 I'm going to kind of break them down by corneal anterior segment dysgenesis and congenital glaucoma. So the pediatric cornea is smaller than the adult one, and it's something we can look at to kind of tell us about the eye, and a kid who can't get to a slit lamp or an infant. The normal corneal diameter of about 12 millimeters, the kids get to that at about age two. A diameter of a newborn is about nine and a half to ten and a half. We can talk a little bit about the disorders of corneal size. Megalocornia is just a kid with a big cornea who doesn't have glaucoma. It's most commonly, excellent, recessive. These kids do have an increased risk of glaucoma. I don't really know the mechanism there. It's probably something, angel anatomy. But you have to differentiate this from congenital glaucoma. If you see a new kid with congenital glaucoma, it's for sure going to be a hazy cornea. So that's usually your biggest clue about checking that pressure as well. This is usually non-progressive. Keratoglobis is when somebody has a thin cornea all the way over. They have a pretty deep anterior chamber. They can get spontaneous breaks and have acute high drops from breaks to decimates membrane. They can be easily ruptured by minor blood trauma. The saddest case I saw in residence, he was a guy who was an attorney in San Francisco doing really well. He had lost one eye as a kid. He got hit in the eye with a baseball and his wife elbowed him in bed and he lost the other eye. He became completely blind in the day. It was awful. But he had airlers down those type 6, so it's associated with that. There's so many types of airlers down those, and I feel like it's getting more commoner. People are just getting diagnosed more, but he did have some hearing loss as well. He had some hearing aids, but pretty sad case. So those people have a really thin cornea and just with minor trauma can rupture their globes and have a lot of problems. Here at a conus is when the central cornea has progressive thinning and bulging. This is usually in families in which it runs. You start seeing it during adolescence, a little more in boys. Associated with Down syndrome, probably because they rubbed their eyes as well as atopic disease. They rubbed their eyes. You guys know a lot about these treatment. Usually we start with RGPs. It's certainly not in kids with Down syndrome. We just kind of watch those kids and manage high drops if we need to. Down can PKP or surgical options, but we don't do those in kids. This usually doesn't happen so much until adolescence anyway. The cute corneal high drops is what you see in those kids sometimes when they have braves and destinies. They're praying from that progressive thinning. In general, you can get this a little more with eye rubbing. Early age or more severe diagnosis, allergic disease is usually self-limiting. They think treating with lubrication, saline drops to kind of try to pull some of that fluid out. People hate those saline drops though because they're so, they sting so much. Psychopathics and toughness steroids. Micro cornea is when kids have less than a nine millimeter cornea. Less than 10 if they're older than two years. This usually happens embryologically after the fifth month of development. Can be autosomal dominant sporadic, bilateral or unilateral. Can also be associated with other ocular abnormalities. Yeah, just for these kids, you got to make sure you get a refraction correction, especially if it's unilateral because they'll be isometropic and treat their associated angliopia. Sometimes they can't have pretty good vision if you treat the angliopia appropriately. Developmental heredity. Just these are just some pediatric corneal opacities that you can see a little bit more rare. Scholaral cornea is when you have an opaque cornea in distinct limbis. In contrast to Peter's anomaly where you have the opacities centrally, usually this one that's clear centrally. Usually non-progressive, don't do well with PKPs, usually bilateral. You know, can be sporadic or hereditary. But yeah, if you transplant that corneal, it will just grow back over because they don't have the distinction of the limbis. So don't usually do so well. So you just try to manage what you can, see if you can get any vision out of it. I had a kid a few weeks ago that I thought he just had a... because I could never get him to the slant that I could have. I always thought he had a cataract because, you know, you would see in his retinoscopic reflex that he had kind of a disc in the middle. And I sent it and then finally we got a little older. He had a really high prescription and his vision is about 2030, 2040. So not too bad, but he's still a young kid. And I sent him to Mifflin. And Mifflin says it's just a really, really mild scholaral cornea. Which is kind of interesting. I've never seen that before. Peter's anomaly is when these kids have a central lukoma. You know, oftentimes that white thing will be connected to the lens, but not always. I have a lot of kids like this who are like an incomplete Peter. So sometimes, and it's usually kind of weird that you see a coloboma, but you'll see a lot of kids just have like a congenital haze in that area. And I think it's just a really mild Peter's. You know, you always wonder when you see kids like that, how much of a workup do you need to do? Like is this interstitial keratitis or whatever? The big thing with those kids is they usually have crazy anisomotropia just because their eyes developed differently. You know, so these kids I have with Peter's are pretty far-sighted, hyper-opic. So they have this central lukoma that's due to a defect in decimates in the endothelium with iris adhesions. And sometimes, you know, it's connected to everything behind it. Often, you know, connected to the lens and everything. They are more likely to have glaucoma probably partially just because they're missing part of that angle on that, you know, over here. Whoopsie. I don't know, is this a, yeah, they're missing, oopsie, or the same angle here too, but they probably have some dysgenesis as well. They can have some other cardiac cardiophacial and skeletal anomalies. I don't see that as much. It can be sporadic and bilateral, map to PAC-6. You can treat these with the PKP. I have seen in residency we had somebody who kind of liked to do that. It's just so hard to manage a kid with the PKP. They often just fail or open up or have other problems. I have seen some people do these optical iridectomies. I know Dr. Jardine had one recently that he was thinking about doing that where they just cut a big hole in the iris and hope that they start using that part of the cornea as well. As far as treatment, you have to just treat their amblyopia. These often get fainter over time. So, you know, although it looks horrible at the beginning, it may get better over time, but that doesn't help with your amblyopia much. Did they tend to have neovascularization? I just had a little kid that nicked you that I got consulted on. It was like a first look out of like, oh, it looks like computers. And then like they had this superior neovascularization. So, like... I don't think so. It's more likely sclerocornia then. I haven't seen that too much, but I know. I don't think they usually do, but I could be wrong on that. The ones that I've seen haven't so much. It was probably more like a sclerocornia. But I have had a lot of kids and I didn't even realize a few of them at the beginning. I didn't realize it's just, you know, kids who just get a funny opacity right in that area. And you'd think, well, when you first start, you're like, what is this opacity? Am I missing something here? And then you kind of realize that it's just kind of a mile of Peters and I have a few of them like, oh. Limble dermoids. You see these a lot in kids with golden hars. They get this choreostoma, the strata limbas, usually in the infotemporal quadrant. Sometimes they can get hairs and things. That usually kind of comes up a little bit later. There's usually no hereditary pattern. They do get a boatload of astigmatism and it usually kind of goes like this, this way against, you know, that one would be kind of going this way. If that makes sense to you, like that your reflex would be more this way and you'd get more with the real astigmatism. You know, you can. Is it flatter? Like so that astigmatism is that? It's like steeper this way usually. I can't explain why. That's just what I know. But yeah, you'll get more, more still. Like if this is infotemporal, then you'd get it like more at like 75 or 70. You can take those off, which most people like to do. It's a little better to wait until people are just a little bit older. They just graft some cornea. They just graft an elliptical piece of cornea in there. But visually it doesn't help them because they still have that funky astigmatism. I mean, it changes, but that's still funky. So that's the big thing. But I have several of these kids that actually have pretty good vision. So even though they'll have like three or four adapters of silk, if you catch it early, which you usually do, because parents bring them in because they have this funny looking thing on their eye. Usually they'll have them on both sides and it's just worse on one side. Yeah, the big thing is that you can graft them. People always want them off, but it's better to wait until they're a little older. Just like I said, PKPs, kids can just open them up and then you lose the whole eye. So it's a little better to wait until they're a little bit older, but they still have some astigmatism. Shed, I've never actually seen this, but they like to ask about it on boards. There's two different types. The recessive, which is more common, presents at births. It's non-progressive, where the autosomal dominant that's a little later progressive, where they have photophobia, progressive, and astagmus can be similar looking to congenital glaucoma because they have, you know, a hazy cornea. It's usually diffusely thickest, thickened, and endemic. Obviously, they'll have a normal pressure and probably not so much make a little cornea. Congenital hereditary stromal dystrophy is autosomal dominant. It's very rare. I've never seen this one either. Non-progressive clavichornia, but they have a normal epithelium. There are a lot of these mucopolysaccharidosis, which they love to ask about on the OCAPS. They're treating a lot of these with stem cell transplants and things now. Herlers, I feel like is a pretty common one. They layer in the disease, get some RPA degeneration and optic atrophy. Most of these are autosomal recessive and have these, you know, later changes in the back of the retina as well. I've never seen anybody treated with a PKP, but they can. I can't get some associated glaucoma. I have a handful of these kids with cystinosis, where they have these deposits in the cornea, and they can treat this with this topical cysts. This drug, I don't really know exactly how to say it, but you have to get it in the mail and you can even get it through CDS. You have to put it on like six to 10 times a day, but it really does work. I have kids who they put it in and it really gets rid of all those crystals, but it's a pain because you have to use it all the time and it has to be refrigerated. And then I had one kid that was kind of getting worse and then mom said that the drug manufacturer contacted her and said the last three batches had been ineffective. Like they had done something wrong to them. So it's a little bit, yeah, and it's exceedingly expensive, but it does really work. These kids have, you know, lots of other issues as well. Usually kind of little kids can have some progressive renal failure. Sometimes they're on some other drug that makes them smell really funny, like you're in their room and you're like, oh, something smells weird, but it can be the drug that they're on. They say they get this, but I haven't noticed that. And I haven't seen it change much when they're on those drops, but they really can get better with this and some of these kids are treated with this later. And I have the kids I have that have this, but they like to ask about this one on the boards too. Syphilis, you always wonder about this and kids who are born with, you know, who have a, who not born with, sorry, who have a, you know, some kind of haze, especially if they have kind of an unknown birth history or from a different country. They have Raffaulica regressive cordial edema. You know, we don't see this very often, but they do like to ask it on the boards. Big treatment is steroids to decrease the inflammation and penicillin. These familial dysautonomia or Riley Day syndrome, kids have a decreased corneal sensation or neurotrophic keratitis. They're kind of like a diabetic foot. They just have a bad cornea. I have one kid right now with Mifflin that doesn't have any other, these other symptoms of Riley Day, but just has no feeling in her corneas at all. She got this huge scar on one eye and now it's lost one eye. And now she's starting to lose the other one and it's just so sad to watch because what do you do? But yeah, she just, you know, gets, has no impulse to blink and just rubs her eye and then starts getting a little abrasion and then it, you know, gets infected and turns into a big corneal scar and then your hose. So pretty sad, pretty weird deal, but, and I've never seen that before in like a normal kid without any other issues, but Mifflin said he's seen it a few times. I mean, obviously you worry in any kid with neurotrophic keratitis about herpes because that's the big thing that can cause it. But, you know, and they ask about this Riley Day syndrome on the boards and things, but I have a really normal kid recently who's really sad to watch. Any kid with haze in their cornea who you don't know why you always wonder about herpes and just start them on a cycle if you're just in case, you know, it's a pretty low side effects profile on that drug. You know, any of these kinds of herpes viruses can cause problems in kids. Yeah, so use, it's spread from your skin and then it stays latent in there. Most people are affected, but, you know, are affected by it by the time they're 70. It's everywhere. People are always worried about it being dirty or whatever, but it's just everywhere. You know, you're more likely to get it and more likely to get it bilateral if you've got atopic disease or things like that or kids who are immunosuppressed. But, you know, it's just so common and if you get it in your eyes, just really bad luck. Congenital herpes is pretty awful. It affects about 1,500 kids annually. It's usually acquired during passage to the infected root canal. These kids look pretty awful. We had one recently. Somebody saw it was pretty nasty. Yeah, you saw that one. Yeah. You know, the big thing is that they get these other CNS disease and it's pretty high mortality. You know, it's increased risk of getting it. If you have, you know, prolonged rupture of membranes, use of scalp electrodes, invasive obstetric procedures where they put those monitors on and things like that. Most mothers are asymptomatic. Yeah, and you just want to make sure that they get on high dose acyclovir. Herpes, it's pretty common in kids. Often asymptomatic primary infections so that, you know, you won't see the dendrite or anything. They'll just come back with, you know, stromal scar. Pediatricians are just remarkably stupid about this one. So, I mean, I've had kids referred for like a three month orbital cellulitis. I was like, no, that's not what's going on. But yeah, just like any red eye with haze, you know. But it's pretty common and it's pretty easy to pick up just with a retinoscope too. You can just see that haze in there. Classically, you know, you get this epithelial keratitis first. I don't see this in kids as much. I don't know if they just don't get it or they don't, you know, you don't see it as much. But, you know, you classically see these nice bulbs and they look really pretty and you see them a lot in residency because people come in because their eye hurts like hell. But usually in kids, yeah, you don't see them as much. You don't want to put these kids on steroids, or these people on steroids. Most results spontaneously. What do you guys do here? You put them on antivirals or what? Just watch them. Do you breed it at all? No, just watch them. Yeah, I don't know, they're different. Different fields of thought on that. I think it's pretty awful to put anything on eight times a day. Some people will treat them as worlds, as like, I can't figure out the head study because I feel, well, we'll talk about it in a minute. We talked a little bit about interstitial keratitis. It's this hypersensitivity of immune reaction. It could get some neobascularization. You got to treat it with a really slow steroid taper. I thought we talked about interstitial keratitis in syphilis, not in this. Discoform, these people, you know, have an endotheliatis get one area that's really swollen. It's also a delayed hypersensitivity reaction. It can be associated with increased IOP and some KP. They can't get a necrotosing keratitis. I've never seen this, but it can be pretty awful as well. You also get a keratitis. I mean, herpes can do everything. You can also cause a keratitis. They often get these trophic ulcers or things later because they don't, you know, they're neurotrophic. It can also be made worse by those topical antivirals, which is why some people don't like using those. There's a little bit about the drugs. In kids, I almost always just use a syclovir because it comes in a nice suspension and it's easy to figure out. The older kids, it can be nicer to do valicyclovir because, you know, you don't have to dose it as much, but it's just easier. Oftentimes, I'll just dose it three times a day and then keep it, you know, for treatment and then dose it back to two times a day when they go on maintenance. And usually, yeah, so I start at 40 to 80, somewhere in there, divide it to TID and then for 10 days and then usually go down to BID for maintenance. These kids usually need to be on it for about a year because they have recurrences common and it's usually when they go somewhere on vacation and stop taking the meds. After they get that, they get some, they get, you know, different astigmatisms so they get some amblyopia often from, you know, the astigmatism or from the haze or from both. And you need to treat that as well. Oftentimes, you know, the amblyopia isn't too bad because this usually comes up later in life and they've already had a good few years of establishing good vision in it. So, and it's usually just astigmatic but it can be several diopters and like against the rule and just can be kind of funky that way. Vernal is just a seasonal allergy. I've got a few kids now that are pretty quiet in the winter and I know it's going to start flaring up in a few months. It's, you know, more common in males, usually resolved by puberty. Usually, you know, I see a fair amount of these like Somali refugees and things or, you know, immigrants from Africa who get these crazy hornetranus dots and I get really bad Vernal. In the Caucasian boys, usually when they get bad Vernal, they'll have the bad cobblestones and not so many of the hornetranus dots. Yeah, it's more common among African-American. It usually gets way better the second you put any kind of steroids on it but the second you take them off, it comes back and so trying to get these people to take Claritin and Patanol and get everything is hard because the steroids fix it so fast and why would I say on anything else? So, it can be hard to compliance wise. The kids with a bunch of cobblestones, oftentimes they'll get some corneal changes and get, drop some of their vision and get some scarring as well in the central cornea. You know, when they get those big cobblestones like that, they get that thick ropey white discharge that they just can't clear out because those cobblestones don't make it so they can't blink very well. The big thing is to, yeah, just get them on an oral hand histamine, topical mastel stabilizer and then use steroids for the acute phase but it can be really hard to do that. A lot of the books say Chromalin. I've never actually used that. Nifflin doesn't like to use it so it's hard to get and things so I usually like to use Patanol because it has a mastel stabilizer and a H1 blockers at it or I think just is an H1 blocker. I can't remember but I usually prefer to use Patanol in these kids. The big thing is it just comes and goes and they kind of have to taper, you know, work on getting their steroids right but you just worry that they're going to overdo it on steroids but you kind of have to, a little, you know, air on the side of doing more because when they start scratching and scarring their cornea you can't get that back. Fluctenules are pretty common in kids. People get all weirded out. I get pictures from my friends who are general ophthalmologists sometimes being like, what is this because they don't see it as much but usually they're, you know, temporally or infratemporally just a white thing. They're just a hypersensitivity reaction. Classically in the books they say or in the tests they want to ask about this because it can be hypersensitivity to TV but most of the time I'm sure it's just a staff. If you put steroid on it for a day or two it goes away right away. Sometimes it comes back but it usually kind of peters out. They get better on like a day or two on steroids. Antioregic segment dysgenesis are bilateral congenital hereditary disorders that affect the anterior segment. They've done lots of genetic stuff on this. I'm not even up to date on that anymore. Post-tier embryotoxin you see commonly in kids just as that white, whoopsie. This white line here, visible at the slit lamp it's a displaced, an anterior displacement of Schwalbe's line but a lot of normal individuals can see it but can be associated with, you know, Axanfel down the mountain when you're allergeals. This GI is diagnosing like crazy these days. I didn't used to but I know I've seen a bunch lately. These kids come in yellow with lots of jaundice. The big thing on them is, yeah, I was trying to check their pressure but usually they get a pigmentary neuropathy that comes in, that comes on later so you aren't gonna see it in these two-year-old kids. They're referring. Post-tier embryo, so Axanfel, so these syndromes. Axanfel's anomaly is the post-tier embryotoxin with iris processes to the sclerosis spur which you can see on gonoscopy but I don't ever do that because you can't get a lens on a kid. 50% of them can develop glaucoma and it's usually autosomal dominoes so you just want to keep seeing kids to check their pressure which is a lot easier with an eye care. Rigors, these are questions they ask on the boards but they're pretty rare disorders. Axanfel's plus iris hyperplasia, 50% of them develop glaucoma, can be associated with foxima and Paxix and these other genetic disorders. Rigor syndrome, these kids have a characteristic appearance. They usually have small teeth, hypospadias, little short and some axillary hyperplasia. Alligials, so this biliary hyperplasia, so I'm seeing a lot more of these kids lately and I really don't know why but they always are wondering about this but it usually doesn't come up to later so I actually haven't seen this in any of the kids that I've been referred. They can't have some of this. They're just someone of these last week who has alligials so she has Axanfel's and coritopia and other kind of funky things. Aniridia, the big thing you're always worried about here and they'll ask about on the boards is it can be associated with Waggar. These kids usually do not see well because of this. Their phobias don't develop so they usually have nystagmus, poor vision, corneal panacea and stem cell deficiency. They start getting hazy corneas. They often have cataracts too that are kind of clumpy and funky. Some can have this. I don't see that very often and they can also develop glaucoma due to a variety of mechanisms or not really knowing why is it because their angle didn't form because their iris didn't form or is the one stump there that's blocking the, you know, the regular mesh work or is there some kind of increased episclerodine pressure because the fluid doesn't drain as well. Aniridia, oh, so yeah, the big thing you're worried about most of the time when you see this is just autosomal dominant due to a Pac-6 mutation and it's pretty easy to get genetic testing. If you can't, you have to screen these kids with repeated abdominal ultrasounds every six months just to screen for Wilton's tumor. These kids are pretty photophobic. Some kids with these, you can get them where you do have an OK phobia. I have a few kids with OK vision with this. They often have a lot of astigmatism. Usually when they need a lumbel stem cell transplant as much later in life, you just definitely want to watch them for a bulk home and get them hooked up with vision services because the nystagmus and the phobia hyperplasia causes a lot of vision problems. I see a lot of kids with colobomas. You know, classically, they can't have problems with pressure just depending on how much of the angle it involves. You know, how much is involved depends on what their vision is going to be. It's part of the continuum that extends to microphthalmosphere and ophthalmos. Can't be surgically repaired, although most people don't. Do you need to look for systemic things? I usually don't unless they've got some, like, other drastic medical problems, but I don't usually send these kids for charge. Bob says that when you have these kids with charge, usually their colobomas aren't as bad, but they can't be associated with many of these other problems as well, but I usually just kind of leave that up to the pediatrician if they have other things. These kids can have really pretty good vision. I have one kid who was referred for surgery as a young age because the coloboma was dragged really down. You know, you can get kids with funky irises and they could still end up with good vision just because they're able to adapt to it. So just because that's pulled all the way down and when you put a reflex there, it's like right in the middle of the iris doesn't mean that the kid will have good vision because they can kind of move their phobia inside their eye and things. So don't give up on vision and most of those kids, even when it's pretty funky displaced, have pretty good vision, especially if you treat their associated refractive error. Sometimes these kids can have some sill just because that eye doesn't form appropriately, so they are much more likely to have a stigmatism. So as long as you treat the anisometropic and, you know, anisometropia, even if their iris is dragged pretty far off, you can still end up with pretty good vision. Neurofibromatosis, I see tons of these kids, you know, and they're always wanting us to look for lesionodules in kids who are like a year or two years which you're not going to see lesionodules. And I often don't even try to get them to the slit lamp because it's a traumatic experience and you're not going to see them anyway. You can look with a 28, but those are hard to see too. So, you know, they're looking for that, those lesionodules as part. These are usually kids where it's a questionable diagnosis and they're looking for, you know, to solidify it. But parents just need to be reassured that these are hammered tomas that are more common in the inferior iris, increase with age, but do not cause any vision problem. And they're only a curiosity for diagnosis purposes. These kids get, you know, the big thing on them is they get optic nerve gliomas, which is not, you know, an anterior segment problem, but they can often, I have at least one patient that I followed for a few years and didn't realize that they'd had glioma diagnosed previously, but she had some anti-symmetropia. So that glioma had pushed that eye and made it more hyper-opic. So sometimes these kids who have anti-symmetropia have to wonder like, is that really true or is there a glioma there that's causing this? And it's not usually a big deal because the ones that are static don't usually change as much, but it's kind of, if you see a kid with anti-symmetropia, you have to wonder if they do have that. The other thing on these kids is, after they're about age nine or 10, we don't worry about those optic nerve gliomas anymore, so you don't have to follow these kids as closely. Cogeneral glaucoma is always the thing you worry about. Pretty rare, but can run in families, especially families have it. You know, these are the classic tears and decimates. Obstrias, they're usually horizontal, just like the eight, the line in age, which is how you can remember, as opposed to vertical, theoretically intact, in cases of forceps trauma. But they're usually just kind of funky, like they aren't necessarily, I think, horizontal. But anyway, these kids, you know, are born with hazy corneas, they can have blusherous plasma, eye rubbing, high pressure. If they have an increased cup to disc, that can get better with treatment. They can have a big corneodameter that stays there forever. This is something we always kind of watch in these kids, and it's hard to check their pressure, and things work to kind of know what their pressure's been, but if they're kind of moving progressive, my OPU, you wonder about that. I have a kid who has a ectropion, like UVA, and I didn't realize that that can be associated with glaucoma, but I had been following her, and her pressure had been fine, and then also her pressure was out of control, and then over the course of like a year, she went three day after as myopic in that eye, and she was about four years old, so they say that that can't happen later, but it can, so that's kind of a good thing to follow, or you can follow, it just can let you know, and you know, if you get a high pressure inclinic, to wonder if it's weird or not, if there's anisomatopia, it can tell you that, yeah, it's pushing on that eye, making it grow bigger. You can also get, you know, congenital glaucoma and these other anterior segment disorders, where they don't drain fluid as well, you can also be seen in some of these other syndromes, one of those, Lowe's, yes, Sturge Weber, yes, not so much. So you check their pressure, if it's high, you know, and when you're doing any UA, you want to do it soon after injection before the anesthesia meds start altering it. Gonioscopy, it can be difficult to recognize landmarks because they have that big membrane that's usually covering the TM, which is what you slice open with agoniatomy. You can have a thick and surbecular meshwork, peripheral iris, stromal hypoplasia. You want to look at refraction, you know, and triambliopia especially, because it's usually a bilateral disease, or even if it's unilaterally, yeah, then you're going to have some differences in anisomatopia and look at the nerve and cornea. When you see these kids in clinic, you usually want to start them on, you know, diamox till we can get them to the OR, one to control their pressure, one to try to, the other one to try to clear their cornea to make the surgery a little easier. I usually do, you know, 15 megs per kick per day and TIDs, so just five megs per kick per dose. You can also use topical beta blockers, can cause some apnea and hypotension. I'm seeing that now a lot more in kids who are on these Timmelala things for hemangiomas. And you want to avoid alpha-2 agonists in all kids just because it can cause some behavior changes and some CNS depression and things, which is actually pretty common. Surgical treatment, agoniatomy requires a clear cornea. You just incise the trabecular mesh work and try to, you know, get rid of that big membrane and open it up. Trabeculotomy, you know, you use when the cornea is, you know, you can enter Schlem's canal with this big trabecutum. You kind of thread it, you know, in here and then pull it in, rip it into the AC. Maybe it causes a lot of bleeding. I think people aren't doing this as much now. They're doing more of these threaded through with the nylons suture and then pulling it in the middle and trabeculotomy using that proline suture. You can't get into the supercoital space and cause a lot of problems. They can decrease that risk by, you know, following that to make sure you're not sticking your probe or what is following that little lighted sensor, which is what they do usually. They can do that at a time or two. You know, if the angle suture repeatedly fails, they can, you know, go to a trabeculotomy with my licensee or tube shut implant kind of just depends on the surgeon what they like to do. Or, you know, they're doing a lot of these, sometimes these ciliary, especially in eyes that don't see as well, ciliary, by destructive procedures. So that TCP or one where they shoot endoscopic. Yeah, transclerone. These kids, you just always want to try to treat their amblyopia. You never know which one's going to end up to be their good eye at the end. And sometimes their good eye is less myopic so can be the morsi in terms of amblyopia. I've had that happen a few times. So you're patching the one that doesn't have as bad a pressure hasn't been operated on and things they start to get amblyopic because it's the less myopic eye. So don't be fooled into thinking that because they have glaucoma in one eye that's going to be the amblyopic eye. And if that's the case, then you really want to treat it because you don't know which one's going to end up being the good one at the end, which one's going to survive till the end. Some of these kids can have pretty awful at disfiguring buphthalmos. I've got at least one girl that has really crazy, couple of kids who have just, you know, crazy buphthalmos from that. In summary, all of these disorders, you know, just require a long-term follow-up. That's the thing about peons. You don't know which one's going to end up being the good eye at the end. You don't know how they're going to change over time. Their imperfections going to change and most of them just need patching and glasses and things because it's not usually symmetric between the two eyes. Sorry, I didn't rewrite my lecture. Next year will be better.