 Okay, so what I want to talk about today is the management of glaucoma secondary to anti-vegeta therapy. We're going to start with a patient. This is a 94-year-old patient that's been a long-time patient of Dr. Zabriski's, who came in for a routine exam as a history of neovastor glaucoma secondary to a BRVO in the right eye. He also has pseudo-exfoliation glaucoma, right eye worse than the left eye, and he's received multiple bevacism ab injections. He says maybe greater than 10, but he can't really remember, and he sees an outside provider. And his pressures have been controlled on max therapy. He says his injections probably started about two to three years ago. We also can't really recall when exactly that started. But his pressures have been controlled. He's on co-sobbed alpha-gan and latana prost in both of his eyes. His pressures were 18 in both eyes in July of 2013, and then slowly over the next two years they started to increase, but still pretty tolerable range, range in the mid to upper teens. But he comes in on December 17th with a pressure of 43 in the right eye, and his vision had slowly dropped over the past few years from 2,100 to light perception in the right eye. So just quickly the exam from the 17th of December, these light perception in the right eye's pressure is 43. He has some corneal edema and a hazy view, some pseudo-exfoliation material by the iris, but no neovastorization of the iris. He's pseudo-fated, has a pretty big cup to disc ratio, and some collateral vessels there and advanced AMD in the macula. The left eye also noticeable for an elevated pressure and pseudo-exfoliation material and a pretty advanced cup in that eye as well. So just some basic glaucoma in the agonioscopy on that right eye did show some neovastorization that day in December. His packies were normal at 560 and 541. And then we'll look at this field. This is his last field that we were able to get in 2012 because of how poor his vision was in the right eye. And you can see the amount of generalized depression and essentially it's a central island, a very, very small amount of field left in that right eye, and then we hadn't gotten any field after this point. The left eye is also significant for generalized depression. Maybe some missed rim points there, but just an early inferior nasal step in that left eye as well. So this day his pressure is uncontrolled. He started on diamox. It's kind of the only option we have left at this point. And his pressure gradually comes down. The next week his pressure I think was 36. The week after it was 28. But he's 94 and can't really tolerate this diamox. He's not feeling so great. But the patient's very hesitant on having any type of surgery. So kind of what are the options at this point? He's supposedly had an SLT in the past in the right eye in 2007 or 2008. But what options do we have for this patient? Clearly a 28 is still too high and he can't tolerate the diamox, so we can't really leave him on it. So just some options. You always start with the least invasive. Can we do a mixed surgery with him? He is pseudo-facic, but is really putting an ice dent or doing a trabecular mesh work surgery really going to get his pressure down enough from how high up it is. Should we do a trabeculectomy? Should we do a tube, either a valve device or a non-valve device? Any thoughts that anyone in the audience has about kind of what to do at this point? So he actually did get an injection on the 31st with an AC tap. Yeah, no, I didn't say it. So he did end up getting that. And the reason he hadn't gotten recent injections was because of how high his pressures had been at the outside provider. Yeah. So just, yeah, no. This is something to... Would anyone do a trabeculectomy as the first, as the primary surgical approach? Usually the majority of these patients end up getting a... Go ahead, Eileen. No. So I think one of the things that we have to think about also for this patient is that he does have active neovastorization and it keeps needing to get injections to control that. So I think that was another consideration for him, that we needed his pressure to be lowered. Could we have considered just doing a diode laser for him? That's also an option with how poor his vision was in that eye. So before we talk about kind of what we did, I just want to talk a little bit about just what is the mechanism of this anti-vegeth is that what's the role of that in creating these increased pressures. So there's a lot of theories. There's the acute rise. It's pretty well-established in intraocular pressure, significant increase in vitreous volume. A lot of... There's some studies that have been shown that the practitioners will use combagane or some sort of an aqueous suppressant when they do do these injections, just the day of and the day after. Some people routinely do an AC tap after they do the intravitral injection to decrease the acute rise in their pressure. And then Leswell establishes, what is this delayed elevation that we're kind of seeing? Is it from the pharmacological properties of the medication itself? Is it from an inflammation, a trapeculitis that's created with these injections? And is there an increase in the amount of residual medication that's in the aqueous after multiple injections that patients get? So, you know, there's...reviewing all these studies, there's probably about 12 to 15 studies that have kind of looked at this. There's really...no one really defines... Everyone defines their sustained increase in IOP very differently. Some people will say it's over 21, others 24. Some people define it as greater than six over baseline and others 10 over baseline. So, a lot of these studies are kind of hard to compare. And what they report is that the incident ranges from 3.45% to 11.6%, with a few patients requiring surgical intervention. One small study said... I think it was just a study with 25 patients, but 23 needed some sort of intervention, but only three required anything surgical happening. And some of the risk factors that these studies have shown include just having a history of glaucoma, fakia status, and the history of steroid use, and then also an extended treatment duration. So, just some of these studies that were... So, in 2014, the study actually had 83 patients that used bevacizumab for AMD with a mean number of injections, about four, and they actually showed no significant increase in IOP. Segal, this is a study from Israel that's much larger of a study size, and they showed a 4.5% of increase of greater than 24 with even up to 70 as high of a pressure. And then in 2014, this very large study with about 1,100 patients, they looked at ranibizumab for AMD, and they showed an increase in IOP in 9.3% to 13% of the patients that they looked at. It's also the... Some studies have shown that it's a number of anti-vegeta injections. Is it, you know... Is there a correlation with the number of patients? Another study showed it was greater than 20 injections would lead to this increase in sustained IOP. So this study showed an 11.6% increase in the patients with treated eyes who had an increase in sustained IOP elevation. And then is there a big difference in the anti-vegeta drugs? You know, we use bevacizumab, ranibizumab. Those are really the two drugs that have been looked at for this. None of the other ones have. And in 215 eyes, they showed an increase in sustained elevation of 9.9% in bevacizumab versus 3.1% in ranibizumab. And some of the theories for that is, is it the fact that the medication bevacizumab is a bigger drug size than ranibizumab, about three-folds larger? And is there some effect it has in the trabecular mesh work? So this is just kind of the interesting things that were kind of reported on this. There's no really randomized control trials looking at this. So it's a lot of retrospective studies that kind of looked at this to see what their rates are. So for our patient, we actually ended up doing an Ahmed valve about four days later. He ended up in the hospital that night because of his reaction to dimox, and he wasn't feeling so great. Surgery itself was really uncomplicated. Post-op day one, his vision was light perception, stable. His pressure was two. Usually with these Ahmed valves, we don't have pressures this low on day one. And then usually if we do, it gets better over the next few days. But for him, his pressure went up to four, and then back down to one, he started developing corrodals. And then on day five, he had severe pain. It was, of course, Saturday morning. He was NLP, and he came in with these kissing corrodals with the pressure of one. So, you know, it's an Ahmed valve. It's not supposed to be, you're not supposed to do as much hypotony with these valves. The acute decompression of the eye, his pressure went from 28 to one. There's no leak around the tube. You always are concerned for that when this happens with these devices. And does he just have serri body shut down from all the drops he's been on chronically for so many years? So, really quickly, just the management of these curatal effusions, we ended up stopping, his luck home of medicines got stopped on day one. We increased, we put him on oral steroids, and we added cycloplegics. And then the big consideration is, do you do surgical drainage for these effusions or do you just watch them? So, one of the things is, should we have done something differently in the operating room? Should we always leave viscoelastic in the eye just a little bit? It's viscoe, but should we have left a kind of a denser device, like Helon GV or Helon 5? Should we have decreased the size of the lumen? Just to decrease the amount of outflow that would go through the valve initially. And then should we have put a non-valve device? Some of these, yes, later on they can cause hypotony, but if you ligate these non-valve devices off, they allow that rate of hypotony early on to be pretty low. So, is that something that we should have considered? So, our patient, you can see here, his pressure went from 46, and he eventually came back up after it went down, stayed between zero and four for about two weeks post-op, and they slowly started coming up. We ended up not operating on him. Like I said, he was really hesitant to have surgery, and he knew he just couldn't see well out of that eye. And now six months later, his pressure is eight in that right eye, but he's back on everything. And one of the big reasons that we kind of brought this case up is we kind of had an interesting series of patients over about one to two months, a series of patients that had really high blood pressure, had been receiving injections under what Ahmed valve placements, and a lot of them ended up with cordial effusions post-operatively. We were thinking, you know, is there something wrong with the Ahmed valve itself? Is it really, is there something wrong with the valve system? It's not working. But we looked at the valves, and they all had different lot numbers, so it's probably not a valve issue. But, you know, is there some other etiology of these patients going from such a high pressure to so low and then getting these cordial effusions? And it's really, we've only really seen it with the patients that have received anti-veget therapy, so anyone kind of seen this or have any thoughts on what could be doing this? So, that's all. Yeah.