During this live webinar, we will discuss the classification and management of patients with angle closure. Questions received from registration and during the webinar will also be discussed.
Lecturer: Dr. Irfan N. Kherani, Assistant Professor, University of Toronto, Canada
DR KHERANI: All right! Thank you for attending. My name is Irfan Kherani, and I’m a glaucoma specialist at the University Health Network at the University of Toronto. And I’m excited to discuss with you today an approach to the assessment and management of primary angle closure disease. Now, this is a topic that has absolutely changed over the past couple of decades. And so our goal today is really to understand how the mechanism driving angle closure can be used to outline the best management for our patients. To start, here’s a quick summary just of my disclosures, none of which are particularly relevant today, but I have received honoraria from the companies that are listed here. Much of what I’m gonna discuss today comes from these two very, very important guidelines: The terminology and guidelines for glaucoma, published by the European Glaucoma Society, have been recently updated, and make reference to some of the newest and most pivotal trials that really guide our practice. Secondly, the primary angle closure disease preferred practice pattern from the American Academy of Ophthalmology, led by Stephen Getty, is a fantastic resource, not only for eyecare professionals and practicing optometrists and ophthalmologists, but also those in training, hoping to get a better sense and some background on the approach to primary angle closure disease. We’ll first discuss relevant background, followed by assessment of primary angle closure disease, focusing first on the staging, and subsequently on the mechanism driving that angle closure. Based on that assessment, we’ll move on to the management, in order to determine the safest plan first, based on mechanism, but after that, based on staging. Many other webinars have focused on the approach to the acute angle closure crisis, or acute angle closure glaucoma, and while I will make reference to it today, it will not be the primary focus for today’s session. So before we start discussing whether or not to shoot lasers or do surgery, let’s start off with some background. When seeing a patient with potential primary angle closure disease, these are the types of risk factors that we want to elicit on past medical history. While there’s no clear cutoff for age, many clinicians suggest that an age of greater than about 50 years is a point at which angle closure becomes clinically relevant. That being said, I’m sure many of us have seen patients with advanced glaucoma that present much earlier than this. And honestly, I can actually think of a patient right now that I’m managing, who presented just a few weeks ago, at the very young age of 17, with very advanced primary angle closure glaucoma, already affecting his central fixation. Females are statistically more likely to develop angle closure. However, it’s certainly not a reason for exclusion. And like most types of glaucoma, family history and genetic predisposition very much play a role. But unlike our classic or primary open-angle glaucoma, racial background plays a particularly strong role in establishing risk for angle closure glaucoma. Patients of Inuit and Chinese background have a particularly high prevalence of angle closure. Up to 4% of Inuit patients are diagnosed with this group of diseases. Now, I’m fortunate to have spent some time in Nunavut, in northern Canada, treating patients of Inuit origin. Their disease is often very pronounced, requiring very thick lasers to help manage. While the Inuit and Chinese populations are more likely to be affected by angle closure, not being one of these races is once again not an exclusion factor. When assessing anyone with angle closure, patients of African or European origin — they can and still are affected by angle closure glaucoma, and as such, even with the prevalence of around 0.5%, we should be mindful of their race and origin. While clinical history is important in all of medicine, clinical exam plays a distinctly important role in risk stratification of angle closure glaucoma. We all look for patterns, so when I see a patient in my clinic with a history of hyperopia, thick glasses, bottle glasses, or short axial length, I immediately start thinking about angle closure. Largely because these patients have a relatively thick crystalline lens, relative to the size of their eye. As such, whenever I see patients with hyperopic correction, shallow or central peripheral anterior chamber depths, steep corneal curvatures, specifically thick crystalline lenses or short axial lengths, and as well anterior lens positioning, I’m automatically thinking about angle closure, and important — complete gonioscopy assessment. Of note, patients that have plateau iris, another mechanism that drives angle closure glaucoma, which we’ll discuss later on, these patients often don’t follow these characteristics. As such, any patient coming in for a glaucoma assessment should be considered a candidate for angle closure glaucoma. With that in mind, direct visualization of the anterior chamber angle with dynamic gonioscopy in a dark room is and will likely continue to be the gold standard for determining angle closure. However, as our imaging modalities improve, our ability to record ourselves and more importantly show these images to our patients will likely continue to change our approach to angle closure moving forwards. Anterior segment imaging, like I’ve shown here, whether through OCTs or UBMs, is proving to be an invaluable resource in the assessment of angle closure. When using these modalities, however, we must be careful not to depend on the automatic measurements and conclusions created by these devices. We must read the imaging ourselves. Whenever using an anterior segment OCT, for example, showcased right here, before even looking at the angle on the image that I have, I first ensure that the pupil is dilated. Indicating dark room completion of the test itself. The last thing you want is to create some sort of false sense of reassurance, because the imaging produced was completed incorrectly. I really refrained from using the automatic IC angle measurements. As you can see on this image, they are susceptible to a significant amount of artifact, and for that reason, I prefer to gonio the patient and then compare it to the imaging that we produced. Now, progression with our imaging, with the increasing use of artificial intelligence, will continue to improve, almost by nature, of artificial intelligence. However, we should always confirm our assessments that are aided by technology. For certain types of mechanisms that we will discuss today, anterior segment OCT will adequately image the anatomy in question. Things like pupil block and lens rise. However, if we are interested in assessing things like plateau iris, we do need to ensure that ultrasound imaging is completed in order to visualize the ciliary body. Anterior segment OCT does not have the required penetration to visualize the ciliary body. As such, dynamic gonioscopy, which I’ve mentioned before, is still the gold standard. And it’s really only the dynamic gonioscopy that can be used to formally diagnose angle closure and its constituent mechanisms. So with that bit of background, let’s move on to our assessment of the primary angle closure disease patient. Our first step in any designation or assessment is to determine the stage of the glaucoma. Whether you look at the general glaucoma textbooks or the Academy publications or the EGS guidelines, angle closure disease is pretty much always subdivided into three constituent diagnoses. The summary table that I’ve presented here is taken from the EGS guidelines document. So level one: Primary angle closure suspect. Primary angle closure suspect patients have iridotrabecular contact observed on gonioscopy without compression, of course, where contact is described as the iris touching the pigmented trabecular meshwork or any structure anterior to that, for at least 180 degrees. Now, there can be no increased intraocular pressure and no scar tissue or posterior anterior synechiae. Furthermore, the patient cannot have any existing glaucomatous optic neuropathy or associated visual field defect. Now, a couple of important notes. First off, for those of us who are still mastering gonioscopy — honestly, this is a skill that is still changing every day for me — I highly recommend gonioscopy.org. It’s a great academic resource on how to approach and diagnose pathology on gonioscopy. So definitely refer to gonioscopy.org if you’re trying to master that skill. And second, a lot of clinicians will ask why we use this 180 degree rule. Why is it that an angle is considered open if less than 180 degrees are occluded? So honestly, in short, the definition of 180 degrees of iridotrabecular contact is really based more off of a consensus agreement. We have no formal scientific reason to argue why 180 degrees put patients more at risk than 90 degrees, for example, but logically, that would seem to be the case. Honestly, the formal diagnosis of angle closure is less important with that 90 versus 180 degree standpoint, but if a patient is only closed at 90 degrees at the age of 45, as they get older and their lenses become bigger, my guess is their risk for angle closure will increase moving forwards. On to level 2. If the patient has 180 degrees of iridotrabecular contact, but there is either increased IOP or some poetry anterior synechiae, we use the term (inaudible). If the patient does show signs of characteristic glaucomatous change, we use the term primary angle closure glaucoma. We add on that last term. Now, a quick note on the acute angle closure crisis. Patients with iridotrabecular contact with an acute rise in IOP are said to have developed an acute angle closure crisis. These patients are the classically described presentation with acute rise in intraocular pressure associated with corneal edema, mid-dilated pupil, and vascular congestion. These patients often have eye pain with headache, nausea, and vomiting. As a bit of a stickler for terminology, you likely will note that I did not use the term “acute angle closure glaucoma”. Patients who present with an acute angle closure crisis, while by definition have closed angles and increased IOP, they may or may not have actual glaucomatous optic neuropathy. And/or visual field defects associated with it. So if managed early enough and the crisis is broken, they may actually never develop glaucomatous optic neuropathy, though of course if there is delay that risk of optic nerve compromise is very, very high. Bringing us back to that summary, PACS patients have at least 180 degrees of iridotrabecular contact. However, there is no associated IOP or PAS. And certainly no optic nerve damage. PAC patients or primary angle closure patients have elevated pressures or some signs of posterior or anterior synechiae. And PACG patients have some level of associated optic neuropathy, whether that be shown through thinning of the RNFL or glaucomatous visual field defects.
Now, let’s move on to kind of part two of that assessment. And in my opinion, probably the most interesting part, which is the mechanism that is driving that angle closure. So far, we have defined angle closure based on 180 degrees of iridotrabecular contact. But what’s the cause of that angle closure? What is the eye’s — why is the eye’s physiologic drainage system closed off and not functioning correctly? So mechanism one is pupil block. So pupil block is thought to be the most common mechanism affecting — it’s estimated around 75% of patients with primary angle closure. And pupil block occurs if there’s a relative seal that forms between the iris and the lens. Trapping the aqueous right here. Behind the iris in front of the anterior capsule. So when assessing for pupil block, we look for this rounding of the iris. And specifically, this connection that connects the central iris and the anterior lens capsule. So while these patients may have peripheral shallowing, as we see over here, secondary to that bowing of the iris, they may have a fairly deep or a relatively deep central anterior chamber. Mechanism number two is lens rise. And lens rise is the phenomenon when the whole lens complex is anteriorly positioned, causing both central and peripheral anterior chamber shallowing. Formally, we define lens rise as a reduced perpendicular — so that’s this here, anterior-posteriorly — distance between the crystalline lens and the angle recess to angle recess line. So these patients typically have both peripherally and centrally shallow anterior chambers. And honestly, I think one of my favorite terms in glaucoma management is the “volcanic lens rise” that we can see in these two UBMs here. And this occurs when, again, that whole lens complex appears to have been pushed forward, typically found in smaller eyes or relatively microphthalmic eyes. So in these patients, look for that iris contour that follows the contour of the anterior lens capsule. Finally, mechanism three that we’re gonna talk about is plateau iris. And in these patients, the ciliary body behind the iris is anteriorly rotated, causing the peripheral anterior chamber to shallow. And in doing so, as a secondary result, causing the angles to close. These patients honestly are far more challenging to identify, because the central anterior chamber is pretty much always relatively deep. And so when we do our quick screens, looking for shallow anterior chamber, they often get missed. Plateau iris is the reason, in my opinion, why every patient undergoing a glaucoma assessment requires low light gonioscopy. Like so many cases in medicine, our patients are often some combination of all of these mechanisms. This anterior segment OCT here that I’m showing you shows the anterior lens positioning. So this pushed forward of the whole lens complex itself, that’s characteristic of lens rise. But also has this rounding of the pupil that, with the small connection, that does show some signs of pupil block. Now, because this is a light-based OCT, we can’t formally assess for plateau iris. The lack of imaging of the ciliary body. However, it could also very much be present. So with that staging and mechanism background, what do we do? How do we manage these patients? Depending on who you talk to, every specialist will likely give you a different way or approach of managing patients with angle closure. Some say in general start with laser peripheral iridotomy. Others say that laser is not really needed because of the low risk of actually developing glaucoma long-term. If a cataract is present, jump straight to lens extraction. My argument and overall thesis today for you is that you should treat the underlying mechanism, and that should largely drive our decision making process moving forwards. So part one of management: How can we use the mechanism to define our treatment? If the mechanism driving the angle closure is clearly pupil block, as is the case in this image here, where we see that rounding and that contact directly onto the anterior lens capsule, we can clearly see how a peripheral laser iridotomy will help alleviate this mechanism by directly relieving the impact of the relative seal between the iris and the anterior capsule of the lens. We can see that by inserting a hole right here in the peripheral iris, we can establish an equalization or an equilibrium between the anterior chamber and the sulcus space, thereby flattening out the iris and hopefully opening up that angle. So if you have pupil block, given the low risk associated with peripheral iridotomy, consider peripheral iridotomy. If the primary mechanism is lens rise, we can see that simply doing a peripheral iridotomy in the peripheral iris likely won’t resolve the actual angle closure. The underlying mechanism is not an imbalance of the pressure between the anterior chamber and the sulcus space. So simply putting in that hole in the peripheral iris will not resolve the underlying mechanism, which is this large lens, pushing everything forward. So truly, to fix or open an angle in a patient with lens rise, really the only underlying option is to consider lens extraction. When discussing the third mechanism, plateau iris, the potential to resolve this mechanism is a little bit less clear. Traditionally we spoke of using a peripheral iridotomy to help resolve any associated pupil block component. Which often honestly presents in combination with plateau iris. Followed by some sort of intervention to reduce that plateau iris configuration, which could be laser iridoplasty, for example. Now, the studies honestly aren’t completely clear, whether iridoplasty has a positive effect in the long term. And honestly, if you complete iridoplasty, there is a concern of developing long-term posterior anterior synechiae. So other options that you could consider for the management of plateau iris configuration could be using miotic agents such as pilocarpine, which could constrict the pupil, pulling this iris away from the angle, or we could consider something called endocyclophotocoaguloplasty, where we treat it with photocoagulation in order to rotate the ciliary body and help the iris to pull back the angle. Of note, ECPL can only really be done in a pseudophakic patient. So either the treatment needs to be done during cataract surgery or needs to be done after cataract surgery if you still have persistent plateau iris configuration. All right. How about the future of plateau iris configuration? So Dr. Ahmed has started doing a midperipheral pupillary cerclage. So in this picture I’m showing how he’s performing a central pupillary cerclage, but if you perform a midperipheral pupillary cerclage, you could pull the iris forward and in doing so hopefully open up the angles. Unfortunately there’s no big study to argue whether or not a midperipheral pupillary cerclage would help, but it does make sense from an anatomical standpoint. So stay tuned. Hopefully we’ll have more evidence in the future. Many of our patients have some combination of these different mechanisms, and as such, we need to determine to the best of our abilities what the dominant mechanism is, and from there, work in a stepwise approach. We must always, however, take into account the risks of treatment. If a patient is PACS, secondary to lens rise, for example, mechanism-based decision making would argue that we proceed with lens extraction. However, does that make logical sense? Should every patient with narrow angles secondary to lens rise undergo surgery to manage a condition that they may or may never actually encounter? Complicating things further, when the angle has been closed for an extended period of time, say the patient is presenting in their 80s, or 75, or 85, the trabecular meshwork itself may develop some secondary dysfunction. So that even if we are able to open up the angle with laser or cataract surgery, for example, it may not adequately manage the glaucoma. And for that reason, many of our primary angle closure patients require more intervention. We will talk a bit about this later on, so stay tuned. For that reason, let’s move on to our last section: Management based on staging. Let’s first talk about PACS. These patients have anatomical changes that put them at risk for high IOP and glaucoma. However, they have no diagnosed true pathology. If the underlying mechanism is pupil block, it seems very reasonable to consider peripheral iridotomy. Though I would encourage everyone to ensure that they’ve reviewed the results of the ZAP trial from 2019. Of the 189 people who were randomized first to laser peripheral iridotomy and observation, only 19 people reached the endpoint of either an increased pressure greater than 24 or some signs of posterior/anterior synechiae, or an angle closure glaucoma in the treatment group. And only 36 reached that endpoint in the observation group. So we’re looking really at a risk of only 4% with just observing patients with primary angle closure suspect disease. And if we do treat them with peripheral iridotomy, that risk drops from around 4% down to 2%. So as such, if a patient presents with PACS, secondary to pupil block, it’s honestly very reasonable to consider observation or laser peripheral iridotomy. Especially if there are any other risk factors, such as family history or contralateral PACG. Or kind of other things. And this is really where that conversation with the patient becomes so, so important. So how about lens rise? Given the low risk, and we talked a bit about 4%, to even just developing primary angle closure, the risk of developing primary angle closure glaucoma, necessitating lens extraction in a patient with primary angle closure suspect disease, seems to be a little bit of an overkill. To me, if there’s some underlying pupil block in my patients with large lens rise angle closure, I would certainly offer a peripheral iridotomy. But I’m really not stepping up to lens extraction for my patients with lens rise who have simply primary angle closure suspect disease. For patients with plateau iris, once again, after managing any associated pupil block component with peripheral iridotomy, you could certainly consider pilocarpine or iridoplasty, though given that the patient doesn’t really have a formal glaucomatous damage or diagnosis… Again, this type of treatment may be unnecessary. So let’s move on to that level two. The patients that are primary angle closure. To review, these patients have closed angles with either increased IOP of greater than 21 millimeters of mercury or some signs of scarring in the form of posterior/anterior synechiae. Now, here’s really where the art of medicine comes into play. So… Observation is still an option. However, I think most of us would probably be willing to offer some sort of treatment, given the higher risk of progression to true glaucomatous damage. So patients with pupil block that are primary angle closure, whether there would be a little bit higher increased IOP, I would be quicker to recommend peripheral iridotomy as a part of a management plan. You doing or completing peripheral iridotomy in a patient with PAS — it’s not going to open or remove the existing scar tissue. However, the hope is by equilibrating the dynamics in the anterior chamber relative to the sulcus space, you can still help open the remaining areas that are not scarred down. Patients with lens rise are a bit more challenging. If they have a pupil block component, once again, definitely consider a PI. However, jumping straight to lens extraction or cataract surgery for a patient that has, let’s say, a pressure of just 22 millimeters of mercury, still seems a little bit aggressive in my view. So we can use the EAGLE study that has been summarized here by a great infographic created by Fang et al., however, in order to be included in the EAGLE study in patients with primary angle closure, they didn’t just need IOP or pressure of 21 millimeters of mercury that we use in our diagnosis. They needed a pressure of 30 millimeters of mercury. So… That cutoff is much higher than we use really to determine normal versus high IOP in our daily practice. So clearly jumping to lens extraction, it’s a step higher, I have to admit, even for me. If they have clear indication of cataract, that’s a clear reason to go to lens extraction. If they don’t have indication of cataract and their pressures are 23, 24, 25, I’m more likely to treat them to drops, and look out into the future. Whether it be pressure-based posterior or anterior synechiae, my pressure to do cataract surgery in them is undoubtedly lower than my patients with open angles. For my patients with plateau iris, once again, after imaging, like lens rise, consider proceeding with lens extraction with some sort of laser to help open or rotate the iris. But like our previous lens rise case… If the pressure is relatively low, again, by definition, there’s no specific signs of glaucomatous optic neuropathy, it would be reasonable to proceed with drops, as a bridge to lens extraction, in the not too distant future. Finally, let’s go to primary angle closure glaucoma. For me, all the options we’ve talked about today are all a consideration. If a patient has true primary angle closure glaucoma, meaning some sort of optic neuropathy, whether thinning of the RNFL or visual field defects, this should be offered as first line treatment. It’s pupil block, plan for PI. With the exception that if they’re planning on lens extraction, a PI may not be necessary. If it’s lens rise, I’m pretty much planning on lens extraction. Especially if it is surgical and there is surgical intervention at this point, I think the benefits of preventing the progression of glaucoma outweigh the risk of lens-based surgery at that time. If the patient is plateau iris, I’m likely considering lens extraction and combination endocyclophotocoagulation. Now, if the angle has been closed for an extended period of time, the patient may develop a secondary trabecular meshwork dysfunction. In these cases, I have a low threshold to even add on a combined minimally invasive glaucoma surgical procedure. Typically something of angle origin. And often I step up to a gonioscopy-assisted transluminal trabeculotomy, described by Davinder Grover and the Texas Associates. It’s a really good procedure that works synergistically with the cataract surgery itself and helps to open up the drainage system as well as open up the angles and approach to the angles. Only rarely will I consider stepping up to a combined filtering procedure, whether that be an anterior bleb surgery like trabeculectomy or pressure flow or a Zen or a posterior bleb surgery such as a tube shunt. It’s really only in the very, very elderly patients that present with very, very high pressures that I will consider doing a combined cataract surgery with a filtering surgery in patients with primary angle closure glaucoma. And really it’s only in the patients where the last thing I would want would be to go back to the operating room in the future. So if I want something truly definitive, I’m really looking to a tube shunt surgery in combination with cataract surgery. But again, I only step up to combine cataract with filtering surgery in my PACG patients in very rare circumstances. So let’s get on to questions and polls to see where all of us are at. So… Case number one. A patient with primary angle closure suspect with lens rise and some pupil block. So why don’t we open up that poll to the group? And let’s see what people think. For that, I’ll give you a couple seconds to answer the poll, and we’ll see where that takes us. Awesome. And we’ll give you again just a few more seconds to put in your choices there. Awesome. So we’re hearing again the biggest kind of option here that we’ve seen is 50% of patients are considering peripheral iridotomy. Some are considering… A small proportion considering lens extraction. So honestly, my counseling of PACS patients really focuses on what the patient’s risk tolerance is. If they want to do whatever they can to really prevent glaucoma, I’ll likely recommend a peripheral iridotomy, similar to what 50% of the group said today. If they are more adverse to intervention, given honestly that low risk of progression — it’s only about 4% — to primary angle closure, I think observation is honestly very reasonable for them. For those that kind of went in the direction of lens extraction, I think that’s also a reasonable choice, especially if they have a coexisting cataract. In which case: Do the cataract surgery and their angles automatically open up and you’ve managed their cataract as well as their angle closure. So very reasonable choice. We’ll move on to case number two. A patient with primary angle closure with a slightly high pressure, just of 22 millimeters of mercury, with what appears to have a plateau iris configuration as well as some pupil block. Once again, let’s open up the polls and see what the group thinks. And again, we’ll give you a bit more time there. And let’s see what people said. Again, this one is a little bit more varied. 37% of participants recommended peripheral iridotomy. 31% pilocarpine. And down to 9% just for observation. For this, again, I think all of these options would be reasonable, depending on the patient’s risk tolerance. I have to say with that rising pressure, I’m likely heading away from observation and moving towards peripheral iridotomy to start. And if the pressure still is high or persists after that, probably pilocarpine, again, if the pressure remains high. But if there was an existing cataract, there would be a reason to proceed with lens extraction, but I’m probably not heading to lens-based surgery just for the management of plateau iris given that there is no true glaucoma at this point in time quite yet. So… Final case. A patient with primary angle closure glaucoma has a pressure of about 35 millimeters of mercury. We can see the mechanism is lens rise. But there’s no existing cataract. And there is moderate visual field changes. So what would be our options? Again, choosing with these various cases here. We’ll just give you a bit longer here. All right. So consensus here is 42% went in the direction of lens extraction. 30% in the direction of peripheral iridotomy. Some in combining with ECPL and some with peripheral iridotomy. So in this mechanism… Given that the underlying pathology really is that lens rise… I’m definitely heading towards the direction of lens extraction. If there was any component that was plateau iris in nature, I would certainly consider doing an ECPL. Though in this case presentation, we don’t specifically outline it. It’s these cases where, if the pressure was 45 or the patient was on multiple drops and the pressure was still 45 with acetazolamide, for example, here you could also consider an attached angle procedure. But once again, proceeding with lens extraction I think is probably the initial point, if we really want to use a mechanism-based decision making process for the management of angle closure. So with that, in conclusion, in the world of primary angle closure disease, we have primary angle closure suspects who have an anatomy with closed angles. We have primary angle closure patients who develop some increased IOP or scar tissue. And finally, primary angle closure glaucoma, who have an associated glaucomatous optic neuropathy or characteristic visual field defect. Our treatment should be based on the underlying mechanism. So whether that is laser peripheral iridotomy for the management of pupil block, lens extraction for the management of lens rise, or miotic agents, or endocyclophotocoaguloplasty with hopes of rotating that iris. The decision to proceed with intervention, however, should be based on a risk analysis that’s specific to the patient. Where suspect patients should consider laser intervention, glaucomatous patients should consider incisional lens extraction, with or without additional angle surgery. So thank you so much for the opportunity to present with all of you today. I’m happy to open up some questions. So we’ll stop sharing here, and I’ll go through some of the questions that people have submitted. All right. So… First question here is: In cases of PACS or PAC with cataract, do you recommend YAG iridotomy before cataract surgery? The answer to this question for me really depends on how soon you’re planning the cataract surgery. If the patient is likely going for cataract surgery in a very, very short term, so we’re talking in the order of a number of weeks or small number of months, I don’t think a YAG peripheral iridotomy is likely necessary. However, if you’re waiting for cataract surgery, which is going to be in the order of months to years, then certainly I would consider a YAG iridotomy and subsequently move to lens extraction and using that iridotomy kind of as a bridge to lens extraction. All right. Second question. How much the drop of IOP after an uneventful lens extraction? Great question. So studies have clearly shown that lens extraction in and of itself, even in open-angle mechanisms, not just in angle closure mechanisms, are associated with a decrease in IOP. You could probably expect a change of about 2 to 3 millimeters of mercury. You probably can’t expect much greater than that in open-angle mechanisms. In angle closure mechanisms, you can even honestly… The impact of just lens extraction with lens rise-based mechanisms can be… Incredibly high. 10, 15 millimeters of mercury of a drop in patients with just lens extraction, if they had a phacomorphic lens or high IOP that raised suddenly in an angle closure crisis. Next question: Which segment of the anterior segment OCT system do you use for angle measurement? Great question. Specifically, in terms of actually measuring the angle, I actually typically don’t use the anterior segment OCT to formally measure that angle in a certain number of degrees. I’m really looking at what the contour of the angle and the iris is. Because that, I find, is more valuable in determining the underlying mechanism. And in a lot of cases, especially the Zeiss-based machines, for example, a lot of that information has to be manually added in. You have to define what a scleral spur is. You have to define where different landmarks are. So I typically actually look for a general contour and say: Is it generally open? Generally closed? And use my gonioscopy to really make that final assessment. All right. Next question. What is the importance of central corneal thickness in vulnerable patients to angle closure? Central corneal thickness is obviously a very important part of the general glaucoma assessment. It has formally been proven… So a thinning of the central corneal thickness of less than 540 micrometers has been shown to predict… Both the diagnosis of glaucoma and glaucomatous progression, specifically in hypertensive patients and open-angle patients. I’m sure there are studies that have looked at the role of CCT in angle closure patients. However, I’m not specifically knowledgeable of them here. But the initial studies that really put forth the CCT were focused primarily on open-angle patients, not specifically angle closure patients. Okay. Could you please show one more time how we define the lens rise on UBM? Okay. What we’ll do is I will just come back to that afterwards. But my best recommendation honestly is actually to search on kind of Google images. There are some incredibly measurements on how to look at the anterior-posterior distance of the… When you measure from the posterior cornea to the angle recess lines. And if it takes up… If the lens is making up greater than 2/3 of that space, that’s really your definition of lens rise. But there are some fantastic review papers that look at both the formal definition and measurement of lens rise, but also what we call lens vault. Which is an associated measurement that can help us determine lens rise. Is PACG due to lens rise the same as phacomorphic glaucoma? Great question. I asked my mentors this when I started my fellowship, because I had a hard time delineating the two, and honestly, in my practice, I put them together. I think primary angle closure glaucoma in a patient with phacomorphic glaucoma — it’s honestly just a large lens in the setting of glaucoma. To me, the management is the same. If someone has phacomorphic glaucoma, the answer for me is lens extraction. Peripheral anterior synechiae will cause angle closure glaucoma? The question here is whether peripheral anterior synechiae will in itself cause angle closure glaucoma. The answer to that is probably not directly. The underlying mechanism that’s causing the creation of the peripheral anterior synechiae probably indicates a likelihood or predisposition to angle closure. And as such, the underlying risk stratification probably suggests that they are at risk for developing glaucoma in the future. So the PAS itself does not define the glaucoma. It’s really the glaucomatous neuropathy — but the fact that you have the anterior synechiae and the scar tissue does suggest that they’re at high risk of developing angle closure in the future. Next question is: Is there any rule for iStent in lens rise-related cataract surgery for PACG? As I mentioned before, patients who have developed angle closure glaucoma, meaning they have developed an optic neuropathy or visual field changes in the setting of angle closure… I do think there is some role for angle-based surgeries like iStent or a gonioscopy-assisted transluminal trabeculotomy, what I had referenced before. Is that the primary intervention? No. I do think the primary intervention is likely… If the underlying mechanism is lens rise… Is probably the lens extraction itself. However, if the patient is elderly and have had closed angles for an extended period of time, which would be consistent with already having developed the glaucoma itself, there likely is a role for trabecular meshwork treatment in the form of angle surgery, whether that be in the form of an iStent or a gonioscopy-assisted transluminal trabeculotomy. All right. Great. So the next question really is to say that there is some argument that most patients have some sort of combined mechanism glaucoma. Where it’s both some angle closure mechanism and some underlying open-angle mechanism as well. And the question is whether or not… How do we prioritize? How do we determine what would be our first course of action? Is it drops like we would in the case of open-angle glaucoma? Or is it… The more interventional approach of opening up the angles with laser peripheral iridotomy or lens extraction? There’s also a combined angle closure mechanism. And for here, I actually go down to the semantics of the situation. In order to diagnose someone with open-angle glaucoma or an underlying trabecular meshwork dysfunction, they must have by definition open angles. I would say… Without question, if I had a patient that I think or feel has both open-angle or closed-angle components, my first priority is actually to fix the closed-angle component. Once we open up the angles, then we can start working on helping those angles to drain better, whether that be increased drainage systems with prostaglandins, or if that’s gonna be treatments with filtering surgery. So if we are concerned about an open and a closed-angle component, I manage the closed-angle first, and then if they still have persistent glaucoma, they become by definition a combined mechanism glaucoma, and for that reason, would start treating the open-angle component. All right. So… Second question is… In the cases of chronic angle closure glaucoma or primary angle closure glaucoma, if the pressure is high with glaucoma drops, would you first go with lens extraction or filtering surgery to stabilize the IOP first? Really looking at a mechanism-based approach. If the IOP is very high, we’re thinking for example angle closure crisis, the patient comes in, 65 years old, pressure of 55, you use drops, the pressure comes down to maybe 40, do you want to go to filtering surgery to create a new drainage system? Or do you want to go with lens-based… Lens extraction… For me, the answer is always lens extraction. If it’s chronic angle closure, open up the angles. Manage the angles first. And leave filtering surgery, whether that be in the form of trabeculectomy, other filtering surgeries, tube shunts, leave that for the future. All right. Do you still… So next question is… Is there a comparative study assessing the effectiveness of iridoplasty and iridotomy in the setting of plateau iris? This is a great question that really again comes down to the diagnosis and definition of plateau iris. So we speak of two different terms. Plateau iris configuration and plateau iris syndrome. Plateau iris configuration is when we have that anterior rotation of the ciliary body, associated with closed angles. And plateau iris syndrome is when we have again that same anteriorization of the ciliary body with closed angles. However, the patient has undergone a peripheral iridotomy. And the reason why we make that differentiation between plateau iris configuration and the syndrome is that the syndrome can only persist, assuming we’ve gotten rid of the pupillary block component. So is there a comparative study? Probably not. Because if a patient is truly diagnosed with plateau iris syndrome, they will have necessarily undergone a peripheral iridotomy, in order to ensure that we’ve gotten rid of the pupil block component. Okay. So a question is… If we don’t have access to UBM or OCTs or lasers, and really you’re doing assessments based on gonioscopy, what is really the highest pressure that you would do a manual peripheral iridotomy in order to manage an acute angle closure crisis? So if someone is in an acute angle closure crisis, and you don’t have access to a YAG peripheral iridotomy, a surgical iridectomy is very reasonable. If their pressures aren’t managed on drops, let’s say… Even to 25 to 30, I think it would be very reasonable to consider a surgical mechanical iridectomy. Because that actually helps to at least stabilize the sulcus, the pressure differentiation, between the sulcus and the anterior chamber. But once again, if they do have an underlying acute angle closure crisis, often these cases present because the patient has lens rise. So really the question is not necessarily are you heading to a manual PI, but for me is: Are they heading to lens extraction? So if you can complete lens extraction in a safe fashion there, that’s the direction that typically I am heading in, in those situations. What are the measures of deciding to restart antiglaucoma medications? This has to do with… Once you managed the mechanism, if the patient’s pressure is still elevated, when do you want to start antiglaucoma medications? It depends on the staging of the glaucoma. So in all of my patients, once I’ve figured out that mechanism, I’ve managed the mechanism, and I’ve determined… They have advanced angle closure glaucoma, I’m gonna do whatever it takes, once I’ve gotten rid of that lens rise or plateau iris configuration, I’m gonna do whatever it takes to get that pressure down to the low teens. So whether that means filtering surgery or that means starting off on drops, whether they be alpha agonists, beta blockers, carbonic anhydrase inhibitors, prostaglandins, when to restart antiglaucoma medications? It depends on the staging. If they’re advanced, anything above 12 to 13, moderate level glaucoma, anything above 15, 16 millimeters of mercury, and if they’re mild glaucoma or preparametric, anything above 19 or 20, if they’re just primary angle closure, meaning they don’t have specific glaucomatous optic neuropathy, anything above 21, I’ll start using antiglaucoma medications. Next question is: What is the role of goniosynechialysis during the presence of posterior anterior synechiae? Good question. It plays a very large role. I would say in all patients that have posterior anterior synechiae that are undergoing lens extraction — please complete a goniosynechialysis. It’s important to alleviate that scar tissue. The hope is, if you alleviate the scar tissue, open up the angles, you can help resurrect the existing drainage system. If you don’t, it may never open and you may be heading in the direction of filtering surgery. So if you can do a goniosynechialysis during cataract surgery, definitely, definitely consider it. For a lot of these patients, when you’re doing cataract surgery, by virtue of opening up… Even with OVD or viscoelastic, that is often enough to open up and release that scar tissue. So… Next question is: In a patient with phacomorphic glaucoma, do we decrease the pressure with mannitol, or just go straight to lens extraction? I try not to do surgery in an acute or emergent setting. The stress level of the situation is quite high. So I do whatever I can to help reduce the pressure symptomatically in the immediate short-term. Whether that means mannitol, acetazolamide, neptazane, I try to use systemic medications to reduce the pressure. I don’t think that a peripheral iridotomy is going to do very much in a patient with phacomorphic glaucoma. However, mannitol and acetazolamide are very reasonable as dehydrating agents to reduce the pressure as a bridge directly to lens extraction. So for phacomorphic glaucoma, patients with large lenses in a lens rise case, I’m really heading to lens extraction. All right. So… Question here is which medications can increase the risk of PAC as a side effect? For example, certain psychiatric medications. Really anything that has anticholinergic side effects. Any sympathomimetic medication associated with dilation and therefore anterior placement of the lens complex. So really there are so, so many. And when we talked a bit about the PACS patients, the patient that doesn’t have truly diagnosed glaucoma, if they are taking psychiatric medications or if they, for example, have ongoing allergies and need to take sympathomimetic medications, my threshold to do that peripheral iridotomy is a little bit lower. If you need be dilated regularly for diabetes checks or you’re on these medications, more of a reason to undergo a peripheral iridotomy to help prevent an acute angle closure crisis in the future. What is your preferred management of malignant glaucoma? Medical or surgical? The studies have shown that 50% of malignant glaucoma cases can be managed medically. Plus or minus in some cases with laser. So for me, my preferred method for malignant glaucoma is really to actually start off with cycloplegia and mydriatic drops, so I use atropine to push the whole complex backwards. If that doesn’t work, I’ll start off with a YAG — not iridotomy, but a hyaloidoiridozonulotomy, to make a connection through the iris, through the zonules, and the capsular bag. These patients have to be pseudophakic at this point. To help equilibrate the pressures in the anterior segment as well as the posterior segment. If that fails, I absolutely will resort to surgical intervention, which typically involves, again, doing an iridozonulohyaloidotomy, to equilibrate the pressure dynamic in the front and the back of the eye. All right. What is the upper limit of IOP that is safe for uneventful lens extraction in the cases of angle closure glaucoma? So… Really this kind of… I think stems largely from what your comfort level is and experience with angle-based procedures. If the pressure… A patient has a pressure of 35, even 40, I would consider doing just lens-based extraction without any attached filtering surgery or any attached angle surgery. And you would be surprised how much the pressure drops once you take that lens out. So upper limit of IOP that’s safe — probably in the 40s would be my general go-to. However, it really depends, again, on your comfort level for the procedures itself. What is the role of GATT procedures in treating patients with angle closure glaucoma? If a patient is coming in with moderate primary angle closure glaucoma, my primary treatment is still the lens extraction, but I would absolutely add on some sort of angle procedure such as a GATT. I’m seeing here… I think I’ve answered the majority of our questions here. I see one here. How do you manage PAS due to uveitis? Great question. Secondary to uveitic glaucoma… Different beast, compared to primary angle closure glaucoma. However, peripheral iridotomy can be considered, if there is posterior synechiae. But if we’re talking about posterior-anterior synechiae, where it really is affecting the angle, I’m not sure how much a peripheral iridotomy is really gonna do to open things up, because really the inflammation is what has caused the scar tissue. If you want to prevent the patient going to lens extraction and goniosynechialysis, it’s possible to try it, but that’s not the mechanism driving the synechiae with associated PAS. With that… I think those are all the questions. So with that, thank you again so much for attending this session, and thank you to Orbis and the Cybersight team for inviting me. It’s been an absolute honor and pleasure having the opportunity to speak to you about the management of primary angle closure! Take care, everyone, and have a great day.
1 thought on “Lecture: Management of Angle Closure”
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