 Of course, this is Louis XIV. This is the magnificent palace that he built when the French Empire was at its peak. And this is the main entrance. This place, like, you know, sets the bar for oculance, I guess you can say. And, of course, there's always all kinds of works with the stonework, with the latticework, with the metalwork. This is the famous Hall of Mears. And so this is where the Treaty of Versailles was designed, which ended the war to end all wars. You know how that one went after World War I, 100 years ago. So this is the famous Hall of Mears. You just have to say it's a busy place. You don't get to get a private tour. You don't get to have it yourself. But pretty spectacular place, if I do say so. And there's the, so I couldn't quite get the roof in. Focus there, there's the Neurals of the Roof, of course, the Grand Chamber of Deers. All right, so what are we going to talk about today? We're going to talk about glaucoma. And any path lecture regarding glaucoma starts with the trabecular meshwork. And so this happens to be a particularly beautiful piece of meshwork. When you guys do your path rotations, you'll see when we get trabeculectomy specimens, they do not have traps on them most of the time. And they're often just sclera. This happens to be a beautiful one. So when we're talking about the trabecular meshwork, there's different ways to break it down. And the first way is you can do the anatomic way of looking at the angle as you're looking at it with agonium here. So when you're looking at it with agonium here, you're looking into the anterior chamber angle. We're going to go ahead and start, say, Catherine. What denotes the apex of the angle? What is the first thing that you'll see when you look in with the agonium there? You'll see the Schwabbi's line. Schwabbi's line. What is Schwabbi's line? It's the end of Decimates membrane. Exactly. So where Decimates membrane terminates, there's a little, sometimes there's a bump, sometimes there's a little line, but Schwabbi's line. And so that denotes the beginning of the trabecular meshwork. If you look, the trabecular meshwork is triangular. This is the apex. And here's the base down here. It's so triangular-shaped. So when we're looking in with the agonium there, also, Sean, there's a couple of different ways we denote the meshwork here. So first, from Schwabbi's line, what's the next part of trabecular meshwork posteriorly? The non-pigmented meshwork. The non-pigmented meshwork. And because it's kind of thinner at the apex there, you don't have a lot of chance of pigment gathering this. When you look in, it'll be a paler line. Theresa, what's the next area here? The pigmented trabecular meshwork. And so that's where sometimes where you get liberated pigment granules. They'll gather up right there. And Rachel, what is the base of the meshwork here? The scleral spur. The scleral spur. So when you look in, you'll see a little line that denotes the scleral spur. Now, when you think of the trabecular meshwork, you've got to think of it in three dimensions. And so the apex is here. The base is here. The scleral spur acts as a little lip. It goes around 360 degrees. And the meshwork sits in that scleral spur. And it almost like a little shelf that the trabecular meshwork sits on. So if you're looking in with agonium here, sometimes underneath the scleral spur, you'll actually see this structure right here. Ariana, that's actually the root of the iris. So you can actually sometimes see that part of the iris are part of the ciliary body when you're looking in. So the other part of the trabecular meshwork we can do is you can also divide it vertically, if you will, for the corneal and the uvial scleral meshwork. But then also, this part of the meshwork right here is particularly important. Allie, what is that called? The juxtacanalicular. And therefore, that means this is what? Schlemz canal, all right? So when you think of Schlemz canal, it's not a round tube. It's kind of an oval area, and this is it right here. And again, you think of the trabecular meshwork in three dimensions, Schlemz canal runs all the way around. And so this is Schlemz canal. It's this juxtacanalicular tissue that is important, because a lot of people think that's where the impedance to flow of aqueous is, and that may be what's involved in open-angle glaucoma. So it's the juxtacanalicular tissue that's important. And here's a close-up. Let's talk a little bit about the flow of aqueous, all right? So we're graced with a senior today. Wow, this is so special. All right, so tell us, where's the aqueous humor made? The ciliary body. Made in the ciliary body. And then how does it get to the trabecular meshwork? So it's made the ciliary body wraps around the iris through the pupil and then into the trabecular meshwork. So here's the meshwork. Here's that juxtacanalicular tissue. Here is Schlemz canal. Chris, good evening. Hello. So it gets into Schlemz canal. Where does the aqueous humor go after that? So it goes to the juxtacanalicular tissue, and then it'll eventually get into the veins. Aqueous veins will go to the veins. Exactly, so here's the aqueous veins, and it will eventually make its way out to the circulation. Here's a close-up. There's that juxtacanalicular tissue. Now, the trabecular meshwork's not just a wide-open meshwork. There actually are endothelial cells lining it, and there is both active and passive transport of aqueous through there. So it's not just passive flow through this meshwork of tissue. All right, so here we're showing that nicely. Here is the trabecular meshwork. Here's Schlemz canal. Here's one of those aqueous veins. And then you see it drains out right into the plexus here, the episcleroplexus. And so I always tell you this every year. Your mission is when you're at the VA or in clinic looking at patients, find an aqueous vein, because we never think about these. We never look for them. So if you're looking with a slit lamp, just beyond the edge of the limus, deep in the episcleroplexus, you'll actually see some aqueous veins and it'll look like there'll be a vessel with bloods in it, but then you'll get box-scarring of the vessels. So you get aqueous flowing there with the little red blood cells in between. So your mission today, find one of those aqueous veins. And you look at it, you go, oh, yeah, they're there. God, why haven't I seen that before? So they're really there. So that's your mission for today. Find them. That's just with a slit lamp, not with gonia. Slit lamp, no, it's actually outside because remember it's on the episcleroplexus. And so the aqueous veins drain it through the, trabecular meshwork through Schlemz canal and then through the sclera to that little plexus that's on the surface of the sclera. All right, so when we're looking right here at an angle, what I wanted to show this is that if you look at a trabecular meshwork and you're patient with open-angle glaucoma, it looks the same as an age match control without glaucoma in light microscopy, meaning that we cannot see the pathology of open-angle glaucoma on pathology. Now the meshwork is different in a 20-year-old as opposed to an 80-year-old, but if you take two 80-year-olds, one with open-angle glaucoma, one without, on light microscopy, I can't tell the difference. And so you really can't tell when you look at that. All right, so when we break down glaucoma, we break it into several different anatomical features. So the first thing we look at is we look at open-angle glaucoma. And then when we look at open-angle glaucoma, you have primary run-of-the-mill open-angle glaucoma not associated with anything else, but you've also got secondary open-angle glaucoma. So we're going to circle back to Catherine. What do we see in here? So you see multiple trans-illumination defects, 360. So this would be concerning for pigment dispersion. Exactly, so there's an entity called Pigment Dispersion Syndrome. And so people used to argue about where does the pigment come from and why does it occur? And if you look at this picture, this tells you you look at the trans-illumination defects in the iris and you see that it has a radio appearance to it. And when you go ahead and you look at the back surface of the iris, you see that that lines up directly with the zonular bundles. So you know the zonules, remember when we talked about lens, they come along here and then they insert onto the cylinder body. Well, this is the back surface of the iris. And so when you have a posterior bowing of the iris, those little zonular bundles will scrape on that pigment epithelium and release pigment, giving you a secondary open-angle glaucoma, what we call pigmentary glaucoma. You know, for some reason this occurs in younger myopes, males more than females, why I don't know. But if you do an OCT of the anterior segment of the eye, you'll see there'll be posterior bowing of the iris. And then you get the scraping of those zonular bundles releasing the pigment. And so when you look, here's a really nice path specimen here. Here's what you're making our measurement. Look at all that pigment. So you can imagine what that pigment's gonna do. It's gonna come up that measurement and cause a secondary glaucoma. Right here, here's the iris. And you can see right there where some of those zonular bundles have scraped off that pigment. So it goes through the pupil, comes around. Predominantly, it's in the inferior angle. Yes. A lot of people have heavily pigmented TM. How can you tell on path that versus pigment deposit in the TM? Yeah, you have a lot of pigments, especially in a darkly pigmented person. You do have a lot of pigment in there. But when you look at the person who's got pigment in the mesh work from just the eraser from normal pigment, it's uniform. Whereas if you look at pigment dispersion, it's usually inferior. Because remember those aqueous currents, they carry the pigment around. And also that pigment deposits on the posterior surface of the cornea. What do you call that? Catherine, the pigment deposit from pigment dispersion on the cornea. Kuchenberg spindle. Kuchenberg spindle. So it's this triangular shape area in the inferior third of the cornea. So the aqueous carries it. So when you go in the ozone with pigmentary dispersion, you'll actually see that the inferior angle have more pigment than the superior angle. And also you'll see the trans-elimination defect. So that's real helpful. All right, there's other reasons for secondary open-angle glaucoma. Sean, what's going on here? So in this picture, there is a big mass kind of growing right across or right below the angle, kind of pushing the iris away. Wrong button. What would you be concerned about? Melanoma. Exactly, so don't forget, if you have a malignant melanoma arising from the ciliary body, it can actually invade forward into the trabecular mesh work. And you see that widely separated area of the iris root and the mesh work as this tumor pushes in here. So that's another cause of secondary open-angle glaucoma is invasion from a tumor, from a ciliary body tumor. And here you can see another one. Here's the cornea, the marcation, the end of dissonance membrane, and here's the iris root. And look, here's this pigmented tumor coming from the ciliary body growing into the trabecular mesh work and the angle causing a secondary open-angle glaucoma. It's open angle. All right, what are we looking at here, Teresa? The picture of the anterior segment with the iris dilated. You can look back and see the lens. There's a deposit more peripherally that kind of has like a scallops edge, so pseudo-expoliation. All right, so pseudo-expoliation or now we call it exfoliation syndrome can also cause a secondary open-angle glaucoma. Why do we have this pattern here, this kind of a bullseye pattern of deposition? The iris acts like a windshield wiper. Exactly, so you get this little deposits on the surface of the lens and as the pupil moves in and out, it scrapes it back and forth so you get a lot of exfoliation material here and you get some in the center and then it's clear in between where the pupil scrapes it off when it goes. And here's a nice close-up view of that scalloped appearance. So you get this exfoliative material and now people have really worked out the genetics. It's the loxal one gene and it causes a defect in how the elastic tissue and the matures and in any event you get extra material that deposits on the surface of the lens and you end up getting this exfoliative material and then of course that can cause a secondary open-angle glaucoma. Now, exfoliation material deposits all over the eye so tell me another place where it deposits Rachel. In the angle, Chris, what's that? Well, she said angle, where else does this stuff deposit? We saw that one, that doesn't count, saw that? It can deposit in the endothelial cells of the cornea. It can deposit in the sphincter and dilator muscles of the iris, it even deposits in the iris pigment epithelium and it can deposit all along the zonules and so unfortunately exfoliation is a triple threat when it comes to cataract surgery. You get deposits on where the zonules insert to the capsular bag along the zonules themselves and where the zonules insert in the cellular body so it makes the zonules triply weaker. Also, it makes the capsule more brittle and makes you more susceptible to glaucoma, makes the pupil so it doesn't dilate as well and it gives you more susceptibility to corneal edema so we see a ton of this here. There's a whole pocket of exfoliation in Utah because it's a disease most commonly seen in people of Northern European ancestors where a lot of Utahns come from. You open the Salt Lake phone book, you see a lot of Sorenson's and Petersons and all that in there so you see a ton of exfoliation here so you guys will see that a lot in surgery and this just shows you nicely on retroalumination that scalloped border. Okay, so this is Arianna, what is this called, this pattern of deposition on the lens capsule? This is showing iron filing. Iron filing, so when you were a kid in shop class, did you ever have some iron scrapings and put a magnet on them and it all stands up on there? Sorry, I come from the non-enlightened era, boys did shop and girls did home act so it was a very non-enlightened thing. Girls were supposed to learn how to cook and clean and things, yeah, see now that you do both and guys did shop manly things, cutting and hammering and manly things so this is the so-called iron filings pattern and of course what we worry about is this exfoliative material deposits in the trabecular mesh work and so it gums up the mesh work and these people can get in trouble relatively early, you can watch them and they're doing fine, doing fine and then suddenly the pressure will really shoot up and so what's interesting is if you do cataract surgery, the intraocular pressure and exfoliation patient will actually drop by three to five points eventually and so I think the reasoning first of all is you widen the angle so that helps a little bit but then you remove all that exfoliative tissue that's sitting on the lens capsule and when you're doing your irrigation and it's floating through there you're actually flushing out a lot of stuff in the angle so even though people with exfoliation you gotta watch them real carefully cause they can have a pressure spike the first day in the long term, especially the first few months after surgery that IOP actually drops so you end up un-gumming the mesh work if you will. All right, yes? Is the exfoliative material more like an epithelial on pathology? No, it's actually a protonaceous elastin tissue, yeah. All right, so this is, I guess who did we end up? Did you answer it? I think Ariana, you answered one, didn't you? Okay, Allie, what the heck's going on here? What do you see here? Okay, and what does that cause? Okay, good, so at least you guys are reading it cause you know I go through this systematically and I'm gonna start like going out of order just to confuse you but at least you guys are reading ahead of time. So classic history here is, you know old rancher from Wyoming, you know, comes in, I hurts, I was like been hurtin' oh, a couple of weeks, it really hurts I can't see anything, well when did your vision get blurry? Oh, it's been there for a while and then of course the spouse always says oh, he's been blurry for years, he hates doctors and so by the time they come in, their pressure's 50, they have corneal edema and what ends up happening is you have a hyper mature cataract, the cortex will actually liquefy oh, the capsular bag is intact, protein will leak through that intact capsule and these are, what kind of cells here, Allie? Macrophages, so you see these macrophages and look, they're just in gorge, they're just stuffed with this protonaceous material and so you can imagine these big fat macrophages can clog up the mesh work but also just the protein can too and so these people can get a pretty significant glaucoma and the treatment is to remove that lens. So that will actually cure this secondary open-angle glaucoma what we call phacolytic glaucoma, it's not really a lysis of the lens but they call it phacolytic glaucoma and this is just a tap of the anterior chamber when people weren't sure what was going on there and you see again, big fat macrophages sitting here. All right, so when we think about glaucoma we've been talking about open-angle glaucoma now where you've got primary and secondary but don't forget there are other causes of glaucoma you can have narrow or closed-angle glaucoma you can have the opposite which is angle recession, dramatic angle recession where the angle is actually wider than normal. All right, so what are we concerned about here? Concerned about angle closure probably. Yeah, look at the, what's the tip off here in this picture? Why would I show both eyes? That's mid-dilated pupil. Exactly, so you look, there's the pupil with light shining in it, constricted pupil. Here's a mid-fixed dilated pupil so these patients who come in with acute attacks of angle closure they'll often have a mid-position iris but it doesn't move well. And of course when we look at with the slit lamp the tip off is you can actually see the forward bowing of the iris. There's the beam on the cornea, there's the beam on the lens and then look at the beam here as the iris narrows in the proofy. So you actually get forward bowing what the French call iris bombay. So it comes forward and really what it amounts to is you get a relative pupillary block. And so when people have an angle at risk they've got a narrow angle to begin with. High hyper-opes, big swollen lens, then you dilate them and the pupil dilates fine. It's when the dilation is just beginning to wear off that you get maximum apposition of the iris to the anterior lens capsule and there you'll get a relative pupillary block. So what's the treatment of this condition? Exactly, so you do laser peripheral adectomy, make a hole in there, it allows the aqueous to bypass the pupil and go straight in. And so for those of you who are younger and haven't done a laser PI on someone with an angle closure, it's pretty cool. You hit that iris and man, you'll get this gush of fluid coming through there and the iris will recede right before your eyes, pretty satisfying. All right, now if you don't treat an angle closure right away, Catherine, what can happen? Exactly, what do we call that? Well, anterior sony. Exactly, so we abbreviate it as PAS. You'll have all the abbreviations in ophthalmology, peripheral anterior synechia. So when you get apposition of the iris sticking to the peripheral cornea, look, here's the measure, we're clear back here and the iris gets stuck. So if you don't break off an angle closure if it just chronically keeps getting worse, you actually can get synechia closing the angle and then those are much more difficult to treat. So this is actually synechia, peripheral anterior synechia closing the angle there. So a secondary angle closure glaucoma. And here you can see again, apposition of the iris to the peripheral cornea and there's the measure, we're clear back there, closing it off. So Sean, what's another cause of secondary angle closure? I'll give you a picture of it right here. Neovascularization, what can cause neovascularization? Those are the top two and you can get a chronic ischemia to the eye just from bad circulation in general, severe carotid disease. And so when you get chronic ischemia, these ischemic factors will go ahead and diffuse into the anterior segment of the eye and you get abnormal blood vessels growing on the surface of the iris. And eventually these blood vessels can grow on the surface of the iris and they'll grow all the way over into the angle so you'll get a secondary angle closure glaucoma due to neovascularization. So it's a neovascular glaucoma. And there you see, here's the iris, iris pigment up thin, you've got vessels in the stroma, that's normal. But you shouldn't have vessels on the surface of the iris here. And so that's called rubiosis eridus, you know, red iris. And so you see these little vessels here and as they grow into the angle, you get a secondary angle closure. And here you can see this is an area where you've got the iris actually stuck to the lens capsule. So what kind of glaucoma does that cause, Teresa? The posterior synechiae. Exactly, so this is now a posterior synechiae. Posterior to the iris, not anterior. And that iris sticks on there. So you can get posterior synechiae, which give you a blocked angle right there. It'll actually, but it's not just that a narrow angle moving back and forth, it's actually the iris sticking down to the lens capsule. So you'll get a secondary glaucoma from pupillary block. And here you can see sometimes you'll even get an inflammatory membrane going all the way across. So they call that an occluded angle. So if it zippers up all the way around, they call it pupillary seclusion. But if you get a membrane growing all the way across, which blocks it off, it's pupillary occlusion. So this is an occluded pupil and you see an inflammatory membrane sticking the remnant lens capsule to the iris causing a secondary pupillary block. And eventually you'll get an angle closure glaucoma. Now, what's going on here, Rachel? And so here's what's left of the mesh work here. Here's the iris root way down here. What's going on here? Exactly, so this is kind of the opposite of the narrow angle of the closed angle. This is an angle that's way wide open. And so this is now an angle recession. And what's the most common cause of this? Trauma, exactly. So it can be automobile accident. Usually this can be secondary to the two dudes. You guys all heard this, how all trauma is two dudes. Never one, it's two. Man, I was just sitting there minding my own business and these two dudes just jumped me for no reason. That's the classic story. They're usually drunk and belligerent when they're telling you this. So they had to run in with a fist or a foot or automobile accident. And in any event, you get a severe blunt trauma to the eye. What is associated with these initially? What's the history, or what do you see on findings often initially associated with this? Hythema, so you get the eye filling with blood. So you really want to be careful once the hythema clears and everything's stabilized, wait a month or so, then go near them and look. So final bonus question. How soon after a severe trauma like this does angle recession glaucoma occur? Yep, seven to 10 years is the average. And so you got to put the fear of God in these guys because these guys are usually young, stupid males. And that kind of is redundancy because young males are often stupid. And so it's a redundancy to say that. You could say that about your own kind. And so these guys just won't show up for follow-up and we see these periodically in the clinic. Someone will come in when they're 40 with blurred vision. And you look at them and their pressure's 45 and they've got a temporal island of field and that's all that's left in that eye. And you go back in the old records and sure enough 20 years ago they had an angle recession. You tell them come in every year and they never do. So I put the fear of God in these guys. I tell them, you know what? You could develop glaucoma and it's really sneaky. It builds up really slowly over many years and you could go blind if you don't come in every year. And so you never say blind to a patient with macular degeneration or optic neuropathy. You say loss of vision because blind is a very limbic word. And so if you say blind, it has a pretty good connotation. So these are the guys you say blind to because you really want them to come in because they can lose vision very slowly as their pressure creeps up over seven to 10 years. This just shows you just the differences. Here's a normal angle. There's the iris root. So technically it's not so much that the iris root tears. It's almost a tear in the face of the ciliary body. So you get a tear that goes, here's the mesh work here. It goes all the way back here. And then eventually over the years that mesh work can become sclerotic and cause you to have a secondary glaucoma. And here's that mesh work. Look at it. It just kind of sclerosis over over the years. You just don't see a good mesh work there. All right. This just kind of shows you, it's a nice picture because we cut it in half. And so here's a patient that's had, look at that angle. Angle recession, cataract surgery. Look at that nerve. Totally cut down there slowly over time. All right, so since we're talking about glaucoma, obviously the place where glaucoma causes its damages at the optic nerve. So what do we see in right here, Chris? You were seeing a nerve that has pretty large cup to disc ratio, which makes us concerned about glaucoma this thing, which is something like this. So where do you think the edge of that disc is? The edge of that cup is, I mean. Kind of hard to tell, maybe right there. This is where you obviously want to look with three dimensions. But boy, that's a pretty suspicious looking cup right there. And this one I think would be a little bit bigger. And so I mean, glaucoma guys are gonna talk to you. There's still an argument to this day. The pathology is in the axons of those ganglion cells coming into the cribriform plate and coming into the laminocrobrosa. Some people say it's block of axoplasmic flow. Other people say it's chronic ischemia and maybe both. And so in any event, you get chronic damage to the axons as they're passing through, then you get secondary death of the ganglion cell. And that's what causes the cup to get bigger. And if you don't treat it enough, you get death. So this is a cup to disc ratio of one. And so this is a totally wiped out, totally wiped out cup with untreated glaucoma. Now oftentimes you can even see an excavation of the cup. So that's even more than one. That's even if you're calling cup to disc ratio 0.6, 0.7. This is like 1.1. So it actually excavates, and this person had a trauma. There is a corneal scar, we call it a glaucoma. And you can see it had a ruptured lens, summering ring there, and then severe glaucoma with cupping. So when you look right here, you'll often see temporarily, look at that nerve fiber layer, completely gone. There's a single fiber left. And then nasally, you'll often get this vessel going in and then it'll dip down. And so it'll often disappear. You see it go into the disc, and then it disappears as it goes down in. And so this is what we call the beam pot. Those of you from Boston, you know the beam pot. And so it's actually got a wider atrophy from the edge of the rim than there is actually the rim itself. So this is a severe end stage glaucoma. And if you look, you'll see that the laminar crebrosa is really bowed backwards. And then of course the fibers in the optic nerve are markedly disrupted secondary to this chronic glaucoma. And there you see another one where, I mean this is totally cupped out, total beam pot. And it's kind of cool looking. It almost looks like those cliffs that Jeff Tabin climbs up and kind of dangle over the edge and climb your way up. All right, this is interesting. This is an optic nerve seen in cross-section and it's got some focal areas of damage. What the heck is that? There you go. And what causes that? Well, this is often an effect from a severe sudden glaucoma. So see you've got someone who goes in and a cute, popular block and their glaucoma goes way up. So you get this kind of cavernous atrophy. They call it schnobbles. Cavernous atrophy. It sounds like something that you would like, you know, used to shoot when you were a teenager. Oh man, let's do schnobble shots, you know? Come on, humor. So this is schnobble's cavernous atrophy and it's usually the result of an acute high-pressurizing. If you do a special stain, you'll actually see that that's hyaluronic acid in there. So people have speculated that the high-pressure literally drives that hyaluronic acid from the vitreous into the optic nerve head focally. The other thing that can happen with acute pressurized alley, what part of the eye are we looking at here? Yeah, so those who are damaged to the lensopathelio cells and eventually they vaculate, what are those called? Glaucomflechin. I love that word just because it sounds cool, you know? Glaucomflechin. And so it can actually with an acute pressurized cause ischemia to the anterior lensopathelio cells and then you get these focal opacities that they call glaucomflechin. It's a great word. Now all right, so what does glaucoma do to the optic nerve? Mix it atrophic and what part of the nerve gets atrophic? Exactly, so the ganglion cell layer, look at the ganglion cell layer here. Totally wiped out, nerve fiber layer. So next week we're gonna do retina path and what do retina ogres and onions have in common? Layers. And so you guys really better know the layers of the retina and there's a lot of them. So know the layers of the retina cause we're gonna talk about glaucoma. The only difference is a CRAO, remember the central artery brings blood to the inner two thirds of the retina. And so you would actually not only wipe that out but you'd wipe out the inner nuclear layer and even part of the anterior part of the outer nuclear layer. Whereas this just gets ganglion cells and then secondary nerve fiber layer. So not quite as extensive of damage. And now here you can see this is an area where they've got damage here. This is the macula of a normal eye. You see the ganglion cells are multiple thick. This is the macula of an eye with severe glaucoma and look how it's even wiped out the macula. So the macula is the last to go and that macula or papillor bundle is really the last to go. And so people will often have that temporal island and that central vision and the periphery gets wiped out and end stage glaucoma, even the macula gets wiped out eventually. All right, we're going to talk about a couple of other different entities that can cause glaucoma that you need to know about. So this is something that you may see with the peed's people. This is congenital glaucoma. And so back in the olden days when I was a resident, they called this Barkhans membrane and they said, well, there's a membrane that grows across the angle in kids with glaucoma and the way you treat it, we used to do what's called a goniotomy. And so now these guys, people have discovered the angle again because the glaucoma guys are putting all these little chunks in and these mixed procedures. And so we would look in there with this funny lens called a kepi lens and you'd look at the angle and you'd go across the cornea with a blade and you'd go, you just cut the angle. The idea would be you cut Barkhans membrane and then magically the glaucoma would go down. And as we study it more, we discover that it's not so much, it's a membrane growing across the angle in kids with glaucoma. It's that the angle just doesn't form normally. So you get this connective tissue here but you don't have a normal angle behind it. What we were doing in essence is we were just cutting a big swath that allowed aqueous to go into either slump's canal, even if it was there, maybe even just the face of the cellar body. So we were just given a way for fluid to go, kind of like people are doing now with migs. So we were just 35 years ahead of our time and didn't know it. And so this is a congenital glaucoma. You get this membrane-like structure over it but you don't really get a normal angle developing. And there you see it. There's the angle, there's Barkhans membrane, there's the angle in congenital glaucoma. So the angle just doesn't develop well. It's just not normal. All right, so there is an entity that we want to talk about today and that is the ICE syndrome. Katherine, what does the ICE stand for? Something to do with filial syndrome. Yeah, irritable, corneal, endothelial syndrome, so ICE syndrome. Sean, bilateral or unilateral? I just mean unilateral. Yeah, it's very, so again, I got to teach you guys now because for oral boards, you say it with conviction. So even if you're guessing, you say unilateral. If you go unilateral, then they know you're guessing, you don't get credit for it. So just put it out there, okay? So it's usually unilateral, it's very interesting. All right, Teresa, so there are three parts of ICE syndrome depending on if you're lump or a splitter. And so what are the, what's the first one? What am I showing here? So essential iris atrophy. All right, so it's called essential iris atrophy. If you look here, they've got what's called corectopia, the pupils abnormal. You even get what's called polychorea, multiple pupils. And so you see a moth eaten iris, multiple pupils here and they can get a severe glaucoma from this. Rachel, what is the common final pathway of all of these three different entities of ICE syndrome? Exactly, so you get this abnormal endothelium growing into the angle which causes glaucoma, but even growing onto the iris. And so the first one, most common one is called essential iris atrophy. Chris, what's the second entity of the triad here? The second one is Chandler syndrome. Chandler syndrome and so these all have common things. Chandler syndrome, you still get polychorea, you still get glaucoma, but what does Chandler syndrome get in addition to that? Cornial edema, so here you see the cornial edema, hazy cloudy cornea. So Chandler syndrome has very similar to essential atrophy, but with corneal edema. And then the third one, Marianna, all right, so you get, it's called coganry syndrome or iris neva syndrome. And so if you look, you see these little pigmented bumps sitting on the iris. So coganrys or iris neva syndrome. And when you look at the pathology and all of these, it's the same and it's called the desmetization of the angle. So abnormal endothelial cells grow all the way across the angle. They close off the angle completely and they start laying decimates membrane even on the iris. And you look right here, look at that decimates membrane. Goes all the way over to the angle, but right there on the surface of the iris. Alley, what stain is this? PAS, why? Why would we do that? Exactly, and that is what decimates membrane is. So you see decimates membrane really thick, covering the angle, covering the surface of the iris. So that's kind of the common denominator in all of these ice syndrome patients. And here we have, this is actually perfilaridectomy that they did. So this is pretty cool. A patient had ice, a perfilaridectomy. The AS stain again, look, here's decimates membrane on the anterior surface of the iris. And then we go to higher power, sure enough, there's the iris, there's decimates membrane right there. And if you look carefully, you can see melanocytes popping through, forming that little iris nevus that you see in these. And so this was cool. This was the cover of the Archives of Ophthalmology. And so it's my only archives cover, so I made the cover with this gulica syndrome. There you can see again these iris nevi on the surface in Cogonry's. All right, now there's another entity you need to know that can be associated with, well, a group of entities that you need to know that can be associated with glaucoma. And the way I like to memorize these, there's a paper George Waring wrote literally 40 years ago about the stepladder classification. What are we talking about here, Becca? Like Peter's anomaly and like... What do we call the whole category, though? Wrongly, by the way. Well, that's what this is, but what's the whole umbrella called? That's another string of the umbrella. So these are called the anterior chamber cleavage syndromes. And so wrongly, we thought that when the eye was forming you'd get this wave of mesoderm coming out and that it improperly cleaved and then left you with these syndromes out here. So they called it the anterior chamber cleavage. Now we know that it's not mesoderm, it's actually neural crest and it really isn't a problem with cleaving. But that name is stuck to the literature. So the anterior chamber cleavage syndromes. And so what is this, Sierra Becca? That's a posterior... Postural embryo toxin. So the first thing you see in these is you see a thickened anteriorly displaced Schwabbe's line. So you see it's thickened and instead of having to look with the gonium or you can actually see Schwabbe's line in these kids, even with a slit lamp. And so you see this anterior displaced Schwabbe's line it's called posterior embryo toxin. They thought this was due to some toxicity during the growth of the embryo and so that's why they called it that. And here you have a close-up. It's the Schwabbe's line. Okay, now what's the next kind of step in the stepladder, Catherine? So you see the posterior embryo toxin. There's posterior embryo toxin real nicely. What else are you seeing here? Scarring over the angle. Yeah, so you've got scarring over the angle. You start to get some thinning of the iris here. What do we call this? Exactly. So we used to split them into two, axon, fel, rigors, and homily. And so the now people just put it together because it's kind of the same thing. So the next thing in the stepladder you still have posterior embryo toxin, but then you start to get these little fibers growing from the decimally membrane all the way across the angle. You start getting thinning of the iris. Now, there is actually a rigors syndrome, if you will. And so these kids are just funny kids that got weird teeth and skeletal anomalies and other funny things with them. And so, but in the eye, axon fel used to be just the things across the angle and then rigors was when you started to get the iris at you. But now they've lumped that together to axon fel rigors anomaly. Now, this is a little bit different. Sean, what is this one? What do we call this one? This is Peter's Anomaly. So Peter's Anomaly is characterized by a central dense opaqueness in the cornea. And they still have the other things with it. But in addition to that, you start to get this. And what Peter's Anomaly is characterized by is you get, for some reason, the posterior cornea just doesn't form well in the center. So you don't get endothelial cells. You don't get this membrane. So you get this dense scarring in the center. You still have the iris at your feet. You've still got this, you know, synechia there. And so what I like, and what these people also have is they'll have a funny anterior polar cataract. And so I like to think of it. It's like the lens went up and took a bite out of the central cornea and pulled it down with it. So there's this little opacity in the lens and then there's this bite in the center of the cornea. And you see Destiny's Membrane, she's gone in Peter's Anomaly and endothelium in the center. So you get this opaqueness in the center and that's called an internal ulcer of von Hippel. And so if you notice a theme here, virtually all iterms were described by Austrians and Germans in the late 1800s. And so von Hippel as in von Hippel Lindau syndrome. And so it's an internal ulcer of von Hippel and that's a characteristic finding in Peter's Anomaly. So again, if you're trying to learn these and memorize these and know them for boards, I find the step letter classification a good way to do that. And everybody's brain works differently. My brain is, I'm not a lump or I'm a splitter. So my brain is like your mailboxes upstairs. Every entity has a little box in there and that's how I keep track of them. So if you think of this, the whole broad umbrella is Antioch chamber cleavage syndrome but you remember the little boxes of the posterior embryotoxin, atcifal rigors, Peter's, then it helps you understand what's going on with these. Okay, and there's the gardens behind Versailles. This is a huge garden. I mean, it could take half a day to walk through these and there's ponds and beautiful flowers and all, but they had a horrible storm in Paris a couple years ago and it took out 10,000 trees in the area around Versailles from the winds. Hurricane winds took them out, so amazing what weather can do. So this is Versailles. So next week, layers. Okay, questions on glaucoma, angle pathology of glaucoma. All right, great.