Lecture: Angle Closure: A Global Issue

DR. PILTZ-SEYMOUR: It is such a pleasure to be here today joining you all across the globe. We have participants here from every continent and every hemisphere. So, it’s just such an honor and a privilege to be here today. I’m gonna just share my screen and then we can get started right away on this very, very important topic. Good. So, today we’re gonna be talking about primary angle closure glaucoma and why it is such an important problem across the globe. Get my screen to move forward… the screen is not advancing. There we go. And let’s start with a question. What type of glaucoma causes the most blindness in China? Primary open angle glaucoma, primary angle closure glaucoma, pseudoexfoliation glaucoma or normal tension glaucoma? And we’ll give just a moment for people to answer that question. And let’s see the results. So, yes. We got 66% of participants wrote primary angle closure glaucoma. And that is true. It may not be the most common form of glaucoma, but it causes the most blindness. And this is why this lecture is so important and why understanding angle closure glaucoma is so important. I’m having trouble advancing my slides. Okay. This is weird. Anyway. Angle closure glaucoma — causes a disproportion that the amount of visual disability. Much higher proportion of patient — here we go. Let’s see if it will work now. Andrew, if you run the slides would that be better? I don’t know why my slides aren’t advancing. Well here, let’s see how it goes for a moment. A much higher proportion of patients with primary angle closure glaucoma are blind compared to normal glaucoma. Half the patients with primary angle closure glaucoma are blind in one eye. In China, 35% of glaucoma cases are primary angle closure, but 91% of the bases of bilateral blindness. It develops into a much more severe glaucoma than open angle glaucoma. And the problem is, globally, the prevalence of angle closure glaucoma is going to increase significantly in the coming days. And why is that? So, back in 2013, we had about 64 million people worldwide with glaucoma and about 44 million from primary opening an and will 20 million from angle closure. So, a two-thirds, one-third split. And what’s to notice here is that while there’s 20 million people worldwide, three quarters of those were in Asia. So, Asia is going to have a disproportionate burden of blindness from angle closure glaucoma. And we can see the projections for population growth over the coming decades that by 2050, population is going to more than double compared to 2010. And that burden is going to be felt, that greatest increase is going to be felt mostly in — great — most significantly in Asia. And — >> Dr. Piltz, if it’s okay, I can run your slides, yes. DR. PILTZ-SEYMOUR: I have no idea why they’re doing this. >> Of course, feel free to stop screen and I will share your slides on your behalf. DR. PLITZ-SEYMOUR: Thank you so much. I’ll just say “Next slide.” So, we’re about slide 9. Good. And if we could get it, yeah, that’s great. Perfect. So, and now we can see the projections for glaucoma worldwide so we — I had mentioned that there were 64 million people in 2013, and 76 million in the 2020s and it’s projected by 2040 that there’s gonna be over 100 million people with glaucoma worldwide. Next slide, please. Next slide, please. And that greatest increase is going to be felt most heavily in Asia. Next slide. But angle closure glaucoma is felt all across the world. In fact, the Inuit of the Canadian Arctic in Greenland has the shallowest anterior chamber depths of awful population, and the prevalence of angle closure glaucoma is almost 3% there, and almost 5% of the adult population have primary angle closure glaucoma in Greenland. Next slide. And I think also, that primary angle closure glaucoma is vastly underappreciated in other populations. A study done in northern Italy found that narrow angles and primary closure glaucoma were much more frequent in whites than previously studied. And primary angle closure glaucoma accounted for more than a quarter of all glaucomas. And two-thirds of those — and this is really important — were chronic angle-closure glaucoma without a prior attack. These weren’t people that presented with angle closure. That presented with acute angle closure. These were slow, in single use angle closures. And we will talk about the differences of angle closure glaucoma. Next slide. Just an overview, we’re going to talk about the etiologies, the stages and then the clinical presentations and what to do from there. Next slide. So, primary angle closure glaucoma is either from a pupil block or non-pupil block. What is pupil block? Pupil block is an impedance of flow of aqueous from where it’s formed in the posterior chamber in the iris to the anterior chamber. The iris is causing a little bit of resistance between the iris and the lens, and is in the chamber, bows that forward and that can cause angle closure. This is most commonly when the anterior chambers are shallow. Next slide. Things that make the pupil dilate and then when the dilation starts to go back, starts to reverse, people can go into pupil blockage. It’s usually not during the dilation process. It’s usually when the dilation starts to diminish that the iris gets stuck on the lens and cause this is resistance. So, it can happen from pharmacologic pew Pi lair dilation, we can cause it. In dim illusion make, from medications, stress, from trauma can make our pupils dilate, intense concentration and illness. Next slide. And it’s very important to remember that laser iridotomy only treats pupil block. It doesn’t treat other forms of angle closure glaucoma. I’ve seen people with neovascular — treated with laser iridotomy, it doesn’t make sense. It only treats pupil block and only when there’s not already synechial closure. If you had an angle closure attack and the angle is already zipped up from synechia, it’s probably not going to undo the angle closure issue. You may need to do the iridotomy, but it’s only going to treat non-synechial angle closure from non-pupil block. Next slide, please. And keep going, next. When do we use a laser iridotomy? For treatment of pupil block, next. For the treatment of angle closure where you’re not sure if it’s pupil block or not. And that’s something if you see something that’s like plateau iris, which we’ll speak about, malignant glaucoma or iris cysts like in the picture, if you’re not sure if it’s pupil block, you can do a laser iridotomy. And next slide. Prevention of pupil block in high-risk eyes. If one eye has had an attack of glaucoma, you need to tweet the other eye. But laser iridotomy is not always a cure-all. It’s very, very important and can really save vision. But it’s not always a cure-all. After iridotomy, this study found that many eyes, by Quigley, anatomical dysfunction, there’s a plateau, increased tendency for choroidal and slow vitreous through the eyes. And there can be residual angle closure glaucoma. In this study of 134 eyes, two-thirds had some app positional angle closure after iridotomy, and the vast majority were plateau iris. Let’s talk for a moment about plateau iris. Next slide. Plateau iris is when you have large, bulky anterior ciliary processes that sit behind the iris and it pushes the peripheral iris up. So, the iris rooting angulates steeply in the periphery, but then the iris is flat. As opposed to pew pile block, the whole iris bows, but you go with your lens and look in the periphery and it’s steep and closing the angle as we see in B over here. So, A is a pupil block mechanism in this picture, and B a plateau iris. It happens more commonly in women. It can happen with any refractive error. One day a pediatrician came to see me. He was a minus 8 in both eyes and he was in bilateral angle closure glaucoma. And from plateau iris. Peripheral iris crowds the angle and it can worsen with dilation. Next. And good. And here you can see a schematic up at the top. And there you can see that same illustration with a UBM. You can see how that peripheral iris is smashed right up against the angle and then the iris comes down straight. Next. So, plateau iris is often diagnosed after the iridotomy fails to deepen the angle. But it’s very common to have plateau iris with a component of pupil block. So, even if you’re suspecting plateau iris, you should do an iridotomy. And it’s the height of the plateau and the tightness of that plateau, how tight it is to the angle, that really dictates the risk of angle closure. If you have just a short plateau that will only cover the scleral spur, you’re not in trouble, but if it’s steep and covers the mesh work when closed, that’s going to lead to glaucoma. You can see that people with plateau iris get a double hump. As you dissent the lens, it humps over the processes and dips down and humps again over the lens. And we’ll have a nice illustration later in the talk. We treat hump with miotics, it pulls it away from the peripheral angle. Some strongly recommend peripheral laser iridoplasty, and cataract surgery typically can be beneficial. Next slide. But as I mentioned, there can be interaction between pupil block and plateau iris in just a big lens, phacomorphic. Next slide. So, what are the stages? So, these are the internationally accepted definitions of angle closure. Primary angle closure glaucoma suspect is basically your narrow angle that — a worrisome narrow angle. These patients have appositional closure for more tan 180 degrees, no actual glaucoma, but just a little bit of risk because of the narrowness and the apposition. Primary angle closure is when you have this appositional closure, but now you have either elevated interocular pressure or peripheral anterior synechiae, that’s one of the first signs of initial primary angle closure. There’s no damage, the disk in the fields is normal. Primary angle closure glaucoma is when you have this appositional closure and then pressure is elevated and you have glaucomatous optic nerve changes. Next. Those are the stages. But patients don’t walk in and say, I have this stage. How do patients present? There’s the pre-glaucoma stage, either your primary angle closure glaucoma suspect or your primary angle closure where you have changes like elevated pressure or PAS, but no glaucoma damage yet. Next. Oh, here’s another question. The most common presentation for angle closure glaucoma is acute angle closure with sudden pain, redness, and decreased vision. True or false? And the results? So, this is very important for us to discuss now. Because the most common form of angle closure glaucoma is not acute angle closure glaucoma. It is a more sub-acute or chronic form. Okay. We can close this and move to the next slide. So, let’s talk for a minute about acute angle closure. But then we’re going to move on and look at other presentations. Next slide. So, this is the one we’re most familiar with. This is the type of angle closure glaucoma that you’re most likely not going to mis-diagnose. Because it’s such a notable presentation. People come in and they’re in distress. They have a sudden onset of headaches, they have eye pain, blurred vision, they’re nauseous, they’re vomiting. The only times I’ve seen it misdiagnosed, and I saw it misdiagnosed twice when I was a resident, so going back a few years. One, a patient was admitted, she was so sick and vomiting that she was admitted for vomiting and dehydration and couldn’t ever localize it to her eye. But that’s where it’s coming from. Another patient had cardiac instability and was in the cardiac care unit when we realized it was coming from his angle closure. But most of the time, these people come in, ow, I’m in pain, my eye hurts, it’s red. They’re really in distress. Next slide. And when you look at them, the pleasure’s high, there’s cornual edema, the eye is red. Their vision is decreased. And their pupil is fixed in mid- dilation with peripheral bowing of the iris. May be vasovagal, brachycardia, may be sweating. Next slide. Later on, you may see Glaukomflecken, not at the time, that’s the spots in the anterior lens, those are signs of prior attacks. And gonioscopy during the attack is difficult. The eye is cloudy. If you’re curious if there’s angles, you can check the other eye. But it’s usually pretty apparent. How do you treat laser — how do you treat acute angle closure glaucoma? You want to lower the pressure and you want to break the block. So, you can give medications to lower the pressure, you can use antidepressants, anti-hyperosmotics if you today to. And the thing to do is iridotomy as quickly as you can. If it’s steamy, treat it medically. Give medicines like aqueous suppressants or inhibitors to lower the pressure and clear the cornea. If you can’t see well and you can’t get the pleasure down, there’s a 30 gauge needle paracentesis that can really be helpful. You’ll need to do this rarely, but it’s a good technique to know. If you have access to 30 gauge needles, you take it — no syringe. Just leave it as an empty hub. And you just put that in the eye and through that 30 gauge, the eye will just slowly decompress. Certainly Betadine the eye first and then you just slide it in. It’s gonna be a little difficult because the iris is right up against the cornea. But if you can slide it in gently, that can really help you if you have a very refractory case of angle closure glaucoma. But I see a lot of people treat medically for a while before they do the iridotomy. For me, as soon as I can do that iridotomy, as soon as my cornea is clear enough, I will do that iridotomy. But you try to break the block medically with pilocarpine and lower the pressure with suppressants. Next slide. Next, please. So, but very important is most angle closure is not acute angle closure. Even back in 1993Wilensky noticed that non-acute angle closure was more than twice as common as acute angle closure and foster in multiple publications found that 80% of primary angle closure glaucoma occurs with an acute attack. If you’re waiting for people to come in with an acute attack, you’re going to miss the vast majority of primary angle closure glaucoma. So, how do people present with angle closure glaucoma if they’re not presenting with an acute attack? Next slide. So, there’s two ways. Either this subacute intermittent form and then we’ll see what chronic angle closure is. Next slide. So, the subacute intermittent angle closure is the most important presentation to recognize. Because when people present here, you have the opportunity as a physician to change the course of their life. So, you couldn’t be a person that doesn’t have glaucoma or you can be a person that has severe chronic angle closure glaucoma. And this subacute is the intermediate stage between not having glaucoma and having glaucoma for the rest of your life. Patients who have this subacute intermittent presentation, it’s important to recognize it. You can treat it and prevent them from having bad glaucoma for the rest of their life. What is it? Sometimes in patients the angle open and closes spontaneously. There can be transient pressure, they can have pupil block and iris, and they interact. The eyes look normal between attacks except if you do conoscope. The way to find people is to do gonioscopy. They will tell you a story. It’s important to recognize the people at severe risk. These people can develop extensive PAS or chronic angle closure or acute. Next slide. Next, please. Yeah. Something is strange about the slides. If we can go back one. So, symptoms may be mild. They may actually be absent. The patients can’t always tell you a story. Or they can be severe. Sometimes they’re associated with fatigue or dim illumination or reading, near work. And it often recurs with similar circumstances at a similar time of day. When you see a patient with narrow angles, ask them, do you have headaches? Oh, yeah. I have a long history of migraines. Because everyone with subacute angle closure glaucoma is either self-diagnosed or has been told they have migraines. Tell me about your migraines? Are they one-sided? No. Sometimes. But I get them every day at 4:00, I’m at my desk and I’m working. And all of a sudden I get this headache and if I close my eyes and relax, it goes away. That is a very, very classic story of subacute angle closure glaucoma. Often at the same time of day and goes away with a little rest. And after the attacks break, they may have a teeny bit of cell. They come in the next day and look at them, you have iritis, and the pressure can be low from the cellular reaction. You can often misdiagnosis them. Very important to listen to their story. Next slide. They can be — some of the symptoms can be headache or a dull ache. They can maybe have even mild, blurred vision. Occasionally halos. Decreases with sleep or rest. Often resolves within 30 minutes and as I mentioned, it often recurs at the same time of day. Next slide. But eventually, if people keep having these attacks, the pressure is gonna become permanently elevated as they develop synechial angle closure. First it closes and opens, closes and opens. And eventually it’s going to start to get P a (S and start to synechially close and then you have chronic angle closure glaucoma for the rest of your life. Often misdiagnosed as migraine, iritis. And delay in diagnose. I have had patients see multiple doctors before a correct diagnosis is made. And unfortunately, the diagnosis is usually not made until they have — angle closure with permanent elevation of intraocular pressures. So, we have an opportunity to prevent people from having chronic angle closure glaucoma if we gonioscope people and listen to their stories. Next slide. And I’ll tell you the story of a patient that I saw. It’s going back a few years. But she was at that time a 50-year-old white woman. She had a 9 year history of intractable headaches. Worse on the left side. And for the last 3 years, her headaches were associated with foggy vision that lasts to 10 minutes and resolved spontaneously. And she was diagnosed with migraine headaches. Erroneously diagnosed. Next slide. She was seen by medical doctors. She saw a neurologist. She saw an ophthalmologist intermittently who found normal pressures and never did gonioscopy and wrote normal DMVP, normal disc macular vessels periphery — you wouldn’t. It wasn’t an examination. After 9 years, finally sent to a neuro ophthalmologist. But by that time she had high pressures in her left eye. For 9 years, her story, and her exam if it had properly been done was trying to tell the doctors that I have intermittent angle closure glaucoma. Next slide. And when I saw her, her vision was 20/20 in both sighs. She had an APD on her left eye, pressures of 19 and 33, very narrow on the left side and already closed for 270 degrees on the left side. Next slide. And these are her optic nerve photos. You can see super healthy right optic nerve on the bottom. And up on the top, you can see how much larger the cup is than on the right eye. So, .8 or more. With intact rim for the most part. But quite a bit of cupping in comparison to the right. Next slide. So, this patient had a long history of symptomatic, sub acute angle closure glaucoma. She had marked optic nerve damage on her left side with a defect and permanent synechial angle closure. But unfortunately, the diagnose was only made after high pressure was noted. There were so many missed opportunities in this patient. Next slide. LPIs — laser iridotomies were performed and she was stable for 4 years on topical therapy. But she wound up needing a trabeculectomy on that left side. When you have 270 degrees of synechial closure, you’re not going to be able to manage that medically. Next slide. So, ideally, subacute angle closure glaucoma should be diagnosed before chronic angle closure with permanent elevation of pressure. Even if they didn’t do gonioscopy, they should have seen that the nerve was changing. It’s important to listen to historical. It’s important to us this subacute angle closure glaucoma into your differential. These are the people you can help the most. These are your high-risk people. Next slide. And we did a small study. We identified 11 patients with a chief complaint of headache who were later diagnosed with subacute angle closure glaucoma and whose headaches resolved with laser iridotomies. These were 11 patients with a presentation of subacute angle closure glaucoma. They were on average about 54 years old. They had more than a 2.5 year average delay in diagnosis. and they had headaches twice a day, most daily. And few other visual symptoms. The main complaint was headache. Any person with headache you have to do gonioscopy. Next slide. All patient HHS-wide prior medical evaluations. They had seen physicians and neurologists and neuro ophthalmologists and none correctly diagnosed. Six ophthalmologists and only one performed gonioscopy. At least they tried, but they didn’t realize the patient had narrow angles. Do gonioscopy and get good at it to know what you’re looking at. Five had narrow imaging. Next slide. And interestingly, only five patients were hyperopic. Don’t reserve your gonioscopy only for hyperopic patients. We need to gonioscope everybody. Gonioscopy revealed narrow, occludable angles in all patients. Six patients had peripheral synechia. Next slide. Next slide. All patients had marked improvement of their headaches with iridotomy. But six patients already had optic nerve damage, three patients had glaucomatous visual field loss. And the patients had the headache duration until they were diagnosed. Those patients without glaucoma damage yet only had the headaches for a year and a. Those with nerve changes were 3.6 years, and those with glaucoma optic nerve and visual field defects had headaches for almost five years before they were diagnosed. Next slide. So, this subacute presentation is the privilege between a benign primary angle closure and primary angle closure glaucoma. It’s that middle place where you have your high-risk patients and those are the patients you want to find. Because you could change the course of their life. They can either go on and be happy people without eye — without significant eye disease– or they can spend the rest of their life fighting primary angle closure glaucoma. Next slide. So, that gets us into the chronic form. The chronic — next slide. The chronic presentation of primary angle closure glaucoma unfortunately looks a lot like — go to the next slide — looks a lot like open — oh. Sorry. I forgot that we have a — we’ll go to the question. Sorry. So, the primary angle closure can look a lot like open angle glaucoma. And we’ll go to the question. So, chronic angle closure glaucoma can be distinguished from open angle glaucoma by checking visual fields, by checking intraocular pressure, by checking OCTs from the nerve fiber layer, by doing gonioscopy, by doing optic nerve photography. So, how do you tell them apart? Chronic angle closure from open angle glaucoma? Excellent. Yes. Gonioscopy. The only way to tell the difference is with gonioscopy because otherwise chronic angle closure is indistinguishable from open angle glaucoma. Next slide. Patients come in, they have high pressures, they have bad fields, they have bad optic nerves. So, it mimics primary open angle glaucoma unless do gonioscopy and see the angles are closed. Once you have permanent PAS, iridotomy is not going to help. Iridotomy is cot not undo peripheral synechial, it can only undo closure. Chronic angle closure glaucoma is more severe than open angle glaucoma. So, it’s going to be more — the pressure is going to be more different to control. You’re more likely to need surgery. And one thing to keep track of is any time you do any surgery on a patient that has chronic angle closure, you need to cycloplegia them post operatively. They have a risk of glaucoma post operatively. Next slide. Even just for cataract surgery. Patient Jane, presented. This is another patient of mine from a number of years ago. Presented complaining of blurred vision in her left eye for four months. She had been followed for more than 6 years with chronic open angle glaucoma. She was treated latanoprost and increasing pressures into her 30s. When she came in, vision was 20/30 in the right eye, 20/70 in the left eye. And interior pressures 35 and 78. 78! She had a deep chamber, angles were terrible. Complete synechial, and nerve changes and end stage cupping with a less than 10 degree island of vision on the left side. Next slide. Laser iridotomies were performed but, of course, it did not help on the left side. Her angle opened on the right side and did fine there. But needed a combined cataract surgery and combined on the left side. You cannot diagnose a patient with open angle glaucoma without performing gonioscopy. I gave a talk years ago and people came up with me from the audience, does that mean I have to gonioscope every patient with glaucoma? Yes. If you’re gonna diagnosis them with primary open angle glaucoma, you’ve got to know that there’s an opening an and will the only way to know there’s an open angle is if you gonioscope that patient. Next slide. So, in terms of preventing glaucoma, we need a global initiative. We need to have an effective strategy. We need to determine the best treatments. And we need to figure out who benefits most from laser iridotomy and other prophylactic treatment. It’s going to vary by country, by resources and by populations. Next slide. We know that it’s — that laser iridotomy and cataract surgery are effective in preventing angle closure glaucoma. Blindness due to acute angle closure in the Inuit was reduced from 64% to 9% over 37 years by screening and performing prophylactic PIs. And in Taiwan, between ’97 and 2004, the rate of cataract surgeries tripled and the admissions — this is for acute angle closure glaucoma — decreased by half. This is significant inverse correlation between the number of cataract surgeries and the number of angle closure attacks. Iridotomy and cataract surgery both decrease the risk of angle closure glaucoma. But it doesn’t mean you could do this on everybody. Next slide. So, and it’s unclear who warrants a prophylactic iridotomy. For instance, 15% of Chinese women over the age of 50 have more than three quadrants of appositional angle closure, yet only 1.5% have glaucomatous loss. It’s hard to know which are going to run into trouble. And LPIs can be difficult. Certain ethnic groups that have thicker irises. For instance, in the Chinese people, their irises are often thicker and then it’s more risk when you do an iridotomy. And does the population you’re treating then have the resources to treat those, any problems that develop? So, if you can induce a cataract from inflammation, does your population have the resources to treat that? So, it’s just things to be concerned about before we think about doing iridotomies on everybody with a little bit of narrow angles. Next slide. So, there were two recent studies, the ZAP trial and the ANA-Lis trial that looked at treating patients with early just narrow angles. Primary angle closure to suspects. They did a prophylactic iridotomy in one eye and followed the other eye as controls. Next slide. The ZAP trial looked at about 900 people in urban China and followed them for 6 years. The next slide. And the ZAP trial looked at about 480 people in Singapore over the age of 50 and followed them for 5 years. Next slide. And they found that treatment with a laser iridotomy decreased the risk of developing angle closure glaucoma by 50%. But what was really interesting is — well, so, we could see that 19 treated versus 37 untreated people in the ZAP trial. And there were 5% of treated eyes with LPI had angle closure versus 9.4%. Next slide. So, treatment with a laser iridotomy decreased the risk of developing angle closure by approximately 50%. But what was also interesting to note is the risk of developing angle closure in that period of time was relatively low. We need to identify the high-risk groups and recognize primary angle closure before primary angle closure glaucoma develops. And that’s where that recognizing the clinical presentation of subacute angle closure is very important. Because we want to try to prevent the development of chronic angle closure. Next. So, also, we — the EAGLE trial reported a number of years back about the effectiveness of early lense extraction for the treatment of primary angle closure glaucoma. This is a little different. The ZAP and ANA-Lis were looking at the trials. These were looking at the treatment of angle closure glaucoma. These people had elevated intraocular pressures or optic nerve damage already. Next slide. And it was a randomized, multi-centered trial. It was done in hospitals on many continents. In Australia, in Europe and in Asia. And they looked at the effectiveness of clear lens extraction versus laser iridotomy for the treatment of angle closure glaucoma. Next slide. Patients had either primary angle closure with apposition and pressures of greater than 30. High-risk eyes and pressures more than 21 and already had optic nerve and visual field loss. Next slide. And they looked at many factors and they followed patients for 3 years. They looked at vision and fields and pressure. And quality of life. So, they did many different studies of quality of life. Next. And so, there were four — 200 people in the clear lens extracap traction group, 200 in the iridotomy. Most had the primary angle closure glaucoma. Next. And it was very mixed ethnicities. So, what they found was that quality of life was better with the lens extraction, intraocular pressures were lower with the lens extraction, and fewer participants that had the lens extraction needed any treatment to control interocular pressure later on. So, in people with chronic angle closure glaucoma, taking out your lens, even if there’s not a cataract there, can be beneficial to the treatment of glaucoma. Next, please. And it was also found to be cost effective. So, over a 10-year period, it was found that it would be more cost effective to take out the cataract than to treat the glaucoma medically. Next slide. And with laser iridotomy. And we can skip this one. So, there is — so, the EAGLE trial has absolutely supported the use of lens extraction, even without a cataract present in the treatment of chronic angle closure glaucoma. So, we have many options now. We have prevention is most important for the treatment. But we have medical therapy. We have lens removal or cataract surgery. When things are — don’t respond just to cataract surgery, we can think about some mixed procedures. We can think about trabeculectomy, glaucoma drainage tubes. Whatever you do, remember cycloplegia post-p to prevent glaucoma post-op. So, gonioscopy is the key to diagnosing angle closure glaucoma. I can’t stress is enough. Next slide. We want to identify high-risk groups within, perform gonioscopy and do optic nerve evaluation. And we want to get proficient at gonioscopy. Next slide. So, what is the biggest obstacle is that people don’t do gonioscopy. We’re just gonna move through it a little quickly. Next slide. Our colleagues don’t do gonioscopy enough. Imaging devices are nice, but they cannot replace gonioscopy. Next, please. And next. So, no, you cannot throw out your goniolens to rely on imaging devices. We need gonioscopy. Next. And next. Just gonna skip through these quickly. The most important thing is to always have your goniolens with you. If you have the budget to have a goniolens, a compressive goniolens, it needs to be somewhere quickly accessible. It can’t be a clinic three doors down under lock and key and you got to find the person that has the key to find the key to get the goniolens. You need to have access to a goniolens. And as soon as, you know, you have resources, that should be one of your, you know, an early purchase. And we have so many things that we can see with gonioscopy that we can’t see with imaging devices. If you can go forward. Next. There’s direct goniolens like the Kepe, there’s indirect. And they can be non-compressive like the Goldmann lens. That’s best for learning your landmarks and becoming proficient so you’re good to do lasers, and trabeculoplasty, and gonioscopy, learn with a Goldmann, get a clearer view. And it makes it more stable. And you can’t compress so you see what the angle really looks like. But have a four mirror lens available to do compressive gonioscopy when you get better because it’s very important to — to know what’s appositional and what’s not. Next slide. So, we’re gonna use gonioscopy to identify our landmarks. Next slide. We’re gonna look at it in the dark. This is a very important slide, let me just spend a moment here. The corneal wedge is very important. You shine a beam of light, a thin beam of bright light on an angle on the cornea and you look at your anterior and posterior beams. And where they come together is Schwalbe’s line is anterior to the angle. If you see that juncture coming at the base of the iris, you don’t have any iris structures. You should see it come together and then you should see your trabecular meshwork and then slow your scleral spur. Next slide. Using that wedge helps to see the pale angle where it’s difficult to see the trabecular meshwork from a closed angle. Next slide. So, perform gonioscopy in bright light to see as much as you can. But then dim the room lights, make your light beam small so it’s out of the pupil so that you can see what it looks like when the — when the pupil dilates and you’ll sometimes see very different changes. You want to check in bright and dim. You can see this UBM in light. The angle is narrow, but open. And if dim, it’s appositional. Next slide. And you also want to check with and without compression. So, on the left side, it’s about compression, I can barely see me angle structures. On the right side, you can see the corneal stria. This is an example of the double hump. You can see the iris has a hump in the periphery and dips down and another hump by the pupil. And I can see a little bit of angle structures peeking out in the corner there. Next slide. Sometimes you can have pigment on Schwalbe’s line. This looks like meshwork, until I compress again. Until I compress. And again. Good. And then I can actually see trabecular meshwork is peeking out down below. So, you can sometimes have Schwalbe’s line get pigmented. It’s good to check for the anatomy, that won’t have the same definition as the anterior angle. Remember that the goniolens is a direct angle. We have so many things that are upside down and backwards. It’s just a mirror. If you’re looking at the top, it’s the top of the opposite angle. If you’re looking at the bottom, it’s the bottom of the opposite angle. It does not — next slide — it does not criss-cross like our other lenses. It’s a direct mirror. That’s important to know when you’re lasering to know where you are. It’s not on an angle, it’s a direct mirror across. Next slide. And have a classification system, I like the Scheie system. It gives it — it doesn’t just say I see scleral spur. Is a it is narrow or super wide angle? Next slide. Andrew, I’m going to run a couple minutes late because of the timing of the slides. But I can stay on for questions. So, why do we do gonioscopy? We want to see the entire angle, not just cross sections. Again, next slide. We’re gonna run through these pretty quickly. We can differentiate appositional from synechial angle closure. Next slide.Week see if there’s pigment in the angle. We have a very pale angle on the left and a densely pigmented angle, most likely from pigment dispersion on the right. Next slide. It helps with our diagnoses. We can see neovascularization. You can see that fine blood vessel right in the center of the slide crossing the — crossing the scleral spur. So, neovascular vessels go from the iris root, they cross scleral spur and arborize so we can see neovascularization. Next slide. We can see PAS. We see little tent-like PAS on the left that we used to see with argon laser trabeculoplasty, and we can see the other problems associated. We can see tumors and we can just keep going through these. Hemorrhage, KP, foreign bodies, blood in Schlemm’s canal, processes and the next slide. Irregular bumpy iris. Here is a video of that double hump. Here it’s flat. Now I’m gonna compress and you see the double hump. The iris bulges in the periphery, and bulges around the lens. We can see into the angle. Here it’s harder to see into the angle. Compress here and you can see deep in the angle. Next slide. And these are courtesy of Lee Alward. Take note of the website, www.gonioscopy.org. A site produced by Dr. Lee Alward, an amazing educator at the University of Iowa. He’s put together a course on gonioscopy. I highly encourage everyone to look at that. You can see post-op and other congenital abnormalities. You can get facility by using a Goniolens and you can learn how to do dynamic. You can see how the angle can change from light to dark and with and without compression. This is here. This little loop again here. We can see the angle structures. Here you could see it without compression — without compression. I can’t see any angle structures right now. And then with compression, we can see the angle structures. And next slide. If we can — oh, that’s good. Let’s skip the questions and just move on. And what all I’m gonna say here is when you do an iridotomy, a lot of times I think when people have episodes of angle closure after iridotomy, that think don’t have a patent iridotomy. It’s very important when you do an iridotomy that you see a black hole, a black opening that you see right through that iridotomy. At many of the finest institutions when I ask people how they check for an iridotomy patency, they tell me transillumination. It doesn’t tell you anything about patency. And think about glaucoma, they have transillumination defects all over the iris. Those aren’t iridotomy or patent. It tells you if there’s lack of pigment in that area. In order to know if an iridotomy is patent, you have to see an opening. I was at one of the resident clinics and I had two people in angle closure glaucoma, and they are patent. They had prior iridotomies but they had transillumination, but their iridotomies were not patent. So, it’s very, very important that you see the opening of the iridotomy and don’t rely on transillumination. I’m gonna just do one slide here, next slide. Linear dysphotopsia after iridotomy is a big problem. If we can go to the next slide. It can develop — people can be very debilitated by there problem. It’s when people see a line of light going up and down as they blink after iridotomies. And what we have learned is that by placing iridotomies nasally or temporally rather than 12 welcome, we can avoid the linear dysphotopsia. And we can skip to the conclusions. I’m happy to go over linear dysphotopsias a little bit more. I will say — we can keep going. And one more. Right there. That’s good. The — oops, if we can go back one more. The best way to treat a patient having a side effect from their iridotomy is not to close the iridotomy. A little corneal tattoo, like is seen here. Other people will just make a little massacre Ralphy — I’m sorry, a corneal pocket and put a little India ink in there. And you can keep having the iridotomy and the patient can stay safe intraocularly, and it takes care of the glare coming in through the iridotomy. Next slide. So, linear dysphotopsia after iridotomy is debilitating. It should be discussed as a risk. And placing it decreases the risk. Not zero. And the last patient had a tattoo over the temporal iridotomy. And that’s the only patient I’ve had that has ever needed that. Next slide. So, in summary, primary angle closure glaucoma is a leading cause of global blindness. We need screening strategies and prophylactic surgery with iridotomies and cataract surgeries can decrease the risk of blindness. But we must customize our care for the specific populations and available resources that we have. Next slide. The rate of blindness is much higher for primary angle closure glaucoma than open angle glaucoma. And most primary angle closure glaucoma is not acute angle closure. We need to recognize angle closure glaucoma that is not acute angle closure. And to do that, we need to gonioscope, gonioscope, gonioscope, and listen to people’s stories if they have symptoms. Next slide. So, gonioscopy is the key to diagnosing angle closure glaucoma and therefore — your goniolens is the key to preventing blindness from angle closure glaucoma. Please go on Dr. Lee Alward’s website and educate our colleagues that we need to examine the angle. Once you are proficient, teach your colleagues how to integrate gonioscopy into their routine. Next slide. The Goldmann is best for learning your landmarks. But a four mirror lens is important. You can keep it with you. You don’t need coupling solution. It’s a simple mirror and know how to record it. The classification lets you record how open the angle is, what your deepest angle structure is. But you can have your own system. Just say what your deepest structure is and whether the angle is deep or narrow and do it in light and do it in dim is simple enough. Next slide. And an iridotomy is not patent unless you can look right through it. Next slide. Look for the black hole. Next slide. This is a patient that has what looks like on transillumination two iridotomies. But only the super one was pay tent. The temporal one was not a patent iridotomy. But it trans-illuminated just fine. You need to actually see the opening right through. Next slide. So, just say no to transillumination. And next slide. And we don’t have to do the questions again. Thank you so much. Sorry for the glitches on the — on the slides. But really appreciate this opportunity. Let’s go to some Q&A. So, if you have a primary angle closure glaucoma suspect, cataract surgery will most often get rid of the risk of glaucoma. And many people are going right to cataract surgery and not iridotomy if they, you know, especially if there’s a cataract present. So, I think that question in Spanish is asking about evidence on OCT for angle closure glaucoma. There are programs that look at the anterior segment and let you see narrowness. But it’s going — it’s still important to gonioscope. But yes there are things on OCT that give the angles, but it’s not the OCT of nerve fiber angle and retina. What do you do in the case of failed API? Will you plan a repeat? Yes. We didn’t talk about the technique of laser iridotomy. But if you’re having trouble with a YAG laser iridotomy, sometimes you can just stop and come back and then a week later go back to the same spot and it will be much easier to penetrate. The other thing you can do if you have access to an argon laser is to pre-treat the area with argon laser, really flatten everything out with the argon laser and then go through. Yes, you can in the case of the failed PI. You want to remember to look for your best spot. Don’t just go in and do a laser. And I always do a laser at 9:00. I’m gonna do a laser at 9:00. Look for your best area at 9:00 or 3:00 that has a small crypt or has an area that looks thin that looks a little bit porous. And those that are areas. So, look for a crypt, a little indentation in the iris. And you’ll have better response. But sometimes if it’s — if things are getting inflamed and fluffy, stop. Let everything settle down, let it scar in a little bit over a week and come back and either pre-treat with YAG or try it a week later and you can often get through. Primary glaucoma suspect with cupping normal fields and normal retinal fiber layer, physiologic cupping… so, you don’t base your — so, this is a question asking about if you have a primary angle closure glaucoma suspect that has a .7 cup but normal fields and normal retinal nerve fiber layer on OCT, could it be physiologic cupping? Yes. Is it physiologic cupping and is PI indicated? It’s based also on the angle appearance. So, if the angle is narrow, an appositional, and the patient has high-risk characteristics, then yes, you should still go ahead. If I see 180 degrees of angle closure, I will often go ahead and do a laser iridotomy. Even without any evidence of damage. So, we know that laser iridotomy in angle closure suspects — and those are people with normal fields and normal retinal nerve fiber layer — will decrease the risk. It’s just how risky was this patient. So, if they’re symptomatic or if they have more than 180 degrees, I will often do an iridotomy. How does cataract extraction treat chronic angle closure? Well, it makes more room. So, if you have true synechial angle closure, cataract surgery by itself does not always lower the pressure. But if you have appositional closure, when you take out the cataract, you — you put in just a small, thin, intraocular lens, you’ve created so much room in the anterior segment that you get rid of the appositional component. Very often, do a synechial goniolysis, and you can break that up. Do you recommend angle examination by anterior OCT or UBM beside gonioscopy? If you have it, it can be helpful. I have not found that it — I do a lot of gonioscopy. And I do not find that the OCT anterior segment gives me a lot more information. It is really good for people that aren’t very confident with their gonioscopy. And so, for starters, also, it can be very good. UBM is really helpful in curious cases. Cases that you’re worried maybe have cysts or other issues behind — that are hidden behind the iris. So, they are useful, OCT and UBM. But as I mentioned, nothing replaces the gonioscopy. And you can if you don’t have access to the OCT and UBM, you can do fine diagnosing angle closure with your goniolens. I’m at a facility where I can’t perform LPI, can I perform surgical peripheral iridotomy and how effective is it compared to LPI? They’re effective, but you need a surgery. You have to have a much higher bar whether you perform it. LPIs are often very easy and accessible. So, you’re not going to want to take every, you know, you’re gonna want to have a high-risk patient or a patient that is clearly in angle closure. But surgical iridotomies are perfectly fine. And so, can we please two over laser settings? So, I — everyone’s laser is a little bit different. Our YAG is a pretty old YAG. I just use the setting of about 6 millijoules or 6 milliwatts, not sure what they are. I think it’s 6 milliwatts for my laser setting and I do a single shot usually. A lot of the irises I see are not thick, fuzzy irises. And when I look very closely on almost any iris, I can find a crypt, a little hole. If you can find a little hole and go to the base of that little crypt, you can often get through without a lot of settings. Most of the time in most patients we get through with one spot in the base of a crypt. And again, we talked about some of the things you can do if you’re having trouble getting through. Is double hump a higher risk? Or just confusing? Dump hump is a sign of plateau iris. So, plateau iris can be a major form of risk factor for — for angle closure glaucoma. So, the two mechanisms are — the two chief mechanisms are pupil block and plateau iris. It’s actually a significant risk factor. So, the question is, and I’m — why placing an iridotomy nasally and temporarily will not have a dysphotopsia. Most people don’t have a dysphotopsias. But those whether get them are really, really miserable. If you look at the linear dysphotopsias people are bothered by. It tends to happen with partially covered iridotomies. Though it can happen with fully-covered iridotomies. The theory is, and I’m sorry I didn’t get a chance to run through the whole section on it. When an iridotomy is partially covered superiorly, there’s a tear meniscus at the edge of eyelid that will bend light. It will come in, shoot through the iridotomy and hit as a focused light. An iridotomy that’s fully exposed nasally or temporally, the light will go in, but it will go in blurred and unfocused and the eye will ignore it. There may be some glare. All iridotomies can cause some blurry vision and glare, but it won’t go in as focused light in most people. So, and there’s often a theory that even with the iridotomy is fully covered by the upper lid, the prismatic effect of the tear meniscus at the edge of the eyelid will bend it and shoot it through. There are cases of fully-covered iridotomies that still have this linear dysphotopsia. There’s a risk of having this, and I’m glad that the attendee didn’t have patients with it. But if you do enough iridotomies, someone is going to have a dysphotopsia. Do I perform an LPI in all narrow angle eyes before dilation? It matters how narrow and their risk factors. The study, the ZAP and the ANA-Lis trials sort of encouraged not to do iridotomies in every patient. But if the angles are very narrow, the patient is in high risk, there’s a good bit of already appositional angle closure or some vague headaches, I would do an iridotomy. I think I already covered the role of anterior segment OCT. How common is the photopsia at the 12:00 position? I think in the study that was done, I think it was around 8% or so. But I could be wrong on that number. But it was noticeably — in his study — it was noticeably more common to have that dysphotopsia at the 12:00 iridotomies than the nasal or temporal. Someone is interested in the normal cup disc ratio. Most are between .3 and .6. But it all depends on the size of the optic nerve. So, if you have a large optic nerve, you can have a large cup and that can be physiologic. So, that’s a whole ‘nother lecture that I love to give. And I think it’s in the archives, actually. I gave a lecture on looking at optic nerves and that should be in the archives. So, this — the size of a normal cup to disc ratio is dependent upon the size of the optic nerve. So, what settings would you use to pretreat with argon? You can use a 50 micron spot or you can use a larger spot. But for a little bit long setting, maybe .2 seconds. And a low power. So, you want to see a low, slow burn and a contraction. So, usually we’ll use like 200 microns, .2 seconds. And then we work up from throw high just to see the iris contract with each spot. Do I see prolong iritis in patients after angle closure glaucoma and laser iridotomy? Not usually, in they have acute angle glaucoma, they take longer to recover. I’m a strong believer in topical steroids. Even when I do a laser iridotomy, I give four times a day steroids for five days. And with trabeculectomy, I treat people for three months with topical steroids. I try to treat the iritis just so it’s not long. I’m not sure I understand what that question is. How do you optimize iridoplasty? The ways to optimize iridoplasty is to get as peripheral as possible. I don’t use the mirror of the lens. I go through the central part of the lens. But I put pilocarpine in first. Then I use a 200 to 500 spot size and again work my way up with the argon laser until I get contracture of the iris and keep it as par peripheral as you can as you go around. How often do we repeat gonioscopy in patients that already have a known diagnosis of open angle glaucoma? Again, so, there’s open angles and then there are open angles. As a friend would say. So, you can have an open angle that’s what we call a D40, a wide open angle. One that I will say, you can drive a truck through that angle it’s so wide open. Then there are angles that are open, but a little on the narrow side. It’s open, there’s no appositional closure. And certainly those patients I will continue to gonioscope in adulthood every year or every other year. As it grows, it takes up more space and people have relatively more pupil block. And the angles request start to narrow over time. A wide open angle maybe every 5 years when it’s wide open. I checked it in light and dim light. You can have nicely open angles in bright light and dim all the room lights and narrow that beam of light out of the pupil and sometimes those angles will markedly narrow. So, make sure you don’t have any narrowness with dimming. And then if the angle is wide open every few years. But if it’s a narrow-ish open angle, then definitely I would go for yearly. Especially as people are aging and their cataracts are worsening. Can sustained release glaucoma therapies be used in cases of angle closure glaucoma? I’m assuming you’re talking about the insert, the prostaglandin insert. And they can. And you can actually put it — you can put it behind the iris even. In relation to laser treatment of angle closure glaucoma, what is the percentage of reduction of IOP one should expect after treatment, so laser iridotomy in — when we do prophylactic laser iridotomies, we don’t see pressure reduction. So, laser iridotomy by itself for narrow angles does not lower intraocular pressure. Whether you have someone with an acute attack, we should hopefully be able to break the attack so you can go from 50 to 10. But if they already develop synechial closure, if they come in within acute attack and don’t wait 5 or 10 days at home, if they come in, you can see a dramatic increase. Laser iridotomy from lower angles does not lower pressure. May I ask what protocol is for managing acute angle closure with a severely elevated — with a cloudy cornea and slit peripheral anterior chamber. Anything you can do to get a laser in as quickly as possible. Myotics to try to break the block, a few rounds. And aqueous suppressants, get your topic carbonic and systemic Hydronic inhibitors. And you can use hyperosmotic agents, Ma any toll, and the oral agents. And to clear the cornea. I mentioned the 30 gauge. It’s tricky when it’s appositional like that. But as soon as you can get that — clear that cornea enough. And try putting a little bit of glycerol on the cornea to clear it. In clinical case, if we have a patient with an acute attack of glaucoma, after drug medication we have to do laser iridotomy in the same day? You don’t. You don’t have to do it in the same day. At Will’s eye hospital, a premier eye hospital in Philadelphia, they don’t do iridotomy in the IER, they send it to us and we do the next day. Once you break the block — but you need to break the block. Even if you it medically, you need to try to break the block. For me, the sooner I can get that in, the iridotomy in, I think it’s safest for the patient. And remember when you have a patient with acute angle closure glaucoma in one eye, you have to plan not emergently, but in the short-term, to do an iridotomy in their other eye. Is there contraindications for prostaglandin analogs in closed angle glaucoma? They just don’t work well. Because things have to get in by the sill lair, the root of the iris, the ciliary body. Please can you shed more light on the pathophysiology of dysphotopsia experience following LPI? Most are benign, a little bit of glare, a little bit of blurry vision. There are lectures that are archived that you can look for the study by Dr. Ahmed that looked at dysphotopsias after done superiorly and horizontally. But the one that’s most debilitating is the linear dysphotopsia. That’s when the light shines through the iridotomy and focused on the retina. People see the horizontal light that goes up and down each time they blink. And it’s very, very bothersome. We have — Prevent Blindness America — has chat groups that patients can go in and chat online. If you look for the chat groups are hundreds and hundreds of posts, it’s always the laser iridotomy ones. It’s not that there are so many cases of the problems, but when people get this problem, they are upset. So, it’s a severe — it’s not a common problem. But when it happens, it’s a very — it’s a problem that really affects people’s quality of life. I’m not sure — I don’t know what that question means so we’re gonna skip that one. Patient with a history of subacute — closure after LPI. Whoops — patent on gonioscopy, complaining of colored halos post laser. These are one of those issues. There can be dysphotopsias of many varieties after LPI. Most of our patients don’t have it, most of our patients never complain. But some people will have problems. And colored halos is one that has been reported. What you can do is some people do better if it’s large — if the iridotomy is large. It’s scary to make it larger. But colored contact lenses, if you have availability to the standard over the — standard colored contact lenses, the ones that are opaque that turn brown eyes blue, they have a dot matrix pattern. If you put that lens in, that dot matrix will often cover the laser iridotomy enough that it will get rid of that dysphotopsia. And they can — if they’re, you know, this is all depends on the resources available. But they can get a custom contact lens with a spot on it that sits over that area. And then also you could always try the little tattoo in that area. So, there was another study that showed no difference in superior versus nasal. So, there was a very compelling study that showed that there was a difference and there was a later study that showed no difference. But you have one study that says yes and one study that says no. And I can tell you from personal experience, I go with the study that was done by Ike Ahmed. But yes, thank you for that disclosure. There was another study that did show no difference. But I really — I don’t agree with that study. So, may I know your experience in doing argon lazier in lightly pigmented irises. It’s hard to do a laser iridotomy in a lightly colored iris. You have to use — it’s just hard. It — because you need the pigment to absorb. If they’re — you can just try using multiple small spots with a 50 micron short duration in the center. But if you have any way to have access to a YAG, it will be much easier to get through and there’s always surgical iridotomies for very high-risk cases. If you persevere, you can often get through. You can try to get some of those compression — constricting burns in first with a larger spot. But you’re gonna have to use higher power for everything. Do you perform cataract surgery for acute angle closure glaucoma and where? Not usually. Usually it’s two unstable a situation when you’re in an attack of acute angle closure. You really want to try to calm things down. Your cornea is going to not be clear enough to do your surgery. Should we do LPI first and then clear lens extraction or cataract surgery and then LPI? During LPI, can it damage a pre-existing IOL? So, a few questions here. So, laser iridotomies do not damage a pre-existing intraocular lens. But you don’t need to do — you don’t usually need to do an iridotomy after cataract surgery. Because usually the cataract surgery alone made the angle deeper. And whether you do an LPI first or a clear lens extraction first depends on the patient. For a high-risk patient that already has glaucoma damage or elevated pressures, you can go ahead with a clear lens extraction. And the EAGLE trial showed there was better intraocular control and quality of life for lens extraction. For lower risk cases, you can do the LPI. I’m not sure of the next one. Do Migs have a role in angle closure? Most Migs procedures are angle-based procedures and you need to be able to get into the angle. So, if you have appositional closure and you do iridotomy and the angle opens or you take out the cataract and the angle opens, you can then do a Migs procedure to lower the pressure additionally getting rid of the mesh. But if you have angular closure — synechial angle closure, you cannot get through. You can try to break it and have access. But very often the iris is very sticky then and it may come back up and close again. For in patients with angle closure — laser iridotomy and peripheral iridoplasty have already been performed, but the angle remains occludable, would you recommend maintaining the patient on pilocarpine, the angle remains occludable — yeah. Pilocarpine can be helpful in patients with plateau iris that are still after laser iridotomy and after the peripheral plasty. If I’m worried they’re progressing, maybe give pilocarpine bedtime, 1%, maybe 2%. But just at bedtime, you don’t need the iris constricted all the time. You just don’t want the iris to sit in the angle appositionally all the time because then it will stick. So, if every nights the pilocarpine pulls it away while they’re sleeping, then they don’t have to use are the pilocarpine all day. Do I stop prostaglandins before LPI? No, I don’t stop prostaglandins before cataract surgery. There’s no need. As long as you can give them a little bit of steroids after it. Oh, we’re getting near the end. Which meds is most appropriate to regulate the IOP with least systemic effects. I’m not taking this as necessarily an angle closure question. But which medications have the least systemic effects. Prostaglandin have little side effects. The ROC inhibitor, has very good pressure lowering with very little systemic side effects. The next on the list would be your carbonic — topical carbonic anhydrase inhibitors. Low systemic absorption. Can cause a little taste, but tend to have low system you can side effects. The most with the most systemic side effects are beta blockers and alpha agonists. Most people are very familiar with the systemic side effects of beta blockers. You have to worry about people with asthma, reactive airways and with people with bradypnea cardiac arrhythmias like bradycardias. But the alpha agonists have marked systemic side effects in many people because they cross the blood brain barrier. People can get somnolent, they can get sleepy, not as sharp. They can have a lot of real quality of life issues. And they can also decrease blood pressure. As can the beta blockers. What is the idealize of an iridotomy? I’m not really sure there’s an ideal size. But it does not need to be giant. But it needs to be patent. So, for me, it’s more about making sure that it’s definitely open. And a little bit less about size. So, if I get an opening I’m — I’m not even sure how to measure because I never measured iridotomies. I would imagine a millimeter would be plenty. You just need enough for fluid to go through and equalize the pressure. So, that’s about it. Well, we have covered all our questions. And we covered a lot of material. And I appreciate you sticking — sticking with us throughout this. Andrew, correct me if I’m wrong, but the lecture will be archived and people can look at it again because we covered so much material. But if people have issues, they can always get through to me through Cybersight. And it’s been a pleasure. And I thank you all so very much for taking the time today in whatever time zone you’re in and whatever climate you’re in. It’s very warm here today. I don’t think you can see. So, I thank you so much. And have a wonderful rest of your day or night.