Lecture: Malignant Glaucoma: From Mild to Major

DR PILTZ-SEYMOUR: Hello, everybody. It is such a pleasure to be here today. To talk to you about malignant glaucoma. And I want to thank Orbis for this opportunity, and for this amazing program where we can reach out to so many people all over the world. Today we’re talking about malignant glaucoma, which is a bit of an enigma. It’s a very difficult problem in many cases. But sometimes it has a more subtle presentation that is not always talked about. So I wanted to talk about the full spectrum of malignant glaucoma, from the dreaded to the mild. I have no financial disclosures about this presentation. I wanted to start by talking to you about a patient I had, probably in the mid-’90s. He was referred to me — and by the way, I call him Mr. Dark Cloud Over My Head. Because everything was just so difficult in his care, first in one eye and then in the other. And it all centered around malignant glaucoma. He was referred for elevated intraocular pressure and he had chronic angle closure glaucoma and he was pseudophakic. He had previously failed non-penetrating glaucoma surgery in both eyes. I performed a trabeculectomy. He was uncomplicated. Great on post-op day 1 and 5, deep anterior chamber, and pressure in the low teens. On post-op day 8, despite having a patent nice wide-based iridectomy, he had prolapsed iris into the sclerostomy. In retrospect, he was on Prazosin. We didn’t know about idiopathic floppy iris syndrome back then. But he was on Prazosin, an alpha adrenergic blocker. And most likely the reason he had this prolapse was because of that. So I gave him pilocarpine to pull the iris from the sclerostomy. He came in with intraocular pressure 45, flat anterior chamber, otherwise normal posterior pole. So he was in malignant glaucoma. And what is malignant glaucoma? It is a secondary form of angle closure glaucoma, and it’s a posterior pushing mechanism, where vitreous pressure pushes from the back of the eye to shallow the front of the eye. It was first described by von Graefe in 1869. He called it malignant because of its unrelenting course, unresponsive to therapy. And people really didn’t know what to do. People just usually lost their eyes, if they went into malignant glaucoma. In the 1950s, Chandler described lens extraction to treat malignant glaucoma. But it turned out that was only successful if there was vitreous loss at the time of lens extraction. So there’s usually an inciting event. Usually, but not always. And it can happen after incisional surgery and it can happen after any incisional surgery. Typically we hear about it after glaucoma surgery or cataract surgery. But it can also happen after lasers. Any laser. Iridotomy, cyclophotocoagulation, even capsulotomy or suture lysis. It can develop if you have a wound leak. And it can develop if you withdraw cycloplegics. So I’m gonna say this a couple times: Beware the patient that comes to you on cycloplegics. Because there are some people who are on chronic cycloplegics, because if you take them off, they go into malignant glaucoma. They may not know. They may not have been seeing doctors regularly. But just beware of a patient who comes to you on a chronic cycloplegic and beware of withdrawing it. It can develop intraoperatively. Say you’re doing a cataract surgery, the eye gets firm and it’s hard to form the anterior chamber. That can be intraoperative aqueous misdirection in glaucoma. And in my case, it started with the institution of miotics. So when I administered pilocarpine, to try to pull his iris from the sclerostomy, it precipitated a full blown attack of malignant glaucoma. And we performed a vitrectomy. We tried to treat him medically and we tried to treat him with laser. But he required a vitrectomy with removal of the anterior hyaloid. And we’ll talk later about how iridozonulohyaloidotomy is the treatment of choice now. But we didn’t understand that at the time. And he still requires chronic atropine to keep his eye formed and to keep him from going back into malignant glaucoma. What are the risk factors? Typically we see this in high hyperopes. And often in eyes that had chronic angle closure or chronic narrow angles. But it can occur with pseudophakes. It can occur in phakic eyes, pseudophakic eyes, even aphakic eyes. Because it has to do a lot with the vitreous space. It can sometimes occur spontaneously or after trauma. And it’s a bit more common in women and people with pseudoexfoliation. But most people with malignant glaucoma don’t have pseudoexfoliation. And the mechanism is controversial. There seems to be usually some type of precipitating event, but not always, that leads to an altered interaction between the ciliary processes, the lens, and the vitreous space. And this causes aqueous not to move anteriorly, like it’s supposed to, through the pupil and into the anterior chamber, but it forces it back into the vitreous cavity. And then these pockets of aqueous form in the vitreous. And expands the vitreous and causes shallowing in the front of the eye. And angle closure. Oh, dear. This changed formatting. Excuse me for a second. The print is very small. So we have aqueous directed posteriorly, which then compresses the anterior vitreous. And when the anterior vitreous then gets compressed, it becomes less permeable, and it creates a barrier for the movement of aqueous anteriorly. So you get this decreased permeability across the anterior vitreous and the anterior hyaloid, and you get this positive pressure building up in the vitreous cavity, which shifts the lens iris diaphragm forward, causing shallowing or flattening of the anterior chamber. And this is really distinguished. This is a very important point. It’s distinguished from iris bombe. It’s distinguished from like… A pupil block. Because the whole center of the iris, the whole center of the anterior chamber, is shallow. The lens shifts everything forward. Usually in iris bombe, the lens doesn’t come forward. You have narrowing and the iris comes forward in the periphery, but the center chamber is still formed. In aqueous misdirection, everything comes forward. You get angle closure and usually elevated intraocular pressure. So what are some contributing factors? Chandler and Grant postulated that zonular laxity, loose zonules, allow the movement of this lens iris diaphragm more readily. With increased vitreous pressure. And it lets people go into this malignant glaucoma more easily. Trope in ’94 described ciliolenticulo block. And he described ultrasound findings that talked about this anterior rotation of the ciliary processes. Having a supraciliary effusion, and that whole supraciliary effusion causes expansion of the vitreous cavity. And Quigley firmly believes that the precipitating event is this choroidal expansion. That’s why Quigley doesn’t like the term aqueous misdirection. I believe he likes malignant glaucoma. But he doesn’t believe aqueous misdirection is the hallmark of the disease. He believes choroidal expansion is the inciting factor. And Liebmann described 6 eyes with UBM and confirmed peripheral annular choroidal detachments. And another mechanism is this impermeable anterior hyaloid. In this study by Balekudaru, he looked at 58 eyes with malignant glaucoma. That’s a pretty big series. And the majority of the eyes had this anterior rotation of the ciliary processes and shallow or flat anterior chamber. He found that only 10% had supraciliary effusion on UBM. And when they tried sclerotomies to see if they could drain this fluid and bring everything back, bring the positive pressure down, deepen the anterior chamber, he found that they couldn’t find supraciliary fluid. So it brings into question this whole notion of whether choroidal expansion is the underlying problem, or this anterior rotation. It’s still controversial, and certain people feel very strongly about it. Thankfully, malignant glaucoma is relatively uncommon. In the tube versus trabs trial of 242 patients, malignant glaucoma developed only in 3% in the glaucoma drainage tube group and 1% in the trabeculectomy group. So making the diagnosis — and like I mentioned, it’s all about that lens-iris family. In malignant glaucoma, there is central shallowing of the anterior chamber, because the whole lens-iris diaphragm pushes forward, and that’s why it’s distinguished, as I had mentioned, from pupil block. Which the lens iris diaphragm doesn’t shift forward. It’s the peripheral iris that comes forward. And there’s a normal posterior segment. On exam. The typical presentation is pain. High pressure. A shallow to flat anterior chamber, particularly centrally. And this is the full blown malignant glaucoma presentation. Poor vision from corneal edema, and refractive changes. Because when that lens iris diaphragm shifts, the refraction changes. And there’s a normal posterior segment. And what we see on UBM here, on the slide on the left, and this is from Dr. Filipe, we see that anterior rotation, those red arrows, are pointing to the anterior rotation of the ciliary body. And then you can see on the slide on the right the forward displacement of the lens iris diaphragm. That’s iris smack up against the cornea in this picture. Right here. And here we can see from this paper… By Gonzalez-Martin-Moro, pre and postvitrectomy. And we look at the difference in the anterior chamber. On the slide on your left, the anterior chamber is a sliver. Everything is shifted forward. And after the vitrectomy, you can see how the anterior chamber is nicely formed. There’s an IOL in the posterior — behind the iris in the posterior chamber. And there’s a nice deep, deep vault on the anterior segment. So the differential diagnosis, when we look at people that have high intraocular pressure and shallow anterior chamber, who have pupil block, choroidal hemorrhage, and malignant glaucoma — and from what we talked about already, we should be able to make this differential. The difference between pupil block is because, in malignant glaucoma, there’s central shallowing, and the difference with choroidal hemorrhage is that in malignant glaucoma, the posterior segment is normal. The intraocular pressure is typically very high. But sometimes in malignant glaucoma, you can have a relative malignant glaucoma, and sometimes the intraocular pressure may not be high. So can malignant glaucoma not be malignant? And the answer is yes. So you can have relative aqueous misdirection. And that’s when the anterior chamber becomes shallow but not flat. So if the malignant glaucoma is starting, and the lens iris diaphragm starts to shift forward, but hasn’t closed off the angle yet, you can have shallowing of the front part of the eye, without actually closing the angle. And the intraocular pressure may not be elevated. The other way you can get high IOP in malignant glaucoma… Sorry, low or normal IOP in malignant glaucoma… Is if you is a functioning filtering bleb. So even if everything is shifted forward and you have closure, you may have a functional filtering bleb draining and lowering the pressure. And let me tell you about Mr. Just had cataract surgery. I had two of these patients right in a row. Very interesting. 60-year-old gentleman with hyperopia. 4.25 in the right, +3 in the left. Moderate cataracts, extensive PAS, normal IOP. Iridotomies at age 50. Short eyes. And we put in some CE and goniosynechialysis for long-term angle health. We put in a 28 diopter lens, so you know it’s a small eye. We gave him atropine in the operating room, which I strongly recommend any time you operate on a high hyperope or anyone with significant narrow angles with compromised angles. So I gave him atropine in the operating room. He had an uncomplicated post-op course. -0.25 in his post-op. Operated on his right eye a month later. He needed a 31 diopter lens. The OR didn’t have atropine that day, so I gave him additional cyclogyl, told him to get atropine, and the next day he came in and he said: Doc, my eye feels fine and I can read great, but everything else is blurry. He was -2.5 diopter refractive surprise. His pupil was still dilated. So it wasn’t that he wasn’t dilated. But with cyclogyl, you can get dilation without adequate cycloplegia. His chamber was formed centrally but shallower than the OS. There was normal fundus, no wound leak. Classic relative malignant glaucoma. We treated him with atropine and dorzolamide. So we’ll get to cycloplegia and aqueous suppression. That’s the treatment. And the next day he says: Getting clearer! He was -1 and his anterior chamber was deeper and only slightly shallower than the other eye. And post-op week two, doing great, -0.25 and with a deeper anterior chamber. I had two cases right in a row. Round two. 53-year-old woman with appositional angle closure scheduled for CE/Goniosynechialysis, 22 diopter lens was placed. Steep corneas. Left eye was treated intraop and post-op with atropine, came in post-op day 1 at 20/20. Other eye received a drop of atropine in the operating room. But she didn’t start it on her own. She came in again post-op day 1, 20/100. But J1+. Clear near vision. Refraction of -3, shallow anterior chamber and pressure of 11. And responded to atropine within the hour. One hour after atropine… Not sure if these pictures do it justice… She was deeper. And one week, she was perfectly normal with normal refraction. And I have other cases since then. So atropine, atropine, atropine. I’ve had a slew of nanophthalmic eyes. You have to use atropine postoperatively. So when I think of diagnosis of low or normal intraocular pressure and shallow chamber, this used to be my differential. It was serous choroidals, overfiltration, or wound leak after trabeculectomy. But now we can add to that… Relative aqueous misdirection. Relative malignant glaucoma. You can have a normal or low intraocular pressure and a shallow chamber. In terms of medical management, we have this stepwise approach. And again, we want to talk about cycloplegia, cycloplegia, and then some more cycloplegia. And atropine if you can use atropine. Or homatropine is really vital. Much stronger than cyclogyl. So cycloplegia is number one, over and over. And aqueous suppressants are also very helpful, as number two. And make sure you discontinue miotics. I’ve seen people come in on miotics and cycloplegics, and that doesn’t make any sense. And miotics can incite malignant glaucoma. So you want to get off of the miotics. So step wise. Atropine or homatropine.

And people may need it permanently. You have to be very cautious. I worked at the Shea Eye Institute and inherited a patient of Dr. Shea’s who was his nurse for years. She needed atropine for the last 30 years of her life. If you tried to decrease it, even every few days, she would just shallow up. Cycloplegia tightens the zonules, pulls the lens iris diaphragm posteriorly. And expands the ciliary body to make it easier for aqueous to percolate through. And it pulls the ciliary body away from that lens vitreous hyaloid interface. We’ve talked about that anterior rotation of the ciliary processes. This pulls — the cycloplegia pulls it back. Aqueous suppressants. So we want to decrease the amount of aqueous that’s maybe flowing back into the vitreous cavity. Beta blockers, carbonic anhydrase inhibitors. And alpha agonists. Possible hyperosmotic to decrease vitreous volume, antiinflammatories, and remember to discontinue the miotics. It’s written that 50% of attacks will end with medical management. Certainly it’s worth giving a number of days. Usually up to five days if people can be moderately controlled with medical management. But lasers can be helpful. And there’s no sense in waiting too long to go with laser treatment. You can perform an iridotomy if there’s not already one. And that’s really important. Just to make sure that there’s not a component of pupil block. But that’s not gonna treat the malignant glaucoma. For that, you need to do a YAG laser disruption of the anterior hyaloid. If they’re pseudophakic, go right through the center of the pupil. Through the PCIOL. If they’re phakic, go through the iridotomy and try to do it more peripherally. There are some reports that say it may be more efficacious to perform it inferiorly. Because that may open up some pockets of aqueous settled inferiorly. In the study, there were ten pseudophakic eyes with malignant glaucoma, first treated with inferior laser peripheral iridocapsule hyaloidotomy. That’s a laser through the iris, capsule, and hyaloid. And 7 out of 10 patients in this group had full resolution of the glaucoma. Three required pars plana vitrectomy, with zonulo-capsule-hyaloidectomy and inferior iridotomy, and they postulate that the inferior laser may better each the pockets of aqueous to break the block. You can also consider — and I haven’t done this personally, but it’s a very intriguing thought. Transscleral cyclodiode laser photocoagulation in pseudophakic or aphakic eyes to shrink the ciliary processes by coagulation to cause the posterior rotation and break the block. In this study, Lin described using low dose CPC and achieved durable resolution of malignant glaucoma. So as I mentioned, the literature states that about 50% of cases will not break with laser and medical management. But we have seen from previous laser studies that their results might be better. We didn’t understand in the past. We thought you could just do a vitrectomy and that would be adequate. But that’s not adequate at all. You need to break that hyaloid membrane and you need to establish a pathway of aqueous from the back of the eye to the front of the eye. Doing a vitrectomy, I can tell you from that first patient of mine, Mr. Dark cloud over my head, vitrectomy did not cure him at first. We need to do more than that. A pars plana vitrectomy, we also need to go from the front of the eye to the back of the eye with an iridozonulohyaloidotomy. So we need to get through the iris, the zonules, and the hyaloid. Get right through there with the vitrectomy. Need to remove anterior vitreous. As it turns out, you probably don’t need a complete vitrectomy, but you need to get a good bit of anterior and central core vitreous. And you need to create a durable conduit to connect the anterior chamber to the vitreous cavity. Most people will usually remove the lens in phakic people. In this study by Zarnowski, ten eyes of nine patients, pseudophakic malignant glaucoma, and they performed anterior chamber approach to a capsule hyaloidectomy with an anterior vitrectomy, and they did this through peripheral iridectomy. So this is not with trocars. This is just going from an anterior approach through a PI, right into the vitreous. And they were all… They broke all the cases, and did not have recurrences. And if you notice, we had 10 eyes of 9 patients. So it is really common if you have a problem in one eye, you may have a problem in the second eye. So you really need to beware. If this study again, by Balekudaru, 58 eyes with malignant glaucoma, in these, the majority of the eyes had the anterior rotation of the ciliary processes. They had success in 86% of patients that just had vitrectomy and lensectomy, but they had success in all the patients who had a connection between the anterior chamber and vitreous cavity. So I should qualify that. So some of those patients that had vitrectomy also had the conduit created between the anterior chamber and the vitreous cavity. The takeaway from here is that they had 100% success when they could create a pathway from the anterior chamber to the vitreous. So when you go in for surgical treatment of malignant glaucoma, a vitrectomy is not what you should be aiming for. You need a vitrectomy with an iridozonulohyaloidectomy. And this just shows a technique, a mini-vitrectomy. And this could be what they refer to as a simple solution to a serious condition. Where you make an incision just through the peripheral cornea. They nicely inject triamcinolone behind the IOL and you can see the vitreous very nicely. They put the vitrectomy probe right through. You can do an iridectomy through the iris into the vitreous cavity. You’ll see you’re taking out the vitreous because of the triamcinolone staining. And then it’s through a simple anterior segment incision. We tend to send these patients to retina, who will do a formal vitrectomy. But we make sure that our retina colleagues are aware that they need to create this conduit from the front of the eye to the back. There will be recalcitrant cases. And it often happens if there’s failure to establish communication or if that communication fails. There are patients that just have intense inflammatory reactions. And they can scar over all sorts of conduits. So if you can’t establish a pathway that stays because of whatever reason, things clogging it, or inflammatory membranes developing, you can be back to square one. What do you do in cases like last resort? What is your last resort? You can put a glaucoma drainage tube — if you have a complete vitrectomy, and you’re still in aqueous misdirection, which really happens, and I have unfortunately seen this, back in the ’90s… You can put a glaucoma drainage tube directly into the vitreous cavity. Because that’s where the fluid is going. And it can drain it right from there. You can also do whatever you need to do to establish a unicameral eye. You can take out the IOL. Leave them aphakic. And make sure… As long as that anterior hyaloid, and they have a vitrectomy with an aphakic vitrectomized eye — will not have malignant glaucoma. Because there’s no barrier. And so if you’re desperate and you have no other way of controlling this, that will always work. So back to my patient. This patient, back in 1995. Which, as you can see, has been very memorable for me… His second eye we said… Well, he’s already had failed non-penetrating surgery in both eyes. That’s how he was sent in to me. I did the trabeculectomy and got the first eye into malignant glaucoma. And he had floppy iris. The second eye, I’m just gonna put in a glaucoma drainage tube and keep that patient atropinized. I did all of that, and he developed malignant glaucoma, unresponsive to laser hyaloidectomy. And it recurred and it was intractable after vitrectomy, and we did remove the anterior hyaloid. But this was back in the ’90s, before we understood about iridozonulocapsular hyaloidectomy. And he was stabilized by IZHV. So preventative measures? What might I have done differently in the fellow eye? Certainly no matter what, we want to discontinue miotics. If someone has malignant glaucoma in one eye, make sure you never use miotics in either eye. And don’t be tempted to use miochol, miostat, or post-op pilocarpine after cataract surgery. There are some operating rooms where the post-op drop routine includes pilocarpine. You want to probably get that out of a routine post-op program. Because if you had people that are on the borderline with pretty narrow angles that you do cataract surgery, that little bit of pilocarpine can put them over. So you don’t likely need it. In a lot of surgeries. And you certainly don’t want to use intraocular miochol or miostat. I’m pretty liberal with using atropine after any high risk surgery. In fellow eyes, absolutely. But if I think the patient is a pretty high hyperope, they have PAS from narrow angles, I’ll give them atropine. Really commonly. I’ve just seen aqueous misdirection develop too many times. Try to avoid shallowing of the anterior chamber intraoperatively. Sometimes that just sets it off. And some people talk about doing the iridozonulohyalovitrectomy prior to incisional surgery in the fellow eye. That’s food for thought right now. What about intraoperative aqueous misdirection? As I mentioned before, suddenly you’re operating. And there’s a sudden increase in pressure and shallowing in the anterior chamber during surgery. First thought is always: Choroidal hemorrhage. And you establish that he’s got a great red reflex, maybe take a look in the back, and everything looks great. But you have a little bit of iris prolapse, try to put viscoelastic in and the chamber gets firm but not deep. You’re having relative aqueous misdirection intraoperatively. And it’s not that uncommon. So what do you do? What will often work is treat with atropine and just sit there. But it’s really hard for us surgeons to just sit there. Because you’ve got to wait a while. You can try some IV mannitol. And wait. But you still have to wait. And I usually give more. I give atropine and I will give neosynephrine also, or intraocular epi, to dilate. But it can take a while. It will often reverse with atropine, but you have to be patient. And most of us really don’t have a half an hour with the patient on the table to wait. You can… If you have a 25-gauge with a trocar, that’s the best. Just go right in with the trocar and it will deepen immediately. If you don’t have that available, you can decompress. The retina doctors aren’t in love with this. But you can decompress with a 25-gauge needle through the pars plana. It’s not ideal. It has its risks. But you go in a little bit, and with very minimal aspiration, the chamber will just… You get some liquid aqueous coming through and the chamber will just deepen. So if you have no alternatives, you can consider that. What are our key takeaways from this? In malignant glaucoma, there is an anterior displacement in both the iris and the lens. And this causes axial shallowing, including central shallowing of the anterior chamber. And that is what distinguishes it from pupil block, which only really has peripheral shallowing. Pupil block, it will look like the chamber is shallow because the peripheral chamber is flat, with iris bombe. But in pupil block, the central chamber stays deep. Whereas in aqueous misdirection, that lens can be right up against the cornea. Medical treatment is cycloplegia, cycloplegia, cycloplegia, and aqueous suppressants, aqueous suppressants. So you just have to really, really treat hard. And you don’t want to give atropine and tropicamide or mydriacyl, because it’s going to compete with the atropine. So you want to give atropine, if you don’t have that, homatropine, and strong cycloplegia, and don’t compete with your cyclogyl. Laser you can try. Medical treatment, one. Laser, number two. And surgical treatment requires the creation of a unicameral eye. There has to be a durable pathway. The aqueous can go from the back of the eye to the front of the eye. Beware of stopping atropine in someone who presents to you on long-term cycloplegic therapy. You’re like… I wonder why this is. They’re pseudophakic. Everything looks good. Just be careful. Not all malignant glaucoma is malignant, thankfully. When we operate on patients with angle compromise, short axial lengths, and shallow anterior chambers, remember, atropine is our best friend. I want to thank you. We have a couple of questions to ask you. And we can discuss those answers. And we can take questions and answers. And we have a nice bit of time that we can have a discussion. So malignant glaucoma always presents with… Serous choroidal effusions. Shallow anterior chamber. Highly elevated pressure. And corneal edema. If everyone could vote… Very good. So shallow anterior chamber. That’s the hallmark. Whether there’s posterior vitreous pressure pushing forward… And so it always presents with some shallowing. Maybe not flat. But some shallowing of the anterior chamber. There are usually no visible serous choroidal effusions. Now, there may be annular ones that we can pick up on UBM. But when you examine the back of the eye, you are not gonna see serous choroidal effusions. So that’s a little bit of a tricky one. Because often on UBM, you can find these annular peripheral choroidal effusions. But you’re not gonna see it on exam. Usually have elevated pressure, but we talked about those relative cases where they’ve shallowed, and maybe they have a myopic shift to their refraction, but they haven’t closed their angle yet. And so they will not have elevated pressures in those cases. Also if it happens in a patient with a functioning filter and bleb, you can have angle closure and a really flat chamber, but still have… Not have elevated pressures. Next question. Regarding the treatment of malignant glaucoma, surgery is always ired to treat malignant glaucoma. Vitrectomy is curative. Pilocarpine should be given frequently. And atropine and aqueous suppressants are the first line treatment. Very good. So atropine and aqueous suppressants are the mainstay of treatment. So that’s cycloplegia and aqueous suppression. That’s the classic way of treating malignant glaucoma. Pilocarpine should be stopped. That can incite malignant glaucoma. That was the cause of the malignant glaucoma or the inciting event in my first patient that I talked about. Vitrectomy by itself is not curative. It may help in some people. Sometimes they’ll relapse. So you need to get a vitrectomy, iridozonulohyaloidectomy. Create a pathway. Surgery is not always required. The literature says about half of cases will break on medical therapy. So let’s look at our Q and A here. So one of the questions is: What is the opinion about malignant glaucoma in normal intraocular pressure? So as I mentioned, you can have malignant glaucoma with normal pressure when it’s relative if the angle hasn’t completely closed yet. Or if you have a functioning filtering bleb. So how do you differentiate capsular block syndrome from malignant glaucoma in a post-op exam of cataract surgery? Usually relative malignant glaucoma after cataract surgery — if it’s mild and you’re trying to figure out what this is, they’ll is a myopic shift. So my patients came in for instance saying: I can read great but my distance vision is not good. And their post-op refractions were myopic. For me, they were both around a -3 or so. And if you look at the depth of the anterior chamber, if the other eye is pseudophakic, you can compare and see that it’s shallower than the other eye. It’s hard when one eye is pseudophakic and one eye still has their cataract. Because they may have similar anterior chamber depths. But the myopic shift is one clear way. I’ll tell you about a patient I had recently. This is a patient who needed 35 diopter lens implants. So this is a nanophthalmic eye. A very tiny eye. So I was really unsure. I did her first eye surgery. Definitely atropinized her. And she came in at a -1.50 in her first eye the first day. And she has a small eye. And her chamber was a little bit shallow. So I was trying to get her ready. I delayed the surgery in the other eye. Because I didn’t know if my IOL calculations were off. Because she’s outside of the normal range that we see when we’re figuring out intraocular lens implants. Or if she was in a little bit of aqueous misdirection. And it turns out she was in a little bit of aqueous misdirection. I let her simmer a little bit with atropine. And she settled down more to a -0.75. So she was in a little bit of relative… But in that case, it was hard. Because she has a tiny eye. She’s not gonna have a big deep chamber. And I was comparing it to her phakic other eye, which also has like a slit-like anterior chamber. How effective is laser iridozonulohyaloidotomy in cases of malignant glaucoma? The results are variable. So there’s a lot of different studies that look at this. I think it’s always worth trying. I don’t think it’s going to be the answer in the majority of cases. I think you should absolutely try to do a laser through the iridectomy. And really get through the zonules. And make a nice opening. And it will break some attacks. Whether they last is a different question. But absolutely try it. If you can. If the cornea is clear enough. You should absolutely try that before proceeding to surgery. Do you recommend iridozonulohyaloidotomy in a phakic patient? Yes, you can do it through a peripheral iridectomy. You can tie it. It’s hard. You don’t always know how deep you got. But you can try to make a big iridectomy, iridotomy, and then go through that. What about pars plana vitrectomy in malignant glaucoma? So yes. You can go in through the pars plana and have your retina doctors do a vitrectomy. Or if you do vitrectomies, through the pars plana, you absolutely can do that. But by itself, the pars plana vitrectomy is not the treatment for malignant glaucoma. You have to — after the vitrectomy, establish a pathway up from your vitreous through the zonules, through the iris, into the anterior chamber. And big enough that it stays open. So this is an interesting question. Regarding intraoperative fluid you misdirection, how do you differentiate it with suprachoroidal hemorrhage when the lens is already obscuring the posterior view, because aspirating the vitreous will precipitate a suprachoroidal hemorrhage. So you certainly don’t want to stick a needle in the back of the eye without knowing what’s going on back there. It’s always good to have a way of looking in the back of the eye, in the operating room. If you have a lens that you can use to look in the back. If not, you can look for a red reflex. So if you have a red reflex, have the patient look up, down, right, and left, and you have a good red reflex, it’s unlikely that you have a suprachoroidal hemorrhage that would be causing shallowing of the anterior chamber. So with aqueous misdirection, you’re gonna get this issue in the eye, but you’re gonna have a good red reflex. It’s not going to alter the red reflex. So I think that’s your best bet if you don’t have a direct in the operating room. What is the disadvantage of transscleral diode laser for recalcitrant patient, versus lifetime atropine? It’s something that really needs to be studied. It’s an intriguing issue. You don’t want to do enough diode laser that you have that popping. You want to contract the ciliary processes. And perhaps there’s even a role for endophotocoagulation, where you go with an endo probe to actually laser the ciliary processes. That’s used for angle closure at times also. So I imagine just changing the ciliary process interface, and you can shrink down those ciliary processes by whatever means. But you have to be careful with this transscleral, because you don’t want to just burst them. You want to do a low, slow contraction burn. I think this is an area that really needs to be studied more. There’s a question… Trab in phakic eye, having risk factors. So atropine, atropine, atropine. When you’re doing a trab in those people, you need to keep them cyclopleged. There are some people… If the patient has had a full blown malignant glaucoma attack in the other eye, then you may want to do a vitrectomy, iridozonulohyaloidectomy before the surgery. But certainly if you do that trab, keep them seriously cyclopleged, and watch them very closely. And the first sign of any problem, you would definitely want at least to do the laser. So the question is: Is the management protocol the same for intraoperative glaucoma in congenital contact extraction? So I’m not speaking from experience. But certainly atropinizing is important. And I would be a little afraid to do your posterior capsulotomy with… When they’re right in this aqueous misdirection. But if you do and go right in with the vitrector, I’m gonna defer that. I can always… If we send a message through Cybersight, I can really get better information on that. When would be the best time to approach that. Can you consider malignant glaucoma in acute angle closure attack… Especially in younger individuals with no significant cataracts? So any time you have high pressure and angle closure, you have to go through the entire differential. So not everyone is primary angle closure. So any time you have an angle closure, you have to go through the whole differential. So you should absolutely consider malignant glaucoma. In people of any age. So… Certainly it gets more common as we get older and our chambers get shallower. But it can happen at any age. Especially in nanophthalmic eyes. Or in any small eyes. With shallow anterior segment. So what are the settings for vitrectomy with hyaloid zonulectomy? High or low aspiration? I usually use low. I don’t want to pull on the vitreous but make a nice hole. So it’s usually high cut rate, low aspiration. Why can’t you stop atropine on longstanding cycloplegia patients? I didn’t say you can’t stop it. The reason I suggested to be cautious is that some people may be on that longstanding atropine because they have a propensity to go back on malignant glaucoma. Sometimes malignant glaucoma is not an acute event. It’s kind of a lifestyle. This person is always going to have a tendency to malignant glaucoma, and may always be a little bit of cycloplegia to keep them out of trouble. That’s not the case for everyone. Most of those cataract patients that get a little bit during the early post-op period, you can taper them off pretty quickly. But occasionally you’ll have a person that has severe malignant glaucoma. That can be fairly intractable. And that person you may need to keep on atropine long-term. Do you recommend prophylactic surgical IZHV in nanophthalmic eyes during cataract surgery?

No. Some do. Some people do. Certainly if you run into trouble in the first eye, I would consider it in the second eye. But most of the time, you don’t get malignant glaucoma. I mean, you can get effusions. Choroidal effusions are really common. Much more common just diffuse choroidal effusions, but not necessarily full blown malignant glaucoma is more common in nanophthalmos. So I do not do IZHV in nanophthalmic eyes during cataract surgery routinely. If the patient had a problem in the first eye, I would definitely go in the second eye. I’m just gonna read this one out loud and we can work on it together. I’ve experienced what seems like a mild form of malignant glaucoma postoperatively in a myopic patient, IOL with 16.5 diopters. Postoperatively 5 days, presented with shallow anterior chamber and corneal edema with intraocular pressure of 49. Resolved on atropine and acetazolamide. Intraocular pressure normal now but have not stopped atropine drops. You can have malignant glaucoma with any refractive error. Because it’s more common in small eyes. And it’s more common with people with high hyperopia. But it has to do with however the relationship with those ciliary processes and the hyaloid zonular interface is. So it sounds… Likely. If there was nothing on posterior segment exam, what you’re describing… Aside from the myopia, it sounds very classic for malignant glaucoma. In this person, you could probably, since it was acute, it was a single episode, over time, you may be able to taper off the atropine. This may not be one of those people that needs to be on it for life. But it may have been this inciting event of cataract surgery. It is unusual in a myopic patient, but it’s not unheard of. I’m trying to think if there’s anything else that would have set this off. But if they had central shallowing and normal posterior segment, there’s not much else. So I think this sounds like malignant glaucoma, and certainly it responded to the treatment, which was so beautifully appropriate. Atropine and acetazolamide. And I think you should feel safe to very slowly taper off the atropine. But watch them. And if they start shifting more myopic, get them back on the atropine. Is it still safe to use pilocarpine before surgical PI when done during a trab? So yeah. I’m not saying you could never use pilocarpine. I’m just saying if you use it routinely, on every post-op cataract, you’re gonna wind up putting it into some hyperopic eyes. Unbeknownst to you, maybe. Maybe they’re the post-op staff or surgical staff will just plunk it in everyone’s eyes. And they’re gonna put it in some high risk eyes. So I’m not saying you can’t use it. But just be careful when you do. And know that you’re doing it. So yeah. If you want to use pilocarpine before iridectomy, absolutely. We still use pilocarpine often before a lot of PIs in the office. Just be conscious that it’s happening. So I was talking more about… Beware of… Unbeknownst to you, your surgical staff has a routine of putting pilo in everybody. Know when you’re using it is all I’m saying. So high pressure in one eye with malignant secondary glaucoma with risk factors for the contralateral eye? I’m not sure what the question is there. So if you get malignant glaucoma in one eye, that’s a risk for the other eye. So you want to be aware. Take necessary precautions. If you’re just doing… If you had mild… Like with a cataract surgery, you want to be sure to atropinize. If you had surgery, you want to be aware and take care before. Is vitreous length on biometry useful for diagnosis and follow-up? So we generally use axial length and anterior chamber depth. So I guess you can sort of compute the vitreous length. But usually if you have a shallow anterior chamber, shallow anterior segment, if you have large lens thickness, high lens thickness, and short eye, those are definitely gonna be risk factors. If vitrectomy is not definitive cure for malignant glaucoma, would you consider cataract surgery definitive treatment? I want to really stress: The answer is no. So cataract surgery is not definitive. In fact, cataract surgery can incite malignant glaucoma. So the only definitive-ish — nothing is ever definitive in eyes, right? The only recommended treatment that has the best results is creating a pathway from the anterior segment to the vitreous cavity and having a fairly nice core vitrectomy. So vitrectomy by itself is not gonna do the trick. Because fluid can still go behind that hyaloid. And once it goes behind that hyaloid, that hyaloid becomes less permeable, and the fluid can’t get back, and the vitreous cavity, even in a vitrectomized eye, can expand. So you need a pathway, a conduit, from the vitreous cavity to the front of the eye. So cataract surgery is not gonna be the answer. Vitrectomy — if you’re going in there to do a surgery for treatment of malignant glaucoma, do not just do a vitrectomy. You’re in there already. Do a vitreoiridozonulohyaloidectomy. Let’s see. So someone asked me about an artisan. And I don’t know what that lens is. If you want to put in another text… Another… Is that an iris lens? Is that an iris fixated lens? Those kind that are in the pupil? If you want to put another chat in. I just don’t have experience with that lens. So just let me know what that is. So there was a question about how atropine and other glaucoma drops affect the heart in long duration. Atropine… You can certainly decrease the systemic absorption of any medication. With punctal occlusion. So… Pressing right in here, to close the puncta. And keeping your eyes closed. So each time a patient blinks, it drives the fluid through the nasolacrimal drainage system into the nose and from the nose and the pharynx… That’s where medications get absorbed. Systemically. They don’t get absorbed systemically so much from the eye. So with any glaucoma medicine, if we can encourage punctal occlusion, pressing here, keeping the eyes closed, you tell patients… Listen to a song on the radio. Or it’s a really nice time to meditate and really rest. And meditation has been shown to be really helpful for glaucoma. So you can really decrease… Increase the absorption of the medicine in your eye, decrease the systemic absorption, and help lower your intraocular pressure and improve your total body health by meditating for three minutes. Like this. With your eyes closed. Or listen to a song on the radio. It’s probably… I tell people it’s probably the only relaxing time you’re gonna have all day. So just enjoy it. So that can decrease, if you have concerns about the glaucoma medications. Atropine… I mean, it can have effects. I’ve seen people that take a lot of atropine have trouble with urination. I don’t think there’s any long-term research that shows it’s detrimental to the heart. Certainly our other glaucoma medicines can have systemic side effects. Particularly beta blockers. And our alpha agonists can have effects on cardiac function. I’m not sure they’re necessarily long-term detrimental to the heart. But we do like to try to decrease systemic absorption as much as possible. And increase ocular absorption with nasolacrimal duct obstruction. So if the artisan lens is this iris claw lens, I think that… That could be a problem in creating a unicameral eye. I don’t know how tightly they fit. I’ve only actually had one patient at this point that has one of these lenses. So I don’t really have good experience with it. But if you’re trying to establish unicameral eye, through the pupil, and that lens blocks… Then that could be a problem. I think it’s unlikely that they’re gonna completely occlude the pupil. Because then everyone that had an artisan lens would need an iridotomy. And I’m not sure that everyone had an iridotomy that had an artisan lens. So I don’t have a firm answer on that for you. But most iris claw lenses that I’ve seen in the past… Had areas for aqueous to percolate. I don’t think it would be ideal. But I don’t think it would be an absolute contraindication. Just because it doesn’t completely occlude the pupil. But I don’t think it’s ideal. (reading question) atropine, aqueous suppressants… And then… If that doesn’t break the attack… You can try… Oral or IV Diamox, mannitol, some other hyperosmotic. But if that doesn’t break the attack in a few days, you’re probably gonna need to go in surgically and do vitrectomy with iridozonulohyaloidectomy. Can you use tropicamide? It’s not gonna give you enough cycloplegia. It’s a much better mydriatic than cycloplegic. The strongest cycloplegic is atropine, next strongest is homatropine. Which I guess is scopolamine. Then cyclogyl and then tropicamide. Tropicamide has much more dilating properties and much less cycloplegia. It’s not enough. One of my cataract patients I treated in one eye with atropine, the other eye didn’t have atropine, I used cyclogyl, that was not adequate. They went into relative aqueous misdirection with the cyclogyl. For a general glaucoma patient… What do you recommend for pediatric patient with two glaucoma drainage implants, two lowering IOP drugs, IOP still in 25 to 30? I’m assuming this patient had angle surgery already. Certainly if this patient did not have angle surgery and it’s a pediatric glaucoma patient… I would do GATT procedure or any other kind of goniotomy procedure. I’m assuming if this patient has two tubes, they already had goniotomy. But if not, I would do that. Other than that, you probably want to do a little bit of diode laser cyclophotocoagulation. This has nothing to do with malignant glaucoma. But this was a question… What do you recommend for a pediatric patient with two glaucoma drainage implants and two IOP lowering drugs. So if they haven’t already had a goniotomy or trabeculectomy angle procedure, GATT. And if not, at this point, a little bit of just a very gentle diode treatment. Is atropine a routine post-op drop for all of your postcataract hyperopic patients? If so, how long and at what frequency? Do you routinely not use miochol on these patients as well? Absolutely no miochol post-op on patients who are hyperopic. You don’t want have a routine of dropping it in everyone. If you drop it in these patients, you may put them over the edge and send them into malignant glaucoma. I don’t use atropine on every hyperopic patient. But any hyperopic patient that has… Particularly small eye, anyone that needs over 30 diopter lens, I will use atropine. And even 28 and up. But if they have angle compromise — so this is assuming that you have gonioscoped every one of these patients. Which you should be doing. Every patient deserves gonioscopy. And especially if you have hyperopic patients, they all deserve gonioscopy. So know what you’re dealing with. Know what your angle looks like. If you have a compromised angle, going into cataract surgery, they have some PAS, borderline… Maybe they have an iridotomy, maybe they don’t, you’re gonna treat their narrow angle with cataract surgery. You want those patients that are at higher risk — you want to treat those with atropine. Sometimes you can just give them a drop in surgery. Beginning of the case, end of the case, at least at the end of the case. Sometimes when I see first post-op day, I’ll put one drop in, and that may be enough. If they’ve had malignant glaucoma or relative aqueous misdirection in the other eye, I will keep them on it for a little bit longer. Maybe a week or more. (reading question at low volume) I’m not sure what the question is. But it’s about someone who has a normal disc but superior visual field defect. So this has nothing to do with malignant glaucoma. But discs can sometimes fool you. You always want to make sure you know about what disc you’re looking at. And if you have a disc that’s small, you always want to know the size of your disc. If you have a disc that’s small, you may miss the fact that there’s glaucoma in there. Because you could have a 0.2 cup and have glaucoma. Because a small disc should have small to almost no cup. But that’s another lecture. And actually… If you look at… There should be posted an optic nerve lecture that I did. That should be posted on Cybersight that will have a lot of answers to those questions. And I think… Have you tried doing a vitreous tap in these cases? Yes. If you have intraoperative aqueous misdirection, you’re operating, everything is going great, all of a sudden you take your probe out, and the iris comes out with you, you try to put some viscoelastic in, and the eye gets firm, right away, but the chamber is still shallow, and you know you have a good red reflex everywhere, you looked in the back and everything is fine, that’s when you start to plunk atropine on the eye. Start to put some mydriatics as well. But definitely… Atropine. Maybe some epi. Or neo. Try to wait a little bit. Maybe give a little mannitol. But ideally, you use a trocar. If you don’t have one, a needle through the pars plana will do the trick. The retina specialists won’t always be happy that you do that, but it’s rare to have a problem with that. You don’t want to pull back hard on the plunger of your syringe. You want to release a teeny bit of aqueous pockets from the vitreous cavity. And a teeny bit. That eye will deepen and soften and be able to finish the case. And then you want to finish your case and keep the patient on atropine. Atropine. I wish I had stock in it! Atropine. Atropine. Atropine. For the treatment of malignant glaucoma and aqueous suppressants. I think we might have come to the end of the talk. It has been such a pleasure to interact with all of you. I can always be reached through Cybersight if anyone needs anything. And I wish everybody a very good day. Or night. Wherever you are. Thank you so much.