 Okay, because of time purposes here, we'll have to go quickly through my travel pictures. So this is the main cathedral in Florence, beautiful architecture. This is the dome inside the cathedral. It's got medieval paintings on the top. I don't remember who did this. Michelangelo did not, so I'm not sure who did this, but very famous paintings. And if you go way to the top, you can climb inside the outer shell and pop out up above there and look around at Florence. So here's a close-up. And it's basically biblical things. There's people being burned in hell and there's people going to heaven. It's very interesting. You can spend an hour just looking at the various murals here on the inside of the dome. And this is, as you go up inside between the outer wall and the inner wall where the dome is, these are old popes that are sitting there inside. These are statues of old popes. Okay, and then the higher up you get, the closer you get to the dome. All right, cornea. Let's go ahead and we'll just start with just zigzag. Now let's go this way. Let's go this way. All right, let's go over layers of the cornea. All right, so starting it underlined that as the epithelial basement membrane. And then there's the corneal stroma and then decimates membrane. Excellent. All right, let's talk about the corneal epithelium. What's the epithelium of the cornea like? It's a stratified squamous. Okay. How many layers thick usually? Five to seven. Five to seven. Exactly. Now, I'm going to ask you one more question. What kind of stain is this and why am I showing it? What is PAS stain? What is PAS stain for? It stains, I think, basement membranes. Exactly. So why would I show you this picture? Well, it looks like it's highlighting the basement membrane of the epithelium. And what is not staining here? It looks like Bowman's layer. Exactly. So it's very important that you remember Bowman's layer is not a basement membrane. So the basement membrane of the epithelium is this thin little line right up here. And so Bowman's layer does not regenerate. So if you're looking at a pathology specimen and there is no Bowman's layer there, it's a historical record that something happened to Bowman's layer. And so Bowman's layer does not regenerate. It's a condensed part of anterior stroma. Now, tell me a little bit about the stroma. What lives in the stroma? So the stroma itself is made up of collagen, collagen fiber wool. It's also keratinocytes. It's dehydrated so it can be clear so you can see through it. And the thing about the corneal stroma is the fibers are all regular. There's a regular array of these collagen fibers and they run limbus to limbus. So if you cut them, even if the cornea heals, it still does not have the strength that it had before they look back. Now, some of the differences between cornea and sclera, why cornea is clear and sclera isn't, the fibers in the cornea all line up exactly the same. So if it's detragested, it allows light to come towards it. The sclera, they're at random angles. And the sclera is not detragest. That's why the sclera is white and the cornea is clear. What layer are we looking at right here? The sclera, cornea is the stroma and then decimation. All right, now tell me a little bit about decimation membrane. What forms decimation membrane? Decimation membrane is the one that can be packed together to protect junctions. That's the endothelial cells. Where does decimation membrane come from? Decimation membrane. Decimation membrane is actually the basement membrane of the endothelial cells. So when there's pH positive, that's important because bowman's is not. Now, if you did an EM of decimation membrane, the anterior layer of decimase is what we call banded. And so the collagen fibers are banded, whereas the posterior is non-banded. And so the anterior part of decimase comes congenitally. Whereas the posterior part, it's thicker with age because it is the basement membrane of the endothelial cell. All right, what are these right here? Closer to the endothelial cells. Now, that's something, take a look at that picture. You never see these in the path lab because the endothelial cells are rarely healthy when you do a cornea specimen. And so this is what a healthy endothelium looks like. Now, tell me one of the functions of the endothelium. That's barrier function. Okay, and what is it about it that forms that barrier? It's been said, but say it again. Exactly, so when you look at these endothelial cells, they are cuboidal when you look at them in cross-section. But if you look at them in 3D, they're hexagonal and they're shaped like a geodesic dome. That's how nature covers the curved surface. And so they have tight junctions between them, which acts as a barrier to keep the fluid from the anterior chamber going into the cornea to keep your gist as the cornea. What else does endothelium do? It dehydrates the stroma. Okay, so does that usually by the barrier, what else does it do that helps it stay dehydrated? Yeah, there's actually some pumping capabilities to that, both directions. So that will lead us to what else? What else is going on here? What else does it do? It can transport nutrients. Yeah, so it'll actually pump nutrients from the anterior chamber into the cornea itself. So there is a function there where it'll actually pump nutrients in. Alright, let's talk about some corneal diseases. What are we looking at right here? Alright, so what is it that forms band keratopathy? Casio. Alright, now here's a close-up. Now it's interesting, what am I showing here on this close-up? Why would I be showing this? What are these little round spaces here? They are actually where the nerves penetrate through the stroma of the cornea up through Bowman's layer. And so in the area where the little nerve penetrates, you don't get calcium deposited, so you get these little lacunar spaces. So that just kind of shows you where the nerves come up through Bowman's layer to the epithelium. And you set it, this is caused by the composition of calcium. So what kind of stain for bonus points do we use for calcium? This one, the alizarin red. Okay, so you can use two of them. One is alizarin red, the other is von Casin. So those are the two, and so this is the red one. And here's epithelium. Here is Bowman's layer, and here's all that calcium. So that's band keratopathy. We'll just swing over. John, I'm showing this picture, and here's all this calcium. Here's Bowman's layer. What is this stuff? So what's it called when you have fibrous connective tissue in between the epithelium and Bowman's layer coming out from the limbus? Panus. And so this is the panus. Now, how do we subcharacterize panesisms? Panesisms. I don't know, what is plural for panus? Panus. Panus. Panus. Panus. Panus. Panus. Panus. Panus. No, no, because that's on the surface. So what kind of panus, what makes up this panus? Panus. Fibrous tissue. Fibrous tissue. Fibrous. This is a fibrous panus. And then we look at this, this is a fibro vascular. So here's Bowman's, here's the epithelium. Here are all kinds of vessels along with the connective tissue so you can get a fibrous panus, you can get a fibro vascular panus. And it all extends from the limbus under the epithelium on the surface of Bowman's from chronic inflammation. And as we showed earlier, chronic inflammation also causes vancaryotopathy so you can get the two of them. Excuse me, running together. Here's epithelium, fibrous panus, calcium along Bowman's and calcium here so you can get panus and you can get vancaryotopathy running together in the same patient. All right, what are we showing right here? All right, so what does that, what is that called first of all? Arcus. Yes. Well, senelus, people don't like that word anymore so it's an aging change but it's another term, it's Arcus senelus. What is the material that forms in Arcus senelus? Lipid. Lipid. And if you look, whenever you see a clear space between the limbus and the deposits, that's a sign that diffusion is what causes it. So it's diffusion of lipid. And what kind of stain do we have to do to stain lipid? Oil red on. Oil red on, what do we have to do to that specimen to get the stain? Keep it fresh. Exactly, so this is a freshly frozen one. It's interesting if you look at it, the deposition of the lipid is power glass shaped meaning there's more of an anteriorly, there's more of a posteriorly and it thins out in the center so if you hallucinate, you know, pathologists are good at hallucinating because we spend a lot of time sniffing formally so it affects our brain cells. And so you can see there's anterior deposition, posterior deposition, it thins out in the middle, kind of an hour glass shape. So that is, is Arcus senelus. Now, it used to be taught in the olden days when I was a resident that this was a sign of high cholesterol. But you had to work up a patient for high cholesterol. It turns out, yeah, high cholesterol could do this, but it's not necessarily that it's high cholesterol associated with this all the time. It's just occurred in normal aging. Sir. For unilateral Arcus, do you guys still consider like carotid occlusive disease? Yeah, you need to work that out because this is by definition a bilateral disease. Something if it's unilateral, something is going on to the supply of nutrients to that eye. All right. What do we see in back here? Who came in here? Tell me. Yeah. All right. What kind of, what kind of material have we put in? What stain did we put in here to take this picture? Fluorescene. So this is a fluorescene stain. And you can see the fluorescene stains areas of denuded epithelium. So when you look right here, you see that this is denuded in the center. It's got these little bulbs. So if you're going to scrape that for a culture, where would you scrape it? Right. So not in the middle where that's denuded, but in the edges where you still have viral fibers that are going on. So you said herpes. Which one? Which one? Yeah, most likely one. There have been reported cases of two. But usually it's herpes simplex one, which is the same thing that gives you a cold sore. So herpes simplex one is usually it. And then we look at the pathology. What do we see on the pathology here? You get a few scattered mononuclear lymphocytes in here. Yes, sir? You just bring the edges. You're talking about the terminal. Well, yeah, you can do it so long as you've got partially next to where the stain is going on. You don't want to take it right in the middle where they're staying because there it's all denuded and you may not pick up anything. So that's what a normal epithelial herpes dendrite looks like. What is different right here? Believe it or not, this is a patient with herpes. I think this geroma looks a little more intact here, but there's still what looks like a little break in the epithelium. A little break there, but what's going on down here? It's an organization in the posterior cortex. So you're seeing a lot of inflammatory cells here. So this has now gone from simply epithelial herpes to what we call stromal herpes. And in fact, if you look closer, sometimes you'll even get giant cells along decimates membranes. So this is actually posterior. So this is inflammation posterior in the anterior chamber here. And these are giant cells along decimates membranes. So when you get stromal deep herpes, sometimes that can be even thought of as an autoimmune disease. Something changes the herpes, change the antigens on there. And even when there's not active disease going on, you can still get ongoing inflammation in the stromal herpes. And this is actually scraping before we had, you know, good immunoproxidized stains and good assays for herpes. And you can see inclusions here, both in the nucleus and also a little in the cytoplasm. A lot of these intra-nuclear inclusions here with herpes. All right, what do we see in here? Well, it looks like there's a lot of information. A lot of contraltidal hypnosis. Maybe what could be like a subconge hemorrhage. Some opacification of the cornea as well. Some kind of discontinuity. Or it looks like maybe the surface of the cornea is... Okay, if this were infections, would this be viral or bacterial looking at this? I mean, I guess it's a little hard to tell because I usually, you know, attend to it for discharge. But I would guess, you know, just taking as bacterial. Yeah, and I believe there's a little bit of discharge down here. So this is a bacterial ulcer. If you see a bacterial ulcer that's this extensive, you really got to jump on it right away because that's a sign of a pretty aggressive bacteria. This turned out to be a pseudomonas from this patient's contact lens. And so this is a pseudomonas ulcer. And the thing about these ulcers is it is really an up-downing emergency because these can perforate a cornea in 24 to 48 hours if it's an active bacteria because the bacteria itself can put out collagen uses and protein uses. But so do the body's immune system. So the body sends in these PMNs. They dump out all of the bacterial that's in their granules, which can melt corneas also. So this is truly an up-downing emergency. And what happened to this cornea? Well, it looks like the whole kind of anterior half. So there's a big ulcer here. What is this? That looks like it's probably a bothic mass perforation. Exactly. So this actually perforated. And if you look right here, you see that's white. That's pale. That's necrotic. It's not the normal pink colors of the stroma in the cornea. And here you see all these inflammatory cells. And when we look closely as opposed to herpes, this is more of an acute inflammation. So this has PMNs in it, but also lymphocytes, but PMNs. So this is an acute inflammatory cell reaction. And unfortunately, if you don't treat these right away, you can get this. So what's happened here? That's how it will be. What's happened here? So this also seems like some sort of perforation of the actual stroma. Okay, what is this thing? Is that like the curling of decimates? Does decimates have pigment? So it's u-yield tissue? Okay, what kind of u-yield tissue? My pars... So we're just pulling, we're yanking, pulling, pulling now. What lives behind the cornea? Iris. Iris. All right. And so believe it or not, here's ciliary body, here's iris. That's iris. So when you get a perforation, the iris can go right up in there and try to plug it up. So this is a perforated corneal ulcer with iris plugging it. And how do we know it's iris? What is unique about the pigment epithelium in the iris compared to the rest of the eye? I'm not sure. Okay. Evan, what's unique about the pigment epithelium in the iris is it's close to the rest of the eye. And by the way, saying you're not sure is good. That's better than just digging deeper. Oh, is it this? Is it that? And when you take oral boards, they'll look at you and they'll go, tell me more. And when you say that, that means, oh my God, I'm getting deeper and deeper. And then you say, I do not know and move on. So what's different about the pigment epithelium in the iris compared to the pigment epithelium, say, of the ciliary body and elsewhere? Both layers of the iris pigment epithelium are pigmented. Whereas in the ciliary body, only the outer layers pigmented, the inner layers non-pigmented. That's how you know it's iris. You have pigment epithelium, both of them pigmented. All right. What are we looking at right here? Short. So for you, Brad, you're as long as Brad. So what if I told you this is a potato farmer from Idaho. This has been going on for three or four weeks. Now it's the fall. I just did the harvest. All right. So the word we use is indolent. And so instead of an acute presentation, it's indolent. It smolders for several weeks. And then stubborn old rancher farmer, then I've got to come in until the eyes coming out of their head. And so finally they come in. You see this. I want you to look, not only is there this lesion here where it's white, but look at that fluffy white video around it. And this is the stain that we did. What does this show? Excuse me. All right. And what kind of stain do we do for fungi? GMS. Gamorimethanamine silver. And so it stains fungi as silverly, silvery black. So if you look right here, you'll see all these little yeasty beasties in here throughout the stroma. So that's a fungal. Also a little bit more indolent than a bacterial, but harder to treat. You know, fungi don't react real well to the antifungals, which are pretty toxic to the eye in any event. What are we seeing right here? So this is an external photograph. Acornia looks pretty diffusely easy. Concentrated essentially there's said to be a ring infiltrate. And then the epithelium looks to be denuded with kind of a whole margin. What gives you a chronic epithelial, denuded and a ring shaped infiltrate? Persona is having a lot of pain. I don't think you can't the meba. If they were amusing topical stear, topical and propericine. Exactly. Now topical and propericine, topical anesthetic use can give you a chronic non-healing also, but it usually doesn't give you that ring infiltrate. So you said acanthamoeba. What stain is this? All right. So we remember gridly because it stains the corneal stroma green. And sure enough, here are the cysts of acanthamoeba all throughout the cornea. So we do a gridly stain. You can actually see these on H&E stain. They don't pick up the stain, but you can see the outline of the little cysts even on H&E stain. Now these are very difficult to treat because you have to get in there. And once they insist, they're a little bit resistant to treatment. So the problem with these is they can get out beyond the cornea even into the limbus and into the stroma and along the nerves. That's why they're painful. So this is acanthamoeba. You want to recognize these because if you treat them early, you can sometimes save a cornea. And it's interesting. We treat them with swimming pool disinfectant. That's basically the drops we use nowadays for swimming pool disinfectant. It kills the acanthamoeba. And here's an EM showing you this triple walled cyst. And so once they insist, they're pretty resistant to treatment. All right. What do we see in right here? An external photograph of the red eye. That's drawn to the cornea. It looks pretty interior. You can see some irregularities of, most likely the epithelium. I'd be concerned for map dot fingerprints. Okay. Let's say we do a slit lamp and it looks like this. Does that help? Not really. If you look at that right there, what does that look like? It looks like little finger prints. It's like a fingerprint. Exactly. So when you have, we call it an epithelial basement membrane dystrophy. It depends on which pattern you get. Map dot fingerprint is literally descriptive. So it'll look like the edges of a map, like this first one, where there's the edges of a map here. It can look like a fingerprint, which is here, or it can look like a dot, which is there. So this is all caused by what? Basically like redundant epithelial tissue. Or specific, not redundant epithelial tissue, but redundant epithelial what? Basement membrane. Exactly. So this is a basement membrane dystrophy. And if you look, I apologize. One of my fellows took this picture. I'm always in the focus. So whenever there's something that's out of focus, blame someone below you. If you're an intern, sorry, you're, it doesn't go lower than you. All right. So this is actually a, what stain? Yes. Yeah, yes stain. And here you see this thickened epithelial basement membrane and you've had recurrent erosions and then the epithelium grows over them. And so the problem with map dot fingerprint is you can get recurrent corneal erosions. And when you treat that, you often have to scrape off all the epithelium and all the basement membrane and give it a restart to grow. And so this is a scraping we had. Here's the epithelium. Look at all this. This is all thickened basement membrane. So this is actually a map dot fingerprint that was scraped. And that is all markedly thickened basement membrane. And so epithelial basement membrane district. All right. What do we see in here? So this is the map photo. What do you have? Diffuse little interior cyst-like deposits. All right. So these are kind of, you know, once again below the epithelium, but they're really almost like specific little whitish deposits. What do you think about here? District B is so short. Okay. Here's the pathology. Again, what kind of stain would this be? So PAS. PAS. You see, Bowmans is not staining. And you've got this PAS positive stuff underneath the epithelium. So this, it's hard because these dystrophies, they all look the same. They're pretty difficult. This is called Miesmann's dystrophy. And it's interesting, the pathologists who first described this call this peculiar substance. So it's interesting that they weren't quite sure what this stuff was. So they call it peculiar substance. So you get this peculiar PAS positive substance underneath the epithelium. And that is Miesmann's dystrophy. All right. What are we looking at right here? Let's see. So again, it's the largest. This is the center. It looks like the entire stoma is based on a slightly passive part. Believe it or not, that's a weird way it's coming off. So this is mostly anterior again, but it's really diffuse and feathery. And what could look like this? I mean, so. So here's the pathology. And what I want you to look at here is the distinct absence diffusely of Bowman's layer and then kind of a condensed stroma underneath it. What dystrophy gives you that? Exactly. And so the Butler's got a, whatever, a lot above it's Buchler's dystrophy. And there are various different types of Reese Buckler's dystrophy. So you need to know those for boards and for corneal lectures. But the pathology is really kind of an absence diffusely here Bowman's layer. So those are kind of the anterior corneal dystrophies that have unique pathology. Now we're going to jump down into the stroma. So, Nama, tell me what the mnemonic is that we use to remember corneal stromal dystrophies. All right. So Marilyn. Macular, Monroe. Euclopolysaccharide. Euclopolysaccharide. Really? Recessive. Recessive. Because that's easy to remember. Now the rest are all dominant. Gets. Now also the really always. Always. Alchemy blue. So which one would this be? If you look in between these deposits in the stroma, there's haziness. So that's macular dystrophy. And then what kind of stain is this? Alchemy blue. Alchemy blue. Stains the mucopolysaccharide. So here is Alchemy blue stain. And it'll stain this mucopolysaccharide, this dark blue color here in the stroma. And that's a close-up again, showing you this granular blue mucopolysaccharide material. Okay. Next one down the mnemonic. Gets. Man. So on track. So here you see granular now. The way you tell granular from macular is there are these red crumb looking deposits, but it's clear in between. So you see the deposits, you see that the stroma in between is clear. And here's your retro illumination. Multiple. Multiple deposits here, but clear spaces in between. And then m. This one's trichromes. Here's a trichrome stain staining this highland material here in the anterior stroma. All right. I guess we come back. L. Ladis. Ladis. A. Amaloid. Amaloid. California. C. Congo red. Congo red. So this is the lattice dystrophy, these lattice lines that you can see coursing through the stroma. And this is consistent with amaloid. And so this is the amaloid stain, the Congo red. Kind of a misnomer. Kind of a bird to orange rather than a red. But in any event, this is Congo red. And why would I be showing you this picture? What does amaloid do under the microscope if we treat it the right way? Yes. So it's got birefringence. So if you take polarized filters and cross them, you get birefringence of, believe it or not, this is a picture through the scope of all these little areas of amaloid lighting up. Now, if you, if we suspect amaloid in there, normally when my technician cuts regular histopathologic slides, they're about three to five microns thick. That's not thick enough to bend the light for birefringence. So if you're worried about it, whenever we do a stain with the Congo red, I always tell my technician, make it a little bit thicker, more like almost five to ten microns thick. And then when you cross-polarize the filter, you end up getting this cross-polarization. You get the amaloid material Now, the other thing you want to remember is amaloid doesn't just occur in lattice. You can also get systemic amaloid or local amaloid effect in the eye. Believe it or not, this is a cornea that underwent a transplant and this turned out to be amaloid. So here again, we're trying to cross-polarize a little bit. Congo red stain, you can see amaloid everywhere in this cornea. So systemic or local amaloid around the eye can also do this in addition to lattice. What are we seeing right here? So it's an image of a cornea. It looks like it's pretty obtusely opaque, but there's also some texture to the surface. It looks like it could be some things like utada. So we go ahead and we do a retro-lumination. It looks like this. Yeah, so again, it kind of looks like I guess I'm not sure which surface that would be based on this. Believe it or not, this is all posterior. But again, it looks kind of textured and bumpy, which again would be considered consistent with utada. And which entity of utada is seen in? Fuchs. Fuchs. Endothelial dystrophy. So we're not working our way through the cornea. We've gone from anterior dystrophy to stromal dystrophy is now a posterior area. And so this is a patient with fuchs and they'll often say this is a beaten metal appearance. So I don't know, in the olden days they would totally segregate people in junior high. Boys would go to shop, girls would go to home act. I mean, how's that? So you guys would learn to cook and we'd learn how to hammer and do manly stuff. And so one of the things we did is we worked with sheet metal. So if you take a thin piece of sheet metal and a ball peen hammer. Now, how do I know this? If you take a round hammer and hammer the heck out of a thin piece of sheet metal, you get this appearance. And so they'll often call it a beaten metal appearance. And so these are utada and what are utada characterized by pathologically? So there's the utada. What the heck is this right here? Oh, so that's where decimates would be. That is decimates. What's different about that? Yeah, so decimates membrane will become diffusely thicken. And then because this is an endothelial dystrophy, as the endothelial cells are affected they start to lay down extra material which then gathers and clumps these so-called utada. And then unfortunately the endothelial cells die off. So the end result is you get corneal edema. But here decimates is markedly thickened. Here's the utada. And if you see them, they're flat top. They look like buttes. On the west, buttes are those things you see when you drive across Wyoming. Flat top, steep sides. That's what these utada look like. So Fuchs endothelial dystrophy. What do you see in here? Oh, pushing. I'm not like, for boards they talk about like the peripheral, like hassle-handling utada that are asymptomatic. What's the difference? You know, pathologically they look exactly the same. Why don't we still get like endothelial? He says they're only at the far periphery. So they're what we call a watershed effect. And so anywhere in the eye where you are kind of at the end of nutrients you can get breakdown as you get older. And so if you think of it, the nutrition in the anterior chamber comes from the cellar body through the pupil up into the anterior chamber and eventually by the time you get to the cells right by the trabecular mesh work all the good humors have been sucked out of that. And so over 50, 60, 70 years those cells start to break down so you get little utada right near the limbis right near the trabecular mesh work called hassle-handling warts. So they're a watershed event. Kind of like at the far peripheral retina where, you know, blood supply before you get to the orserata the good humors are all taken out of that. And so in older patients you'll often get little schisis, little splits, little cysts from the peripheral retina, same idea. So when you look at hassle-handling warts they're exactly the same as utada. It's just they're an aging effect in a watershed area in the far peripheral retina. All right, what are we seeing right here? This is an external photograph of a patient looking down gaze attention drawn to the right eye you can see there's some indentation of the lid crease because it's all the monson sign. This is monson sign. What is this a sign of? Cardiconis. So it says to be pretty severe you can actually see the cone when you look at it but this is what they talk about. You'll often hear people talk about monson sign and so this is a sign of severe caroticonis. Of course now with good topography we can pick up caroticonis a much earlier degree of differentiation than this and so that's severe caroticonis. What is caroticonis characterized by pathological? So it's a breakdown in decimace we can see here pathologically. Break down in, I know your brain set up decimaceous. You always say what you think not what you said. I tell the nurses that to give me the instrument I need not what I asked for. So I knew you meant bomins. It's a discontinuation of bomins here and so it's thought to even be a bomins dystrophy so you get these focal breaks discontinuities. Now the stroma is thin in these areas which is why it poaches out and you often will get these breaks in bomins. All right Abbey this patient comes in they're wearing contacts for caroticonis and they say wow my vision suddenly went really blurry. All right? All right so hydrox. So if you get a break in decimace and the way I think about it is when you have severe caroticonis it stretches it stretches it stretches it stretches and finally decimace breaks and then you get a gush of fluid into the corneum so you get an acute corneal edema and here we have what kind of stain is this? Yeah yeah so sure enough here's bomins layer that broke and you can see bomins has got some elastic properties too so it curls up and then the fluid gushes into the corneum so you get corneal edema. So here's a close up of decimace and you can see that acute break and so you get what's called acute hydrops acute corneal edema. Okay what kind of stain are we doing with our Prussian blue and what is Prussian blue stain? Iron how do we remember that? Dr. Patel is not the only one who asks you history questions. Who are the Prussians? Exactly so they were the German militarists and so Prussian blue stains iron and I always equate that to iron iron is what tanks are made out of and bullets and guns and things so Prussian blue stains iron this is a Prussian blue stain so now you guys know all of the various iron depositions in the cornea that will stain but this is the staining that you can get and so let's pretend this is the base of a cone keratoconus patient and this epithelium has iron in it what is this called? I don't know. A pleasure ring exactly so there's various different rings that can stain the cornea but the bottom line is they're all due to iron deposition alright we've got a cornea right here it's got a bunch of sutures on it and we've cut it in half before we process it and it's totally white. What would you be concerned about here? What makes a cornea turn totally white infusely? Corneal edema exactly so when we look right here what are we seeing here? Deporated from bones. Alright so you can see what we call a bull eye which is a nice way of saying just a blister so there's endothelial damage for whatever reason and then the fluid will start percolating through it will gather in these epithelial cells on the base the cells will eventually pop in the form of a bull eye look right here this is actually epithelial basement membrane which is different than bull minds and so technically these bull eye don't dig underneath the epithelial basement membrane there in the basilar layer of the epithelium which then pops. You leave the basement membrane still on bullmen's layer but then the epithelial layer is popping and you eventually get this bull eye and so bullish keratopathy a sign of diffuse damage to the endothelium and then we say goodbye to the dome on the Dromo and floras. Questions in two minutes. Yes I was on a transfer center call of the emergency department physician used the term Wesley you ever heard that term? Wesley's immunering is literally just a deposition of we think it's immune cells that make it term white but I don't know we really don't ever use that term so I'm not sure what that means First it's a ring it's a ring infiltration due to infiltration of white blood cells usually mononuclear cells in the cornea but we usually don't use that term much but when you get a call from the ER and they tell you something just go look at it yourself please you don't know what they're seeing so just go look at it yourself other questions do we still do like anterior stromal puncturing from all these like EVMD or current erosions or is that like crystal? Well no but it is a way to get it to stick down and so if they're getting recurring erosions from say a map dot fingerprint or something similar you want to help it scar down a little bit and the way we used to do it is micro puncture in Bowman's layer and that will actually diffusely get it to stick better nowadays we will often remove the epithelium completely put a bandage contact lens on and let it regrow from the lens out or you can even use an eczema laser to remove all that abnormal base membrane and kind of caramelize what's left of Bowman's layer they're hopefully allowed to smoothly but if you have recurring erosions and you've tried everything and nothing is worth micro puncture you just take a band 25 gauge needle it almost looks like a little cystotone that you used to make an antiochepsalotomy and cataract surgery make a bunch of micro punctures and that will again get it to stick down better