 All right, well, I apologize. We're not going to have a pointer again. So I'll just have to point to things. And so this is a really depressing site, because this is what Notre Dame looked like before the massive fire almost took it out. And you can see that's the spire that collapsed when the roof was on fire. But the tour boats go on the sand, and Notre Dame's actually on an island in the middle of the sand. And so it was beautiful to see. Let's see if this works. Well, none of this works. So this thing, even though the green light's on, it has to be put in here. So, sorry, Mike. I didn't know that. I didn't know that. That's good to know. OK, works great. And so again, here you can see that this is the back of Notre Dame again from across the sand. This is the front, and these are the two towers that, again, thank God they were able to save them, because if those gone, the whole thing would have collapsed in on of itself from a little loss completely. And again, this is the spire that fell through the roof when the roof was on fire. This just shows you the side part that's coming on. That's all stained glass. It was beautiful. They claim they're going to get it back up within five years. That's pretty optimistic, but hopefully they'll be able to bring it back to its old grandeur. All right, today we're talking about lens. All right, here's the first one sitting there. Tell me about the pathology of the lens. What embryologic layer does it derive from? So it's a surface ectoderm. All right, so you can see on the top how the lens forms. Remember the first lecture we talked about embryology, much of the important parts of the eye come from neuroectoderm. So the neuroectoderm outpouches from the neural tube. It then touches the surface ectoderm, and when it does that, it induces the surface ectoderm to invaginate. And so basically, the surface ectoderm invaginates. And I like to say it's like you've got a balloon, and then someone puts their fist in the balloon. So the surface ectoderm invaginates, and then that little piece of surface ectoderm gets pinched off and becomes the crystalline lens. And so you can see these are chick embryos. But interestingly enough, chick embryos look exactly like human embryos, but the same stage of development from four to five weeks of gestation. And this just shows it again in a schematic. Now, once the lens vesicle pinches off, it's an empty circle. But what happens is, is the lens of epithelial cells will grow from the posterior surface anteriorly. And these primary lens fibers, all the way forward, they fill the lens completely, and that's what forms the embryologic lens nucleus. From that time on, there should normally be no lens epithelial cells along the posterior capsule. So that's something pathologic going on if you see those. And so then they go out to the equator, and as the lens grows throughout life, it will grow from those epithelial cells at the equator. And this just shows you, this is actually a human embryo. And this just shows you, again, those cells from the posterior surface coming forward. And those lens fibers then make the embryologic lens nucleus. This just shows you what the nucleus looks like in a normal adult dye. So throughout life, what happens is those fibers keep growing. So you end up getting a fetal nucleus, eventually an adult nucleus. And then also throughout life, as those fibers keep growing and growing, the lens comes from round to more oval, as we're used to seeing now, the oval shape of the lens. This just shows you in an adult dye. Again, this is the lens bubble where those fibers are, the nucleus, the cortex, the lens capsule, and then it's schematic. All right, Rachel, what am I showing here, and what's the stain? What is it staining now? Look and see what it's staining, and then I'll tell you what the stain is. Okay, and so what stains, lens capsule that, bright magenta color. This is PAS. So remember, the lens capsule is the thickest basement membrane in the body. And so we always claim that the eye's the most important part of the body. So the lens capsule is the thickest basement membrane in the body. So anteriorly in the front, you see the lens capsule, you see that lens epithelial cells underlying it posteriorly on the bottom. We see the posterior capsule, and you do not see lens epithelial cells. Now, for those of you who are just starting surgery, the posterior capsule's only two-thirds as thick as the anterior capsule, it's five microns thick. So it's all that is there between you and vitreous. So when you have that 40,000 Hertz ultrasound in there, be really aware of what it can do to the posterior capsule. What are we looking at right here, Marshall? So we was showing about lens equator. What's the bowing of the lens? So this is the lens bow. So again, those lens epithelial cells don't extend posteriorly, but you look at them, they're all through there, so they kind of go along the rim of the nucleus. So you think of the lens almost like a flying saucer. Those lens epithelial cells go to the periphery, and when you're growing, they grow under the capsule, they start laying concentric pieces of capsule, and they send fibers anteriorly and posteriorly. So when the lens is growing anteriorly and posteriorly, and then they tend to meet in the middle, and so you get the lens becomes denser and denser and denser as we grow older. What are we looking at right here? So this is a zonular fibers attaching to the lens. All right, now I really wanna point out here what's interesting is the zonules attach not exactly at the equator, but they go somewhat anteriorly and somewhat posteriorly. So when you guys are starting to make your capsule over excess, you know, if you take it out to eight millimeters, you'll be getting into the zonules, and so you don't wanna do that. But the second thing is, you notice the zonules, they insert to the ciliary body, but look at some of these guys. They come clear back here, in fact, some of the zonules almost insert to the parsed planar. So we've got a pretty strong insertion there, anchoring the lens in place. Now, what are we seeing here, Ariana? We're looking at the sutures where all these fibers come together. And they form the letter? Y. Y, so, and that's because again, it's not a perfect sphere, it's more oval, and so those fibers, as they come around, instead of coming to a single point, they form a Y. So you've got a Y at the front of the nucleus and at the back of the nucleus. So you'll see it, you know, right side up, Y, and upside down Y. So again, you mission today, you never even think about this when you're looking at the lens nucleus of the slit lamp, find the Y sutures, okay? So that's your mission. Think about it just for a second and find them because they're there on everybody. And that just shows you how the fibers come together. And this just shows you the lens nucleus here in an H and E stain. It's not really very interesting. And so oftentimes we don't even stain these nuclei. So if you've got a patient with a really hard nucleus and you do an extra capsule or surgery and you send it to us, we look at it grossly, but microscopically there's really nothing interesting to see. This is interesting because this looks like a honeycomb. These are actually the lens fibers in cross-section. So you see they're hexagonal. And these fibers are interesting because they start to lose their nuclei in the cells as they start getting packed in. And they've got lots and lots of proteins in there. And again, their regular array allows light to come through. So it almost looks like a honeycomb in cross-section when you look at the lens fibers. All right, Allie, what do we see in here? All right, so they're wearing an AFIC kit contact. And when you say it's, well, actually sublux, yeah, because sublux means down. But again, it's luxated superiorly, but not only superiorly, but what other direction? Superior temporal. So what entity do you get superior temporal luxation of the nuclei or the lens? Marfans. So this is a Marfans patient. So I don't know why, but Marfans go up and out. It doesn't make sense because it's a diffused zonulopathy. So you think that the lens will sink down, but it doesn't in Marfans. It goes up and out and haven't been able to find a good explanation for that yet. So you see the patient's wearing AFIC spectacles. Here's the patient. This is a really old picture. This is one of our old texts. This is when the clinic used to be in the main hospital. So this picture is about 30 years old now, but this is a Marfans patient I took care of for years. Look at his, he's seven foot tall. Look at his long spindly fingers. What's one thing you need to know for boards about Marfan? What disease, what entity could kill a Marfans patient if it's not watched closely? Disorders of the aortic root. Exactly. So they can get, this is a connective tissue disease, they can get aortic root dissections. You can get acute failure of your valves that are coming out. And so you want to be really careful with Marfans people. Look at his long spindly fingers. So this is actually that patient. This is one of the first patients I saw with Marfans. All right, what do we see in here? Back to you. Yeah, so there's some photographing. What's the other one? This looks like it's an infrared nasal. So which entity is inferior nasal usually? It's gonna be homocystinuria. Homocystinuria, that's just a board question you really want to know about. So superior temporal is Marfan's inferior nasal is homocystinuria. Again, I don't know why, but that's what it is. And homocystinuria people can be kind of tall and spindly too. So that really doesn't help you discern them. But again, they're diffuse zonulopathies. They're weaknesses of the zonules that cause this to happen. Rachel, what do we see in here? It acts in the anterior chamber. So how do you get a dislocated lens in the anterior chamber? What's an etiology that could cause that? Okay, so this could be a zonulopathy. But in this case, it looks... Exactly. So, you know, wild Marcazani is an entity where you get this small spherical lens. And the people are different than Marfans because they're not tall, spindly. They're kind of short and have little stubby fingers. Kind of short stubby instead of long and spindly. And so you can get spontaneous dislocation of that small spherical lens in the anterior chamber. What's the most common reason for a lens to get in the anterior chamber? Trauma, yeah, so trauma hit to the head, car accident punched. And so you can often see traumas as the cause of doing that. So you guys know the story. Every patient who comes in with eye trauma, what happened? Two dudes. Okay, so you haven't heard the two dudes story? I was just sitting there, minding my own business. And these two dudes just jumped me. They always said it's never one, it's always two. I was just minding my own business and they just jumped me. And so I had a friend from the South, I guess they didn't realize that the South had carried even further. I saw my front portrait in the Bible and these two dudes jumped me. And so the two dudes can cause a dislocation of a lens into the anterior chamber. All right, and this just shows the path of the lens dislocated in the anterior chamber. All right, now, this is a younger child. What are we seeing on this globe that's been cut in half? Marshall? We're seeing that the globe itself looks a little small and also the lens is also more spherical. So what other entity can you get a small spherical lens in a young child? Can general rubella. Can general rubella, this is a good board's question too. And so when you look at this, what's interesting about congenital rubella when you look at the lens, not only is it small and spherical, but the nuclei tend to be retained more in the fibers. So you'll see nuclei throughout the lens itself more so than you would normally. All right, what are we seeing right here? We see a cataract right in the center of the lens and it looks like it's probably like a congenital cataract seeing as it's confined to just the center of the lens. Exactly, so you can see that's kind of the fetal embryologic lens nucleus. This is a really interesting one because if you look carefully, here's female sign, up top is the male sign. So I call this the prince cataract. Remember when prince stopped being called prince the singer and he became this male female symbol? So this is the prince cataract. And so you can see it just, at least smile or something. I'm trying to keep these from being too boring for you guys. So you can see it involves both the central nucleus, not the entire nucleus. So this is a congenital cataract. Here's another one that's not quite as easily seen but you see this slip beam is coming from the side and you can see it just involves the central nucleus. So this is a congenital nuclear cataract. Now you can have other congenital cataracts. You can have congenital polar cataracts anterior and posterior early. So a whole variety of those. Now what are we seeing in right here or not? This is a liquefied vitreous here and some condensed vitreous there. So this is just showing us kind of a dense adult nucleus. So this is just an adult nucleus, just a real dense one. And here you see it from behind. It's both nuclear and cortical but you see the yellowish nuts. So this is what we think of as our standard adult nuclear sclerotic cataract. It's yellow, we grade it depending on the pacification, depending on the color. This is your standard nuclear cataract, if you will. What is this, Ali? Yeah, prunescent, it literally means brown-like. And so you go through this progression from yellow to orange to brown to even black. And so it's rare in the developed world that we see black nuclei like this. But in the developing world, this is not uncommon that you guys will see these. So if you're going on trips with our international outreach, you'll often see nuclei like this and you can see why VACO is gonna be difficult on a lens like this, where this would be an ideal patient for a small incision, extra capsular surgery. So this is a dense prunescent nucleus. And you can see now on the pathology, the nucleus here is denser staining than the cortex here. What kind of cataract are we seeing right here? I guess we're back to you. All right, so the cortical cataract, it's kind of spoked or pie-shaped. You know, start in the periphery and then come centrally. So this one happens to be pretty advanced. So it's kind of an advanced cortical cataract. And then from behind, this is our same picture we had previously, but you can now, I want to accentuate here, the cortical spokes coming in. In addition to the nuclei. So this is a cortical cataract. And how is cortical different than nuclear when you look at the path? Exactly, so it kind of liquefies. And hopefully I can show you guys when you're doing surgery with me and you've got these people with the cortical spokes. Oftentimes when I'm doing the rex, I'll just touch the capsule and you'll see the little bubbles will like be pushed away like little fish eggs. And so you'll get this focal liquefaction of the fibers in the cortex. And so there'll be a lot of liquid in here when you get a cortical cataract. Here you can see it again, liquefaction of that cortex. And so that's what gives you the white spokes starting the perforate and moving to the center. Rachel, what the heck is this? Okay, so what kind of cataract is this? It's called more gagmy cataract. And so when you get end stage cortical cataract, the whole thing will turn to liquid. And the nucleus will sink down into that liquefied cortex. And so you'll get it sinking down and then you'll have the capsule be kind of wrinkled because the fluid starts to leak out of the capsule. So you'll actually get it shrinking down a little bit. And I always thought this looked like a sunny-side-up egg. So that's how you remember the more gagmy cataracts. Looks kind of like a sunny-side-up egg. And this is actually one we did here. Here's the lens capsule with that. Just not much cortex left, totally liquefied. Here's the dense nucleus in the center. So these are really almost a hyper-mature type of cataract. So again, you don't see these usually except in, you know, people from Wyoming or something from the ranch, you know, like doctors and they'll come in right away. What is this, Marshall? Here you see a pacification of what's most likely the posterior aspect of the lens. So a posterior subcapsular cataract. Exactly. So this is the light shining through. And this, believe it or not, is one of my old fellows. And he said, you know, when he was applying for residence, he said, you might look out my eyes. Someone told me, you know, years ago when I was young that I had a cataract. Sure enough, he had a central posterior subcapsular cataract since childhood. So this, you can see the beam shining in. And this is right in front of the posterior capsule. So this is a PSC, posterior subcapsular cataract. There it is against retroalumination. You can see a little bit better against retroalumination. A little bit of a close-up. Again, it almost looks like kind of granulated fish eggs on the inside of the posterior capsule. And there's another one you can see on retroalumination. So pathologically, what is this characterized by? So you have nuclei on the posterior capsule there. So what's wrong with this picture then? It's upside down. It's upside down, exactly. What else happens beside those nuclei extending posteriorly? You get those, like the swelling of the cells. What do we call those? Ladder cells. Ladder cells. And I guess the Germans describe them. Vado. Vado cells. W-E-D-L. So vado cells are bladder cells. And so swollen cells and eventually they can even become fibrotic. So you get this fibrotic plaque on the posterior capsule in a PSC. What are we looking at here, Brad? So this is a picture of the anterior lens capsule. It looks like we have an anterior capsule or cataract. So this is what we call an anterior subcapsular. So these are much less frequent than posterior subcapsular. But what's interesting about these guys is that they are characterized by almost like a fibrous differentiation of these lens epithelial cells. And I don't know if it's a focal trauma that sets these off or you can even see these congenitally. But what stain is this now? Tri-chrome. Tri-chrome. So you see it stains, the tri-chrome stains like collagenous tissue blue. So instead of the lens here, painting the color it should and you see it's got a bluish tint to it. So these lens epithelial cells will undergo a metaplasia and they will become like fibroblasts. And so they'll start to grow this plaque underneath there and you'll see the capsule on top of it. Some normal cortex underneath it. So this is what we call an anterior subcapsular cataract. All right, what do we see in here Ariana? Okay, so what do we call that? Summering. Summering dream. And so it's not spelled summer like the season, it's S-O-E-M-M, summering dream. So he's just the pathologist that described it. And so this can occur from two different ideologies. What are the different ways that you can get a summering dream? Exactly, so if you have a trauma and the lens gets ruptured, you can lose a lot of lens content and the lens epithelial cells that are left in the periphery will grow in this donut. Now, when we started doing extra cap surgery, we would do it manually. You'd manually express the nucleus and you'd go in there with a handheld suction cannula and you'd suck out the cortex and you can't open a capsule on them. You said they're irregular edges so you really couldn't get a lot of the cortical and the lens epithelial cells out of there. So it's not uncommon you'd get a summering dream. Today you can get it after many, many years but it's just less frequent that you just see a big summering dream. This is what it looks like. This is an old eye. We've cut it in half. We're sitting at the optic nerve looking out. This is a Maoki view. And you can see a lens implant in the bag there. And then you see this proliferative cortex around the periphery forming this ring. It's like a donut. Is it a separate entity from when you see like the anterior capsule and it's like really thick? Correct, the anterior capsule, you get the anterior lens epithelial cells undergo a fibrotic change. So you see that the anterior capsule will turn white and you'll get some pymosis. The lens epithelial cells in the forenecks are different and they are made to lay cortex. So they'll lay cortex where the anterior capsule cells that are left over the periphery of the capsule rexus, they're the ones that undergo the fibrous metaplasia. So here you can see now a quote modern surgery. This is a Maoki eye from 20 years ago as opposed to 30 years ago. But you can see this patient had a capsule rexus and a three-piece lens in the bag and you do see a summering dream but not as prominent. And here you can see it in cross-section. Cross-section, it looks like a dumbbell. So these two round areas of proliferative cortical material and the center is clear. And this just shows you what can happen. Sometimes the anterior capsule and posterior capsule fuse at the edge and you get this proliferative cortex around it. Alley bonus points. What stain is this? Actually, the PIS, remember, it stains basement membranes that are pretty magenta. Here it stains it blue. Tri-chrome. Tri-chrome, good. So this is a trichrome stain. And again, look how thick the anterior capsule is as opposed to that thin posterior capsule. So the posterior capsule is only about, well, this is exaggeration. This is a rabbit, actually, just to kind of show you guys. But the posterior capsule and a rabbit's even thinner. All right, so you get credit for that, so. What are we seeing right here now? We see all whitish material. So not only in the periphery, but even in the center here. So this, you know, I guess now we're supposed to say exfoliation syndrome, but again, it's sort of exfoliation. And so what happens is, is this material gets deposited on the lens capsule, and then as the pupil moves in and out, it's like a windshield wiper. So it sweeps it out so you get the little central deposition and the peripheral deposition. It's kind of clear in between where the, where the uterus rubs. So here you can see a close-up. This is the so-called scalloped edge look. So you see that this exfoliative material gets deposited in the periphery and it looks, it looks scalloped when you look at it. Here you can see it nicely on retro-lumination. Now, they're not always this prominent. So you know, exfoliation can be very subtle. Sometimes you see a patient, their pupil just doesn't quite dialy as wide as you think it should. You look really carefully. You'll see some little, you know, white ruffle stuff right at the pupil area border. So sometimes it's a lot more subtle than this. And what does it look like pathologically? What do we call this? Do you see the material sitting on there? No, well, you can actually get by with the world boards on that, but they call it iron filing. And so if you ever take a little shreds of iron and you put a magnet on them and they all stand up on the edge of the magnet, so that's what it looks like. These little areas of this exfoliative material just kind of stand up on the edges. And you know, I'm gonna go back. Now, the reason why, it's through exfoliation. Okay, we're gonna actually do several reasons. Why does exfoliation syndrome make cataract surgery more difficult? Rachel, give me one reason. Vortilation, martial. Zonular weakness. Zonular weakness, good. Right, when you're doing the capsular rexis, it tends to tear out. Well, not only tear out, but the capsis is more fragile. So it's actually more fragile. Oh boy, we're almost down to maybe one other problem with when you do cataract surgery and exfoliation. Do you build on that? Is starting my anterior capsule, posterior capsule also more fragile, so more risk of rupture? Well, I guess everything combined. So the small pupil, the weak zonules, the weak of capsule, maybe one other thing. What else does, this will be another lecture. What other thing does exfoliation cause beside the lens problems? Beside the capsule problems? Pressure. Pressure, I'm sorry, misunderstood. Yeah, so it can cause glaucoma. So you gotta be really careful when you do cataract surgery. People with exfoliation, if you don't watch the, you don't watch them real careful the first day or so after surgery, they can get a pressure spike. But believe it or not, after cataract surgery, if you just remove the lens and then you flush down all that exfoliative material from the anterior chamber, the pressure actually drops and it can be significant. So you have a patient with exfoliative glaucoma, you can get a three to five point pressure drop just by removing their cataract. So you gotta be, remember when you have exfoliation syndrome that they are more susceptible to developing pressure spikes afterward. So, and I don't have enough time in this lecture, but I've got some beautiful EMS that I got from a pathologist in Germany and they actually show the exfoliation material on the lens capsule, where the zonules insert to the capsule, on the zonular body, and where the zonules insert to the ciliary body. So it's like a triple whammy. So if you guys come up to, are they letting you go to the ASCRS, the old Crabble course at Deer Valley into the month? Okay, so they actually gave me 20 minutes to talk about exfoliation. So if you are going up, you'll be able to see that. What the heck is this now? This, they're not staining any material there, almost looks like a cataractless lens as well. It's consistent with exfoliation. Yeah, so this is true exfoliation. So they used to call exfoliation syndrome pseudo exfoliation, you know, to discern from this. You hardly ever see these. This is a case Sam Mascot sent me. This was a woman with no other history. She's like 90 and she had this, see that little scroll up there on the top? That's actually a split, a schisis in the anterior lens capsule. And here's the, this is before he's done any capsule autonomy. So you can actually see it in the operating when it gets red reflex, that little scroll of material. And this case was so cool, he actually sent us the lens capsule. So we wrote it up and it was on like the cover of the INET. So we made the INET cover with this just cause people don't even see this. Historically, what kind of job did people with true exfoliation do? Yeah, glass blowing. So you remember that you see these pictures of the glass blowers at Moten, Juan blowing on this and spinning it around because it's that intense heat and also the infrared radiation that comes out of it. So you actually saw it in people who used to work in these old steel mills before they were automated and they were gonna be like throwing coke into the blast furnace and they would get these. So you see that the capsule actually splits. It doesn't go all the way through but you get a lamellar split, a schesis if you will. So here you could see the lens capsule, those lens epithelial silt's on the inside, you get this lamellar split on the outside. So this is true exfoliation. And so I've seen one case pathologically and one case in clinic in 32 years. So I mean, this isn't something that you may or may not see in your career but you have to know it for boards because they love testing minutiae on boards. There you can see again, beautifully the split, the schesis of the anterior capsule. What's going on here, Rachel? So it felt like there's like something. Why is that, I really bad and why is that cornea looked kinda swollen? I don't know, it's due to you. Exactly, so this is a patient with ficolytic glaucoma. So again, old rancher, doesn't like doctors, wouldn't come in till the eye started hurting. And so you ask him, well, when did you start to lose vision? Oh, a while ago and then the wife goes, oh yeah, I didn't see none of that eye for like years. And so, you know, you always bring the spousal on to tell you the true story. So basically, this is a hyper mature counteract and it's so mature that the cortex not only liquefies but the proteins from the liquefied cortex leak out of the lens capsule into the anterior chamber and they'll cause a severe glaucoma. So when you look at it, Marshall, what kind of cells are these? Macrophages. Macrophages, and if you look at it, they're all that granular and they've been ingesting protein. And so they're just all gobbled up all this protein like little Pac-Man, you know, they're gobbling up this protein. So those fat macrophages clog the mesh work but so does the protein. And so the treatment for this is remove the lens, wash out the anterior chamber. And so they call it fakeolithic. I mean, you don't really lice the capsule. The capsule's actually intact in these but it leaks out and so you get this fakeolithic glaucoma. All right, what's going on here, Brad? A lot. Looks like it's a pretty inflamed eye. We've got, I think that's, is that the lens material left in? All right, so there's some lens material right in here. Yeah. And then coming out of the iris here, it looks like we have a haptic. Yeah, so how does the fit, yeah. Half of that eye welds in front of the iris. And so complicated surgery but this is what we call a fakeotoxic uveitis. And so if you leave a lot of lens material, so you have a capsular tear and you can't clean it up real well and didn't do good retracting me, you leave a lot of cortical material in there. Plus you don't put the IOL behind the iris. What could happen is, is this leftover cortical material can cause a severe glaucoma. And so again, you get kind of a fakeotoxic reaction. And so you'll see these I'm referred in, you know, Cranwell get these once in a while where they'll say, oh, we've got this terrible glaucoma, we can't control it. And you look and you see that there's a tremendous amount of this leftover cortical material, which can then incite a lot of inflammation that can lead to a secondary fakeotoxic glaucoma. All right, what's going on? You did that Brad, are you on it? Cornia, they're whitish deposits that look that they're. Okay, what do we call those? Mutton fat. So again, I guess I don't quite know what mutton fat looks like, but I guess it looks like big globs of stuff. And so this is large carotid precipitates. So they're not just little lymphocytes that are in here. What cells are in these mutton fat KPs? Necrophages are giant cells. And so this is, and then we looked at the lens itself and I want to point out, not only did they have an organized opion, but look at what's going on in the lens capsule here. What is this? It's a white material, also collected and superiorly. It looks similar to the opion that you put. So what entity is this? I'll give you a hint, it's a double misnomer. This is one of the two double misnomers you need to know. This is fakeo-anaphylactic endothelmitis. So double misnomer. First anaphylactic means IgE mediated, it's not. And endothelmitis means infectious, it's not. But what it is is it's a reaction to a very badly done surgery where there's so much cortical material in there that it incites a granulomatous inflammation. Now these were common, believe it or not, in the 1920s people were doing crude extra caps, wearing loops and kinda pulling the lens material out manually. And so this was commonly seen. And then as people discovered, if you remove the whole lens with the lens caps itself, what we call an intracap, there was nothing left in there. So this disappeared for several decades. And then in the 70s, we started going back to doing extra caps. And again, we weren't very good at doing it. People were just transitioning to using scopes. You did a canapar caps a lot of me. So we actually saw this resurge again. And interestingly enough, this was a case I saw when I was a Dave Apple fellow. And people didn't know what the heck was going on here. And so we wrote it up. And so this was the first feculonophilactic endothelmitis reported from like 1924 to the early 80s. And so there was this gap in there. People didn't know what it was. And then after we recognized it, we started seeing it a lot. And of course now it's disappeared again. Because why we do capsular rexies? We have good microscopes, we've got good IA equipment. We don't leave a huge amount of cortex behind. But remember when I talked the first lecture about inflammatory reactions, we talked about the three different types of granulomas. So this is more the zonal type of granulomatis inflammation where it's actually an immune reaction to the lens material that's left over. Now this is another reason you can get feculonophilactic endothelmitis. This poor guy got kicked by a horse. He was trying to push the horse into the trailer and the horse gave him one of these. And so he ended up rupturing his lens capsule. So believe it or not, this is what's left of the nucleus. And here's some cortex and he just totally ruptured the lens capsule. And then had a raging granulomas inflammation around it. Here you can see again. Here's what's left of the lens material. Here's the lens capsule. And ruptured dramatically. And here's a close-up. And if you look right here, there's little macrophages starting to come up inside here to try to munch up that cortical material that's there. And then this is the lens capsule again, macrophages. And you can even get giant cells on this. And so this is called feculonophilactic endothelmitis double misnomer. Not anaphylactic, not an endothelitis, but that's what they call this from the 1920s. And again, it sticks. And here we have what gives a giant cell sitting right at the edge of the capsule there, munching up that cortical material. All right, we say goodbye to Notre Dame from the river. Any questions on lens? You guys know all there is to know. Okay, next week is at IOLs or is it about coma? I don't know, does anybody have to schedule? Next week is nothing. Nothing, yeah. Oh, there's no lecture? Two weeks after's IOL. All right, so two weeks after's IOL, you guys get to chill a little bit because we're gonna talk about its history of IOLs. And so the reason we do this is because people are always coming up with new ideas of why don't we do an IOL like this? And it's the answer as well because we did that 40 years ago and it didn't work. So I just wanna give you an appreciation of a little bit about history of IOLs. So you'll be able to just kinda sit back and enjoy it. There'll be no reading assignment. All right, great, thanks. Thank you.