 We're going to do dress down Tuesday. So I'm going to do dress down Tuesday. I'm going to do dress down Tuesday. Sorry, but these are my traveling clothes. I got to go right to the airport. If I'm going to be on a plane for the next, God knows how many day and a half, you got to dress comfortably. So we're going back to Paris. So of course this is the Eiffel Tower. A little plaza where you can like look over it and see it. And then this was nice. This was at a restaurant and we actually stayed there in typical French meal. It's a four-hour meal. And so the nice thing is the Eiffel Tower lights up in the dark and then every hour on the hour the lights go crazy. And so I tried to catch that, but it's really hard with just a regular one. Yeah, hard to catch it doing that. But at any event, you know, you're there for like four hours. So you get to see this happen four times. So it's worth at least seeing at once to see the lights every hour. They did this for the millennium. And then people liked it so much they decided they're just going to keep doing it. So they keep doing it. So every hour from like whatever, seven until midnight, it goes off and goes crazy. So people love that. Okay, today we're going to talk about the cornea. So we've got, wow, ophthalmic pathology fellow, bright-eyed and pushy tail. Neon, tell me about the layers of the cornea. So again, what's our main theme about ophthalmology? It has layers. Okay, so what are the layers starting from out to end? So there's the epithelium. Okay. And then there. So what stain is this? P-A-S stain. And how can you say that? Because bowman's isn't stained, but it does amaze. Exactly. So it's a good way to remember, you know, bowman's layer is not a basement membrane. Decimacy membrane is. And so if you do a P-A-S stain, you see that decimacy membrane stains this nice kind of magenta color, whereas you see bowman's layer up at the top is still pink. All right. So let's talk about some of the layers here. All right. Arianna, tell me about the epithelium. It's a stratified, squamous, non-carotidase. How many layers thick is it? Okay. So you can see it's about five to seven layers thick. Carotid or no? No. No carotid. All right. And then what layer is this right here? Bowman's layer. And so, you know, as you see, bowman's layer, it's really a condensed, almost stroma. And the important thing you remember is bowman's layer does not regenerate. And so if you have an injury or an infection or something that causes either break or loss of bowman's layer, it does not regenerate. So it's kind of historical record of what's happened to that part of the cornea. And we're looking right here. Rachel, why are we doing this stain again? What stain is this? P-A-S stain. Why would I do this? It doesn't. But what does stain on here? Exactly. And so what this shows is it shows the epithelium has a basement membrane. So right under the epithelium, you see that line of staining. And then bowman's layer underneath that does not stain. So bowman's layer is not the basement membrane of the epithelium. The epithelium has a separate basement membrane. And so this P-A-S stain shows nicely that thin layer under the epithelium, epithelial basement membrane, and then bowman's layer underneath that. Now, let's go back a little bit to... Obviously, that's not going to happen. So stroma. All right. Pretty unexciting part of the cornea. Marsha, what is the stroma comprised of? Curls and fibroblasts also. Well, it's actually keratocytes. So these little spindly-shaped nuclei are the keratocytes, which are normally quiescent in a cornea. So they're spindly-shaped. You have these lamellae of collagen. Now, what's interesting is they run from limbis to limbis. That's why the cornea is so strong. So they run from limbis to limbis. It's very strong. Now, if you injure the cornea or disrupt the cornea, these keratocytes can become like fibroblasts. And so they can start laying down collagen. But the problem is, is once you do that, collagen will not be that nice, regular limbis to limbis collagen. It'll be shorter and it won't quite be as strong. And so once you've made an incision in the cornea, even though it re-healed, it's never as strong as the original cornea. And so there's some other things. There's some glucopolysaccharides and some other material that's in there. But mainly, it's collagen and it is these keratocytes that are in there. Now, why is the cornea clear? A couple of reasons why the cornea transmits light. Because it's the appropriate hydration. So exactly. So it's dehydrated. So it's not full of fluid. And so if you get any fluid in the cornea, of course it becomes cloudy. Chris, what's another reason why the cornea is transparent? The stroma. Exactly. So if you look at them on, say, electron microscopy, they're very regularly arrayed so light can come through them. And the sclera, on the other hand, is white, but it's made up of the same stuff. But the sclera fibers are not regularly arrayed and the sclera has fluid in it. And so it's not detergent. So that's why the sclera is white and the stroma is not. All right. Now, we're looking at the posterior here. Alley. So again, what layer is this right here on the posterior? And then what's outside of the endophelium? Decimase membrane. So if we look at that closer up, there's the endothelium, there's decimase membrane. So remember we said decimase membrane is PIS positive. It truly is a base membrane. But if you look at decimase membrane with electron microscopy, there are two different layers. There's a banded and a non-banded. So the anterior banded part of decimase membrane is the part that's there from early on. And then throughout life, those endothelial cells lay down more decimase membrane. And so it becomes what we call non-banded if you look at EM. And so throughout life, decimase membrane actually thickens a little bit. Looking at the endothelial layer here, the endothelial layer is a very busy layer. There's lots of things. Teresa, what are the junctions like in the endothelial layer between each of the cells? Tight. They're tight junctions, exactly. And so this is where you get a barrier to fluid pouring into the cornea. So you've got all the aqueous fluid in there. If you didn't have tight junctions here, the cornea would be constantly edematous. And so those tight junctions really help to keep the cornea detergesse. Now, if you look at them in a sagittal section like this, they look cuboidal. But if you look at them in 3D, they're actually hexagonal. And in fact, if you look at the corneal endothelium, it's like a geodesic dome. And geodesic dome is nature's way of covering a curved surface. And so if you look at these, they're actually hexagonal, and they interlink together nicely like a geodesic dome does. Now, not only do they have tight junctions, say, hey, what else do endothelial cells do? Did you make decimation membrane? Okay, man. Did you think of that? Yeah, that's a good answer. All right. Well, that counts. Arianna, what else do they do? Exactly. So they actually try to pump fluid out of the cornea. So if you start, then they pump fluid out. Rachel, what's another thing that they do? They actually transport nutrients from the aqueous into the cornea. So there's truly transportation going on. So they'll transport nutrients in there also. So in order to have a clear cornea, you've really got to have a good functioning endothelial layer. All right. Let's look at some different diseases here. Marshal, what do we see in here? So there's external photograph of the left eye. You see a hazy, almost grayish covering what looks to be covering the epithelium of the cornea in a band-like fashion. Not sure what it is, but it could be band carotopathy. Okay. What is band carotopathy? It's the deposition of calcium in the cornea. Where in the cornea does the calcium deposit? I believe it's above moments. Or even in moments. And so it's along there. It's down below the epithelium and along Bowman's layer. And if you notice, it's in the palpebral fissure. It forms a band. And so there really is calcium depositing from the tears into this area. And this is really nonspecific. This can be a sign of any kind of chronic inflammation. And so you see it's in a band in the palpebral fissure where the tears will deposit their material. And so when we look at it, Chris, what are these little dark spaces here in the band carotopathy? Those are the spots where the corneal nerves come in. Exactly. So the corneal nerves come into the anterior stroma, kind of along Bowman's, and they pop up to the epithelium. So those little round areas where the corneal nerves pop up, there's no calcium right in there. So there'll be these little blank areas that do that. And I'm sorry this is sideways. I should have turned it around. But there's the epithelium there. There's some connective tissue underneath it. And then that's all along Bowman's layer, both above and below it. Allie, what stain is this? That would stain oil. So what is this material? Calcium. There's red in the stain because it is red. Lizarin red. All right, very good. So this is a lizarin red which stains for calcium. So you can see band carotopathy here. But often band carotopathy is secondary to some kind of a chronic inflammation. Not only do you have band carotopathy, it's very rare to have just band carotopathy. But you've got this area right here where there's this kind of dense fibrous tissue between the epithelium and Bowman's layer. What do you think that could be? Now, a panacea. All right, so as we look right here, sometimes during chronic inflammation you can get material growing out between epithelium and Bowman's layer. And it's called a panacea. You can have a fibrous panacea where it's mostly fibrous tissue. You can have a vascularized panacea. You can even have an inflammatory type panacea or a mixture. So this is what we would call a vascular panacea. So epithelium on the top, Bowman's layer underneath it, and all this vascularized material in between, again, a side of chronic inflammation. So often you'll see band carotopathy and panacea running together because they're both sides of chronic inflammation. Here you have band carotopathy here, some calcium granules up there, and then this dense fibrous tissue in between. So fibrous panacea with band carotopathy. All right, what are we looking at right here, Ariana? Just at the limbus there. The cordia is not clear. There's a whitish, easy part there. Okay, so what do you think that is? Exactly. So this is like an archicinillus, the word senile is bad now, so we just say arcus. What's it made of? Lipid. And so whenever you see a clear space and then something, it's a deposition. And so it's coming from the limbus and then it diffuses and then deposits in the stroma. So you see a little clear space between that limbus. You know, if you look at people as they're older, I mean, almost everybody has an arcus of some kind. So you see an arcus. And double bonus points. What kind of stain is this? Oil-red-O. And what do you have to do with the tissue in order to get it to work? It has to be fresh. Exactly, it has to be fresh. And so interestingly enough, you get deposition of the snippet. It's more anterior and more posterior and not quite so much in the middle. So if you hallucinate, you know, pathologists sniff a lot of formalin and so they're good at hallucinating things. They say this is an hourglass pattern. So it's kind of wider at the bottom and then less in the middle and then wider at the top. And so this is the deposition of lipid and the stroma is kind of an hourglass pattern. All right, Rachel, what are we seeing here? All right, so what is usually the cause of this dendritic staining like this? All right, more specific. And then type one or type two? Type one. Type one, but it could be two. I mean, it could be. So again, I'm going to give you guys some pearls here. So whenever anybody asks you a question about anything in the cornea, they say what's in the differential diagnosis and you say offhandedly, well, of course, herpes. Just say it offhandedly because herpes it and they'll go, oh, yeah. So if you don't know what the answer is, just say, well, of course, herpes because that's it, every differential diagnosis. So these are pearls now, remember these, but you have to say it offhandedly, like, well, of course, herpes. And then they'll say, well, simplex or zoster. And you say, well, simplex, but could be zoster. You know, sometimes zoster can cause these. Although if you see the dendritic pattern with the little kind of raised bulbous edges, that's usually simplex. But zoster can give you some staining, but it doesn't look like this. So this is usually herpes simplex that causes this. And when we look at it, you'll get a little area of ulceration in the epithelium. And then you'll get some stromal inflammation, but you can also have a more of a stromal herpes. And then this is thought to be more autoimmune than actual active infection. And if you look real carefully, you'll even see epithelioid cells down here in the deeper stroma. And so you can get a more epithelial herpes. And the cornea guys will talk to you at this at length because, you know, the different ways that herpes can present it, whether it's infectious or it's an immune reaction. And there you can see the giant cells down there along decimage membrane. So this is the more stromal herpes that you can see. And that's just kind of cool because this was a scraping they did. And you can see the epithelial inclusions that you see in herpes. Now you guys have, you know, PCR tests. You can just scrape it and send it off and you get them right away. But, you know, before we had that, you'd do scrapings and you'd look at them. This is almost like a papstain. And so you'd look at them and you'd see these inclusions that would be signs of herpes involvement. Marsha, what do we see in here? Diffuse injection, some pemosis, and neovascularization, 360, as well as a cloudy cornea with a regular surface. Not sure what the diagnosis is. So this is actually a corneal ulcer. And so this is a really nasty looking one. This turned out to be pseudomonas. So this is a patient that didn't take care of their contacts and got them contaminated. So this is a bacterial corneal ulcer. And it's very important to recognize these because especially an aggressive bacteria like pseudomonas elutes collagenases, proteaneses, things that melt corneas. And so you can melt a cornea in 24 hours with a nasty corneal bacterial infection. So you've got to recognize these right away. Look at the pathology. What happened to this cornea? Looks like the epithelium is gone. Most of the half of the stroma is gone also. It's severely thinned. What else? There's almost like a penetrating wound. Exactly. So it perforated. So if you look right here, you can see that there is an actual area of perforation here. And if you look, it's not that nice pink stroma. It's white and it's pale. And so what's happened is it just completely melted. And so this had a severe bacterial ulcer in the cornea melted and then perforated. And what kind of inflammatory cells do you usually see in a bacterial ulcer? PMNs usually. So acute inflammatory cells. And so you can see in here lots and lots and lots of neutrophils, PMNs. Now, you can still have lymphocytes in here or plasma cells, but there's acute inflammatory cells. There's lots of PMNs in here. So it's an acute infection. So when you treat it, not only does the bacteria cause the cornea to melt and become a pacified, but the PMNs that come in to fight it, they dump out a lot of materials from their granules that can also cause the cornea to melt into a pacified. So, you know, that's good if it's in the skin that an infection in the body's immune system attacks it and cleans it up. But in the cornea where you want it to be clear, that's not good. And so you want to really kill those bacteria as rapidly as you can. And so this is truly an ophthalmic emergency. You know, you want to treat them with fortified antibiotics or antibiotics. We're talking every hour to two hours for the first, you know, 24 to 48 hours where you can melt the cornea. All right, Chris, what are we seeing here? There's a little photo of cornea in the cloud, essentially, and there's this white specification. It looks like it could be another infiltrate, potentially another ulcer. Yeah, so there's an ulcer on the infiltrate and then you see this little rim of haze around. Now, I'll give you a hint. This is an Idaho potato farmer. His eye's been irritating him for about a week. So you think it might be about something more indolent or something like fungus could do this? Okay, so when you see a more indolent ulcer like this, you think something less than bacteria, but something more like fungus. And so when you have more indolent, especially someone who works, you know, farmers, ranchers, or sometimes people will say, oh, I was a high king. I don't know, I was in the garden. Something got in my eye. And so they'll often have some kind of a vegetative exposure. What is this stain? GMS. So Camori methenamine silver. So it stains fungi, silvery black. So you see the little yeasty beasties or the little one staining black up there. So this is a chronic fungal ulcer. Alley. This is a patient treated by an ophthalmologist for herpes for about two or three weeks. Didn't get better. Hurts. Lots of pain. Lots of light sensitivity. It's not even a fluorescence stain, but you can see a chronic area of epithelial abrasion there. You think this could be? All right. So this is a classic acanthamibus, the ring infiltrate, chronic non-healing ulcer, often misdiagnosed early on as a herpes infection. And what's the stain? I don't know if I even showed you guys this in our staining talk. Well, bonus points if you know the stain for acanthamibus. Gridley. Gridley. Because gridley stains green. Okay. So gridley green. So it'll stain the stroma green, and it'll stain the cyst walls kind of a silvery black. And the problem why these are so difficult to treat is that they insist. So once they insist, it's really tough to get the medicine in them to kill them. They're very resistant to that. So you want to recognize these early on because these beasts can get into the nerves. They can start to go in beyond the cornea into the sclera. And so you really want to recognize this early and treated. Nowadays you've got good treatment available. Basically your swimming pool disinfectant drops is what you use. But there is another material that you can order. You have to order it from England, from Pamidine, from Berlin. But usually now you can get the swimming pool disinfectant and that will treat this. And so this is the gridley green stain that stains the acanthamibus cysts. And usually the patient will have some kind of exposure to standing water or something. Don't put your face in a hot tub, by the way. You can do this. I had a young kid who was a wrestler and wore contacts. And the reason I say that is, you know, wrestlers, these guys will like not wash their sweats for the whole season. So he had acanthamibus growing in the case. We actually swabbed his contact case and he had acanthamibus in the case. So, you know, he ended up getting a really nasty infection. And this is an EM showing you it's actually a triple walled cyst and so very, very resistant to treatment once it insists. All right, I guess we're back around to Sneha. What do we see in here? So I think we're seeing... Yeah, so this is actually under the epithelium. And so this is, we're going to start talking a little bit of some kind of dystrophies. And so this is an epithelial basement membrane dystrophy. And I'll often call this map dot fingerprint. And so you'll see you can kind of hallucinate some little map lines or some fingerprint lines there. Then you go here, here again with the light on the side. It looks like fingerprints. So this is an epithelial basement membrane dystrophy. They'll call it map dot fingerprint dystrophy because that's what it'll look like. The previous one looked like a map. It looks like fingerprints. There'll be little dots in there. Here you can see against retro illumination, the little dots. The reason that these are important, and I apologize, this is a bad picture. Actually, I shouldn't apologize because the fellows took this and so on. If it's bad, the fellows did it. If it looks really good, I'll do it. So that's how we did it. Same thing when I show surgical videos at a meeting. The case looks great. I did it. If it's a complicated case, I was the resident doing that. I was the smile when I see it. All right. So basically this is a dystrophy where the basement membrane gets thickened, it gets irregular, and because of that, you can get chronic recurrent erosions. So these people will often wake up at, you know, five in the morning and they'll open their eyes, and then suddenly they'll get an acute pain and watering, and so they'll get erosions from this. So this is an epithelial basement membrane dystrophy. Yes. What are all those layers it looks like as if there's like basement membrane repeatedly? Exactly. So you'll get an ulceration that'll pop, and then you'll get cells that'll heal over that. So you'll get actually duplication of basement membrane in several different layers when this happens. This is a sign they've had multiple recurrent erosions from the epithelial basement membrane dystrophy. And this just shows you, this is a patient who had a scraping. And if you look at it, here is the epithelium that's scraped off. Look at the basement membrane. Remember I showed you the general path, the basement membrane, a little tiny thin ribbon. Look at how thick that basement membrane is. And so when you have the basement membrane dystrophies, it's tremendously thickened. There's a close-up. All of that material underneath there, that pink material, is thick basement membrane, so massively thickened. What do we see in here? We see all these little dots. Yeah, so there's multiple little dots all over the place. So this is a little bit deeper than the epithelial basement membrane, but still really anterior. What could this be? Another dystrophy. Which dystrophy is characterized by anterior dots? Miesmann's. Miesmann's. And Miesmann's is interesting because you get this weird basement membrane-like stuff deposited and the clever pathologist years ago called this, and I quote, peculiar substance. That's the name of this stuff. So it's called peculiar substance. And so it's a dystrophy where you get deposition anteriorly of a basement membrane-like material that forms these little dots. It's Miesmann's dystrophy. Rachel. Yeah, kind of a granular, irregular, not really dot, still anterior. What's another anterior dystrophy that can give you a picture like this? Not usually. Still more, and this is still anterior. We're still not quite in the strongly yet. It's called Riesbuchler dystrophy. And so this is a more anterior dystrophy, and you will get deposition of material anteriorly in the area of Bowman's layer. And so this is, again, anterior type dystrophy. There are different types of Riesbuchler. And so when you get into cornea, you'll study the different types. But really, it's a deposition of material that kind of takes over Bowman's layer. It's an anterior dystrophy. All right, so now I want to talk about stromal dystrophies. And, Marshall, there's a mnemonic that we have you guys all memorize that tell us the stromal dystrophies. What's the mnemonic? Something about Marilyn Monroe getting her way at LA? Not exactly. Write this down, because you'll do this on... I can remember sitting on boards going... So if you don't know this, write it down. Marilyn Monroe really always gets her man, LA, California. So, Marilyn, what does that stand for? M, macular, Monroe. Mucopolysaccharides. Yeah, mucopolysaccharides really... Riesbuchlers, no. Recessive. So, always... Oh, so you gotta know these. So another thing, if you're ever on overboards, don't guess. The guy who does it will go, mm-hmm, tell me more, and then you just get deeper and deeper. So the key thing, when you're in a hole, the first thing you do is stop shoveling. All right, so, always Aussian blue. So the nice thing is it tells you what it is, it tells you what the material is, it tells you what the stain is, and that really gets thrown in because this is the only one that's recessive. So that's all you have to remember. The other two are dominant. So, macular, mucopolysaccharide, recessive, Aussian blue. So macular, you can get little round-like deposits, but if you use them, the key thing is it's not clear in between. It's hazy even in between the deposits. So this is macular. The material is mucopolysaccharide. The stain is Aussian blue. And so it'll stain the mucopolysaccharide material blue. And there's another stain of this mucopolysaccharide material in the stroma. Gets. Manular. Highland. Man. So this is now granular dystrophy. It looks like little cookie crumbs all over the stroma. The key thing is in between the cookie crumbs, it's clear. Also, the deposits are more central, and there's a clear zone in the periphery by the limbus. And so it's a granular dystrophy. It's more specific focal granules. And this is on retroillumination showing you these big cookie crumbs that are all over. And then the stain is Basad's trichrome. And so it'll stain this deposition red. The trichrome stains the stroma blue, but the deposition will be red. All right. Alley. L, lattice. A, amyloid. California. Combo red. Exactly. So you see lattice, very descriptive. It's got these little lattice lines all through the stroma. And if you stain it with Congo red, Congo red's kind of a misnomer. It's not really red, it's more orange, but in any event, burnt orange. And so you see the amyloid deposits that are in the stroma. And then, what's a fun thing I love to do at the microscope, you haven't been with me, but any of you guys, what can you do with Congo red stain? What does it do? Exactly. Cross-polarization, so if you put Polaroid filters on there and you cross them, you will get the amyloid will light up. And I thought this was a cool picture. It's kind of hard to get a good picture of that. But this is the amyloid lighting up with cross-polarization. So if you remember that mnemonic, you will know what you need to know about corneal, stromal dystrophies. So put that to memory. Marilyn Monroe really always gets LA, California. Theresa, what the heck is this? It looks like limus to limus. There's like a classification of the corneal with like in growth of blood vessels. Yeah, so just this is really hard to tell because this doesn't signify anything. But the reason I showed you this is not all amyloid deposition is lattice. And so you can actually get amyloidosis causing corneal deposition either systemically or locally. You can see a cornea with severe amyloidosis. And this is all amyloid deposited throughout the cornea. And again, this is a congo red stain and I'm trying to cross-polarize. It's kind of turned yellow instead of lighting up. So you can get amyloid that's separate from lattice dystrophy affecting the cornea. What do we see in here now? Yeah, almost like there's little granular dots on there and then you look at retroillumination. If you look at the beam, these are deep. So this is really deep now. So this has gone beyond the stroma. This is actually now in the area of what we call an endothelial dystrophy. So what do you see that's got all these little irregular dots posteriorly? And this is fuchs, exactly. So these are gutata. Little deposits on decimies membrane from endothelial cells that are affected by this dystrophy. So this is fuchs dystrophy and what is it characterized by pathologically? So these are gutata, these little excrescences on decimies membrane, but look at how thick decimies membrane is. So you get massive diffused thickening of decimies membrane and you get gutata and endothelial cells eventually break down. And so you'll get corneal edema as kind of the final issue with fuchs dystrophy. And so thick and decimies membrane multiple excrescences which are called gutata and then the endothelial cells eventually die off. Now there is a condition called gutata-less fuchs. There can be fuchs without gutata and that can be diagnosed only by professor corneal chairman attendings. And so Randy Olson is the only living human I know who can diagnose gutata-less fuchs at a slit lamp. Mere mortals can't. It's equivalent of the S1 murmur that the cardiologist or somebody else can. So Dr. Olson can diagnose gutata-less fuchs but mere mortals we have trouble doing that. But there is such a thing we've actually seen fuchs where there's thick and decimies membrane and no gutata. So rare but usually you see the excrescences of the gutata. What are we looking at here Ariana? This is one since science. So this is a gentleman looking down and look at the eyelid or outside part of the eyelid how it's cone shaped instead of round. So this is severe keratoconus. It's called monson sign. So if you look at and look down you can actually see the cone shape. Obviously we've got superficial topography now. We can diagnose this at a much earlier stage but this is keratoconus and it's still lumped into the category of dystrophies. So we're not sure what it is. Some people call this an anterior dystrophy or a basement membrane dystrophy. But if you look at it what's the pathology that characterizes keratoconus? Here we see. Okay so that's the classic sign a little focal break in Bowman's layer. Now you'll also get thinning of the stroma especially inferiorly and then you'll get that cone shaped outpouching but when you look at it pathologically there'll be multiple areas of little focal breaks in Bowman's and that's why people think that this should be classified as maybe an anterior Bowman's dystrophy. So this is keratoconus. Boy along that line what's going on here Rachel? Okay so this is a keratoconus patient and he was going along doing fine with his special contact lenses and then said wow. Suddenly yesterday my vision became totally blurry in that eye and you see this. Hydrops. So what is hydrops and what is exactly the event that happens that causes this? There's a break in decimates membrane so what stain is this again? PAS and so here you can see a patient with hydrops. There's a break in decimates so the way I think about it simplistically is that it's usually not in early keratoconus. It's in advanced keratoconus so that cone stretches and stretches and stretches and stretches and stretches and finally decimates just breaks and so because decimates is pretty elastic when it breaks it curls in and then you can imagine that fluid from the anterior chamber just pours into the cone so you get acute edema. Now if you can get the patient through this you don't have to do an emergent cornea transplant. I mean fortunately they did here so I could get a good path picture but you don't have to do that. Eventually what can happen is the endothelial cells adjacent to it can slide over and fill the gap and then re-establish that linkage and it'll deter just that cornea eventually but that could take months for that to happen and so stop that. Quit yawning. It's contagious. All you guys, both you two stop that. So this can eventually get better if you give it enough time but often times you know the edema takes a long time to get better so you get that focal break in decimation look at the close-up. Decimase is elastic. It curls around on itself but they're still viable endothelial cells so eventually they'll slide over and fill the gap. Now we're going to talk a little bit about some other different things that can occur. Marshall what's going on here and what kind of stain is this? Tri-chrome stain? I'm not sure. In terms of what's going on there seems to be um extra cellularity in the epithelium. Well you've got some staining some positive staining of some stuff that's kind of in that epithelial basement membrane and actually this is a Prussian blue stain. What is Prussian blue stain? It's in the epithelium but what is it stained? Specifically material? Not sure. Iron. So this is an iron stain blue stains iron. How do we remember that? Who were the Prussians? They were the militarists from eastern part of Germany that really built up Germany and started World War I so when you think of Prussian blue you think of iron and what does iron make? Tanks, you know shells, cannons and so iron and so Prussian blue stains iron. So this is an iron stain. Now why would I be showing you an iron stain of the cornea right after I showed you keratoconus? Exactly. So you can get an iron stain in a ring at the base of a keratoconus called a what? Pleischer ring. Exactly. Now remember anywhere you get stasis of tears where there's an irregularity next to what tears can pool you'll get an iron stain. So you can get an iron stain at the head of a teridium you can get the iron stain where a bleb comes over you can get just an iron stain normally where the lid sits. Those are called Hudson stolly lines and so you can get iron stains anywhere that you get as I said an elevated area and then some pooling of tears next to it. So this happens to be an iron stain at the base of a keratoconus of Pleischer ring. Chris, what is this thing? It looks like an external specimen of probably a failed corneal graft is what it looks like. Yeah so you can see all the little sutures that were on there and of course this has been cut in half we're going to process the other half and you see that it's markedly edematous. It's opaque, it's thickened and so this is a sign of just chronic corneal edema. So corneal edema what's the final common denominator that leads to edema? Exactly, so chronic endothelial damage so failed graft high pressure, inflammation for whatever reason the endothelial cells get damaged enough and then you end up getting edema and so you get a corneal edema there and when we look at the actual pathology on this specimen what do we see and hear? So you're seeing them break. Exactly, so this is bolea it's just a big blister so this is bolus caretopathy and it's important this is a PIS stand, look the basement membrane is still on bonements and so the fluid percolates through the cornea it causes swelling of the basal layer of the cells eventually those cells will swell they'll pop and then you'll get a boli or a blister so this is bolus caretopathy and again it's kind of an end stage of whatever's going on to you know to cause that endothelium to dysfunction and then eventually you'll get swelling in here so this is bolus caretopathy it's a sign of corneal edema now you can't call edema by looking at the stroma because during normal processing the stroma will shrink and there will be these little spaces in between so you can't call edema by looking at the spaces in between you call it by looking at the boli and the edema and the epithelium so this is bolus caretopathy say goodbye to the Eiffel Tower Paris at night questions regarding cornea