 All right, so we have to continue our world tour. These are the streetcars in Lisbon. And it's interesting because the streetcars, there's some really steep hills there. But it's like San Francisco, but they're not cable cars. They're actually motorized streetcars. So it's kind of fun to ride on them. They're refurbished, but they're all about 100 years old. And this is the Castillo up on top of the mountain. And this is the view you get, one of the cathedrals, and then looking out onto the river here, which then goes into the Atlantic Ocean. So you get a nice view of the whole harbor. Obviously, that's why they put the fortress up there to protect the entrance to the river. And then this is looking back into the city, very, very dense, old city, and very Mediterranean looking bar-tile roofs. And then, of course, that's a suspension bridge across the river. OK, so we're going to talk about the lens. And so let's see. Teresa, were you here earlier when we did embryology? No. Lee, tell us a little bit about the embryology of the lens. Where does it come from? Which layer does it come from? And how does it form? Is it official? OK. So if you remember back a month and a half ago, we were talking about embryology of the eye. And the neuroectoderm pouches out from the side of the developing fetus. As it goes forward, it touches the surface ectoderm. And it induces the surface ectoderm to thicken. You'll get invagination of the neuroectoderm. And then that surface ectoderm will pinch off. And it will form that primary lens vesicle. And then the fibers will grow from back to front to fill that and eventually form the fetal lens nucleus. This just shows you, I believe these are chick embryos, but very, very similar to human embryos. This just shows you the various stages from four weeks to five weeks. And so this happens very early in gestation between the fourth and the sixth week of gestation. This just shows you more of a schematic. So once you get the lens pit forming, and then it pinches off and forms the vesicles, those cells will then grow across and fill the lens. And the reason that that's important is in a normal lens, you don't have epithelial cells posteriorly. So once those posterior cells grow across and fill that lens, then the cells will go to the equator. And then they'll fan out. And then they'll send fibers anteriorly and posteriorly. So you normally don't have cells and lens epithelial cells inside the posterior capsule, unless it's a pathologic state. And this shows you this was a fetus. And you can see that the lens epithelial cells go to the equator, then they fan out across the equator like a disk of a flying saucer. And they send fibers both anteriorly and posteriorly. And so this just shows you the lens itself, looking at a slit lamp. And so for those of you at the VA, this is what a clear lens looks like. And so I know you never see them at the VA, but this is what it looks like. And here you see the lens pathologically. Here's the nucleus. So what happens is the lens will grow concentrically throughout life. So you'll still have a fetal nucleus. You'll have an embryologic nucleus. You'll have the adult nucleus cortex around it. And as you get older and older, the lens becomes less round and more oval. And so those fibers condense more in the center. The lens nucleus gets harder and harder as time goes on. And here you have that again in a schematic. The embryologic nucleus, the fetal nucleus, the adult nucleus, the cortex, and the lens capsule surrounding it. All right, Teresa, tell me a little bit about the lens capsule. Okay, which is thicker, anterior or posterior? Okay, so here's the anterior lens capsule. Which stain are we using here to show it? Nope, nope. You said the one thing. What did you say, the first comment you made about the lens capsule? It's a basement membrane. So what's stain, stain, basement membranes? It's the PAS stain. And so this is a PAS. And so it'll stain, basement membranes, it's bright, magenta, and don't forget, the anterior lens capsule is the thickest basement membrane in the body. So you see, the anterior capsule is about 50% thicker than the posterior capsule. And what's the second way we can tell the difference between anterior and posterior capsules? Exactly, so the lens epithelial cells are present anteriorly, but not posteriorly. So that's the way we tell them. So this just shows you the equator. Here's anterior lens epithelial cells. They come out to the equator and then they fan out, sending fibers both anteriorly and posteriorly. And normally there should not be any cells along that posterior capsule that's there. Chris, what are we looking at here? Okay, and where do the zonules insert? Besides anteriorly they insert in the capsule. Where do they insert posteriorly or peripherally, I should say? Okay, so what I wanna show you though is people think about the zonules inserting the ciliary processes, but don't forget they also go between the ciliary processes and some of these guys insert almost back at the paris plana. And so remember the ciliary body, the wrinkle, the folded part is called the paris placata, placated, the flat part is the paris plana. And you can see some of those zonular fibers come, clear the heck back here. And so they insert a lot more posteriorly than you would think. Now what do we show in here, Niko? And what forms the Y suture? Exactly, so you know those lens fibers they come around both posteriorly and anteriorly. The lens is not a perfect sphere. And so because of that they don't meet at a point they form a Y. And there's an anterior and a posterior Y suture. So your mission today when you're looking at patients with a slit lamp if you do is look for the Y sutures, because you'll find them. You'll be able to see them, they're subtle, but they'll be shaped, usually the front one is more inverted and the back one is normal like a Y. And so your mission today is to find the Y sutures when you look. Now here you can see the individual fibers that are in there. And what's interesting if you look at these in an EM, what does this remind you of? Like a honeycomb, exactly. So you see that they are hexagonal. And so you see these hexagonal cells and a lot of time as the cells mature they start to lose their nuclei and they're left with a lot of protein. There's a lot of protein in the lens and other materials that are in there. So this is what the cortical fibers look like in the lens. They look like a honeycomb. All right, Shrav, what do we see in here? Okay, so see a red reflex. What's funny about this picture? What is that? What do you think that ring is? All right, so there's the lens and which direction is that lens luxated? All right, so this is the crystalline lens right here and so it is superior and temporal. What the heck is this thing? That's a contact lens, exactly. And in fact, more specifically it's an aphakic contact lens because this patient's crystalline lens is dislocated leaving them effectively aphakic, meaning without lens. And so they need about a plus 10, plus 12 lens in there to help them see better. So that's an aphakic lens. And so which disease process classically leads to a superior temporal dislocation? Marfans and so this is indeed a Marfan's patient and here he is. So you see he's about 6'11". This is one of our old techs here in the old clinic. This is a great picture because this was in the old hospital. And so before there was a Moran I, let alone a Moran II, the entire Department of Ophthalmology was crammed into one little hallway in the old ER of the main hospital. And so this is where we used to function and he was 6'11". Look at his spindly fingers. So if we have a patient who has Marfan's syndrome, Tara, do we have to worry about talking to our colleagues and other services if we make this diagnosis? Why? Exactly. And so remember it's a disease of connective tissue which is why the zonules are weakened. One of the areas of connective tissue that's weakened is the aorta, especially the aorta crude. And so minor detail, these guys can be playing basketball and having a aorta group dissection and die. And so it's important that they be hooked into other resources, make sure somebody's looking at their aorta, looking at their heart, making sure they're okay. Well, I guess we can ask pathologists pictures. Now this is a different picture. Why is this lens different than the one in the other one? It's inferiorly and a little bit nasally, so kind of almost the opposite of Marfan's. It's either, I mean that seems to be some sort of material that's colored. Believe it or not, these are what's left of the zonular fibers that have all broken. So this is another thing you have to memorize. You don't have to for boards, but ophthalmology residents do for boards. This is homocystinuria. And it's very weird. Marfan's, it dislocates superior temporarily. Homocystinuria, inferior nasally. Why I don't know, because they're both zonulopathies. And in fact it makes no sense to me that if your zonules are weak that something would move up. That's anti-gravity, so. But in any event, that's where they go. And so homocystinuria, they love asking you that on boards, the difference between homocystinuria and Marfan syndrome. This is an even stranger looking picture. So back to Theresa. What do we see in here? What is that white thing? Yeah. Yeah, I'm looking for it, and it's known like the anterior chamber. Yeah, believe it or not, that's an entire lens in the anterior chamber. So this was one that you may have seen on New Year's Eve, you know? I was just sitting there minding my own business and these two dudes just jumped me, you know? I was minding my own business, so. I heard a different variation of the two dudes, a friend down south that told me this one is, I was sitting on my porch reading the Bible, you know, and these two dudes just jumped me. And so this is always the two dudes and he's always minding his own business. No, I wasn't doing nothing, man. And so this is somebody, this is a traumatic lens dislocation. And so it has to take quite a trauma, you know? But the eye is tough. I mean, to rupture an eye, you have to have some pretty significant trauma. And so this is actually a lens that is dislocated into the anterior chamber. So it's actually right behind the cornea. It almost looks like it's on top of the cornea, but it's behind the cornea in the anterior chamber. And pathologically, here we go. Here's the iris. And sure enough, here is the lens in the anterior chamber. So total dislocation in the anterior chamber. Now there are some other entities. I'm not gonna go into this yet. Let's go back here. Lee, let's say you have someone who did not have two dudes jump in. And spontaneously his lens dislocates into the anterior chamber or he gets a spontaneous pupillary block of a lens. What's another entity you have to remember that's susceptible to a pupillary block with a lens or dislocation of a lens totally? Exfoliation does make the zonules weaker, so that puts you at risk. But how about if you have a pupil block with a lens? You get a lens that's really mobile and really small and it pops forward and blocks the pupil. Well, there is an entity that you guys have to memorize also that has microspherophakia. And it's called wheel Marcazani syndrome. And so because there's not much pathology in the lens, to be honest, they really have to search for things they can ask you on boards. And so wheel Marcazani syndrome is a syndrome where you get microspherophakia and you can get spontaneous dislocation of a lens anteriorly or spontaneous pupillary block. And these people are different than Marfan's. Because remember we showed you the picture of Marfan's? Really tall people, long spindly fingers. Wheel Marcazani are very short people, short stubby fingers. So almost the opposite of Marfan's. And so that's how you tell them apart, but you do need to know that for boards. So wheel Marcazani. Okay, let's go. Chris, we've got an eye here. And I want you to first of all, look at the eye, see how big it is and then tell me a little bit about that lens. So she's pretty small. One and a half centimeters in diameter. So pretty small eye. What do you make of the lens? Yeah, so it's kind of round. What's another word we use for round? Sphero. So we've got a small eye. Microspherophakia. What's another disease can cause microspherophakia, especially in young children? Something that's almost was wiped out in this country. Close, rubella. So rubella is an interesting disease. Rubella can cause small eyes and can also cause small round lenses that form cataracts. And so rubella. Rubella is a disease we almost had wiped out, but surprisingly enough, there are resistant groups to vaccines, not people in poorer places who don't know better, but people in like Park City who are not letting their kids get vaccinated. So I find it fascinating that college educated people are not vaccinating their kids. So, you know, you can't use an excuse. Well, you just don't know better. So, but we almost had rubella wiped out in this country, but there are now pockets of it still alive because people refuse to vaccinate. So rubella is a disease, hopefully you guys will never see. Can general rubella. But again, for boards, remember that can general rubella can give you small eyes with small spherical lenses. Now, the other thing that rubella does is you have the nuclei retained within the actual cortical fibers. So I'm not sure why the rubella gets into the nucleus. It does something to the mechanics there and it keeps the nucleus from disappearing from those cells. What are we seeing here in eco? All right, so this is a congenital cataract and you can tell because it's just in the fetal nucleus. So it's not in the entire nucleus. And this is interesting. It's kind of got the female and the male symbols there. And so it's kind of like, I call this the Prince cataract. You know, remember Prince, the guy who just died? He became that little male female symbol. So this is a Prince cataract. And so the male symbol and the female symbol. But this is a patient, she's now in her 70s. It's very interesting. She's had this forever. And in the other eye, they tried to do cataract surgery when she was a young child when the surgeries were really crude. And so she had a really crude extra cap and didn't do well and wears an aphasic contact lens and refuses to let me touch this eye. And so she's about 2,400 and been functioning for 50 years with that. So this is a congenital nuclear, we'll call this a fetal nuclear cataract. And here's just another view on the slit lamp. If you notice only the center part of the nucleus is opacified. The peripheral part is clear. And so this isn't your normal adult nuclear cataract because it's only the central fetal nucleus that's involved here. All right, Becca, what are we looking at here? This is one of my fellow's cuts, you know? Actually when the residents are learning to cut globes, this is their oblique cut that you guys make on your first cuts. And you get your vitreous visible there. Yeah, believe it or not, look, there's a pocket of liquefied vitreous back here and some condensed anterior vitreous here. But what do you make of that lens? That lens would be spherical. Yeah, so this is a very opaque, kind of almost the ultimate cataract. I mean, this is kind of a white, opaque, hyper mature type of cataract. But this just brings us into the realm of adult cataracts. And so what we wanna do is spend a little bit of time talking about the various types of cataracts that we have that can affect the eye more in an adult. So that was more of an adult nuclear type cataract. Now it's interesting, I don't think I've got path. Yeah, well I do have a dense one. But we often don't send the lenses for pathology nowadays. Well first of all, we do FACO. So we chew up the lens and so there's no lens. But occasionally we'll do an extra cap but we usually don't send the lens for pathology because there's really nothing interesting on a lens that you've got. So this is a opacity of the central lens here from behind and so that's a nuclear cataract. All right, Shraab, this is indeed a nucleus. What can you tell me about this? So this is the ultimate nuclear cataract. This is what we call a brinescent, brinescent meaning brown-like. Sometimes in the third world you even get black nuclear. So third world or parts of Wyoming, you can get, you're allowed to slam your own kind. That's allowable. So you can get these dense, dense black nucleon. So as you can imagine, FACOing one of these is very difficult. And so what you end up doing is you can do a small incision extra cap and remove this hole. So this is a brinescent, brown-like nucleus, the ultimate nuclear cataract. And I was trying to show you kind of a nuclear cataract here. This was one that actually was sent to us an entire lens. And you can see in the center of the nucleus, you've got this dense, dense fibers that are really, really condensed. And then they become almost calcified at this point. And they become very, very thick and very dense. All right, what do we see in right here, Tara? All right, this is a cortical type of cataract. And you see the spokes or the pie shape where they come from the periphery to the center. And we look at that from behind. And again, you see the pie-shaped spokes. So you can see these pie-shaped spokes. And what's different about the cortical cataract as opposed to the nuclear cataract? Exactly, so they actually liquefy. And so when you look at these, I try to show you guys when you're in surgery with me, you can sometimes see they've got the little dots, the cortical fibers under the anterior capsule. When we push on the capsule to start a capsule on me, those little dots move to the side because they're actually liquid. And so cortical cataracts, you get not only a pacification, but you get liquefaction of the cortical fiber. So you get a lot of liquid in there. And here we can see, again, a very liquefied, very mature, almost hyper-mature cortical cataract. And what do we call a cataract that is so hyper-mature that the cortex is completely liquefied? More gagny in cataracts. So this is a more gagny in cataract. And what's happened is is that the cortex is totally liquefied. And in fact, it's liquefied so much that that hard nucleus has sunk down. And so you rarely see these again because these are hyper-mature cataracts. So the cortex completely liquefies, the nucleus sinks down into the capsule bag. And it reminds me of a sunny-side-up egg. And so here's the nucleus. The nucleus is the egg. And of course, the cortex is really runny, really runny white, so not a kind of egg that you want to see on your plate. And so more gagny in is the ultimate cortical cataract where the cortical cataract, the cortex completely liquefies. The nucleus is hard and sinks down to the bottom. And this shows you one. This was a more gagny cataract that was removed. Here's the hard nucleus. Here's the remnant capsule or bag. And this liquefied cortex just oozes out. I mean, there is no cortex left in there once this happens. All right, again, you haven't seen slit lamps before, but if you look, here's the beam hitting the anterior part of the lens. So where does that tell us this opacity is? In the posterior lens. All right, so this is an opacity in the center part of the posterior lens. And when we do retro illumination, this is what it looks like. So what do we call this kind of cataract? This can actually be associated rather, it can be with aging, but there are other entities that can cause this cataract. This is called a posterior subcapsular cataract. And this can be associated with diabetes, with medications, especially steroids. So this can be a steroid induced cataract. It can be diabetic induced. It can be aging, but most commonly these are due to something else. So this is along that posterior lens capsule inside of it. And there's a close-up. It almost looks like dense, fibrotic fish eggs that are in there when you see this. This is a close-up retro illumination on the posterior capsule. Now you can see it even better. So when we look at these, what's wrong with this picture? Let's go back to, so what's wrong with this picture? What if I say this was the capsule from the patient we just showed you? Exactly, so what's wrong with this picture? Exactly, plus it's upside down. You know, remember we always orient pictures so the cornea's up and the optic nerves down? So this is posterior here. This is anterior down here. So you said it, there's cells along the posterior capsule in a PSC cataract that shouldn't be there. What's going on here? Yeah, in fact, these are really swollen cells. They call these bladder cells. Or from the German VATAL cells, I guess. W-E-D-L, VATAL, VATAL cells. And so these are swollen bladder type cells and this is a posterior subcapsular. So believe it or not, this is the posterior capsule. These cells have migrated along the posterior capsule and you get these swollen bladder cells. And so this is what a posterior capsule or PSC cataract looks like. Lee, what are we looking at here? All right, here's the anterior capsule. Here's the cortex. What's going on here? What do we call this? Exactly, so don't forget, we've got the posterior subcapsular cataracts. We also have anterior subcapsular cataracts. And what's interesting about these guys is in these guys, here's the anterior capsule here, the lens epithelial cells are down here and these lens epithelial cells have been transformed. And so they have become almost like fibroblasts. They've undergone fibrous metaplasia and they start laying down fibrous tissue. And so what stain are we using here to show that? Trichrome, very good, this is the trichrome stain. And so it stains collagen-like tissue, fibrous-like tissue blue. And stains normal lens, this pink color and the lens capsule lightly pink. And so you can get those anterior lens epithelial cells are almost pluripotential. And if you stimulate them just right, they can undergo a metaplasia and become like fibroblasts. So you get this fibrous metaplasia of the anterior lens epithelial cells forming this anterior subcapsular cataract. What do we see in here, Chris? Okay, what do we call that? Summering's ring. A summering's ring, and how is summering spelled? Close, S-O-E-M-M, so summering's, not summer the time of the year, but summering's after the guy who first described him. And so a summering's ring, and what are a couple of ways summering's ring cataracts can form? Okay, do you see an IOL in here? I don't. Okay, what's the second way that a summering's ring can form? So same concept, but in AFAKIC patients. Okay, and that can be surgically AFAKIC, or dramatically AFAKIC, exactly. So summering's first described these in trauma. So when I would have severe trauma, and the lens nucleus would be extruded beyond the cheek of the patient somewhere, they'd put the eye back together, and you'd get these peripheral cortical elements would start to grow in the periphery, and they would form this donut-shaped ring, so-called summering's ring. And here you see the second way, this is an old, old IOL in here, and you see a large amount of periphery of cortical material in the periphery. And so this is a summering's ring in a pseudo-FAKIC eye, and this is where we would see these most commonly. And here you can see another one. Here's a three-piece acrylic lens in the eye, and sure enough, here's all that lens epithelial cells proliferating the periphery. So remember when you do cataract surgery, we try to take out all that cortex, but we still can't get to the forenecks and kill all of those lens epithelial cells. So where the anterior lens epithelial cells can undergo a fibrous metaplasia, give you fibrosis, and even contractile properties to it, the lens fibers in the forenecks try to make new lens. And so you get proliferation of cortical material here in the forenecks. It's interesting, one of our old PhD researchers from here who went to San Diego, who's doing some work in China, is now claiming they can regrow lenses in children. So they do a tiny capsulotomy, suck out all the lens contents, and just leave it alone, and then the lens fibers regrow. Which is absolutely true, rabbits do the same thing, and you'll hear me say when we do research, rabbits behave much in the same way as children. And so in a rabbit eye, if you don't put an IOL in there, and you just take out the lens, it'll regrow a new lens, and it'll grow a summering drink or a new lens, and they're trying to do that now in kids. My problem with that is the research has all been done in China. It's not been published in peer review journals. And who knows the clarity of that regrow on lens, the power of that regrow on lens, and the functionality of that regrow on lens, but yeah, it does happen. And so, very interesting idea. You have to do your whole lens removal through about a one millimeter capsulotomy, so you can't make a capsule, or it'll form a summering drink instead. So there you see a large summering drink, and here you can see it pathologically. This was an eye that had a traumatic cataract, and there you see the summering drink. And here is the close up. What stain is this, Nico? Tri-chrome. Tri-chrome, very good. So here's the anterior capsule, here's the posterior capsule thinner, here's where they've kind of fused together, and here's this growth of proliferative cortical material in the periphery. And so this is what a summering drink looks like. Becca, what are we looking at here? Okay, so what do you think this could be? Probably pseudo exfoliation. Pseudo exfoliation, or I guess now we call it exfoliation syndrome, okay? This is a very common entity in Utah, and so you guys are gonna see tons of this. The population base where this is most commonly seen is Northern European. I mean there are pockets of exfoliation elsewhere. We just discovered our Moran outreach in Guatemala. I discovered a whole bunch of pseudo exfoliation there that we didn't expect to see. But usually it's from Northern European, so I call it the Yahshur You Betcha Belt, you know? So yah, people from Sweden and Norway and Denmark, oh yah, you betcha. And so if you ever look in the Salt Lake City phone book, I tried this once, my neighbor's name is Peterson, so I was gonna look up his phone number to call him. This is before we had Google, and there's like 14 pages of Peterson's and Sorensen's and Jensen's and all. So a lot of people in Utah have their roots from Northern Europe and Scandinavia. As do a lot of people in Minnesota, and not by coincidence, Minnesota and Utah are the two places in the US that have the highest rate of exfoliation. And so we see this very commonly, so you guys are gonna see this a lot, and you know, you'll have to probably know a little bit about the genetics of pseudo exfoliation and the genetic defects. Do you know anything about the genetics of exfoliation? What's the four letter enzyme you have to remember? Anybody? Loxal 1, and so that's a genetic defect and it's got to do with making of the proteins and the elastic nature of the proteins. And so they're finding that there's a Loxal 1 gene defect that's associated with these, and so keep looking at that because we're unraveling the genetics of this entity now, but why do you get this clear space with exfoliative material there and exfoliative material in there? Shrop. Exactly, so as the pupil moves in and out, as light hits it, it almost acts like a windshield wiper. So it's like you have this pupil moving back and forth and it scrapes the exfoliative material, so there'll be some at the edge where the pupil was and some peripherally and in between when that pupil moves back and forth, it actually scrapes it clean. So that's why you kind of get this double ring pattern. And if you look, here it is in the periphery, this scalloped material that's actually on the anterior lens capsule. And of course, in retro illumination, you can see it really nicely, this kind of scalloped material that's deposited on there. And here we actually see the material on the lens capsule. Shrop, what stain is this? PAS, so PAS stains the lens capsule, and these are the lens epithelial cells inside of the capsule. This is kind of flipped over here, but you see the material, this exfoliative material on the lens capsule, they call this an iron filing pattern. So if you ever had shavings of iron, you put them in a magnet, I don't know, they used to make, in the olden days, boys had to take shop and girls took home, of course, because girls are supposed to make cookies and things and guys are supposed to like grind things and do shop. And so in shop, you'd be grinding things and then you take a magnet and it would just grab all these and the fibers would stick up. So this is called iron filing and that's what it looked like. Okay, we're looking right here, Tara, a little bit different view here, a little more subtle. It's kind of scrolled and curly here. What could cause that? Exactly, and so the reason the term pseudo exfoliation came up is there is an entity called true exfoliation where the lens capsule itself splits and folds up. It's almost a schesis rather than exfoliation, but the term pseudo exfoliation came up so that you wouldn't confuse the true exfoliation with the pseudo exfoliation. And interestingly enough, this is from Sam Masket, this is actually that patient and this is in the operating room and he saw that patient, he saw this really funny scroll here and so he was sharp enough to recognize that that was part of a split in the anterior capsule. I've actually seen people peel that off and do a rexis on there and then they go into hydro dissect and for some reason it won't hydro dissect. The reason is it's because the anterior capsule is still intact and so this is that patient and so he recognized that and so he went peripheral to that and did a full capsillotomy and the nice thing is is he sent us the path, we actually had this in the eye world as a case in the eye world, thus you see the arrows here, but here's the anterior capsule, these are the lens epithelial cells, so this is inside, this is outside and you see that the capsule is actually split. So it's split like a schesis so it's called true exfoliation and it was weird, this was described in people who are glass blowers and I know if you've ever seen these people in trade shows or something, they have this big glob of glass and they blow it and they spin it around and make a bottle out of it, well, that emits this intense infrared hot gas and that'll actually split the lens capsule. This was seen a little bit later in the industrial age in people who worked in steel mills in the blast furnace. Same thing, this hot infrared air is coming on and so you would get this exfoliation. What's weird is this lady was like an 80 year old normal lady, she'd never blown glass or worked in a steel mill so you can get this to a curse spontaneously but the key is it's actually a split in the anterior capsule and these are very, very rare but that's why this is called true exfoliation as opposed to the deposits which are pseudo exfoliation and now we just call that exfoliation syndrome. Here's a close up, here's the lens epithelial cells under the anterior capsule, there's the split. In the anterior capsule there, the exfoliation. Okay, what do we see in here? Just to kind of describe it. Yeah, so that eye is really red and really angry and in fact, this patient comes in and his eye hurts like heck. He says, man, my eye hurts. Say, well, how long has this been going on? Now it's been hurting for a couple of weeks. He finally comes into clinic. You say, well, have you got any history, any trauma to that eye? No, no, but then the wife always pitches in and says, oh, he hasn't seen for years out of that eye. And so, you know, he's a tough old, you know, Nevada rancher or something. And so he finally comes in, this eye is really painful. You check the eye pressure and it is 50. So you've got a patient with a pressure of 50, opacified lens, real red hot eye and you look inside and believe it or not, this is the anterior chamber angle. What kind of cells do you think these are? Do I have an answer that I actually know? Okay, answer, go ahead. These are macrophages. They're macrophages. Almost, almost, but it is a secondary glaucoma and what happens is, is when you have a hyper mature cataract, like we showed one of those Mogagni ones, hyper mature, the lens proteins actually leak out of the intact capsule into the anterior chamber and these are indeed macrophages and so the macrophages come in and gobble up this, look how fat they are. I mean, those macrophages are just gobbling it up. They're getting really big and even the protein itself from those cortical cells that have liquefied clogs the mesh work. So you get a severe glaucoma, it's actually an open angle glaucoma but it's a severe glaucoma and the treatment is you take out that hyper mature lens, you flush out all of this protein and these macrophages in here and you can actually get, you know, cure the glaucoma. So the history is usually that the vision's been poor for a long time because you have to have a hyper mature cataract. You can't just have, you know, just a regular cataract for this to happen and so this is called phacolytic glaucoma and so secondary glaucoma due to the leakage of that protein that's there. Okay, wow, what's going on right here? Theresa, what are we seeing here? Yes, that lens is supposed to be behind and so you see that part of that lens is in the anterior capsule. We call that an optic capture, meaning it's caught in front of the iris and it looks cloudy behind it, exactly. So this is a case of a difficult cataract surgery. They probably ruptured the capsule. Weren't quite sure where the lens was going in. Part of the lens pops anteriorly. You get proliferation of all this cortical material. It's got vitreous mixed in it and so you can get a significant inflammation. We call this a phacotoxic uveitis or a uveitis that's induced due to difficulties with the lens and so we see these not uncommonly in a cataract surgery where there's been difficulties. The cataract, when they're trying to take it out, there's a rupture of the lens capsule, vitreous comes forward, you don't get the cortex out and you can get a significant uveitis from this. Again, they call us like a phacotoxic uveitis. So this is that all that proliferative lens material that's still left in there, that can induce a lot of inflammation. So these patients get inflammation, they get glaucoma, they even get an entity that we call UG syndrome and what does UGH stand for? Lee, exactly. So you can get a secondary UG syndrome and so you can get an UG syndrome from various other entities but uveitis glaucoma hyphaema is not uncommonly seen in this entity, this phacotoxic uveitis. All right, Chris, what are we seeing here? Why would I be showing this picture in a lens lecture? All right, so on the posterior cornea you've got these KP, what does KP stand for? Karate precipitates and this is a specific type of KP. Big greasy looking Karate precipitates, what do they call these? Mutton fat, so mutton fat I guess is big and greasy and so this is big and greasy, mutton fat KP. And then we look at the lens inside. Now this is an eye that's been cut in half sagittally. What is this right here? Give you a hint, the iris is back here. Yeah, what do we call an inflammatory material in the anterior chamber, anterior anterior chamber? Hypopia. Or hypopia. So not like hyphaema which is blood but you can get white cells so they've got a hypopia on. What is going on here where the lens was? All right, so this is a sagittal cut, this is where the lens was. You've got this big white area here. So it looks like you get a cataract there. Well believe it or not the IOL we removed it when we cut in half but there was an IOL in there. Okay, so you get a cataract that's nested inflammation after the surgery. So you see a tremendous amount of this white, inflammatory membrane around what was left after they had the cataract surgery. Now, I'm gonna have you guys have to memorize this term again. This is one of those double misnomers that you have to memorize. This is called feco-anaphylactic endothelmitis. Now it's a double misnomer, why? Because anaphylactic assumes it's an IgG mediated allergic reaction which it's not. Endothelmitis assumes it's infectious which it's not. So this is one of those double misnomers. But in any event, this is again a toxic uveitis condition if you've ruptured the lens capsule either surgically or dramatically. So this is a patient with a severe trauma. This guy got kicked by a horse. So watch out for horses hooves because they can do some serious damage. And so the lens capsule ruptured here internally inside the eye and he had a tremendous amount of inflammation. And here you can see this, believe it or not, is what's left of the cornea, the iris. This is the lens. Here's some lens cortical fibers. Look at all those inflammatory cells around that ruptured lens capsule. And here we have a close-up. What kind of cells are these down here? All surrounding that lens. Yeah? Macrophages. There are macrophages in there but there are also these smaller ones with the smaller- Lymphocyte. Lymphocytes. And so you get, they call this zonal granulomotus inflammation. So you get some lymphocytes and then you get some macrophages. You can even get multi-nucleated giant cells in this entity. So this is a focal granulomotus inflammation. And here you have a ruptured lens capsule and you see these inflammatory cells are some big macrophages in here and they even form, what is this? Niko. Giant cells. Giant cells, exactly. And so double misnomer, FACO, anaphylactic endoplamidus. So it's not anaphylactic, it's not an endoplamidus. It's an immune reaction to lens protein. And so if you rupture a lens capsule dramatically, you get a tremendous release of those lens proteins and you get this immune reaction. The original entity of FACO-anaphylactic endoplamidus was described in the 1920s and believe it or not, in the 1920s people were beginning to do crude extra caps wearing surgical loops and making big cuts and kind of pulling stuff out of the eye and then putting giant sutures in them. And so these patients would get a pretty raging inflammation. Well, after that, the technology evolved such that people were removing the entire lens. And so you do what was called an intracap so you wouldn't have any cortical material left around to cause an inflammation. But in the late 70s, early 80s, people went back to starting to try to do extra caps. And some of the extra caps were very crudely done and were leaving gobs of protein behind from the lens cortical material which would cause the FACO-anaphylaxis. It is. It can occur after trauma. It can occur after trauma. It can occur relatively acutely. So after trauma it occurs right away. After surgery, I haven't seen a FACO-anaphylactic endoplamidus for a while now. I mean, sometimes if you again had a difficult cataract surgery, you've ruptured the capsule, there's still gobs of cortex in the peripheral you could get, FACO-anaphylaxis. This comes from the first report of FACO-anaphylactic endoplamidus in 50 years. And this was in 1984, written by a Dave Apple fellow who had brown hair and a really big mustache at that time. And so, believe it or not, this wasn't reported for like 50 years. And then it started making a comeback in the early 80s. As we got better at doing cataract surgery with circular capsillotomies, instead of irregular canopiners and good IA's sucking out the cortex, this is pretty much faded away. You don't see this very often. But, you've got to know the name because FACO-anaphylactic endoplamidus is confusing because again, it's a double misnomer. So it's almost like, what's the other double misnomer we talk about?