 Okay, everybody, we're ready for Brank-Hurley-Bakoma-Path. So unfortunately, I haven't been to an international meeting now in almost two years, and so I've got no more pictures to show you. So this is Sun Valley at Labor Day. I uploaded these last night. So you guys get to see Sun Valley. This is the resort really early in the morning. Very pleasant place to be because it's about 35 degrees in the morning, but about 75 at night. So I mean, vice versa, so very, very nice. So this is Sun Valley early in the morning. And what they do on Labor Day is they do the wagon days parade. And so this celebrates the old wagons that brought the ore down over the mountain. And so they do a parade there. And so this is the wagon that used to bring the food and the water to them. And so everybody dresses up like cowboys and people sit on the side of the road and cheer. And so this is the actual ore wagon. It's got 20 mule team, literally. So they hook up 20 mules to it. And I always find it fascinating that these ore wagons were filled with iron ore and then came down this incredibly steep mountain pass in the turn of the century. And so they restored these and come on by and everybody cheers. And these things are huge. I mean, those wheels are as tall as I am. And so imagine those filled with just tons of ore coming down a mountain pass. And then they go by and everybody cheers and they go into town. Sorry, didn't erase these. My bad. OK, so we're going to talk about trabecular mesh work today. So the key thing is we want to know what's the pathology of the trabecular mesh work. And so one of these days you'll learn not to sit in the front seat here, but when you guys start gaming it, I'm going to switch it around so you can't not be called upon. So tell me about the trabecular mesh work. What are some of the main landmarks that we look at? Let's say we're going to look at it with a Goniomir. So we're looking with a Goniomir and we're looking at the trabecular mesh work. So what's the first part right here, which is not on this particular picture? Well, what's the separation point between corny and trabecular mesh work? Where does the decimus membrane end? Schwabbi's line. Exactly. So when you're looking with a Goniomir at the trabecular mesh work, there'll be a little white bump or white line here, which is where decimus membrane end Schwabbi's line. And then we start looking down and what do we call this part of the mesh work? Looking in a Goniomir. Non-pigmented mesh work. And what do we call this part? The pigmented mesh work. What is this right here? That's where you start seeing this. Scleral spur. And then lastly, you can sometimes see part of the iris root or part of the ciliary body when you're looking there. All right, now, there's another way to divide the trabecular mesh work up. And that is kind of these functional zones of the trabecular mesh work. How do we divide that up? All right, so we can divide them longitudinally into areas, the cornea scleral, the UVL. And the most important area is the juxtacanalicular. And that's this area right here. And that's where a lot of people think the pathology of open-angle glaucoma resides. And in the juxtacanalicular. So when you look at the trabecular mesh work, it's these bars of collagen with elastin in it. They're lined by endothelial cells. So you get some passive transmission of aqueous. But you usually don't get just passive transmission. There is some active transport of aqueous across that juxtacanalicular tissue that's right here. And so that's the important area when we're talking about open-angle glaucoma. What is this structure right here? The schlemz canal. Schlemz canal. What does schlemz canal do? So schlemz canal, the aqueous percolates through here, goes through the juxtacanalicular tissue, goes to schlemz canal. When you look at schlemz canal, it's not round, it's kind of oval and almost flatten. But now remember, in your brain, this is all 360 degrees. So this goes all the way around. And the aqueous goes into schlemz canal. What is this thing right here? Well, more specific, it is in the aqueous sclera and it's a vessel, but what do we call that vessel? Ah, I got it. Well, I'm excited, because I know you guys all read up on this and look at the old lectures and all, so I gotta put something out. We actually call these aqueous veins. But indeed, it does drain to the aqueous sclera. And so it is an aqueous sclera vein. Tell me about the sclera spur. What the heck is that? So that's a little extension of the sclera that's a bit of a shelf of the trabecular meshwork. Okay, so if you think about it again in three dimensions, the trabecular meshwork is triangular shaped and this piece of sclera spur sticks out and it almost gives kind of a shelf for that trabecular meshwork to sit on. So it sits on here and that sclera spur comes out. Now, what structure in search to the sclera spur that's important in glaucoma? The longitudinal muscle fibers in the sclera body. Okay, and why is that important? Because you can manipulate the angle opening it with certain medications. So one of the first, in fact, the first medication that we had to treat glaucoma for 100 years now was pylocarpine. And what pylocarpine would do is it stimulates the sclera muscle to contract, which then pulls on the sclera spur and opens up the meshwork. So it opened up outflow. Now, there were problems with pylocarpine. I know you don't really use it much anymore unless we're in a peripheral erudectomy or something, but pylocarpine also causes myosin, so people would be really small. When you get the sclera muscle contracting, you get a whopper headache from it. If you use a high dose of pylocarpine and you have to use it four times a day. So not really a very effective glaucoma medicine, but it was the first one we had. And so it works by constricting the luncheon mucillary muscle, which then pulls on the sclera spur and opens up the meshwork. Here's a close-up. There's the cells that line Schlemzkanal, the juxtacanalicular cells, and then Schlemzkanal here. Schlemzkanal is interesting. It's not wide open. In fact, there are almost little valves in there, almost like veins going all the way across, and there's a little septate across it. So it's a little bit more complex than we know. All right, so we're going to track aqueous from where it's made to where it goes. So where is the aqueous made? The aqueous is made in the nonpigment epithelium of the ciliary body. Okay, and then once it's made, where does it go? It goes kind of around the iris through the pupil into the anterior chamber, where it's absorbed by the travecular meshwork, and then it goes to the juxtacanalicular tissue, is absorbed by Schlemzkanal, and then goes into the aqueous veins. And in fact, that's just what we're showing right here. So here's the anterior chamber angle. Here's the travecular meshwork. Here's Schlemzkanal, and sure enough, here's one of those aqueous veins, and it pops out and it drains right in the episcleral tissue. So you could actually see these. We never look for them, but so when you're in clinic today, your mission is to look for aqueous veins. What you can see is you can see a vessel there, and then you'll see boxcarrying of the blood vessels. And so you'll actually see little squirts of clear fluid going in between the RBCs. And you can see those, a couple of millimeters from the limb, but it's deep in the episcleral. Look for those. And you'll find you go, oh yeah, there they are. So that's how the aqueous drains out. Bonus question, what's that? What the heck is that? Yeah, no, that's good. I always say, if you don't have any idea, don't say, oh, I have no idea. That is actually a haptic of an IOL that's sitting in the ciliary sulcus. And so we just happened to get a beautiful picture here, and this is a patient who had an IOL on the sulcus. Look at that. IOL just digging into that iris root right there. So that's, believe it or not, the haptic of an IOL. All right, so when we're talking about open-angle glaucoma, the interesting thing about open-angle glaucoma is when you look at the angle with light microscopy, it looks no different than an angle with that's normal for the age. So there's some aging changes in the trabecular meshwork, but if you have a 70-year-old with glaucoma and a 70-year-old without, you do light microscopy. It just doesn't look any different. So you really can't tell much on the path about the etiology of open-angle glaucoma. Now, if you look with EM, there's some subtle differences in the trabecular meshwork, but with just light microscopy, there's no difference. Now, all right, so I wanna look at some secondary open-angle glaucomas, and I'm sorry, I have lights in my eyes. I can't even see who's a resident and who's a student, so. I'm not a resident. All right, you don't count. So in here, you can see in the iris, there are trans-illumination defects, 360 degrees around, they shape like spokes. What do you think could cause that? So this could be pigment dispersion syndrome. Exactly, and so when you look at a picture like this and you do retro-illumination, you see the shining through these pigment defects in the posterior iris, and if you look, they're shaped like spokes. What do you think that is? Why are they shaped like spokes? So the iris would be rubbing on the zonules as it goes backward, and that rubbing causes... Exactly, and here's a piece of iris from a patient with pigmentary glaucoma, and you can see here's the bundles of the zonules coming through, and these zonular bundles rub on this because for some reason in these patients, the iris bends backwards instead of forwards, and so it scrapes on there. So what's the most common sex and most common age group for pigmentary glaucoma? Or even younger, and you can see these 20, 30-year-olds, what's their refractive error? They're usually hyper-opes. Actually, you would think that, but they're not. They're actually moderate to mild myopes. So it doesn't make sense because you'd think with hyper-opes it's more crowded, and it would do that, but they're not. So something is weird. If you do an OCT, that posterior iris literally bends backwards, and so some people have advocated doing a perfilaridectomy, which is kind of the opposite of what you do it for an angle closure glaucoma to let the aqueous flow through and maybe let that shallow a little bit and get away from the zonular bundles. So what happens is, is you look right here, here's where one of those zonular bundles rub. Here's the iris, there's the pigment I've been feeling behind it, and look, it's all been scraped off. It floats with the aqueous, and sure enough clogs up the meshwork. So there's a meshwork just full of pigment. And so that's a secondary open-angle glaucoma due to pigment dispersion. If we have any other, you guys all students back there? Okay, coming back. What the heck is this? Iris, here's the cornea. What could cause a pigmented mass in the ciliary body going up into the angle? So this could be a melanoma, it's a secondary open-angle glaucoma from the ciliary body invading into the angle. So you can get secondary open-angle glaucoma from tumors arising from the ciliary body and invading forward. And here you see another picture, there's cornea, there's iris, and right here there's this big tumor coming from the ciliary body forward into the anterior chamber angle, causing a secondary open-angle glaucoma. All right, what are we looking at right here? So why is there a clear space right here? So you think about it, the iris is almost like a windshield wiper on a dirty windshield. And so when the iris constricts and dilates, constricts and dilates, it scrapes that exfoliative material from the surface of the lens. And so you've got some in the center where the pupil is small and in the periphery where the pupil is big, and in between it scrapes it off. So that's exfoliation syndrome. Here's a close-up, that classic scalloped-edge deposition of this exfoliative material. And here's a nice, now these pictures look familiar because we talked about this when we talked about lens, but there's a lot of overlap here. So here again in retro-illumination, the classic scalloped-edge of exfoliation syndrome. And then what's the pathologic finding? How do we describe this? I don't know what you're not mean. Lens capsule, and then you see these, that material kind of up on end, like iron filings. Iron filings, and so I don't know if you've ever taken a magnet and stuck it in some iron, they stick up on it. So it's like iron filings, they call it, and that's what this material looks like when it deposits on the lens capsule. So the problem with this material, it just doesn't deposit in the lens capsule, it deposits in the trabecular meshwork. So you can get a severe secondary opening of glaucoma and exfoliation syndrome. And the problem with this is people could be going along fine for a lot of years, and then suddenly their pressure goes up. So you really wanna watch exfoliation patients closer for potential glaucoma developing. And this is interesting because it's a genetic disease, they've found the locus of what causes this, but also it's a disease seen in people of Northern European ancestry. So people from Sweden, Norway, Denmark, Northern Germany, England, that's where a lot of exfoliation comes from. And so where do a lot of people from Utah trace their ancestry from Northern Europe? So we have a ton of exfoliation in Utah. The other place in the U.S., they have a ton of exfoliation is Minnesota. Again, where do people from Minnesota come from Northern Europe? And so we've got two big pockets of exfoliation, but it's interesting because as our outreach people have gone all over the world, there's pockets of exfoliation in Ethiopia, in Guatemala, very interesting. So there's these other pockets of exfoliation syndrome that doesn't quite fit that Northern European ancestry. But the key thing is, you can get a significant glaucoma with this. Now, taking out a cataract, believe it or not, is very helpful for secondary open-angle glaucoma from exfoliation because first of all, you remove all that material that's on the anterior lens capsule. But again, all that fluid circulating through during a cataract surgery flushes a lot of this out of the angle. And thirdly, when you put a thin implant in the capsule bag instead of a thick capsule, it opens the angle up wider. And so if you've got people with exfoliation and you do cataract surgery, their pressure can drop three to five points. So it's pretty good treatment for exfoliation glaucoma. All right, we're looking right here. Sally, what are we seeing here? See some white. Some white, fluffy stuff in the inferior angle. So we've got a dense, mature cataract. You've got some white, fluffy stuff here. What if I tell you that patient's pressure is 45? Exactly. And we talked about this again during the lens, but we really want to hit it again here because another rare cause for secondary opening of glaucoma is what's called fake-olytic glaucoma. And so it's in the setting of a hyper-mature cataract where the cortex has begun to liquefy. You actually get leakage of protein out through an intact capsule or bag. Macrophages come in, they munch up that protein. They clog up the mesh work, and you get a really severe secondary open angle glaucoma. Here's a slit lamp view, and there's that hyper-mature cataract. And look, here's that material, all those macrophages stuffed with protein in the inferior angle. So you can imagine all these macrophages, they're just stuffed. I mean, they've just engorged themselves with all this protein. Now the protein clogs up the mesh work also. So you've got this protein here, which you've got all these fat macrophages here, clogging up the mesh work. So again, you can get a pretty severe acute secondary open angle glaucoma due to fake-olytic glaucoma. Now, hopefully we don't see this very often in the first world, but sometimes you see it in the developing world or parts of Wyoming. And so that's the kind of developing world. You're allowed to slam your own kind up from Wyoming. I'm allowed that, isn't it? A little slam, but some parts of world Wyoming, you know, you might see these. And believe it or not, this is an aspiration of the anterior chamber. And these are macrophages just stuffed with pigment. All right, now this is just a simple schematic drawing, but I do like to show this, especially for the students, because we've got our normal angle. You can also have a narrow or a closed angle, or you can have a recessed or wide open angle. And so those are some different types of angle anatomy that can cause glaucoma. So the first thing we want to talk about is this patient. So the thing is the medialated pupil at the right eye, it's also injected. What would your concern here be? So they'd be worried about acute angle closure. I'd be worried about angle closure. This was a patient that, believe it or not, had a GI procedure. They gave him atropine, and then they're in the hospital about a day later. The atropine starts to wear off a couple of days later. They get a severe headache. And so what do they do? Of course they give him Tylenol. And so, you know, two days later, they still got a severe headache on that side, and they did notice that the eyes were red. So they sent them over for a consult. And sure enough, the pupil's mid dilated, and the eyes really injected, and the pressure's 50. When we look with the slit lamp, what do we see here? It looks like the iris is pushing forward. Yep, so iris bombay. So the iris bombay is bombay, B-O-M-B-E, accent, a goo coming up from the, not the Greek, from the French. Okay, so from the French. All right, so it's bowing forward. You can see there's the beam on the cornea. And look at this coming forward. It's almost touching in the angle. And so, you get this angle closure glaucoma. What is the actual etiology of this? Yeah, so basically you have pupillary block. So you have a mid dilated pupil, and you have posterior opposition of the margin of the pupil to the anterior lens capsules. You don't allow for the aqueous flow. So the aqueous just builds up behind them. What's interesting, it doesn't happen when you dilate the pupil. It happens when the pupil is just coming down from dilation in a susceptible eye. Hyperopia, they'll have a narrow angle. And so you dilate them, and they're okay. And then the dilation starts to wear off. They come to that mid position, and for some reason it sticks. So you get that effective block there, and then you get aqueous building up behind it. What's the treatment? Drops in the lasers. Yep, so you wanna bring the pressure down, make sure the cornea is clear, and then you do a laser peripheral aridectomy. And it's pretty cool. I don't know if you guys have done a PI in an angle closure. It's pretty cool. You set the yag on. You do a couple spots, maybe five millijoules each. You just blast it, and you go pow! And you literally see the aqueous flowing through, and the iris goes back down. So it's pretty cool to do when you actually do it. Yes? So if this was like uveotic, and you had like sneak it down, and you had like a hot AC, would you still shoot a laser through that? You know, you wanna try to calm the inflammation if you can, because otherwise the PI will seal off more frequently. So if you've got a hot eye, try to calm it first. Calm it as in like steroids? Calm it as in steroids, and then give them anything it takes to bring the pressure down, including oral medications. You may even have to give them dimox and give them as many drops as you can to suppress aqueous. Then once it calms down a little bit, then you can do a definitive laser. All right, so this just shows you what the result of chronic angle closure of glaucoma is, and what are we seeing here? They are PAS, Perifal, Ontario's, Nike. Exactly, so here's the mesh work clear back here, and you can see Iris is stuck to the Perifal cornea here. And so if you let angle closure glaucoma go on too long, or if it's a secondary angle closure, go to inflammatory mechanisms, you can get Perifal, Ontario's, Nike or PAS as we call them. This just shows you a broader PAS. Here's the Iris stuck to the Perifal cornea there, blocking off the mesh work. So for a secondary angle closure, there can be some other causes of this, aside from just chronic angle closure. What is another, what's another, what's the cause for secondary angle closure? You have vascularization, you can see the blood vessels. All right, so there we see the Iris stuck to the Perifal cornea, and there are abnormal blood vessels on the surface of the Iris, so what could cause that? So I think causing vessel growth from usually ischemia, so that could be diabetes, vein occlusion, ocular ischemic syndrome. Exactly, and those are the top three. So those are what you need to memorize for boards. Most commonly diabetic, but then central retinal vein occlusion or even peripheral vein occlusion in the retina. And finally, ocular ischemic syndrome. And so those are the causes. Chronic ischemia produces vascular growth factors. These vessels start to grow on the Iris and then eventually grow into the angles so you get secondary angle closure glaucoma due to neovascularization. Here's a close up. Here's the Iris pigment epithelium posterior. And look, you should not have those fine little vessels on the surface of the Iris stroma. So that's Iris neovascularization. All right, what the heck is this? So what is this called? Iris adheres to the lens back there. Exactly, so posterior scenicia. So you can get secondary angle closure glaucoma due to the Iris sticking to the lens surface, probably secondary to inflammation and forming posterior scenicia. And then you can see this was actually broken. I don't know if they're broken by dilation or whatever, but that Iris pigment was still just stuck to the anterior lens capsule. So secondary angle closure glaucoma due to posterior scenicia. We abbreviate those as PS. Here's a close up of an Iris here. Now you can see that the Iris not only were there scenicia, but there's a little pupillary membrane here. So you can get secondary angle closure with an inflammatory membrane across the surface of the pupil, which sticks things down and doesn't allow aqueous to flow through. So again, secondary angle closure glaucoma due to a pupillary membrane. All right, what are we looking at right here? Instead of the normal architecture of kind of where the Iris meets the cornea with the trapezoid. So what do you think happened to this patient? Exactly, so this is an angle recession. So if you look real carefully, this is a trabecular mesh where clear up here and you're actually looking into the face of the ciliary body. So when you look at a traumatic angle recession, it really is a tear in the face of the ciliary body. So it tears down. And you can see that right here. If this patient were to get glaucoma, how long after that acute injury would the glaucoma develop? Yeah, so like 10 years. And so this is the one time you gotta put a fear of God in these people because a lot of these people are young. Young males of course, who else does dumb things that allows you to get a lot of trauma to the eye? You know, fists, feet, wrecks, whatever. You get a blunt trauma, you get a tearing of that, but you don't get glaucoma immediately. You get it up to 10 years later. So we always tell these people, you have to come in every year because pressure will build slowly and you may not even notice it. So I had one really sad case. Guy came in, he was probably 40, and he had had a trauma a year ago. I mean, not 10 years ago, it didn't show up. He came back because of blurred vision. Well, the reason his vision is blurry is he had a temporal island of vision out here and that was it. Total 0.9 cup, you know, lost his eye slowly, but surely because he didn't come in. So you really have to tell these guys, and this is the one time I never used the word blind in ophthalmology because blind is a very visceral word. And so I tell people you can lose vision, you can do that, but if you have a young guy with an angle recession, I use the B word. And I say, you know what? You can go blind from this. And if you don't come in every year, you could go blind. And so that has a more visceral effect on people and we'll hopefully get these young guys to come in because the glaucoma will form up to 10 years later. And this just shows kind of a compare and contrast. Here's a normal angle. Here's an angle recession. There's the angle, look at that tear right into the face of the ciliary by now. These often will occur in the setting of a traumatic hyphaema. So when you've got some with a traumatic hyphaema, you don't want to put a gonio lens on there and have them squeeze and bleed again. So you want to wait, let the hyphaema clear, let everything settle down for about a month or so, and then bring them back and gonio them to make sure that there's not an angle recession in addition to the hyphaema. What are we looking at right here? Oh, actually no. Yeah, that angle just doesn't look normal. You just don't see a developed angle there. And so this is kind of a almost like a scarred angle that didn't really develop well. So that can be the secondary features from a chronic recess angle. You just get scarring in there over the years. All right, and this is, what the heck does this show? Yeah, so if you look right here, look, there's the mesh work up here. There's the mesh work up here. So big traumatic angle recession. They had a ruptured lens, summering ring here, and then unfortunately a total cut. And so this is years later, unfortunately they didn't come in and they actually lost their vision completely due to the severe glaucoma. All right, so we want to talk about glaucoma. We can't not look at the optic nerve because obviously that's where the, you know, vision loss occurs from glaucoma. So what are we looking at right here? This is a color-focus photo. Looking at the optic nerve. I'd say a cup to disc ratio is probably 0.8. Right here, the cup to disc ratio maybe 0.7, 0.8, but definitely an enlarged cup. And sometimes hard to appreciate on a flat picture. This is where you want to look with your 90-diopter lens or you want to look with, you know, stereo photographs in order to see this, but significant cupping. And that's kind of the end stage of glaucoma. Now we look at this, even more cupped, it's symmetrical, but pretty significant cupping here. And so any glaucoma, open angle, angle of recession, narrow angle, bottom line is when the pressure's high enough for long enough time in a susceptible nerve, then you can get a severe cupping, which can lead to the glaucoma to stand. And of course, this is a total, you know, 1.999 cupping. And so you can get in the long-term severe glaucoma to just changes total cupping. And here we can see, again, what do we think happened here? I have some summerings ringing. I don't know what's going on. The AC looks like the iris is, like, attached to the cornea, optic. Nervous, completely excavated out. Looks like this guy's got an RT or a PVD as well. So this is artifact, you know, with the post-mortem artifact. But if you see severe cupping, which end is this? Is this nasal or temporal? So actually, when you get this sloping a little bit, that's temporal. When you get the excavation, that's a little bit more nasal. So you see it's actually excavated. And so you can see when you look at these, you'll actually see a vessel going around the edge of the nerve, and then it just disappears, you know, into the big cup, and then it comes down. So this looks like a Boston bean pot with severe cupping. But this patient had trauma. There's an adherence scar to the cornea and to the people called a lucoma, and of course a summering drink. So traumatic glaucoma, leading to severe angle change. So here's that bean pot we talk about. So this is a severe end stage glaucoma. You actually get excavation. And so this is temporal. Look, there's not a single nerve fiber left there. And then nasally, here's that vessel just dipping around the corner. So you can see it completely excavated, posterior bowing of the lamina crebrosa, loss of all of the fibers here. So this is an end stage glaucoma desoptic nerve. Here you can see another one. Look at that excavation. There's like a little cliff right there. And then it goes out. And again, widening here of the subarachnoid space so that nerve is totally atrophic with end stage glaucoma. There's a close up. So you can just imagine Dr. Tabin, you know, climbing that cliff there and going over the edge and scrambling over it. You guys probably know who Dr. Tabin is. So one of our old faculty has climbed Mount Everest several times. So you can imagine climbing a cliff looking like that. I had a patient in the hospital the other day that Dr. Tabin picked up hitchhiking and they went skiing together. Did you ever meet Dr. Tabin and he invites you to go skiing? You know, unless you have a death wish and say, oh, I hurt my knee the other day. So he is an incredibly good skier and he loves going through trees and off cliffs and down ravines and things. So unless you really, you know, value your life, say no. All right, we're looking right here and this is interesting. So this is an optic nerve and cross section and there are vacual depositions that we call Schnabel operos optic enter. Exactly. I assume Schnabel's German. All right, so if you have an acute glaucoma, like you have an angle closure and the pressure shoots up to 60, you can sometimes get this acute change in the optic nerve and people even speculate that it's got a little bit of hyaluronic acid in there and a little bit of fluid. It's almost like that high pressure drives stuff into the optic nerve head. So it's called Schnabel's cavernous atrophy. Is the atrophy from, like is the white stuff from the atrophy or like the material itself? It's actually the material that's there and then eventually get an atrophy. So this from hyaluronic acid in there, that's why they think it may come from the vitreous and there's some fluid in there. Then eventually it damages the fibers and you get this focal kind of cavernous atrophy. And there you can see the stain. This is a mucin stain. And so you can see you've got this mucinous material that's, I'm sorry, it's a stain or hyaluronic acid, I apologize. So you've got this hyaluronic acid material in there. All right, we're looking at a lens capsule here. Medium power, high power, anterior capsule. What are these little focal, again, almost swollen spots in there under the anterior capsule? Greatest space is Glockum Flecken. Glockum Flecken, exactly. Here we got two German words in a row. So Glockum Flecken, that just sounds cool. And so again, in a setting of acute high pressure, these would be usually people with an acute angle closure or whatever, pressure goes suddenly high, you'll actually get swelling and ischemia here in the anterior lens epithelial cells and you get these focal little swollen areas called Glockum Flecken. All right, what are we showing here? Oh, did we do, oh, I'm sorry. We go in there, there, yeah, yeah. So you can see that there's lots of ganglion cells in the retina and that's the inner layer or the top layer of this picture here. All right, so when we get to retina, which is in October, I will really wanna know your layers of the retina. That's really important, so you gotta know your layers because there's all kinds of layers in the retina, so know those cold. But the key thing here is, you see here's your outer nuclear layer, here's your inner nuclear layer, right here the ganglion cell layer is completely absent. So that's a sign of glaucoma because glaucoma affects those axons going out through the optic nerve, then you get secondary cell death of the ganglion cells. And so you get a selective loss of ganglion cells in the retina and in stage glaucoma. And this just kinda shows you the difference. There's a normal area in the macula where there's tons of ganglion cells and here we're in the macula and a patient with severe glaucoma and even in the end the macula is affected. So severe drop-off of ganglion cells. What are we looking at here? There's no real developed angle there and there's kinda this stuff here kinda covering the angle, what could this be? What if I tell you this is a two-year-old? Exactly, so congenital glaucoma, when you look in there with agonium ear, you don't have to put these kids to sleep obviously because you're not gonna let you put a mirror in their eye, but you look in there and you'll see it almost looks like a little fibrinous membrane almost across there. And in fact, they called it Barkhant's membrane and Barkhant had described it. And so one of the earliest treatments of congenital glaucoma is you go in there with agonium knife and you just slice this membrane you know, 180 degrees and people thought if you cut Barkhant's membrane then make the glaucoma batter because the trapezoidal mesh would be okay, but if you really look at these kids that meshwork is not properly developed. So even if you cut this membrane, you'll get a little bit of an effect because it just kind of increases UVL scleroflow but you don't have a good well-developed Schlem's canal and trapezoidal meshwork in these kids with congenital glaucoma. So that's the so-called Barkhant's membrane. Here's a close-up, this little membranous material here but you just don't see a well-developed trapezoidal meshwork behind it. So congenital glaucomas can be very difficult to treat because you just don't have a well-developed, you know, meshwork, Schlem's canal, the whole drainage system of the eye. Okay, now Abby, I bet you wish you had that other one instead. What are we looking at here? There's many areas. There's also injection of the conge since we're talking about glaucoma. All right, so what entity do you think this is? About one of the ice syndromes. All right, so what does ice stand for? Okay, so you really need to know about the entity of ice, irritocornil endothelial syndrome. And lumpers lump it all together, splitter split it up into three different areas. And so it just depends. If your brain likes to lump or likes to split, I'm a splitter, you know, I like little mailboxes where you can put all your things in that you memorize. And so ice can be split up into three different presentations. So the final common denominator is that it affects the endothelium abnormally and gets secondary glaucoma. Now is ice unilateral or bilateral? Thank goodness, it's usually unilateral. So this first one is called a central iris atrophy. And so you get literally polychoria, multiple pupils. You can get the iris stretched out and thin and pulled. And so that's a central iris atrophy. What is this one? All right, so what does Chandler's have that's in addition to the essential iris atrophy? So there's the iris atrophy, the polychoria, the multiple pupils. But if you look carefully here, look, that's hazy. And so you've got corneal edema in addition. And so splitters call this Chandler's syndrome. And so you've got significant corneal edema in addition to the iris atrophy and to the high pressure. And then finally, the third entity in ice. Iris, nevus, former Cogan reese. Yeah, so Cogan reese were the, they're both famous pathologists while Cogan was, reese did pathology. So Cogan reese, and you see these multiple little, almost like little nevi sticking up on the iris. But if you look in between, you see this velvety looking almost like a clear membrane on the surface of the iris with these neva cells popping out. And so when you look at this pathologically, what's the final common denominator in all these ice syndromes? Exactly, so the endothelial cells almost become epithelialized. I mean, they grow, normally they shouldn't. And so you'll get endothelial cells will grow across the angle onto the surface of the iris. And so that'll cause a severe closure of the angle and it'll cause all those problems you're seeing with the iris. So you get an endothelialization of the angle and of the iris. That's in all three of these. And here's a close-up. Look, that's decimates membrane on the surface of the iris. So you'll literally get decimates membrane going all the way across on the surface of the iris. Look at that decimates membrane here. Look, it's like four times thickness. So you get this really abnormal, very actively growing endothelium. It grows across the trapezoidal mesh, it'll work onto the iris, gives you secondary closure of the angle and then gives you the iris atrophy, the corneal edema, and then also in the cog and reese, the iris neva, you get little neva cells poking through. So here's a peripheral aridectomy in one of these patients. And this is the anterior surface of the iris. What kind of stain is this? This is, I mean, it looks like it's staining and it's been membrane, so is this a PS? Yeah, yes. And so what are you seeing here on the anterior surface of the iris? What about the decimates? Yeah, so you actually see decimates membrane on the surface of the iris. So here you see desmetization of the iris in a patient. This patient happened to have cog and reese. And the nice thing is, is we're able to look right here and here is that decimates membrane on the surface of the iris. But this is kind of cool picture. There's the little neva cells popping through. So you see this velvety membrane on the surface of the iris, then you see these little mushrooms popping out. And this is the iris neva. And so this is the third part of the ice syndrome, the iris neva, cog and reese. So you gotta memorize those because they love those on boards. Yes. Specular macroscopy, do you get like a characteristic appearance like that endothelium? Or are they still like normal looking? You get a lot of drop off of endothelium because endothelial cells aren't normal. So you get a decreased number of endothelial cells and then you get, again, the pleomorphism and some of the weird shapes and sizes that can come when the endothelium is affected. But the count actually goes way down. Here's a close up of that iris neva popping out on the surface there. So ice syndrome, any questions on ice syndrome? All right, well, you're up anyway. What are we seeing right here? What the heck is that? That looks like a thick and unfolded over that's amazing numbering. So what do we call that? Posterior embryotoxin. All right, so there's another kind of lumped together group of things that you need to memorize. And so this is part of what's that group called? Anterior cleavage syndrome. All right, so anterior chamber cleavage syndrome. That's really a misnomer because initially we used to be taught in the olden days when I was a resident that this wave of mesoderm would come out and form the anterior chamber and then it would cleave and form the angle and that abnormal cleaving would leave to this syndrome. So they call it anterior chamber cleavage syndrome. It turns out it's really not a wave of mesoderm. What is it that forms it embryologically? Norocrest. Norocrest, exactly, it's not mesoderm. It's norocrest in it. And you'll get waves of this form that doesn't really cleave, but that's how we know it. And so back in the 1970s, we're talking now almost 50 years ago, George Waring came up with what's called the stepladder classification. And again, it's a good way to memorize a lot of information going on that you need to know for boards. Well, for patient care too. And so the first thing you'll see in these anterior chamber cleavages is you'll see a thickened, anteriorly displaced shrobby's line. And so that's called posterior embryotoxin because early anatomists thought that this was due to some toxicity in utero that would cause this. And so posterior embryotoxin is the first part of the stepladder. There's a closeup, that abnormal thickened shrobby's line. But then you have abnormal thickened shrobby's line and what do you have right here? There's just some scarring and some connective tissue that is garrulous. Yeah, so what do they call this one? Exactly, so axinfeld rigors and it depends on if it's the anomaly or the syndrome. There is a syndrome where these kids get this axinfeld's rigors anomaly in the eye but they also get funny teeth and bone things, all kinds of funny things with them where you can get just localized to the eye. And so you have this posterior embryotoxin which you've got these little filaments of almost like Irish tissue growing up to that area and you can get a secondary blockage of the angle. And so you can get a secondary glaucoma with axinfeld's rigors. Yes? An exam does it just look like gas? It'll look like, well no, the angle will still be open. It'll almost look like a congenital angle because there'll be this little thin membrane over the surface but the iris doesn't come up and close it, the iris is down there but these strands come across it. And so you can see that it's almost like that angle's open but there's still all these strands across it. Eventually it'll close it off but early on you'll see almost like a membrane across it, blocking it off. You can see it external too, right? Like that cornea where it's like. Yeah, and you can actually see the posterior embryotoxin, you'll look, you'll see it's almost like a white ring coming a little bit in from the limbus in these kids. All right, this is the third part of, oh my, I thought I was skipping the intro. Okay. Looks like the corneas. Yeah, so you see this white opaque cornea and since this is, obviously I go, we'll see DUIs from one step to the other so the next entity in the anterior chamber cleavage is? Peter's anomaly. Peter's anomaly, okay. What happens in Peter's anomaly? You have loss of the posterior cornea leading to corneal edema. Exactly, so you get, when you look at pathologically here, it's interesting for some reason in the center part of the posterior cornea you don't get endothelial cells, it just doesn't form properly. So you don't get endothelial cells, you don't get decimals of embryo forming there, you get secondary edema. In fact, some people call it an internal ulcer. You'll almost get an internal ulcer in the center of the cornea. Now you'll still have the XFL rigors changes, you can stop with your embryotoxin but then you get this secondary almost internal ulcer. In fact, von Hippel going back 100 and higher along that's been 140 years, describe it as an internal ulcer. And so you'll get in Peter's anomaly, significant corneal edema because of that internal ulcer. And here you see a close up, you see decimals of membrane and endothelium are just gone, they just don't form there centrally. So that's kind of the third part of this, this step ladder classification of the anterior chamber cleavages. And so on boards they love ice, they love anterior chamber cleavage because they're rare and there's a lot of material and there's minutiae. So, you know, really know those before you guys take Ocaps and take boards. So for the Exenfield rigors, I know you can get like the polychloria and caractopia as well. Is that from like the irstrands actually pulling? Exactly, it's almost like you see in the ice because it pulls on the iris and so you can get the iris pulled over to the side, the corneal copia, but you can also get polychloria with these too. This is typically like younger kiddos, bilateral ices, ices, unilateral. Exactly, exactly. And these are younger, especially Peter's anomaly. These kids are young when you see them and it is an abnormality in the anterior chamber development. So it's a developmental abnormality. But I do think if you look at wearing step ladder classification, that's a good way to memorize this. And so I found that very good way to fill up the little mailboxes and allow you to know what's going on with these. And we say goodbye to the wagons as they're heading toward the ski area and Sun Valley. And you see, we line up, people put their chairs out the night, the day before. You have to put them out in the afternoon to get a place to sit. And so we get that yellow almost white crime scene tape and we put chairs out and put tape around it and everybody dibs their places here along the road so that they can see the parade. And then the parade goes all the way into town, around the corner comes back. So there's the ore wagons leaving as we say goodbye to Sun Valley. Okay, questions? All right, so retina is in October. And again, what does retina, ogres and onions have in common? Layers. Layers. So you really want to know your layers of the retina when I'm gonna do the retina later next month. Okay, thanks. All right, thanks, Dr. Vamos. You're welcome. Dave, where are you thinking?