 It goes through the mnemonic that you just have to know all of these because they're highly testful things. So you get the Marilyn Monroe macular bucoplysaccharide, that's the substance that's in the stroma and it's going to sting with alchamblue, granular for the gits, hyaline for the herd, and then manned is the centricrone, and then lattice for the amyloid and the cungerbid. I love that amyloid with the apple-bire fridgens to show you pictures of those to kind of remember those. Okay, so those are kind of the big ones. Okay, so let's switch, we're going to go all the way down to the, what are the posterior corneal discrophies? What's the biggest, one most common one that we do with? So foox. Okay, what are the other ones? Rachel? Yeah. Good. Posterior polymorphous. Just a little bit more common than you think, it's, you can find it on a lot of people, just kind of these subtle, tiny little nests of endothelial cells that look like epithelium. We have a couple of families in Utah that have pretty bad PPMD that you'll see in Hoffman's Clinic. They're probably getting into their 20s now, so maybe they're kind of falling out of the Pete's Clinics, but those are kind of the two big ones, what's the last one? Ched? You've got Ched 1 and 2. If you look at all of the corneal discrophies, let's go into these lecture slides just a little bit. When you think about the genetics of it, what are you thinking always? What's kind of your default genetic sort of inheritance for these corneal discrophies in general? Autosomal dominant, right? So if you ever have a question and you're not sure what it is, just guess how the somal dominant, because that's what a majority of them are, and that's how their inheritance patterns come in. So you always want to just organize it by layers. You've got to remember that mnemonic for most of the stromal discrophies. When you look at thinking about what is a corneal discrophy to try to parse these out, so you have degenerations of the cornea, you have discrophies, you have ectagias, so it's always inherited, right, and so what a discrophy is, it's inherited, it's bilateral, and it's not inflammatory, okay. So inflammatory things are not going to be something that you're inheriting as a discrophy. They're typically in the center of the cornea. They usually don't go out to the periphery, there's a few exceptions to that. But when you think about like Fuchs' discrophy, like where is it affecting the cornea initially, it's just right in that dead center, right? Same thing with like immaculate discrophy, granular discrophy. The center is what is affected the most by it, okay? So if you have some lesion in the peripheral cornea, your first thought is not going to be this is a corneal discrophy, okay, it's going to usually affect the center. So you see a patient with whatever corneal discrophy you're always just going to kind of guess that it's autosomal dominant, if you're not sure. So think about the layers, we talked about this anterior, we've got the Miesmans, the EVMD and the re-spooplers. Miesmans is pretty rare, it's these tiny little epithelial vesicles that you'll see in the central cornea, usually not symptomatic until they get into later generations and then they'll start to become symptomatic with it. EVMD is so common, you guys deal with this all the time, on call with recurrent erosions kind of being the biggest one, a lot more common to affect females and Caucasians. So let's see Marshall, if you have a patient with EVMD, they come into your clinic, they have no idea they have it, what might they be complaining about, or what's usually going on with them clinically? Overcurrent corneal erosions. Okay, that's usually kind of a, it's not that common if they have anterior base membrane dystrophy to have erosions, what's kind of the main symptom that they're going to have? Blurry vision. Okay, vision might be blurry, right? Because what's it going to cause on the cornea? Cause like separation of the epithelium. Yeah, so you get a little bullie that can form, right? That's kind of the pathology behind it is that the epithelium isn't very tightly adherent, that's how you're going to get it tearing off, but if you think about like skin having like peaks and valleys in it, what's it going to do for astigmatism? Oh, make it irregular. It's a pretty irregular astigmatism, right? And so that's why they're not going to C grade is because their cornea is not very smooth. Okay, what else might they be complaining about? Eye pain from what? Like you're talking about recurrent erosions, right? You're going to have eye pain from that, but what's even more uncommon than that? Pretty much everybody has almost every patient dry eye, right? So you're going to manage these patients like they have dry eye because that's going to be their main symptom and their main issue. And so optimizing dry eye, Michael, what are you going to do? Drugs, ointment, drugs. My first go to on these patients is plugs. I get plugs in them. And if plugs keep falling out, get them cauterized. I'm not somebody who does all four punctal occlusion on most patients. I usually just worry about the lowers because the uppers aren't really doing that much. If I can't keep lowers in these patients, then I send them to Dr. Patel to do cauterine remarks or Chrome. So you just have to optimize the tear film, plugs are the go-to. Patients kind of get lax on artificial tears, so plugs just kind of boost that. So kind of a primary treatment for this. And then you're obviously doing everything else to optimize it. So adding tears, ointment at night, what about the ointment at night? Like what could you do for somebody who's maybe decompensating a little bit with EDMD that's struggling? So what does muro do, Marshall? What is it? It's like hypertonic saline solution to help draw water out of the cornea. And so kind of dehydrates those little epithelial cysts or the bole that they're trying to form, trying to help keep that cornea nice and compact. Every single night when you go to bed, your lid and your cornea stick together. And there's a war going on of who's going to win the battle when they wake up. Because it's a really, the cornea gets swollen every night. And so when you first wake up, is that skin going to tear off or is it going to stay down? And so optimizing that while they're asleep at night's really important. Okay, so now you have a patient with a recurrent erosion. How does that change management? What are you going to do now, Riz? Initially I treated like a corneal abrasion, so you treat it like that. These patients you can give them bandage contact lenses, they can help with pain and stuff too. And if they're more recurrent than that, then you can think about doing some more invasive procedures. So things like what you could do, anterior or strong little micropubture would be another thing we could do for these as well. What's like our go-to? What do we do first, if we're doing a surgical procedure, do you know? What do you do first? Yeah, pretty much cure it in most cases. Superficial care, tectomy, right? So you're just going to remove all the skin, leave a little one millimeter skirt of limbis, and then what you're going to do is you're going to polish moments. And you're trying to create little micro scars. So just really gentle, diffuse polishing of moments. You're trying to get that skin to grow back and heal down. That can be curative in most patients. It's just trying to get rid of all that abnormal skin and letting the stem cells regrow. Okay, so this is important because it's really common that you're dealing with this on call. The skin is always really loose, right? You have a patient that comes in and that you can see this little elevation of the skin. Or maybe they have a complete FB defect where the erosion's happened. Sometimes it's very subtle. You might just see these little tiny cysts sort of low in the cornea or in an area that's ripped up. So you have to stain them. And I usually, if I have somebody with a cornea problem, I usually don't put a whole drop of fluoresce in. Because it usually just kind of washes out everything. You can't really see what's going on. So I usually put a little properacanin, use a little fluoresce strip. Just have a tiny bit in there and give it some time. So you want to wait a while for all the fluorescein to kind of wash out of the eye. And then you can kind of see some of these more subtle things. So I know you're always in a hurry on call to like get going and figure out what's going on. So just get a small drop of that in there, give it some time. Let it kind of rinse out so that you can kind of examine the cornea well. If you have a big bole that looks really loose, then it's probably a good idea to actually debride it to get rid of it. Because it kind of delays the healing if the skin is there, but it's like dead and it still has to die before the new stuff can grow back. So just taking a little cotton tip swab with some properacanin on it and just kind of cleaning it off is sometimes helpful to speed it up. So usually it's just medical management, right? You're going to do antibiotics, you're going to do lots of moisture drops. Make sure I would get them on Muro pretty quick. But if you're going to put a contact in, you wait on any ointment. So if you put a contact in, just put new drops only. But they have to have an antibiotic for sure. I've got a couple of patients that in the past have had really bad infections when they've had any erosion and they've lost some vision from it. These are patients that I inherited over the years. I haven't seen an infection in a recurrent erosion myself. So just make sure you're getting them on, usually big amox, good strong antibiotic without preservative in it. So that's how you're going to medically manage them. I use a lot of bandage contact lenses in them and I usually leave it in for a good three, four weeks just to try to get the skin to heal really well. One of the big problems is they're in clinic with you and their erosions heal and you're thinking, okay, I'm going to take out this contact and you take out the contact and rip their skin off again. And so you have to make sure that contact's nice and mobile. And so I put usually a drop appropriate cane in the lower lid, one in the upper lid, have them squeeze really tight, blink a few times. And I want to see that contact moving on their eye before I take it out. And then I usually grab it on the upper part of the contact, have them look down. And I kind of just gently kind of move it a couple of times and then bring it off. Some people are in a lot of pain and they just don't like their eyes being touched. And so sometimes you have to take it off from the bottom. And you can kind of do the same thing, just have them look up and just pull on it from the bottom. So questions about that medical management stuff on that? You B.M.D.? So you put the contact in right away and then have them do like four times a day drops for it just until it's closed. It all depends on how bad it is. But usually I think a contact lens is really good first line therapy for it. And then once the contact's out, they have to put mirror in every night. And I usually have them do it for a year. When you get an erosion happening, they usually cluster. And so they're going to keep having them over and over again over the course of a few months. And then a lot of cases they'll just kind of go quiet and be fine for a long time. But I try to keep them on that mirror for an entire year before we switch them off of it. Okay, so we talked a little bit about some of the surgical options. These are just a few pictures. I need to get some of my own better pictures, but that's like a classic sort of matte dot fingerprint thing on that top right. Some of them can be more subtle. So this is like a more subtle finding that you would see where this one's almost probably a little bit healed. And there's just a few little areas where there might be an erosion with the ABMD. This is what a path slide will look like. You'll just have a little gap in the epithelium, not really stuck down while the bowman's. So we talked about the Miro, the Debreedman. You can do stroma, micro puncture. What you're doing is you take like a 30 gauge needle. You just bend the tip of it just a little bit. And usually just do this at the slit lamp. Just put an eyelid holder in. And you're essentially just poking down through bowman's, just trying to create these little scars. And again, the goal is you're trying to get that epithelium to tack down into the stroma. And so that's how that micro puncture works. You can't really do it with central erosions. Usually you're doing this if somebody is having recurring erosions in the same location. In a lot of cases, you'll see this more commonly in recurrent erosions where patients have had an injury to their eye, like a fingernail injury or something. So there's an area of the cornea that's struggling. And you do a little micro puncture in that area, as long as it's peripheral. Works pretty well. PTK or phototherapeutic keratectomy in comparison to photorefractive keratectomy is essentially a laser that you'd apply to the cornea, you remove the skin, apply a laser to the cornea. It's usually, you're usually doing a myopic ablation. So you have to kind of think about what is a myopic ablation when you're doing a LASIK or PRK? What does the laser actually do? It treats where? It treats the end of the steeper, right, steeper. Opposite. So I think in myopic refractive area, usually you have a steep cornea. And so you're trying to flatten the central cornea. And so myopic ablation works pretty well because you're going to remove the central cornea. And it'll treat kind of the central 9 millimeters. So if somebody's like a plus 2 and you do a myopic ablation on them, what are you going to do? You're going to force them more hyperopic, right? So it doesn't work great in patients who happen to be hyperopic. But in myopic patients, it actually works really well. So a hyperopic ablation is just going to treat kind of the peripheral cornea mostly. And so you don't get a great treatment. The EX-500 that we have, the Aligretto laser, is a rapid flying spot beam laser. So it's these really rapid pulses. And so it actually doesn't have a PTK setting on it. So in these patients, we're just doing PRK. There actually are lasers that have a really slow, long pulse laser that you can do like true PTK on like the BizX laser. So we just do PRK on them. You want to kind of just get through moments. You might treat just like a minus 1. You might just treat their refractive error. So just depending on what's going on with it. What's that? This is like a refraction. Yeah. And I had a case where a patient was like a minus 6. And I was like, I had a treatment sheet ready. And it was like a minus. I was doing like a minus 2. And Mifflin was like, just treat a refractive error. Like what, why aren't you just treating a refractive error? I was like, OK, whatever. This doesn't matter. It's the same card. So we treated her, got her out of contacts. Respooklers, again, it's not something you're going to see that often. It kind of creates this weird little honeycomb pattern. They'll test you on that big H3 gene a lot. Recurrent erosions is kind of how you're going to go. You'll have problems with it. There's this other one that's kind of a variant of it that looks a little smoother. But kind of this honeycomb pattern. I don't know if anybody's ever seen haze after PRK. Has anybody ever seen that on a cornea? So this is kind of like an extreme case of haze, is what it actually looks like, where you just get this weird, reticular sort of honeycomb pattern on the cornea. You'll get kind of this little thickening of the, just underneath the epithelium. So kind of similar treatment. You might do a lamellar keratoplasty, or you might do some of these other things that we already talked about. OK, so stromal dystrophies, we kind of went through that. I just want to show you some pictures of them just so you can kind of think about them. So a granular dystrophy is going to be very central on the cornea. And it's just granules. It just looks like granules on the cornea. So it typically spares the limbis. It's how you kind of determine that this is granular. So there's the deposits of hyaline, staining with mason trichrome. Treatment is, you're just going to get rid of the stroma in most cases. But they can have recurrent erosion stuff. So you might do, some people will do PTK on them, like a laser treatment first. Usually, these are kind of in a superficial stroma. So lattice dystrophy is this amyloid with congel red. And so it just kind of looks like a little, I don't know, I don't know how to describe it, other than, what does lattice actually look like in a garden? Yes, lattice is a little more pattern than this, but just lines, lattice lines. Congel red with the birefringence pattern. That's kind of what you're looking for. There are some different types of lattice dystrophies that they'll sometimes test on. The biggest one is that meritose syndrome that has the systemic amyloidosis. So that one's like a big one that you don't want to miss. Treatment, again, all the treatment for all these is pretty similar. They can get recurrent erosions. The stroma gets too dense and not very clear that you might have to do PTK on them. All of these, they can recur. Avalinos is this weird combination of granular plus lattice. You kind of get both of them in there. This is kind of a picture. Avalino is really rare. So you get these weird little linear thing deposits and these little round deposits. So macular is kind of the big one that doesn't fall into that same genetic inheritance pattern. So that's when you have to kind of remember the Marilyn Monroe add in really. So you have that recessive and then always for the alchemy blue. And the biggest thing with maculars is it's limbis to limbis. So all the way across. So that's how you're going to distinguish macular from the granular. And again, a lot of these are really superficial in the corneas. So sometimes doing an anterior lamellar caratectomy would work for it. A DALK would work for it. D-bantear lamellar carioplasty, PK works for it. Any of these, again, can recur. So other rare ones, you have Sniders. It's associated with a lot of cholesterol. So you want to check cholesterol and triglycerides. Stains with oil, oh, you have to have a fresh specimen to stain fat. So those are kind of the highly testable things about Sniders. It's usually like this. They have a dense arcus, which is kind of this peripheral corneal deposit of cholesterol here that you'll see in a lot of patients. But they'll have a dense arcus along with these central cholesterol deposits. And that's what oil would look like, or that the fatty tissue would kind of look like throughout the corneal. I don't have a very good slide of that. I need to get a better one. K, they always ask about what's more common to have recurrents in a PK. I don't know, I guess just memorize it. This is one that you'll see fairly commonly, and you're like, what is going on here? What's wrong with this cornea? I can see too much corneal. Like usually you can't really see the cornea when you're looking at an eye. It's just kind of clear, right? Not much to it. But if you're seeing too much of the cornea, we have a couple of patients at the VA that have this. Or it's just this little clouding of the cornea. It's usually very central. Usually no symptoms that the patient would have in it. This is what we would call it, is this central cloudy corneal dystrophy of French wall. Or some people would call it like a crocodile chagrin. So you might see that on some patients at the VA. Fluct dystrophy is just these little gray, white opacities in this trauma. Usually not really progressive. It can be anywhere in the cornea. Usually an incidental finding that they're not really having a lot of symptoms on. Gelatinous drop-like dystrophy is kind of weird. Cause it'll look like there's something inflammatory going on with the cornea. But the eye will really look inflamed. So there's no redness, there's no inflammation in the cornea. So it's like these little stuck-on lesions that are on there. Okay, so the posterior dystrophies are, again, Fuchs dystrophy is the one that, you just have to know everything about Fuchs dystrophy. So it's autosomal dominant. It's 40-year-olds, they'll start to see it in. Sometimes you'll see it in 30-year-olds. You'll start to see these little gutata. If you see somebody who's 70, and they have some gutata in kind of the peripheral cornea, do they have Fuchs? What are those? You've never heard of the name of those? I think they're called the Haspel Henley bodies. Right, that's how I felt. I'm blanking on it now. But you'll sometimes see these little gutata that are nasal on the end of the, they're not central. So don't call that Fuchs. Just maybe put a few peripheral gutata. But Fuchs dystrophy, the youngest transplant that I've done on them is a 40-year-old. I just had a 38-year-old come in that has a corneal edema from Fuchs dystrophy. So we're doing a transplant on her. It's not that common. It's usually like somebody who's in their 60s or 70s that you're about to do cataracts, or do you find out that they have Fuchs dystrophy? Okay, so tell me everything you know about Fuchs dystrophy. What is the finding on the corneal? What are you seeing? Yeah, you're seeing some. They're called? Gutata, okay. So what's the mechanism of their edema? Do you know why it happens? Close. What's right inside decimates memory? What's the layer of the corneal just below endothelium? Yeah, good. Okay, good. So this is kind of a weird thing because the cornea just lets fluid into it openly. It's not an energy-dependent process. So there's actual fluid just constantly flowing into the cornea from the anterior chamber. It's a passive transport of fluid, okay? And then you have an ATP-driven process to drive the fluid out of the cornea back into the eye. And so these endothelial cells are working their tails off all day long to keep fluid out of the cornea because the cornea wants to be at a certain hydration to stay clear. And so as you lose these endothelial cells, typically wherever those gutata are, they're forming on the decimates membrane and kind of pouching out into the endothelium and they're just causing the endothelial cells to kind of die off. And so one of the big things that you'll see in Fuchs dystrophy is you'll see endothelial cell loss. So you might get an endothelial cell count and find out that you're low on endothelial cells. And so some patients will have no gutata. So you can have gutata-less Fuchs, which sometimes you'll see in the path lab with Dr. Mamelis, where decimates membrane will just look thicker, but you won't really see that many gutata. But typically you're seeing gutata. Gutata is kind of the finding. I have plenty of patients who present with corneal edema. It's clearly endothelial dysfunction, but I don't see any gutata. And so they may have Fuchs, but they may have something else going on that's damaged their endothelium. But that is the primary thing you're seeing. You're seeing gutata. And when you get this beaten bronze metal appearance or whatever that they're talking about, it's when you have confluent gutata and you can't tell that there's one, two gutata with some space in between. They're just like all over. And so you just can't really see anything specific that there's gutata there. And typically when you have that, you're gonna have some stromal edema. And you may have bole, you might have epithelial edema, microsystic edema, okay? When you have stromal edema of the cornea, you may not be able to tell. When you look at enough corneas, you can kind of start to predict or guess what the pochymetry is, how thick it is. But one of the ways that we follow these patients is we actually take pochymetry measurements, right? So we check their central corneal thickness to see how much swelling they have in there. That's how we would judge response to treatment. We put them on murals, right? Murals gonna draw fluid out from the front of the cornea while the endothelial cells are pumping it back into the inside, right? So you've got two ways that you're kind of getting into the swelling. So we're gonna follow that pochymetry to see if it's getting thinner, to see if it's helping. When do patients complain about their vision in foocustitrophy? In the morning. In the morning, right? What did I talk about at night? What happens to your cornea? It swells, right? There's this hypertonic state when your eyelids close of the cornea itself, so it kind of draws fluid into it. And then when you first wake up, you're gonna be blurry because your endothelial cells haven't been able to keep up overnight. Okay, so when am I gonna do a transplant on somebody who has foocustitrophy? Marshall? What are kind of the indications for transplant? At least when they're having persistent blurry vision that isn't connectable with glasses or contacts. You could consider doing it around the time that they're getting counteract surgery. I guess when you've got a conflict cut at the center. Okay. Let me know what the most common complaint is in a patient with foocustitrophy. It's actually not vision, blurry vision, it's glare. That's the most common thing. So I have these couple of 40, 50 year olds who they have pretty significant gutata, but their vision's still fine. So their vision is 20, 20, 20, 30. They're still doing pretty reasonable. They have some swelling in their cornea, but not that much. They haven't really decompciated in the swelling part. Their contrast sensitivity's very low. They have a hard time with contrast. So night driving, usually they're telling you I can't drive at night. It's driven by that low contrast and then the glare. And so those are kind of early indications for transplant. And then late indications are bolus carotopathy, right? So they just fall all the way over into decompensated edema of the cornea that you can't get to go away. Okay. All right, what are our transplant options, Rob? So we just want to replace that endothelium. You can do PK on them. And I've had patients that have had to go that far into PK. You get some really complex eyes when you're doing endothelial carotoplasty. But for Fuchs, most of the time, there's not a whole lot else going on. And DMEC is probably your best option. And that's probably the go-to. It's gonna give you just a replacement of just decimase membrane plus endothelium. DSEC is giving you a replacement of a little bit of posterior stroma with that endothelium and decimase. So DSEC surgery I think is easier because that's what I learned. If you talk to fellows now who are just primarily learning DMEC, they say DMEC's easier. I think it just depends on what you start with. But they're both kind of finicky and tricky, but they both do the job. And that's kind of the main way that we would go. So a couple of pictures of some gutata. Kind of that, this is kind of that beaten bronze metal type appearance, that sort of sheen that you'll get on that left side. Those are the gutata that you'll see coming off of decimase. And you can see where the endothelial cells are, how they're just kind of in between those gutata. You kind of lose the ones where there's a gutata. So that's how it works. Blowdryer, what about a hairdryer in the morning? So I don't really like this idea, but I've told some patients I could try it. I mean, what's the arm right? Just hold a blowdryer out there until it hurts. Give it some of the edema. I'll occasionally come across a patient that just doesn't want surgery. So they don't want to do a transplant. They're old, they're not healthy, whatever. They just don't want to do it. And so sometimes a bandage contact lens is very helpful. You can actually do a conch flap. You can do AMT, like amniotic membrane transplants to kind of help with pain. So there's lots of ways to sort of approach it if they don't want surgery. But the go-to obviously is just replacing that endothelium. PPMD, autosomal dominant again, bilateral. This is really variable in presentation. Like I saw a patient again with Dr. Hoffman in his clinic that just his entire posterior cornea was just hammered. Like he just, all the endothelial cells just looked funny. And then you get patients who, I'm doing a lot of refractive screening on patients. I'm really looking closely at tons of healthy young corneas. You'll occasionally see these little sys in the posterior cornea is kind of what it looks like to me. It's this posterior sort of extension of what looked like epithelial cells off the back of the cornea. So if you have your slip beam go on and you're just kind of zooming across, if you see anything bumping off the back, you might see this. Sometimes they can be kind of linear, where it'll almost look like somebody's had like a penetrating injury to their cornea and they've got endothelial changes in like a linear fashion. So I think it can present pretty variably, but it's not that uncommon actually. So you'll see it quite a bit in some of the more mild cases. I need to get some pictures from Hoffman, but on the top left, you've got just these little tiny endothelial type looking cells off to the side. Okay, so Chad, so there's Chad one and Chad two. Chad one is on a somal dominant. The way I always think of this as a one, I can just put a D on it. Finish the D to make it dominant. This is something that you're usually gonna see in a very young age. And they usually, they do have corneal swelling. And so it's something where their cornea is gonna be thick, they actually have swelling going on. And they're not very comfortable. So it's usually not a comfortable thing for the kids. Autosomal recessive for Chad two. So with two, I just think I can add a line to that two and make it look like an R. So that's how I kind of remembered it. It's typically present at birth, but non-progressive, whereas Chad one is gonna kind of progress as the edema gets worse over time. So it's these epithelial bowl A. So you can see on the front of the cornea, the skin's lifted up. And then there's no endothelial cells. So this is where they might show you, they might show you a cornea where they've decompensated the bolus carotopathy, right? And what you're really focusing on is what is the endothelial looking like? So in this case, there's no, you're taught I just say this is Fuchs distrovi, but there's definitely no endothelial cells. So that might be the picture that they show you to try to get you to. Okay, questions about any of those? Yeah. You were saying that as in there too, see a patient with, are you seeing an exam to that? So it's usually a patient who's fake it and they haven't had any intracular surgery. So I can't blame it on anything. Could they have like, have had like a viral endotheliitis at some point? Yeah, but they're usually gonna know that they had that. Like they had an episode where their vision was crazy blurry for like two months and they were on lots of medications. So they have no history of any injuries to the eye, no surgeries and they're just coming in with a failure of their endothelium. That's where you might come up with it. Otherwise your diagnosis is gonna be, if they've had surgeries, you're gonna call it like a pseudo-fake-ic bolus carotopathy is where you're gonna put them. And then you may send it off for path to figure out is this Fuchs or is it really just bolus carotopathy? And if they don't have gutata, again, it's gonna be a thickening of decimates membrane that might make doctor man, let's call it a Fuchs distrovie. So what's that at the bottom, at the bottom, that's slide there if it's not gutata, like the separation, yeah. Also, so this is decimates, right? This could be swelling or it could just be processing artifact. It's what, this is stroma. The hard thing about stroma is when they cut a cornea, that stroma, it's usually pretty swollen because it's kind of a, you know, they take it off the eye, it's been sitting in fluid. And so you'll get this little stroma edema in there or just artifactual separation of those layers. So did you see the picture of the gutata? Yeah. Kind of have us a comparison. So it's just those little bumps. So these are the gutata right here. And these are the endothelial cells in between them. You can see how thick decimates membrane is. Like that's really, that's like twice as thick as, as even in that Chad picture, which is way thicker. And it's not just because the zoom is in, you can actually tell it's quite a bit thicker on them. Okay, so those are all the dystrophies. Yeah. Is there really cloudy at birth? Yeah, I mean, if their cornea is really cloudy, you're kind of stuck trying to get something going for them, right? Because they usually develop nystagmus and other issues, but it kind of just depends on how you think their vision's doing, which is really tricky to know. So sometimes you're doing a cornea transplant on an infant. They typically have a very, very poor prognosis of vision. I don't think that they do. I think it's mostly just the cornea issue. Like I don't know of any comorbidities with it on the eye. And I don't know, actually, I haven't been, obviously I've never been involved in a Chad case. I don't know if they're just doing like a, like Chad one, I know, I have heard that people will do just endothelial caretoplasties on kids. And then in Chad two, it's mostly just that you get a cloudy stroma, which not really swelling typically, that's usually that bad. And so it's just kind of trying to decide. They usually need a transplant right away. PK usually, okay? All right, page two. All right, you're gonna write down everything you know about caretoconus in five minutes. You would say, hey, I need a book chapter on caretoconus. Okay, should we start? So let's just start over here and just kind of go through, kind of sneak her in a little bit. Okay, so just start by some, like say one clinical finding. Months and sign. Okay, months and sign, which is? That's when they look down and see like a bump from the cornea poking out at their eyelid or their little lid. Good. So caretoconus, right? Cone-shaped cornea. So if they look down, they're gonna displace that lower lid and do a cone shape. Okay, good. Yeah, that's cool. Brazutis? Yeah, brazutis sign, okay. Again, you're just kind of looking, and you'll get used to this when you're looking at corneas, kind of understanding what's a normal curvature of a cornea versus what's a steep curvature. You can kind of start to pick some of that up as you're looking on exams, but yeah, those are some of the sort of, these are some of the external things that you can do. You can see scissoring if you try to do retinospin. Okay, so scissoring and the red reflex. If you have a caretoconus patient, a clinic who's dilated, go check that out, just do a retinoscopy, and it just causes these lines to kind of go back and forth like this. Just kind of weird reflections off that apical cornea. That's why they can't see well, and they're just getting weird sort of reflection of light. Traumatic feeling. Yeah, perfect. So thinning, thinning's a big one. So when you're thinking about a thinning disorder of the cornea, what do we call that in a general sense? Ectasia. Ectasia, right? So these are the ectatic disorders of the cornea. So ectasia means that it's a progressive thinning of the cornea. Okay. Vox-stria. Okay, vox-stria, or vertical, B for vertical, vox-stria in the cornea. So those are stress lines, essentially, compared to what's the H1 that's horizontal. Hops-stria, which come from what? Lachoma. Yeah, congenital glaucoma. So you have hops-stria, horizontal, vox-stria, vertical. So Rob. Okay. It's asymmetrical, it's a period. Well, let's talk a little bit more about topography. Well, let's keep going. We'll fill in what we don't talk about. Good. So that's why they can't see, right? Like patients with mild keratoconus do just fine because they haven't quite developed that high irregular stigmatism. Okay, good. You can see like the Kaiser-Fleischer ring, like the covered models. Good, so you've got, it's actually iron, like an iron ring that's in the circle. Usually you can see that best on a cobalt blue light. That's pretty much present in anyone that has probably a cornea over 48, 49, or you're getting a really steep cornea, you'll see that. So a blue light on the cornea will help to show you that. It's just a round circle in their central cornea. So here are the cases you can get, scarring or breaks in the flare. Good, so breaks in bowmen's is kind of the pathology diagnosis that you come up with for keratoconus, disruption in bowmen's, and you'll get these little scars on the cornea, okay? Any others? I believe the thinnest part of the cornea usually correlates with the apex. Where, in any case? Good, and where is it usually at? It's usually dead center on the visual axis. Where'd usually be apex and keratoconus? Slightly low, right? Just a little bit inferior. Okay, so the comparison for that is like a pollucid marginally degeneration where the thinnest spot is below the apex of the cone. Shade that you're getting in the pollucid. Pollucid's really interesting. We have a couple, I don't have that many pollucid patients. We have a couple, and they're really interesting looking for corneas. Okay. Shot of my cell on a call. Fidget, nice. Coming in percent complete. So to diagnose keratoconus, typically you're gonna have to have a topography, and hopefully a tomography, which, so topography is just a corneal surface mapping, like a, I just forgot to name it right, topography. Yeah, just a front surface map is what topography is. And tomography is three dimensional mapping of the cornean. So tomography is what we use in refractive surgery screening to make sure that patients don't have keratoconus, because you can sometimes have a normal topography, the front surface of the cornea looks fine, but the back of the cornea is gonna look really funny in somebody with keratoconus. And then tomography also gives you the chemistry measurements to tell you the thickness. So if somebody has an ectatic disorder, they're gonna be thinner, they're gonna be steeper. The usual finding is inferior steepening. Red flags that you're kind of watching out for is if somebody has against the rule of stigmatism at a young age, you're gonna be a lot more careful with them. Corneas that are below 500, Cays that are above 48, 47, you're kind of worried about that. Okay, what about some of the historical things in the patient's history that might make you worry about keratoconus? I rubbed, right? So that is the biggest risk factor for keratoconus progression. The other one would be diagnosed at a young age. So those are kind of the two things that would cause it to progress quicker. Obviously a family history of it. But I rubbing is the one thing that will make keratoconus progress. And it progresses after PK, it progresses after crosslinking. No matter what you try to do to stabilize the cornea, it's gonna progress if they continue to rub their eyes. There's a big campaign down in South America where they're trying to teach people how to appropriately rub your eyes because they just know that people are gonna rub their eyes. And so they want you to rub your eyes the right way. I don't know why I can't find the campaign, but it's an actual campaign that they're advertising in the media. So if you rub on the eyeball and there's people who rub with their palm, there's people who knuckle rub, that's probably the most common one. If you're pushing on your eyeball, that's gonna progress your ectasia. So that's the biggest risk factor. So okay, eye rubbing is if you pull your lids down, you're gonna get floppy eyelid, but Dr. Crumb will love you. You just rub on the bone. That's the way I always think of it. If I'm rubbing in here, I don't really care. That feels so good, right? Just right on the bone, not touching the eye at all. And so as long as you're not pushing on the eye, then it's fine to rub that way. So that's what I try to tell my caretaker. If you tell a caretaker on a station not to rub their eye, you're crazy, they're not gonna stop, let you try. So you just try to get them to rub it, okay? So eye rubbing, so if you think about all the reasons that people rub their eyes. What was the biggest one? That's a bit cheaty. What's that? What'd you say? Oh. Yeah, so allergies, right? So atopic disease, so that's easily the most common one. You'll also get in people who don't have good vision, right? That digital sort of stimulation to help them see, and so they can develop it. And then there's a lot of people who have some sort of a mental handicap where they struggle to sort of inhibit behaviors, and so they have repetitive behaviors in one of them is eye rubbing. So a down syndrome patient has a really high risk of keratoconus because of eye rubbing. There's a ton of them. I was reading through the AEO's like preferred practice guidelines, which are pretty good resources to learn about what people like to ask on tests. And there was this slide, here's this paragraph that had all these like genetic associations with keratoconus, and so any of this stuff is pretty highly testable, so it's kind of cool to see all that on there. Another common one is obesity, and people who sleep on their face. So they're gonna develop really floppy eyelids and they're putting a ton of weight on their eyes when they sleep at night. For some reason, obese people like to sleep on their face. I don't know how they do that, but I've learned that over the years that they just, I'm like, how do you sleep on my face? That's why you have keratoconus. So they really floppy eyelids, and that's why all your sutures are loose after I did a PK on you three weeks ago. So that's a common thing to think about too. Is somebody with floppy eyelids or that has sleep apnea and they sleep on their face? Go figure. Okay. Other things on keratoconus, history, clinical findings that you can think of. Another big one they like to talk about is hydrops. So what's hydrops? Corneal hydrops. Breaking decimates, right? Yes, you actually have decimates just ruptures because of stress, right? Decimates isn't growing to factor in that ecstatic process. Like the corneal is actually pushing forward and decimates is under stress and so sometimes it'll just rupture. And so you get this big rush of fluid. It's typically just dead center on the corneal and it's usually right over the cone. So it's kind of inferior. It's just a stress thing. I can just think about it. That corneal is pulling away, it's gonna pop that decimates membrane. So how do you manage it? Am I gonna jump to PK? Do you have surgery on it right now? It's hard to suture into a boggy cornean and I think that's probably the main reason why we don't do PKs on hydrops. The other reason is because it usually resolves and just leaves like a little scar. Sometimes it can be a bad scar but sometimes it's kind of a mild scar and you don't really have much vision issues with it. So decimates will kind of find its way back and reattach. What if you want a speed recovery? Any thoughts? So Murrow, I'm gonna put everybody on Murrow and it's kind of inflammatory so I usually put them on bread and some cycle penalty because it's painful so you dilate them. You wanna be careful with infection risk too because they usually have some boolean. Skin can be unhealthy. What else can you do? Yeah, you can lower their pressure. Can I put something in the eye? Can you act something? Put a needle in your cornean, put something in the anti-air chamber to reattach decimates. Your bubble. That's even put air in. So that speeds recovery. Usually these patients are kind of like tricky socially and so it's not really like feasible to put an air bubble in. If I had somebody who was pretty cooperative, I'd be fine to put one in at the slow lamp and just get an air bubble in there to kind of reattach decimates. Hope speed it up. Usually takes like two to three months for it to clear with medical therapy. So with an air bubble in there, you can sometimes get it to clear after a few weeks or a month, okay? All right, what's the next one on the list there? Clinical management, okay. So how are you gonna manage somebody with keratoconus? What are you gonna do? What are our optometrists gonna help us with? Okay, so yeah, what are our goals? So goal number one of any patient, what's their goal? To bring vision. To see, right? I wanna function in life, so I wanna see. So we have all the way from patients who have really bad keratoconus who have 20, 20 vision. Their cone's really low, they're just looking right over it. They can see fine. To glasses, to contacts, to what are some of the surgical things that we can do for recovery of vision? PK is probably most common or DALC, right? Or what about in-tax? You're seeing in-tax, intrastromal segments. You can put in cornea and kind of reshape it. That's not that commonly done. We used to think that that was slow progression, doesn't really, it seemed to still progress, but it can help with vision. So again, main goal is vision. So it's glasses, it's contacts. And goal number two, stabilize it, stabilize it. We don't want this to progress. So what they can do, no eye rubbing, don't sleep on your face. So you're gonna treat allergies, teach them how to rub their eyes, talk to them about the dangers of eye rubbing. It's worse than smoking. Yeah. Then if we want to do something to their cornea to stabilize it before we go into PK, then collagen cross-linking. Like these patients, care-to-conest patients, they should all get collagen cross-linking. And they should get it as early as possible. And so we wanna try to find them early so that we can cross-link them right away, okay? So post-PK management, right? They've had a surgery, they've had a DALC. Biggest thing is we're trying to prevent rejection, infection, so we get sutures out as soon as we can to prevent infection as broken sutures lead to infection. Rejection, we're gonna treat with topical steroids, sometimes oral steroids. Every PK that we repeat on a patient increases their risk of rejection. And then suture removal, you're removing sutures at steep axis all the time, right? Wherever there's a steep axis on topography, you're removing sutures from there. Usually takes about six months to a year to kind of recover vision after a PK. And then the biggest thing that I talk about with my PK patients is to avoid eye trauma. So they've gotta protect their eyes because that can cause them to lose their vision completely. Okay, questions about that? Okay, we're gonna blitz through something else real quick. I want you guys to practice looking at topographies. So the corneal refractive power of the anterior average corneas 43 diopters, or the total corneal power 43. Fronts 49, backs minus six. This keratoscopy, we actually have kind of a keratoscope for some reason I can't think of the enamel band clinic where you can actually look through it a little hole and it's shining a rat, like a placebo ring on the patient's eye and you can look at their stigmatism. So it's really helpful when you're trying to remove sutures and topography looks really crappy and you don't know where the steep corneas is. So if you look at the top picture, it's kind of subtle, but you can tell how the rings are a little bit closer together inferiorly and they're a little wider superiorly. So they're wider in flat parts and closer together in steep parts. So you kind of use that on the cornea to kind of help you decide. On the bottom one, what it's trying to show you is that there's an area of distortion in the lower cornea where the rings are very crisp. And so it can help you find like surface disease, dry eye, salmons, nodules, stuff like that where the cornea just looks kind of funny. So Marshall, describe this topography. It's like there's a relatively regular stigmatism with the steeper and the vertical axis and maybe it's about a diopter sort. Okay, so this is a little bit steeper superiorly than inferiorly, right, if you look at these numbers. So out here it's fine, like 42.7, 42.6, right? If you look more central, you're 42.6 versus 43.4. So it's a little bit irregular in that central cornea. Yeah, this is, what kind of a stigmatism is this? If it's vertical, what do we call it? With the rule of stigmatism. Okay, good. What this is trying to show you is that if you scale, these are the same pictures, but the scale's different. So on that right side, if you look at the scale on the topography, caretometry readings, it goes from that 12, 12 up to 60. And so it just kind of white washes out the normal cornea, whereas if you change the scale from 35 or the range to 47, see how it sort of shows the stigmatism a little bit better. You gotta be careful, because sometimes your natural instinct is to look at a map and just see the color of the map, but you also have to look at the numbers sometimes to make sure that the scale's not weird on you. So kind of a similar thing here. This is a posterior corneal mapping. And you can see that there's some big numbers, like a plus 33 on that left side, plus 30, but the colors are just washed out because the range is too big. You change the range on the mapping that kind of shows you some of the steeper spots. So you gotta be careful when you're looking at topography to make sure that it's good. So if you look at this right eye topography, this is something weird with the data calculation on a topographer, where it'll show you a blue spot and a red spot right next to it. So you don't really have a lot of pathologies where you've got a steep spot right next to a red spot, or a steep spot and a flat spot, blue and red. So this is some parallax, I call it a parallax. I'm gonna miss calculation, so it's a bad topography. You repeat the scan, it looks fine. You'll see these all the time at the VA, and we just need to repeat the scan to make sure that we get a better topography. So kind of similar here, just a bad topography, like what is going on with this cornea. We just have a steep spot next to a really flat spot. That's a bad topography. What about this one? I'm gonna do what's going on here. So look at the Ks, the Ks are like 44.6, which is pretty normal, right? So why does it look like it's so steep? Again, it's just the scale. So if you adjust the scale to more, what the scale should do on an auto adjust is it should take the average corneal power, put it in the middle of the scale, and then broaden from there. On this one, the scale is down to 39 and only up to 45, and so that's why it's looking so steep. Okay, so you have to kind of look at both to make sure that you know what you're doing. So that's what the topography should look like. It's normal. Okay, so this is what it would look like in Karatecona, so you've got this inferior steepening, right? Big red spot, lower the cornea. On Pentacam, you've got, this is a topography map on Pentacam, the top left, so that should always look the same as a regular topographer. A tangential curvature is just gonna amplify some of these measurements, so you might see that steepness a little bit easier. Relative to Chimetry, so the cornea is thinner over the apex of the steep spot, right? So relative to the rest of the cornea, it's getting thinner abnormally in the center, and so relative to Chimetry means the progression of the cornea is abnormal. And then a posterior float or a back elevation, what that's trying to look at is what is the inside layer of the cornea doing? So endothelium, this, amaze, what's the shape of that? And this is saying that if the cornea is like this, his cornea is going like this, a plus 30 microns above what the curve should be, okay? So that's what a posterior elevation map is. And then you get a Chimetry map that kind of shows you how thin it is. So this cornea is very steep, 51 diopters. It's very thin, 430, I can't quite tell. And you've got posterior float changes and relative to Chimetry changes right over the apex. So that's carried on this, right? That's how you define it. Is it 805? Why does it say 757? That's wild. Sorry, we're done.