 This is Glaucoma, but before we get to Glaucoma, we have the pleasure of going back to Lisbon and here again we see the Dr. Zeus Castle here in Lisbon. And it's a very interesting mixture of Dr. Zeus, maybe a little Gadi in there and the Moors and you name it. So that's the castle. Well, the pointer works. All right. We'll just go this way. All right. So this is the main dining room. As you can see, it kind of looks like the dining room in my house. Very similar. A bit, I mean, you know, as expected, you would expect the dining room to be kind of ornate and so very ornate dining room. This was the part of the chapel and again the theme is, but interesting, but again kind of Moorish tiles around it. So very interesting mixture of different influences, you know, in Portugal for through the centuries. And then you just go through the living quarters and this is just one of the handmade closets and the vases, excuse me, if you want to sign it, tell you to say vases, the vases, some of the vases that are in there. And again, this is Jade, by the way, a very ornate Jade. You've got this Jade lion over here. So again, very, very ornate fixtures as you wander through, except this was put in in the turn of the century, a telephone. So they did bring it up to speed. You've got a telephone right here. It's just a little bit different than the cell phones that you guys carry. But imagine answering pages on this call, this phone. Okay, so we're going to talk about the glaucoma and we can't talk about glaucoma without talking about the pathology of the anterior chamber angle. So I'm going to, I always go randomly here because you guys won't know where to sit. So Teresa, you are sitting here. What are we looking at right here? All right, we're looking at the trabecular mesh work and the structures of the anterior chamber angle. So when you are looking at the angle through a goniomere, you put a goniomere on there and you're looking into the angle. What's the first thing you see here as the cornea ends? Shwabbi's line. Shwabbi's line. And then as you go down here, you'll see a little more whitish line, a little bit lighter colored line. Well, this is where it's membrane is where Shwabbi's line, that's where it ends. So we're looking here at the mesh work. So they've divided it into non-pigmented and pigmented mesh work. And so when you look with your goniomere, the part that's closest to the cornea will be lighter colored. The part that's further posteriorly closer to the IRS will be darker colored. So there's Shwabbi's line, the non-pigmented trabecular mesh work, the pigmented trabecular mesh work. Becca, what is this structure right here? If you look in, that will look like a little white. That's the scleral spur. So if you think about it, the trabecular mesh work is shaped like a triangle. So the apex is here, the base is down here and the scleral spur sticks out and makes a little shelf for it. So if it goes around 360 degrees, the trabecular mesh works like a triangle sitting on that shelf. So here's the scleral spur right here. And then we've kind of cut it off here, but what is deep to the scleral spur? Chris? So, well, first before the scleral body, if you look into the angle, you may see part of the iris root. Exactly. So the iris root and then scleral body, and so that's what you'll see when you look in there. So the toughest part is, you guys are going to have to do gonioscopy a good, you know, several hundred times, because when you look in there, it's not like the book. All those little lines don't really define themselves easily like it does in the textbook. So it makes it a little bit more difficult. So you've got to really look inside because you need to know, is that angle open? Is it closed? You know, is it recessed? I mean, you really got to know your landmarks when you look there. Okay, so one more structure we're looking at right here. Fellows get pinned too here. So Josh, what is this structure right here? Is that Schlem's canal? Schlem's canal. So, you know, and for those of you who have followed the old movie, Schlem was the fifth stooge. You know, there was molary, curly, shamp and then Schlem, no. So Schlem's canal, interesting name. So this is Schlem's canal and then what is this structure right here? That's actually right here. Okay, just an aqueous vein. It's an aqueous vein, exactly. So let's go to a little bit of a higher power here. All right, so Nathan, we're zooming in here and Josh mentioned a tissue. Exactly. And so what's important about the juxtacanalicular tissue here? Exactly. So you need to remember that when aqueous flows through the trabecular mesh work, it's not just passive. There's even some active transport and it's interesting that glaucoma is probably the second most common disease that we treat, yet we don't understand it fully, you know, open-angle glaucoma. So the bars of trabecular mesh work have collagen in them. They've got elastin in them. They do have endothelial cells around them, but this area right here, the juxtacanalicular tissue, there is more than just free flow. So there's some obstruction there and so people are really coning in on this area because we really think that when you have open-angle glaucoma, this may be where the pathology is. So slums canal, if you think about it, it's like a flattened, like an inner tube that goes all the way around. Again, it goes around 360 degrees. It's this flat tube and again, here's an aqueous vein that we're looking at. There's a close-up. There you see the endothelial cells in the juxtacanalicular tissue that line slums canal. It's almost like an emphatic channel. It's not got a complete endothelial lining around it. All right. So, Rhys, what we're going to do is we're going to trace the path of aqueous. Where is aqueous made? All right. So it's made in the ciliary body and then where does it go? Okay. So then it goes through the angle, the juxtacanalicular tissue, slums canal. And then what are these right here? Aqueous veins. So, aqueous literally drains out through the veins, through the sclera and then there's some areas, some little veins that are right on the surface of the episcleral tissue here. So I always give you guys this assignment every year and we always forget about it. But every once in a while, look at the area just behind the limbus with your slit lamp and focus deep and you'll see little vessels there and then you'll see some boxcar. And so you'll see a little bit of clear fluid squirting through there and then you'll see some RBCs in it. So you'll actually be able to see the aqueous veins if you look carefully. So I mean, this is one reason why you can get a secondary glaucoma from increased venous pressure. So see, you've got a disease, you've got an AV malformation, you've got something going on. You can get glaucoma from increased venous pressure which causes a backup of that aqueous flow out of there and causes increased pressure. All right. So we're talking about open-angle glaucoma here and what the point I wanted to stress here is that if you look at the trabecular mesh work in a patient with open-angle glaucoma, you cannot tell any difference with light microscopy from glaucoma to an age match control. Now, trabecular mesh work changes from 20 to 70, but if you take a 70-year-old with glaucoma, 70-year-old without glaucoma, they look the same. Now with EM you can find some subtle differences, but with light microscopy they really look the same. So you don't really see any differences there. All right, Tina, what are we looking at right here? All right, so you see these radial spokes here with transillumination, so there's being pigments scraped off the posterior iris and it's in this radial pattern. Why do you think there's that radial pattern to it when you see pigment dispersion? Exactly. So it's where the zonules rub. So what we want to do when we're starting to look at glaucoma, we want to characterize it. And the first thing we do is you say, is it open-angle? Is it closed-angle or whatever? So when we look at open-angle glaucoma, we first look at primary open-angle glaucoma, where it's open-angle glaucoma with nothing else going on, but there are secondary open-angle glaucomas. And one of the secondary glaucomas is pigment dispersion syndrome, pigment dispersion glaucoma. So what is thought to happen in this entity is that, for some reason, the iris bows backwards. And we're looking at the posterior surface of the iris here, cylinder body here. And if you look right where the zonules run, those zonular bundles scrape on that posterior iris that's going posteriorly. And so you get pigment liberated there. And then, of course, it floats through the pupil and deposits into the trabecular mesh where it's causing pigment dispersion glaucoma. So it's an interesting entity. It occurs in younger males who are moderately myopic, not high myopes, moderate myopes. And for some reason, their iris pushes posteriorly. And before we had OCTs, it was really hard to judge that. Now you put an OCT on. You can see it in a second. And the treatment is you actually do a laser iridotomy. And the iris will actually come forward a little bit. And you can help decrease the pigment dispersion with that. So I have to show path pictures to path fellows. And so what am I illustrating here? There's three things right here I want to show in this one picture. So pigment in the stroma. And look, what's happening here? Actually, so pigment scraping off here. What's the second thing we see? Pretty much you can say all through the mesh work. I mean, there's pigment on there. So if you put a goniomere on there and look, you would just see dark, really be dark with pigment. There's a third thing on here. Hard to tell thickness, but if you look closely, you even see pigment dusting on the corneal endothelium. And so it's interesting, because of the patterns of the way the aqueous flows, you get a deposition in a certain pattern. Thresa, what's the pattern you see when you shine a slit lamp on a person with pigmentary glaucoma and you look at their cornea? That's so exfoliation. Kuchenberg spindle, exactly. So Kuchenberg is just the guy who described it. And if you look, the pigment will deposit kind of in the lower third of the iris in a little triangle, almost. So it's called the Kuchenberg spindle. So you see the pigment on there when you look with your slip beam. You'll see little pigment deposits all over. That's, again, a sign of pigment dispersion. And then eventually, you can get pigment glaucoma. All right, now, Becca, this is another potential cause of secondary open-angle glaucoma, which we're showing here. It's actually kind of stretched out there. What's going on right here? Believe it or not, those are pigmented cells in there. So what could cause a picture like this? We've got a whole bunch of pigmented cells in the ciliary body moving into the angle. Believe it or not, this is a melanoma. And so you can get a secondary open-angle glaucoma from a tumor invading the anterior chamber angle from behind. So here's the iris. Here's the cornea, trabecular mesh work here. And you've got a large, ciliary body, heavily pigmented tumor invading the angle. So this is a secondary open-angle glaucoma due to a tumor invading it. So don't forget, you can get a tumor invading it. And here's just another view. Here's the iris back here, cornea up here. Look at the space in between these. You've got this tumor in the ciliary body invading forward into the mesh work and into the anterior chamber angle. So secondary open-angle glaucoma from a malignant melanoma of the chloride. Chris, what are we seeing right here? Pollution. Why do you have that particular pattern where there's some in the periphery and some in the center and clear in between? You've got the windshield liper effect of the iris contracting and invading. Exactly. So that's why you see this. The iris, every time it goes in and out, looks like a windshield liper. It sweeps the exfoliated material more toward the center to the periphery, but there's a relative clear spot that's right there. And here you can see. We call this the scalloped edge look. You look in the periphery. You see the scalloped edge of this exfoliative material that's deposited on the anterior lens capsule. Why would I be showing you pictures of exfoliation on the lens capsule again in this lecture? Exactly. And so you can get a secondary open-angle glaucoma from exfoliation syndrome. And the thing about exfoliation syndrome, you guys need to remember, when you see these people in clinic, you've got to watch them really close, because they can go downhill very rapidly. So you can watch them, and the pressure's OK, pressure's OK, and then suddenly the pressure will shoot up, and it's pretty rapid. So you've got to keep a close eye on people with dense exfoliation. And so again, here's the classic, what do we call this, pattern again, Chris? The iron filings. And so here you see lens capsule. Which capsule is this? The anterior capsule. And how can we tell that? Exactly. You see, you were awake for that lecture. This is a good sign. So here's the anterior capsule, lens epithelial cells under it, and the iron filing pattern exfoliation. What are we looking at right here, Josh? Exactly. So you see exfoliative material here actually clogging up the angle. So there's a couple different mechanisms that you can get glaucoma from sort of exfoliation. One is it just physically clogs the angle. But you also get, you can even get little exfoliative material even into the trabecular meshwork, into the bars of the meshwork, even into Schlem's canal. And now this stuff is all over. So when you're on board exam and they're asking you about exfoliation in the eye, it's not just on the lens capsule. It gets into corneal endothelial cells. So you have more chance of corneal edema. It gets into the iris cells. It even gets into the iris sphincter and dilator muscles. So this stuff gets everywhere when you look at it. But the one thing that you want to be concerned about is the fact that it can cause pretty significant opening of glaucoma. And this is one of the glaucomas that has really helped by doing cataract surgery. Because when you remove that whole scaffolding of anterior lens capsule that's got exfoliative material on it, that helps to decrease the burden. But also when you take out the crystalline lens from behind, it opens the angle wider. So you can get a 3 to 5 millimeter drop in pressure just by doing cataract surgery in a patient with exfoliation syndrome. So you can literally help the glaucoma by taking out the cataract. All right, Nathan, what are we looking at right here? All right, so what's the lenticular cause of glaucoma? This guy complains of severe pain, hasn't seen through that eye for a while. It's been blurry a long time. My wife drags him in. Exactly. So this is, again, a case of a secondary open angle glaucoma from protein leaking out of an intact lens capsule. It's a hyper-mature cataract. And then what kind of cells are these that gobble up the protein? Macrophages. Macrophages. And so you get these big, juicy macrophages clogging up the meshwork. You even get just the protein itself in between the macrophages clog it up. So this is, again, a glaucoma that is curative by removing that hyper-mature lens. You take that lens out, you flush out the anterior chamber, and the glaucoma gets better. But, again, these people can show up with a pressure of 50. And their eye really painful and red, and the cornea demidas. And so this can be a pretty acute glaucoma, but it's due to a hyper-mature cataract with leakage of the protein outside the closed capsule. And this is just a little aspiration that was done just to confirm it. And these are macrophages that were just aspirated from the anterior chamber. All right, so I wanted to go over, again, just in this crude drawing a little bit about the angle. Because when you've got open angle, normal angle that will look like this, when you've got a closed angle, you look in with your goniomere. You may not be able to see any structures in the anterior chamber angle. And then, lastly, you get an angle recession, which is deeper than normal. And you look in with your goniomere. You may actually see a big band of ciliary body underneath there, because the iris is pushed way back. OK, Reese, what are we looking at here? And it's painful. All right, so this patient was on the GI ward and had some procedure. And then had this severe pain. And, of course, first thing they do is they give them maybe Tobardex and Tylenol for treatment of this. What would your concern be? An angle closure. Exactly, so when you see a mid-position, usually fixed iris, it's not dilating, it's not constricting. The eye's very red, it's injected. Pressure's really high. You go in there with your slit-lamp exam, and what do you see? Iris Bombay. So here's the iris bowing forward. Iris Bombay, B-O-M-B-E, with an exxon, a goo, going up. The iris Bombay. But look at the beam on the cornea. And look at the beam on the iris. You can literally see that coming forward. So what do we think the mechanism is for a primary narrow angle glaucoma? So you get what call it a relative pupillary block. So it's interesting, when you have someone with an angle of risk, so they've got a narrow angle to begin with, maybe they're hyper-opical, they've got kind of a big lens in there. It's not when you dilate them that they're widest that they go into angle closure. It's when the dilation is beginning to wear off and you're just beginning to constrict a little bit, but you're still moderately dilated. That's the point where you have maximum contact between the anterior lens and the iris. And it doesn't take much to get a relative pupillary block. Aqueous builds up behind the iris. Then it blocks off the angle. So you get angle closure glaucoma secondary to that. Tina, we talked about now kind of a primary angle closure glaucoma. Now we want to look at areas that can cause secondary angle closure. What do we see in here? So here's the angle back here. It's pretty much scarred down here. What do you think could cause that? More specific. Exactly. So what we abbreviate as PAS, peripheral anterior synechia. So you'll get the peripheral iris stuck to the peripheral cornea and you get it blocked off. And so that can be secondary to an acute angle closure or even like a chronic low grade angle closure. Now we don't see that much angle closure here. In Singapore and in Hong Kong, we have a lot of ethnic Chinese. Up to 40% of their glaucomas are chronic angle closure. So just a different patient population, different configuration to their eyes. And so we just don't see it much here. But you see there's a peripheral anterior, meaning in front of the iris synechia, blocking off the angle there. And here you see a broader one blocking off the angle. And I'm going to show you a close up here. What do you think is going on here that could cause this angle to close off? So we actually call this neovascular glaucoma. So when you have a disease that causes neovascularization of the iris, then you can get abnormal blood vessels growing along the surface of the iris and then actually into the angle and then closing it off. And so, I don't know, extra bonus points. What are entities that can cause neovascular glaucoma? Actually, that's probably not a fair question. Exactly, and so what are, name me, three good causes of chronic ischemia that could lead to neovascularization. Diabetes is the first one. Central vein occlusion, second. Usually, but just ischemia in general. So I mean, people can have severe carotid artery disease and they can just get ocular ischemia in general. But what's interesting is it's not really something focal to the iris that causes this. It's ischemia elsewhere in the eye that creates humors that circulate forward and cause abnormal blood vessels to grow. And so the key thing is as you treat the retinal ischemia or the ocular ischemia before you get permanent changes in the anterior chamber angle from the neovascularization. Yes, we get anything that decreases the ischemia. We can now use anti-veg F injections, we can do laser treatments, and we try to get it before it closes off. Yes, usually not. No, in fact, usually not. It would have to be a significant diffuse ischemia more of the retina than anything else. And here you see a close-up of an iris again and there's those fine vessels on the anterior surface. So iris neovascularization leading to a secondary angle closure. All right, boy, don't worry, I'll come back to Chris Josh. So what are we looking at here? It kind of looks like a dinosaur, you know, he's going, ah, he's coming in and. Yeah, it's stuck right there, so you think that's not an artifact? So was there posterior synechia before? Exactly, so you can get angle closure from posterior synechia. So say you've got chronic inflammation especially and you get the iris stuck to the lens capsule. Again, you get build-up posteriorly of aqueous and you get a secondary angle closure. So this is a posterior synechia, meaning posterior to the iris and it's right at the pupillary border. And this is an extreme example. This is where you've got a completely occluded pupil. So you've got this little inflammatory membrane going all the way across the pupillary space and just closing it down and then you get a secondary angle closure with that. So one of the first things we do when we have someone with an acute iris, especially if it's a bad one, we give them a dilating drop. First of all, to help stop the ciliary spasm so they feel better, but secondly so that that iris doesn't get stuck. Close so that we can open it up a little bit and make it so it doesn't get stuck. All right, Nathan, what are we looking at right here? Exactly, so kind of the opposite. Look, here's the mesh work up here and there's the iris root and so it's clear down there. So what's the most common cause of angle recession? Trauma. And so usually it's a blunt trauma, not a penetrating trauma. So blunt trauma, common cause of angle recession, blunt trauma, there's a couple of causes of the two dudes. So whenever you're assaulted, it's never one guy, it's two and you never started it. Oh man, I was just there, minding my own business and these two dudes just jumped me. So the two dudes can cause this. Automobile accidents, especially unrestrained, anything that gives you a severe blunt trauma, you can actually get recession of the angle. It's interesting, it's actually a tear in the face of the ciliary body. So it's as if, you know, the iris, it's uncommon, surprisingly, for you to get an aero dialysis, you know, where the iris just tears off at the root. It's more common for it to tear into the face of the ciliary body. And the problem with this is you can, and I'm just showing you normal angle below, recessed angle here. Look, there's the mesh work. Look at tear right into the ciliary body. So for extra bonus points, if you were to get glaucoma from an angle recession, from a blunt trauma, what time does it normally occur? How far after the trauma? Yeah, seven to 10 years. And so that's really important. And so you gotta put the fear of God in these guys, cause these guys are usually 19 and stupid, you know, they have that Y chromosome and all that testosterone. And so, you know, the eye is not gonna hurt right away. And so you gotta tell them, you have to come in every year and I see these, you know, not uncommonly every year or so, someone will come in and their claim will be blurred vision. And so what's the matter? Oh man, my vision's really blurring. You'll look, their pressure will be 45, 50. But it's been going up a couple of points a year for several years, so they don't even notice it. And the visual field from glaucoma starts in the periphery where you don't notice it. So by the time it comes down to where they've got just tunnel vision you'll notice that it's too late. So you gotta put fear of God in these guys and tell them you have to come back every year or you could go blind. So again, this is one of the times I use the B word, the blind word. You know, if you don't come back every year you could get glaucoma and you could go blind. So it'll maybe work for a year or two, but do your best, try to get them to come back. And what happens for some reason is when you've got a recessed angle, for some reason that mesh work over time becomes sclerotic. And I'm not sure what exactly the etiology that is, but it almost becomes sclerotic and closes off. All right, Reese, what are we looking at right here? Kind of the front and back of an eye. Kind of? Significantly cut. And then what are we looking at in the front? So you got a little bit of a summering or in cataract here. Whoa, that's bizarre, okay. Again, $60 million building, $200 computer system. So what's happening here in the angle? There's Slim's Canal. No, there's actually just severe angle recession here. And so this was actually someone who completely lost their vision and the eye was intractively painful and lost their vision, so it became a nucleated. And this again was like 12 years after the trauma. So recessed angles, severe glaucomodus cupping. All right, so we're talking about that. Tina, what are we seeing here? Yeah, you look right there, certainly 0.6, maybe even bigger. Look, where's that rim there? Hard to tell right there, but definitely an increased size and you can't see 3D on these flat pictures. So you really wanna look with your 90 diopter looking 3D, but that is definitely cut. So it's an enlarged cut and that's one of the signs of glaucoma. Now, I mean there's an entire literature on what exactly causes glaucomodus cupping. And one argument is that there's focal ischemia in that area and then it causes the nerve fiber layer to the cells to drop out from the nerve fiber layer, the ganglion cell layer that's putting their axons there drop out. The other thing that people have looked at is disruption of axoplasmic flow and it may be both because what happens is if you look at the trabecular, if you look at, I'm sorry, the area where the laminar crebrose is where the fibers leave the eye. Laminar crebrose is an interesting area. You know, you don't wanna just make a hole in the back of the sclera for the nerve to go out because that wouldn't have any strength. So how the body is designed is you have again, almost like a mesh work where these axons go through the laminar crebrose and somewhere in there, there's either ischemia or there's disruption of axoplasmic flow and you'll get posterior bowing and it'll push against those axons. But in any event, you lose those axons and eventually you get cupping and eventually you get the changes that cause opening glaucoma. This one's probably a little bit more prominent. This is one even a pathologist would recognize so you can see enlarged cupping. Are there still a decent rim around there? You can see a decent rim around there. You do, and in fact, you get, the vessels will move a little bit nasally and they'll kind of arc around that so they'll be pushed nasally. Now this is, you know, we usually rate, you know, the percentages of 0.5, 0.8. This is one. I mean, this is an eye that is severe end stage glaucoma. There are no intact fibers right here. And so when we look right here, we've got an eye here, look at that, severe cupping. And in fact, sometimes the cup will actually excavate underneath it so it's almost like it's more than one. You know, I mean, it'll actually excavate it like a Boston beanpot. And so it'll excavate it. Now for extra bonus points, what happened to this patient that caused this end stage glaucoma? I'll point to it. What's going on up there? That sure looks weird. All right, so that you're half correct. That's a summer injury. It's not then Gorge boat vessels. That's just the cortex that's there. And in fact, that's a severe, that's actually an area where you've got fibrosis coming through actually adherent from behind the iris to the cornea. So this patient has had a severe penetrating trauma. It ruptured their lens. So you've got a summer injury and you've got this adherent white connective tissue. So they call it an adherent glaucoma. Glaucoma means white band. From which language? From the Greek, of course, glaucoma, so white band. So you've got this adherent glaucoma. So this patient had a penetrating trauma, ruptured their lens, caused scarring and then eventually led to this end stage glaucoma. All right, so what do we show in here? Back to, what do we show in here? So I like this picture because oftentimes when you look at these totally cupped out discs, you'll see a little blood vessel coming up to the edge of the disc and then it just disappears because it literally dives around the corner and this bean pod excavates even more so that you can't even see it. So it'll look like that nasal. So it's pushed nasally. This is nasal. This is temporal where it's always flatter and more sloping and that blood vessel dips around and then here is the laminar corbrosa back here. And so you'll get this posterior bowing of the laminar corbrosa also when you get this severe end stage glaucoma effect on the optic nerve there. And here you've got, look at the excavation there and now you've totally killed off all of the fibers here. Look at the atrophy of the optic nerve. Here's the optic nerve sheath. Here's the optic nerve fibers. Look at that space right there. So this is a severe end stage glaucoma. You've pretty much killed off all the axon so that optic nerve is just dead. There again, you can see the, just the severe excavation that's there. All right, guess this one's gonna be yours Becca. First of all, what kind of tissue are we looking at right here? Okay, so it's optic nerve kind of in a cross section on longitudinal section. Now you're seeing some areas here where it's kind of pale and white focally here. So it's kind of a trophic, but it's interesting it's in a focal area here. So you've got some good fibers here. You've got some areas here where it's almost got this little focal degeneration. And I don't know if I put the stain on here or not. Ah, I did, okay. So this is a special stain. Special stain in that area where you've got this focal disrupted nerve. What could that stuff be? Mucin, exactly. So this is a mucin stain. So in what entity do you get a focal degeneration of the optic nerve with kind of mucin material pushed in there? Exactly. So these are usually secondary to a really high pressure. So you get some with an acute glaucoma. Pressure may shoot up to 50 from 20. And this has got kind of a cool name to it. So again, named by the guy who described it. Extra points. Schnobbles. Again, schnobbles, cavernous, optic atrophy. So again, schnobbles. It sounds like, you know, that really, that colored liqueur that, you know, you shoot once in a while, you know, just do some schnobbles, you know, so schnobbles. So it's due to an acute rising pressure. A sudden acute one. It could be angle closure. It could be an acute glaucoma. And you get this mucin stuff. I like to think of it as the pressure's so high it almost pushes vitreous into the nerve. I don't know if that's what happens, but that's the way you can remember it. Now it does some other things. I'm Chris. Boy, this is your day for this. What kind of tissue are we looking at right here? And through your lens capsule again. Why am I showing you this? So you get these little focal vaculated areas right under the lens capsule due to high pressure. And again, bonus points for what you call them. Let's see, I'm skipping the T now. German name. Glaucomflecken, all right, so glaucomflecken. So again, cool-sounding word. And so basically it's little flecks under the anterior lens cap. So the little focal areas where they think the high pressure disrupts those lens epithelial cells. Then they get these little swollen focal areas. These will go away when you treat the pressure. But you'll see these little focal areas are called glaucomflecken. So you know, literally, flecks not from the Greek, by the way. You can see them. Yep, yep, they look like little kind of vaculated areas, little white vaculated areas right under the capsule. All right, back to Joshua. Why am I showing you this picture? What are we looking at here? Picture of the retina. Retina, what's wrong with this retina? So you're looking in here, what cellular layer should there be right here? Ganglion cell, and if you look at it, it's really markedly atrophied. So does that tell you anything? No, probably. Glaucoma, very good, okay. So when glaucoma causes damage, it damages the axons from the ganglion cells. And so you get loss of these axons, and eventually you get the ganglion cells dying off. And so when you look at it in a person with glaucoma, the retina externally is totally intact, but it's this inner neurofiber layer and ganglion cell layer that's affected. So that's what glaucoma does. And if you're looking here, here's a top and a bottom, what? Nathan, what part of the retina are we looking at now? Normal on top, severe glaucoma on the bottom. Josh said the ganglion cell layer. So where, what part of the retina are we in? The macula. So if you look at the top one, you see the ganglion cell layers, multiple cell layers thick, we're in the macula. You come down here, the macula, some of the severe glaucoma. The last thing to go is the macula. That's the last thing, but once the glaucoma gets severe enough, you even start to lose cells in the macula. Got it, all right. So we're gonna switch gears a little bit here. So, Rhys, we're gonna talk about some specific types of glaucoma. So looking at this angle, this angle just looks funny. Tell me what you're seeing here. And this is really disturbing. Yeah, it almost looks like there's kind of some little fine bands of fibrous tissue coming across. You really don't see that much of a develop mesh work behind there. How old is this patient? This could be a kiddo. It's a kiddo. So this is what we call a congenital glaucoma. And so I hate to keep making you guys memorize these names, but again, there's a guy who described this when you look in with a goniomere. It's called Barkhans memory. Now, it's weird because people at one time thought that the mesh work was normal and you treat congenital glaucoma, you put a lens on the eye, you're going with this big blade and you just slice it all the way across 180 degrees and you would slice this Barkhans membrane and then the iris would drop back, the angle would open up and the glaucoma would be magically cured. It's a lot more complex than that because what we're finding is, is that the angle in congenital glaucoma is just misforn. And you do get this little fibrous tissue over here. And if you open that up a little bit, it helps a little, but unfortunately, the mesh work underneath it in congenital glaucoma is often not normal. So even though they used to do this goniotomy, they'd go in with a blade and slice it open. That's not really that successful because you, this Barkhans membrane, it's not really a membrane, it's an area of just not well-developed trabecular mesh work. Here's a close-up. Here's that Barkhans membrane and here's supposedly where the mesh work is and I don't know if my eyes are bad or not, but I just don't see well-developed mesh work on these kids with the congenital glaucoma. All right, Tina, what are we looking at right here? So we call this polychorea, literally, multiple pupils, polychorea. What entity would you think about when you see an iris that looks like this? What does ice stand for? Exactly, so people who are lumpers like to put categories all together, people who are split or split them up, but there's an entity called ice syndrome, irritable corneal endothelial syndrome, and the ice has kind of three different ways of presenting, but they all have the same final pathology and so this is called essential iris atrophy. So the first part of the ice syndrome, it's called essential iris atrophy. You see corectopia, you see polychoreas, you see pupil pulled to the side, you see multiple pupils, you see this ratty, eaten appearance to the iris that's right there. Now there is a second part of it. Again, I don't know if you've even heard, have you ever heard of these in altruistic? So we'll swing over, three so the younger here, yes. All right, so hazy cornea, but what do we see with the iris here? That's kind of thinned, kind of moth eaten here, some holes here, but there's corneal edema, so what's kind of entity two under the ice umbrella? Chandler syndrome. Chandler syndrome and so Chandlers, again you have the iris atrophy and the polychorea, but you have corneal edema. So Chandlers, you have more corneal effect. Becca, what's the third thing you got to know under this umbrella? Iris Neva syndrome, or again two more names, Kogan Reese syndrome, there you go, Reese and Kogan, so Kogan Reese syndrome. And so you see these multiple little knobs on the iris. It's kind of cool looking when you see it, it's kind of velvety in, there's multiple little knobs on there and we see them on there. And the problem is is that these entities are all caused by kind of the same disease process. So Chris, what's the common unifying theme in all these ice syndromes? Well, yeah, that's really a vague term, but what specifically happens here? Different group, different group. That's the next group, okay? This is where you get endothelial growth on the uval tissue and desalination. Exactly, so the whole common theme to these is you get endothelialization of the anterior chamber. So for some reason, these endothelial cells are abnormal and they will literally grow across the mesh work onto the iris, even behind the iris, and then as they do that, you'll get decimage membrane growing with them and you'll get severe glaucoma, you'll get the iris changes, the corneal changes. And so what you're looking at here, what kind of stain are we looking at right here? PAS. PAS, so here's decimage membrane a lot thicker than normal and it's coming around the corner and the mesh works clear the heck down here. So you get this decimage membrane growing onto the surface of the iris and it literally closes off the angle. So that's kind of the common theme to all three of these different entities is desmetization of the anterior chamber angle. And if you look, look at decimage membrane, it's like quadruple thick in there. And then it comes around the anterior, the inner surface of the iris where the angle would be and then on the surface of the iris. So you see decimage membrane growing along here and then closing off the angle growing on the surface of the iris. So all three of these entities, it's a desmetization of the anterior chamber and that's what causes the three of these. Now what's kind of cool is when you look at a PI from a patient with the iris nevis with Kogan re-syndrome. And so this is a little peripheral erudectomy in this patient, this is cool because this is my only archive cover. We got, what's the archives called? JAMA ophthalmology, so this was our only cover on JAMA ophthalmology. We had this cool patient with Kogan re-syndrome. If you look at it, you can see here again is decimage membrane on the anterior surface of the iris but you have these little pigmented cells popping through. So the reason it looks velvety is because you've got decimage membrane on the surface of the iris. But in between here, you get these little mushrooms popping out and they're these little benign melanocytes. And so this iris nevis syndrome, you get these little mushroom outpouchings of melanocytes through decimage membrane on the anterior surface of the iris. So again, pretty cool entity, pretty cool entity there. There you see a close-up again, anterior surface of the iris, little iris nevis there. Okay, Nathan, what the heck are we seeing right here? What's that? More specific, which base of membrane? Decimage, exactly, so you see decimage here decimage is thickened and there's almost a little fold and not only that, it's coming out from the irregular measure would be over here and so you've got decimage membrane thickened and even a little fold. And so when you looked in there, you would actually see decimage more toward the center than you would toward the periphery. So what do we call this? Exactly, so there's a second big umbrella that you have to memorize called the anterior chamber cleavage syndromes. Now it's a misnomer again because we used to think that this mesoderm would come into the anterior chamber and then form the anterior chamber and cleave and then you'd get the trabecular mesh work. We know now it's not mesoderm, what kind of tissue is it that forms kind of the, it's neural crest. So kind of what you thought of as mesodermal cells is actually neural crest and instead of this massive tissue coming in and then cleaving, what happens is they think there's successive waves of migration of these neural crest cells. So it's kind of different but the way to remember it is very easy and George Waring, who sadly just passed away last Christmas, came up with what's called the stepladder classification of these anterior chamber cleavage syndromes and he wrote it 40 years ago. But it's still a good way to memorize it. So the first thing you see in these anterior chamber cleavage syndromes is you see a prominent Schwabbe's line, they call this posterior embryotoxin because people would theorize there was something toxic going on. So posterior embryotoxin. Now you see a close up. Okay, going down the stepladder here, Reese, what's the next thing you can see? Here's posterior embryotoxin, what's going on here? You actually see little bands kind of coming down from this posterior embryotoxin to toward the iris but more in the periphery. So what is the next one? Yeah, almost like, but like a longer, broader anterior synechia. So what is the next entity in the stepladder? So it's called axonfels. How do axonfels ride? Axonfels reiger. And so they used to separate them but now they're lumping them a little bit more to get to the axonfels reiger anomaly. Basically, you see posterior embryotoxin but you start to see little bands of connective tissue kind of coming down from that onto the iris. So you'll see some funny iris abnormalities. Now this isn't just an eye abnormality. These kids can sometimes even have funny teeth and funny bones but axonfels, axonfels slash reigers anomaly and you see these changes and then there is a third one, Tina going further down. This is Peter's anomaly. So as you come down, you've got posterior embryotoxin and then you've got axonfels reigers with bands coming to that and then you go to Peter's anomaly and what's interesting about Peter's anomaly is Peter's anomaly is in addition to the other things that you have, you get this central area where decimates membrane and endothelium just don't form. And so you get this little central area where you just have this internal kind of ulcer in the cornea and you get corneal edema. Now sometimes with this Peter's anomaly you can get a focal anterior subcapsular cataract associated with it. So again, the way I remember it is is when it's trying to form and that lens is coming off, it kind of grabs the posterior cornea and pulls it down with it and you get a little focal cataract underneath here and then you get this central ulcer that causes corneal edema. So again, people call this a step ladder because it was these successive waves of mesoderm. That's not what it is, but this is a good way to memorize them because these are all very rare entities. You may see one or two of these in your career depending on where you end up. So Peter's anomaly, you get this central ulcer. Central ulcer of Von Hippel, another nice Greek boy. Come on, wake up guys. Come on, it's not that early. So as a result, you look here, you get corneal edema, there's the boli. You have this central area where there's no decimase, no endothelial cells. So these kids get severe glaucoma, but you still have the other, I mean severe corneal edema, but you still have the other things. You still have the little bands coming down. In fact, if you look at the peripheral part where this central ulcers, you'll even have bands coming down from the cornea to the iris. And so you'll get all three. It kind of goes in a step ladder from milder to worser. Milder to worser. Okay, and we say goodbye to the, see it's up on a hill looking out onto the ocean eventually out there. Sir. Where does scleropordia fit in with Peter's anomaly? People will often throw that in with Peter's anomaly because the cornea kind of loses its normal architecture and it becomes a lot more fluid in it. It turns white like sclera and it even looks like sclera. So people will chuck in sclera corneal in there somewhere too. So it's kind of a, it's an offshoot. Yeah, that is actually a true Peter's. Well, you get eventually peripheral sclerilization of these. You do, exactly. So they often will run together. All right, so I believe next week is retina. I'm pretty sure so please be on time because retina is really tough to cover in an hour. There's a lot there. So please be on time next week. All right, thanks for your attention. As usual.