 1 (00:50): Awesome. I'm very glad that you're here, uh, as someone who, uh, does, uh, both of the topics that we're going to talk about today. Let's delve in directly into the case. We have a 34-year-old woman who presents to your clinic with blurry vision and mild eye discomfort in the right eye for two weeks. She has a history of HLA-27 associated recurrent anterior uveitis and ankylosing spondylitis on intermittent and set therapy, uh, that she takes systemically. Vision is 20/40 in the right affected eye, 20/20 in the left eye. IOP is 38 in the right and 14 in the left. Slit lamp exam shows conjunctival injection, inferior fine KP, one plus AC cell, posterior synechiae from four to six o'clock and pigment on the anterior lens capsule of the right eye. The left anterior segment is unremarkable. You perform a gonioscopic exam before dilation, which shows patchy peripheral anterior synechiae (or PAS) in the right eye.

(01:43): A dilated fundus exam is unremarkable except for a cup-to-disc ratio of 0.6 in the right and 0.3 at the left with no disc hemorrhages in either eye. Dr. Rivera Grana, what are your initial thoughts about this case?

Speaker 2 (01:56): Yeah, so great case. So every time I see a patient like this in clinic, I create a flow chart in my mind on two sides. One side, I have uveitis, and one side I have glaucoma and I merge them together. So this is a fairly young patient with what seems to be a unilateral uveitis. So I want to characterize what type of uveitis the patient has. Is it anterior, intermediate, pan-uveitis, et cetera, because this will also give me more of a risk assessment for developing ocular hypertension or glaucoma. Um, and then I also, it's very important in the history, you know, we're uveitis specialists, so our history is very important. We know that she has been on non-steroidals, but I really want to know if she's been on any steroidal medication, what dose frequency, uh, and timing of this medication. Um, and then, you know, in the glaucoma aspect, I don't only want to know what the pressure is.

(02:51): I also want to know what her prior pressures have been. Has she ever had any prior episodes of elevated pressures before her inflammation? Did this all start after her inflammation? Did this start after any particular medications that she started on? Um, and then, yeah, I think it's very important also in the physical exam to get a pachymetry reading on every patient with uveitis and borderline or elevated pressures. And I love that you guys did a gonioscopy exam right off the bat, because that's very important. And, you know, sometimes we see patients with eye inflammation and we focus on the inflammation and we forget to do a gonio exam. So that's a very, very important thing to do. Um, yeah, so that's the things that I try to characterize uveitis and try to figure out when the IOP started to get high.

Speaker 1 (03:42): Okay. Awesome. Yeah. I think, uh, you summarized it really well. You know, there's a very complex, uh, association between inflammation and glaucoma. So this, you know, likely is maybe inflammatory uveitic glaucoma. There's some AC cell, there's some angle findings, you know, the cup-to-disc ratio’s a little concerning. Um, and then as you said, kind of getting control of both cases, so getting the IOP down, um, but also, um, controlling inflammation. And so going on to the different types of glaucoma that uveitis can cause, we know that it's a multifaceted problem. How do you classify uveitic glaucoma in your mind?

Speaker 2 (04:23): So in my mind, even before I classify uveitic glaucoma, I want to classify uveitic ocular hypertension and glaucoma. That's something that sometimes people think is the same thing and it's not. So ocular hypertension is a pressure of more than 21 mm Hg without any glaucoma optic nerve defects. So then you have uveitic glaucoma when you have elevated pressure and you have optic nerve findings. And that's very important to differentiate. So in this patient, we already know that she has an asymmetric cup-to-disc ratio, so I'm thinking more about uveitic glaucoma. Um, so, you know, there's different mechanisms why uveitic glaucoma can happen. One is an open angle mechanism. This is usually when we think about, for example, herpetic etiologies when we have trabeculitis and the pressure gets high, but your drainage system is open, but not necessarily only limited to herpetic diseases. Other anterior uveitics can also get it, especially HLAB27 patients tend to get it a lot.

(05:24): And it's mostly because, you know, you get all this inflammatory debris and protein debris when these eyes get inflamed in the aqueous and there can be some clogging mechanism to it and the drainage is still open. And I'm also a strong believer that especially in recurrent or chronic anterior uveitis, you, um, uveitic patients, you can also get scarring of not only the trabecular meshwork, but also the downstream canalicular channels, and that creates an outflow resistance. So we have our open mechanism. We, then we also have our closed mechanisms. This is when we get, uh, PAS, so anterior synechiae. Um, in patients like, for example, VKH patients, they get a lot of posterior synechiae, which ultimately can develop into a bombé, which means that the iris holds forward and blocks directly the trabecular meshwork. Um, sarcoid patients and also VKH patients can also get ciliochoroidal effusion.

(06:18): So, uh, fluid accumulates behind the ciliary body and it pushes everything forward and you get, um, a blockage of the trabecular meshwork. So we have to think about the closed angle mechanisms. And then we also have mixed mechanism. We can have PAS. We can also have, you know, canalicular outflow restriction and we call this a mixed mechanism. And this is actually the most common type of mechanism in uveitics because you get, you know, everything, a little bit of both. And also, every time we talk about inflammation, inflammation is mostly treated with steroids, so we always have to keep in the back of our mind steroid-induced responses, especially in a young patient. Yeah. In a young patient like, like the patient that we have here, young, the younger the patient, the more risk of a steroid response that they have.

Speaker 1 (07:05): Yeah, that's excellent. I think you outlined the different classes really well. Um, you know, I think open angle, closed angle mix mechanisms and a lot of people tend to think of uveitis, um, causing a decrease in the IOP, you know, due to the inflammation of the ciliary body. Um, but you can have trabeculitis as you mentioned in herpetic disease or other types of anterior uveitis or in V27, as you said. So I think those are great points to make. Uh, and you mentioned that, uh, some patients may be predisposed to uveitic glaucoma you wanted to, uh, look at, you know, whether they have anterior uveitis or panuveitis. Are there particular uveitics that are more predisposed to this?

Speaker 2 (07:44): Yes. Even though everyone can get it, any type of uveitis can get uveitic glaucoma or hypertension, definitely anterior and intermediate patients are the highest risk followed by anterior and then panuveitis. The reason why anterior and intermediate are more at risk is because usually those patients get more of a steroid burden because of the intermediate component as well as they also get the anterior component. So those patients are the ones that I get more worried about and then also the anterior and panuveitis. Intermediate uveitis, solely intermediate or solely posterior uveitis have a, lesser risk of developing, uh, uveitic glaucoma, but they can also get it. So another patient that I'm always very, you know, very meticulous about looking for glaucoma are JIA patients because they're very young. They get exposed to a lot of steroids or also have a chronic anterior inflammation. So JIA patients are patients that we really, really have to be on the lookout for.

(08:42): Um, Posner-Schlossman syndrome, for example, that they get this recurrent very severe bouts of inflammation. They also get trabeculitis. So these are patients that because of the recurrence of their inflammation and IOP spikes, are more predisposed to getting glaucoma damage. And then, you know, any sort of chronic, uh, anterior uveitis because of the scarring and PAS formations are going to be more at risk of developing uveitic glaucoma.

Speaker 1 (09:11): You mentioned, uh, that this is a spectrum. You know, you have patients with ocular hypertension, uh, you know, what we call maybe a glaucoma suspect, and then you also have the glaucoma. In some cases, uh, when you look at the, uh, primary angle closure, uh, classification with the primary angle closure suspect, primary angle closure, primary angle closure glaucoma, PAS, uh, is actually one of the definitions of primary angle closure. Um, you know, you do not necessarily need to have, um, you know, high IOP if you have the iridotrabecular contact and PAS that, that is not a suspect anymore. Do you classify the presence of PAS as angle closure without glaucoma and uveitic eyes as well, or do you think of it differently?

Speaker 2 (09:54): No, I use the same criteria. Uh, you know, I start with PACS, which is primary angle closure suspect, which means, um, you know, there's more than 180 degrees of trabecular meshwork contact with the iris, um, but there's no IOP spikes or no PAS formation, that's the S. Then you get your PAC patients, which is the primary angle closure, that's when you have more than 180 degrees of iridotrabecular contact, but now you're having either the IOP spikes or you have PAS, which most of our uveitic patients are going to fall into that criteria. And then primary angle closure glaucoma is when you have the contact, the IOP spikes or the PAS and you have your optic nerve damage. Another thing that I think is very important to talk about is—that it's mostly, you know, negated when we talk about uveitis—is the flare. The flare tells me a lot about the chronicity of the uveitis and also, you know, higher flare amounts doesn't necessarily translate to active uveitis, but it translates to me to a risk factor of these patients developing posterior synechiae and PAS, which ultimately will drive the patients into uveitic glaucoma.

(11:05): So I look a lot at the flare and, um, I use it more as a risk stratification for these patients.

Speaker 1 (11:11): Mm, that's awesome. Yeah. I think in addition to the cell, as you said, the flare and how, how dense that anterior chamber is filled with the aqueous and the debris, uh, the, the protein material is, is really important. And so that I think segues really nicely into the clinical exam signs, um, in these patients. You talked about posterior synechiae, you talked about iris bombé. Do we see PAS maybe in different locations compared to a regular primary angle closure, um, person? Uh, and, uh, what other findings, uh, can you find maybe on gonioscopy or in your dilated exam otherwise?

Speaker 2 (11:48): Yeah. Great question. Um, yes. The pattern of PAS formation in uveitics differs from primary angle closure non-inflammatory patients. In uveitis, uh, most of the PAS will be in the inferior angle because by gravity, most of our inflammatory debris will accumulate in that area versus our non-inflammatory, uh, angle closure patients usually start superiorly. So by looking at the gonio, it gives you a lot of information also. Another thing that will also, it's also different in uveitic patients compared to, like, for example, pigment dispersion, uh, patients is that the, uh, pigment is going to be mostly located in our inferior angle in our uveitic patients versus in our pigment dispersion patients are not necessarily only in the inferior angle. So yeah, that definitely is very important. It gives us a lot of information.

Speaker 1 (12:42): We talked about the importance of imaging, uh, modalities, uh, in these patients. You know, we always get, uh, nerve fiber layer. We get the Humphrey visual field. Those are classic imaging modalities to, uh, monitor for the glaucoma. Uh, but do you, uh, obtain any additional imaging in your clinic, uh, apart from the RNFL and the visual field?

Speaker 2 (13:02): Apart from the RNFL and the visual field, depending on the uveitis and how I see the gonioscopy exam, I might lean towards doing either, uh, UBM. I think UBMs are essential, especially in panuveitics or anterior intermediates looking for ciliochoroidal effusions. Um, and yeah, I think it's also very important to note that for this particular patient at presentation, I always get, try to get everything, but I know, for example, especially an RNFL reading might be in the green or might be elevated because some of these patients get retinal edema as well, even if they don't have active CME. And a lot of people, you know, see the RNFL and they're like, "Oh, it's great." And then once the patient gets quiet, the RNFL drops significantly and they're like, "Oh no, it progressed." It's not necessarily that it progressed, it's just that now our glaucoma is manifesting because that edema went away.

(13:57): So I think that's also very important to keep in mind. I usually take both and I have both baselines and then after the inflammation is quiet, that's the baseline that I'm going to start tracking looking for active progression.

Speaker 1 (14:10): Mm-hmm. I think that's a phenomenal point to make, um, that disc edema can accompany a lot of our different uveitic conditions, even anterior uveitis, uh, and, uh, that can really make it difficult to interpret it in the setting of, uh, glaucoma for these patients. We briefly talked about corticosteroid associated glaucoma and how it is an open glaucoma subtype and there's a very fine line between steroid response and controlling the inflammation acutely. I've had several, uh, colleagues or junior residents, uh, get very concerned when they see a high IOP with inflammation and they're worried that they're going to make it worse by adding steroids. When should we suspect steroid response and what is your thought of treating in these acute cases?

Speaker 2 (14:54): Yeah. Excellent question. So steroid responses usually don't develop before three weeks of steroid therapy onset. So I am never really that concerned only in very young patients if someone started them on like difluprednate, which is a very high potency steroid. Um, usually before three weeks, I wouldn't expect any IOP, uh, steroid response. Um, when I said in the beginning that I create a flow chart in my mind, it, it's at the same point that I'm treating my flow chart at the same time, you know, we have to treat the inflammation aggressively concomitantly with the pressure. We can't, you know, stop treating one to treat the other. We always have to treat both. So if there is a very active inflammation, I'm going to be very aggressive with the steroids. Um, and then I usually, if I'm giving very aggressive steroids, you know, like every one hour prednisolone or every two hours or difluprednate at high doses, I, I'm going to see these patients back in three to four weeks.

(15:52): I usually don't see them before unless there's one exception to this rule. If I already know that the patient is a steroid responder, if you've already had a steroid response, then you can get it earlier. But still, I would treat aggressively and just manage the pressure medically if, if possible.

Speaker 1 (16:09): Mm-hmm. I think those are great points. Uh, you mentioned that, uh, some topical agents are stronger through difluprednate because it penetrates into the eye more than prednisolone. That's more at stake and same with our local steroids. If you give intraocular steroids like, um, a dexamethasone implant or a fluocinolone implant, obviously more than in comparison to a, um, a subtenon kenalog, for example. So, um, and, uh, we also know that oral prednisone can cause a steroid response in some patients but not very aggressively. So if there is a concern and you're worried that someone's going to get a steroid response, you know, oral prednisone can be a good option, uh, like we talked about. So, um, at this point, um, we're going to take a short break. Uh, we'll be back after hearing about our sponsors.

Speaker 1 (17:06): Okay, welcome back. Uh, we talked about, uh, steroid associated glaucoma and the intricacies. Dr. Rivera Grana, do you have anything else to add before we talk about treatment?

Speaker 2 (17:16): Yeah, I think it's very important to clearly note that, uh, steroid induced responses are dose dependent and, um, potency dependent. So a higher potency like difluprednate will create a higher response than, for example, an FML drop. So patients that are topically treated are going to have bigger responses to a patient that's using like a topical skin cream and that's important to note.

Speaker 1 (17:39): Okay, great points. Uh, moving on to the treatment of uveitic open angle glaucoma or angle closure, uh, how do you think about stratifying these treatments? Uh, when do you escalate from topical treatment? When you have an open angle in front of you versus angle closure from posterior synechiae versus angle closure from extensive PAS, uh, how do you consider different treatments in your mind?

Speaker 2 (18:04): I try to stratify what mechanism is the primary mechanism, although this can be quite difficult most of the time. So as a rule of thumb, if I'm seeing more than 180 degrees of PAS, I'm classifying them more as a closed angle mechanism. Um, for these patients, you know, all patients, open angle, closed or mixed, I'm going to start medical treatment. Um, so I start with IOP lowering drops. If the drops, I try to max it out if they are maxed out and by maxed out, I mean usually a four-drug treatment regime. Then I consider adding, uh, systemic medications like acetazolamide or methazolamide. Um, and if these fail or if I know that I'm going to have to keep them on all these medications, including systemics, then I start thinking about surgical management. So, um, and what I do is I differentiate between open and closed because that will guide my surgical management differently.

(19:01): Um, usually for an open angle mechanism, um, I would try to do, uh, minimally invasive glaucoma surgery first. Angle-based procedures work wonderfully for uveitic patients, in particularly patients not only with open angle mechanism, but steroid-induced responders. It's a beautiful surgery and it's less invasive. We're not leaving any hardware in the eye, which is always a great idea for uveitic patients versus, uh, chronic, a mostly chronic angle closure. I know that even if I create a goniosynechialysis, most likely that trabecular meshwork is going to be scarred and it's not going to work even if I unroof the most superficial area with the trabeculotomy, most likely the outflow canalicular channels are going to be restricted so most likely, uh, goniotomy won't work. So in those patients, I'm going to think more into like the glaucoma drainage devices.

Speaker 1 (19:53): Awesome. And what are your thoughts about CPC and SLT in these patients?

Speaker 2 (19:58): So CPC to me is a big no-no. CPC is very pro- inflammatory. Um, it creates a lot of CME, which in patients with uveitic CME, now you're basically dealing with an entirely different beast if they don't have CME before. So I always, I don't even consider CPC on uveitic patients, unless it's a patient that's been inactive for more than two years and flare-ups, you know, were pretty mild maybe, but otherwise it's a no-no. SLTs, on the other hand, um, it's a, if a patient has been very, uh, well-controlled and by well-controlled, I mean off steroids, either on IMT or off IMT, but no steroids, um, or if it's mostly a steroid-induced response and I know that I, you know, I'm going to have to start steroids soon, I might consider SLT. But still, you know, I don't use it as first-line like I would do on a non-inflammatory open angle glaucoma.

(20:52): Um, I think, yeah, so SLT, I might use it, um, but it's not first-line.

Speaker 1 (20:59): Those are great. I think it's important to know that the, the cyclophotocoagulation, the destructive procedures can be, uh, very harmful and accelerate, uh, as you said, macular edema, hypotony. It can lead to ptosis in some of these patients with worsening ocular inflammation. So it should really be reserved for, um, a very, very small subset of eyes. Uh, and, uh, like you said with SLT, uh, it's important to kind of pick the patient, uh, accordingly. Uh, you talked about topical drops and different antihypertensive drops that you use in the acute setting. Uh, do you have any particular ones that you like? Do you have ones that you avoid? Uh, and what about chronic treatment?

Speaker 2 (21:41): Yeah. Let's first start with the ones I avoid, because that's the most important thing. Um, I always avoid miotics. Miotics and uveitics, first, it's usually they're pro- inflammatory, so you're not helping the inflammation. Secondly, you're, you know, you're constricting the pupil, so you're helping the posterior synechiae formation to happen and also you're also, you can also push everything forward from the ciliary body to the front and, you know, you can, you can also create a closed angle mechanism now with miotics. So miotics to me are a “no” for uveitics. Um, then when we're talking about, uh, IOP lowering drops, there, you know, there's no real consensus of which one is best and which one should be first-line for uveitics. I personally love timolol as a first line and it's mostly because it's on ... I only use it as, uh, every morning and it's once a day so it's, I get a better compliance from patients with these doses—after timolol then I might add dorzolamide.

(22:39): Um, as a third-line, then I'm talking to brimonidine. The reason why I use brimonidine as a third-line, it's because even though it's a very small subset, brimonidine can cause, uh, granulomatous anterior uveitis. Um, so I don't want to help the uveitis at all, so that's why I use it as third-line. And also out of all of the topical medications, it’s the one that can cause the most allergies to it. So I try to avoid it if I can, but I still use it. And then as a fourth-line, I use prostaglandin analogs. You know, in the past we, we used to hear like prostaglandin analogs, uh, no-no for uveitics. We have a lot of data now showing that it's really not pro-inflammatory as we thought in the past. So I still use it. It's also once a day dosing so it's easier on the compliance.

(23:26): Um, the only patient I wouldn't use it if it's, if it's a herpetic patient, because it can, it can increase the chances of a flare-up. So that's the only patient I would never use it. Um, and then after that, then we start with the systemics like acetazolamide and, uh, methazolamide.

Speaker 1 (23:43): Mm-hmm. That's a great summary. And I think that, uh, segues well into the different surgeries and the surgical procedures. You already talked about, uh, the different MIGS options and, uh, the glaucoma drainage, uh, devices and some of the incisional surgeries, but, uh, what do you think about the timing of surgery for these patients in relation to uveitis quiescence? Uh, what are, uh, some surgical options apart from drainage devices that we can use? Like, could we do a trabeculectomy in these patients? I would love to hear more about that.

Speaker 2 (24:16): We always hear, I remember as a first year medical student, uh, resident, people telling me, "You never do a surgery on a uveitic if it, if it hasn't been quiescent for more than three months, for less than three months." You know, this, uh, saying, and this data was taken for cataract surgery in uveitics or glaucoma, we throw that timeline off the window. Um, ideally, I want to have the best inflammatory control that I can before going into surgery because active inflammation, um, you know, could lead to further complications after surgery, such as hypotony. Um, the ciliary body in patients with uveitics is very labile and it tends to go into shutdown. So, um, if they're active, the hypotony can get worse. Uh, CME is also a very, uh, increased concern in these patients. So definitely you want to have the best inflammatory control, but if the pressure, you know, it's in the 30s or you're seeing, um, more pattern loss in your RNFL or in your visual, in your Humphrey visual field, don't wait until they're quiet.

(25:19): You just have to go in and, um, do the surgical procedure of choice. And with me, like I said, open angles, I try to do an angle based procedure. Uh, I try to do a goniotomy or, um, trabeculotomy with viscodilation. I feel like that's the best one. I try to go always for the 360 degrees. It's very important when I talk to a patient about these surgeries, I tell them, you know, the, the IOP is going to be up and down the first few weeks, and that's okay, that's normal. Um, and also I, I tell them about the risk of hyphema. You know, these patients, especially if they're actively inflamed, they're going to bleed. You know, as a glaucoma specialist, I see hyphema all the time, so it's not that alarming, but you, you're going to see some degree of hyphema. Um, so, and that's okay. And you try to minimize it in the OR by putting cohesive viscoelastic and create a little bit of a tamponade for a little while and it helps sometimes, but yeah, you're going to see hyphema.

(26:15): Just let the patient know because that way they're not scared afterwards. Um, we talked about the glaucoma drainage devices, but I think it's very important to note that for uveitics, I tend to go with valve mechanism devices, um, and that's to decrease the risk of hypotony. And even me personally, even if I put a valve glaucoma drainage device, I always leave at least a third field of viscoelastic to prevent hypotony in the immediate post-op, uh, period. And then other surgeries that we could, we could consider, you know, trabeculectomies, they're relatively contraindicated, yes and no. And the reason is if the patient is actively inflamed with very severe inflammation, the chances of the trabeculectomy failing earlier is higher. So that's why we try to avoid it, but it's not really a, uh, you know, an absolute contraindication. Some patients, we might need to do it.

Speaker 1 (27:06): That was a great overview and I think the studies really corroborate, uh, your, uh, your style as well. You know, valve surgeries, uh, based on, uh, most recent studies, you know, you can control IOP with maybe zero to one medication and 75% of patients even after four years. So do they fail? Yes. Um, and I've definitely seen patients who have, uh, multiple tubes in the eye. Uh, and, uh, as you said, the hardware becomes a concern. If you especially have scleritis or more surface inflammation, it can be very challenging, uh, to control these patients. You can get erosion of the tube through the conjunctiva, you can have valve migration, uh, you can get corneal decompensation and a lot of other retinal complications. So I'm glad that, uh, we kind of weigh the risks and benefits of those. And similarly, in trabeculectomies, I was surprised in the literature they showed IOP control with zero to one medication in maybe 62, uh, percent after five years.

(28:05): That was a lot higher than what I was anticipating. I thought that a lot of them would fail, but as you said, I think it's important to, uh, tailor it to the patient. You know, if they've been inactive for a long period of time, uh, clearly there are, um, areas of success and obviously early and late bleb leakage, the increased risk of endophthalmitis, uh, choroidal effusions, hemorrhages can, um, also be a concern. But, um, I'm glad that you weighed both options and, uh, seems like the glaucoma drainage devices, uh, are more so the treatment of choice in the acute stage.

Speaker 2 (28:38): Yeah, I think it's, you know, there's no one size fits all for uveitic glaucoma. So, um, another thing that's very important that I forgot to mention, especially if you're thinking, you know, of a trabeculectomy, it's also looking at the mobility of the conjunctiva. You know, like you said, scleritis patients, they get very thin tenons, so you know, that, that closure might be a little bit harder, they're higher risk of bleb leakage, like you said. Um, another thing, uveitic patients, if they're receiving recurrent intravitreal injections, that conjunctiva might be pretty scarred down. So that's also something that you have to take into consideration. Um, patients with uveitis, uh, especially with valve mechanisms, can get a lot of hypertensive phases. So I try to start them at least on one IOP lowering drop in the immediate post-op period if their IOP is higher than 10. That's my cutoff and that's why I use, you know, the, the lower you keep the pressures in the early post-operative phase, the less chances of, um, hypertensive phase you're going to have.

Speaker 1 (29:35): That's a great point. Yeah, thank you. That's, it's a good cutoff to have, especially if you're doing these surgeries in these patients. So, uh, going back to our patient, you started her on, uh, Pred Forte every two hours while awake. You started cycloplegics, anti-hypertensive drops. You see her back, uh, in a week or two, the AC's now quiet, IOP is well-controlled, you get an RNFL and a visual field, that shows some mild glaucomatous changes in the affected eye, not surprising. Um, how would you treat and counsel this patient long-term? Would you consider starting immunomodulatory therapy in this patient if maybe this is their first flare, maybe it's their second flare, you know, if you don't know, um, does the fact that she has ankylosing spondylitis play any role in your discussion, uh, and other thoughts you may have?

Speaker 2 (30:24): Usually in patients that develop uveitic glaucoma, especially the younger the patient, I am going to push more aggressively towards starting immunosuppressive medications earlier because I don't want to give them the chance to develop a steroid response even if they haven't yet. So in this particular patient being a 34-year-old, especially that we know she has a systemic associated uveitis, I would definitely talk to our rheumatology colleagues and try to get her on an immunosuppressive medication to use it as a steroid sparing agent. So definitely, yes. If this was just a plain, you know, an idiopathic anterior uveitis first episode, I might wait, but as soon as they start developing a steroid response, I would push forward for immunosuppression to, uh, use it as a steroid sparing. Um, you know, glaucoma is a, you know, you're, you're pretty much racing against time and against the disease. So the younger the patient, the more aggressive I am, because I don't, I don't want them to be 75-year-olds with a 0.9 cup in, you know, just a central field. So yeah.

Speaker 1 (31:30): It's really important to think about the glaucoma as a structural complication of uveitis, like posterior synechiae, like the cystoid macular edema. I think all of those are important in consideration of, uh, initiating IMT, um, in these individuals. So, um, that, that was great. Let's summarize what we learned from Dr. Rivera Grana. Glaucoma is very common in uveitis with anterior and panuveitis being the two most common subtypes. It can be open angle from trabeculitis, from clogging or steroid response, or closed angle from PAS, posterior synechiae, and iris bombé, or a posterior push mechanism where the lens iris diaphragm comes forward from etiologies like uveal effusion. Always think infectious uveitis first when you're seeing a hypertensive, uh, uveitis, but that it could also be from trabeculitis in non-infectious uveitis. Baseline gonioscopy is crucial for all patients with uveitis involving the anterior segment as well as a baseline OCT RNFL on all patients with uveitis to monitor the nerve exam over time.

(32:31): Steroid response rarely occurs like we talked about before three weeks on steroids. So remember to treat the uveitis aggressively with topical steroids early on as this is likely the source of the high IOP. Treatments based on the underlying cause with control of the uveitis, tapering steroids if this is indeed a steroid response, a surgical iridectomy, possibly if this is an iris bombé, um, or steroids and cycloplegia for a posterior push mechanism. Avoid CPC and miotic agents in these patients, but you can use prostaglandin analogs with more recent meta-analysis showing little association with worsening uveitis, um, as Dr. Rivera Grana said. Uh, still be very careful when you use it in your herpetic patients. Valve tubes are preferred over trabeculectomies or non-valve devices for most patients and no need to wait three months if it is urgent. MIGS, uh, is emerging as possible, um, great options, especially for steroid-induced glaucoma.

(33:29): Perioperative and intraoperative steroids are paramount to control the inflammation as much as possible and glaucoma at the end of the day is a structural complication like we mentioned of uveitis and IMT and should be strongly considered in these patients to ensure optimal control of uveitis and the associated glaucoma. Dr. Rivera Grana, anything else you would like to add?

Speaker 2 (33:50): I would just like to add that when I take a patient with uveitis to surgery, even if they have a steroid response, I am going to give them perioperative and post-operative steroids. I don't shy away from the steroids. So that is important to know. I want to clarify that.

Speaker 1 (34:05): Yeah, that's great. And we didn't talk, uh, in detail about, uh, you know, iris bombé and we, uh, both know that laser peripheral iridotomies generally do not stay open in these patients. They're very pro- inflammatory so, uh, in most cases if you have a, if you have a bombé picture, it, it may be best to take them to the operating room to do a surgical, uh, one. I know in some patients if you can't have the operating room access, some people will do multiple LPIs in multiple locations, uh, but I know that's not your preference. Uh, what, what are your thoughts on that?

Speaker 2 (34:40): You said it perfectly. I try to avoid laser iridotomies because they're pro- inflammatory. The opening that you do with the laser tends to be small, so it'll, it'll mostly get clogged with the inflammatory, uh, debris that the uveitis causes and also there's something that's called the PI paradox. It was described, uh, UCLA and some of our colleagues over in England and it's that patients that have, you know, less than one o'clock hour of opening with posterior synechiae. If you do a PI on those patients, now you're taking the, all the outflow that the patient had was going through that little tiny opening. So now you're creating another opening so the outflow will decrease through that opening and the iris will now get opposed and you can cause a 360-degree posterior synechiae, and then when your PI gets clogged, now you're on full bombé. So on patients, you know, that have little, tiny openings of posterior synechiae, I leave them alone unless if it's a very aggressive, active uveitis, I might go in and just do a surgical iridectomy.

Speaker 1 (35:44): Mm-hmm. Yeah, that's a great point to, uh, to mention. So thank you so much for, uh, adding that. And Dr. Rivera Grana, before we end each episode, I ask all of my guests a question. My question for you is if you could go back in time and give your younger self one piece of advice, what would it be?

Speaker 2 (36:01): Uh, wouldn't it be nice? Would it, we could go back in time. So I think I would tell myself, take a deep breath, relax. Um, you know, we sometimes have these role models that we aspire to be and we look at their trajectories and we're like, "I want to do that. I want to, you know, emulate this person." But in reality, you know, we can't achieve our goals and we don't necessarily have to follow a similar path. You know, we can take a completely different route and still achieve our goals and, you know, and that's okay and that's beautiful. So I would just say, you know, stay concentrated, work for your dreams and it doesn't matter, you know, what life throws at you, just keep working towards your dreams and you're going to be okay.

Speaker 1 (36:46): That was great. Uh, we, we really appreciate that insight and I'm sure a lot of our, uh, listeners would echo that sentiment as well. Uh, Dr. Rivera Grana, thank you for joining us on this episode of the Pupil Pod.

Speaker 2 (36:58): It's been a pleasure. Thank you so much for having me. It’s been great talking with you.

Speaker 1 (37:02): And thank you to our listeners. See you next time on The Pupil Pod.