 Hopefully they've improved pictures for you guys, but let's just jump in and get started. Okay, crappy picture. Okay, so conjunctivitis. So you have kind of two main types of conjunctivitis that you're having to figure out. So which one do you think this is? So look at the size of the bumps is kind of the idea, which again, it's always hard to tell. So right here if you look at this slip beam, and you can kind of see these like slump areas here, so it's a fullicular conjunctivitis. So anytime you see a fullicular conjunctivitis, there's almost always... I turned it on. So you're always gonna have like a little papillary where it's just kind of this bland redness over here, and then you're gonna have like larger follicles. So if you want to know what a follicle looks like, just pull any patient's conjunctiva, their lower lid, just pull it down really, really far, and you'll always see a few follicles in the forehead. So you can kind of get an idea of what one type of conjunctivitis is. Okay, so patient presents with chronic fullicular conjunctivitis. All the following could be the cause except. So HSV, definitely, right? Holoscope? Definitely. Stevens-Johnson syndrome. Chronic ocular environmental allergies? What do you think? Probably Stevens-Johnson, right? Stevens-Johnson is just gonna kind of cause it's like an irritation, like kind of a like papillary conjunctivitis, and you'll usually see membranes, right? With Stevens-Johnson syndrome. So the term chronic in kind of a follicular reaction is technically over four weeks, and somebody came up with this BAPMAP lap, kind of tried to try to remember them all. I never was very good at remembering these lists of things, but these are kind of all the ones that the main ones are gonna be viral, and then you've got like things like trachoma, like chlamydia, moluscum. You're always gonna want to look at the lip margin looking for moluscum lesions, and then there's a bunch of other random ones that don't come up as much. Okay, another question. So patients after hyphema, so they've had a trauma, they've got an intracular hyphema, are more likely to develop corneal blood staining due to all the following except. So what can cause corneal blood staining? Imagine like sickle cell trait, are they getting that? Because if the re-bleeds, it just kind of leads to maybe a prolonged course. So the idea is if the blood doesn't clear quickly, then you'll get it, or if they have high pressure they'll get it, or if they have some other endothelial condition, they can get it as well like these. And the method of injury has no bearing on it, right? Okay, alright, CIN. So you've got a patient that comes in with CIN, how do you treat it? What is CIN? So we're thinking this is some sort of lesion growing on the congenitiva that's in the spectrum of a squamous cell carcinoma, right? So you can have all the way from benign growths on the congenitiva, which are like a pinguecular atorrhagium all the way to squamous cell cancer, right? So that spectrum sort of in between those is a CIN. And you can have any variation of this. A lot of vets have this, so you'll see a lot of these at the VA. And you have to kind of decide, okay, how am I going to manage this? So you've got to the point on this patient where you probably want to do something. Does mitomycin C work for this? Not very well. You'd usually actually do what for it? What topical treatment might you do? So interferon alpha works for it. Mitomycin is actually not the treatment of choice for CIN. Mitomycin might be a treatment of choice for what other ocular kind of growth on the eye. PAM. So it works well for PAM, that melanoma kind of spectrum of pigmentation, okay? So you either have simple excision, which is the least good option up here. Mitomycin C, not a great option. So you've got wide local excision with topical steroids. It's going to help prevent what if you do topical steroids after this? Scarring, right? So it's going to be helpful a little bit. But what you really need to do is wide local excision with cryotherapy. And what's the term that they like to use for the cryotherapy technique that you use when you're doing cancer killing? So no touch for sure. But the cryo part, double freeze thaw. So what that means is that you freeze the edge of the conjunctiva where you excise this and you let it thaw. So you kind of just move all the way around it and then you repeat it. So you do it twice. And what that essentially does is it kills any cells that you didn't excise. And you're trying to excise everything that you can see. We haven't gotten to the point where we're doing mows for this on the surface of the eye. So we usually just, you can't really take, you know, like the classic for even four millimeter margins are kind of big on on some of these. And so you usually try to take a couple of millimeter margins on. Okay, another really crappy picture. I did it on purpose just so you know, because I feel like OCAP sucks at their pictures. And this is what they all seem to look like. They were all grainy and crappy. Okay, so somebody help me describe what you see just to kind of get an idea of what's going on. There's a classification at the limbis with a lot of vessels. Okay, so we got congenjection, maybe some whitening here, hallucinate that it's a little elevated to. So just right at the limits. No contact lens wear, no trauma. What's your diagnosis? You got to come up with something. And this usually the question will kind of help you sort of get an idea of what they're maybe leaning toward. So a little inflammatory lesion of the congenitiva, what type of hypersensitivity reaction is happening? Get a jump, get a jump even further. So these are usually in kids that they'll come in and they'll have this little elevated red spot on their congenitiva flictenual. Yeah, good. So flictenual is what kind of hypersensitivity reaction? Type one, type two, type three, type four, type seven, I don't know. So it happens to be a type four hypersensitivity reaction. So this is a little bit of a better picture of what they'll look like. It almost looked like a, like a necrotizing scleritis is what you're kind of like worried about initially. But it's going to be just almost like a little ulcerative lesion on the congenitiva. It reminds me of what like an ulcer of kinker would look like in the in the mouth. So we don't have great information about these because they can sort of just be anything that can cause this, but they can be infectious. So you have staff is probably the most common cause of them. And obviously, you're you're always worried about tuberculosis when you see somebody with this, you're asking about exposure and travel and all that kind of stuff. It's a, it's a lymphocytic sort of collection of inflammation. And so really, the treatment is topical steroids. And usually you do like it tobermicein or something with it. So like a toberidexerum, acetrol would usually get these to melt away pretty nicely. So if it doesn't seem to respond to this treatment, you'd want to culture it and kind of go from there and see if it's something else. But they're trying to get you to test for tuberculosis when you have a flictinule. Okay. All right, another funky picture. It's kind of blurry, but it helps you understand sort of what's going on. You can describe what's happening. What is this? The lower lid. Okay, lower lid. And we have what appears to be a large corneal abrasion. Okay, so we've got missing skin, right? Yeah, rolled up edges. It's a rolled up edges. What's this? Okay, so we've got the upper limbus here, right? Okay, so where is this going to be? Superior. So superior up underneath the eyelid, right? Okay. Shield ulcer. Okay, so good. So you kind of have to sort of take a step back and say, okay, where am I? What's the most likely thing that they're trying to give me to think of here? So if you have, if you take a step back and say, so what causes abrasions on the upper corneal or what causes the skin to break down in the upper corneal? So you talked about a shield ulcer, but a foreign body is a big one that they'll want you to think of too. Okay, so they're kind of the two made ones. So you'd always want to flip that upper lid and see what's going on up there. Okay, so this patient presents with the following finding after years of battling allergies, what is the cause of this finding? So which one of these is kind of an allergy type appearance, right? So if you look at these other ones, you could have any of these, right, recurrent erosions, it could be herpes simplex, it could be a traumatic epithelial defect, it could be a foreign body in the upper eyelid. But it's kind of that location of it being up underneath the lid in somebody with kind of an allergy type appearance or look. Okay. Shield ulcer. So vernal keratoconjunctivitis is a type one and a type four hypersensitivity reaction. They're usually young people. And we don't have a lot of them here in Utah, but we do get a fair amount of them. They usually present with just this really nasty, beefy, tarsal conjunctival sort of inflammation. Typically, it's better on its own. This is kind of your link to it. So somebody who has like a really bad sort of atopic dermatitis, they're going to kind of go down that path of trying to get you to think about more systemic issues. There's kind of two types. There's some that are just right at the limbo sort of involvement and then some that are more on the lids. So it's kind of this cobble stone papillae is kind of the big one. And they have these huge septic kind of in between them that separate those papillae out. Okay. So that's a vernal conjunctivitis. All right, Marshall. What's wrong with this guy? Major things are very floppy eyelids syndrome, potentially very large with acidity. Okay. So don't do this to yourself too much. But if you try this, you can't do it to your eyelids because your eyelids are normal, right? I try to tell patients like I can't like flip my eyelid over just by doing this. Whereas in somebody who has really bad floppy eyelid syndrome, you can. Right? Okay. So they're always going to think about what's the scariest thing with floppy eyelid syndrome. This patient has the font chronic medical condition, sleep apnea, right? So that's going to kill him because it causes pulmonary hypertension and heart disease and chronic oxygen deprivation. And they're tired at work all the time and they might fall asleep while they're driving to work. You know, so it's the thing that's going to kill them is the sleep apnea. And so that's what they're going to get you to think of. So how do you treat floppy eyelid syndrome, Marshall? I'm a steroid ointment like Mastrol, especially if they're having crusting of their eyes. And if they feel like the antibiotic ointment is helpful, but then they get crusting back and they can do eyelid surgery to tie them up, tie up the lids. I'm also a treat sleep apnea, okay, so what's the mechanism of their sort of ocular inflammation? What happens? At least what do we think is happening? Are you just getting under the lids because the lids aren't tightly opposed to the globe? And sometimes these guys, they'll actually like flip their lids will actually flip over, they'll get like tarsal plate inversion while they're sleeping. And so that they'll get kind of that chronic sort of mechanical irritation on their lids. For some reason, a lot of people with sleep apnea actually sleep on their faces. It's like the strangest thing. I can't breathe, and I'm going to suffocate myself at the same time. So okay, there's a ton of sort of other issues with this. So what, what's a cornea problem with floppy eyelid syndrome? Anybody know the cornea connection to floppy eyelid syndrome? I mean, I would think like some like lag maybe some just like surface disease like recurring. Yeah, you've got you've got all that kind of chronic irritation stuff, right? There's something different structurally with the cornea. So I don't know that we know the exact mechanism, but I mean, I tell my care to come this patients to stop sleeping on their faces to try to get keep their it's crazy like if you talk to young kids or like teenagers or 25 year olds with the care to come as they sleep on their face. It's like the strangest thing. I don't get it. Just like face down. Yeah. Like I don't know how you sleep that way, but they seriously sleep on their stomach on their face. And then they'll have like a little opening for their mouth. That would be a good approach. Okay, so this is a papillary conjunctivitis. There's typically no follicles. And you're not seeing like a filamentary caretitis with it. So it's kind of easily averted upper eyelids. So you have to touch your patient sometimes to kind of figure this out. And the underlying problem seems to be this decrease in elastin in the tarsal plate. So you've got obesity, sleep apnea, eyelid, rubbing, careticonis. So the treatment really is to protect that eye. So either wear a shield at night, take the eyelid closed at night, obviously do some sort of a lubrication on it. If you can just lubricate the inflammation will go away. Sometimes it does need a steroid to kind of calm it down like Marshall was talking about. Like chronic erythromycin ointment is not that big of a deal in a patient like this to try to keep some of that crusting away. And then you have this, what is the surgical lid tightening procedure where they call it? Wedger section. You guys ever seen one? Kind of weird. They seem like so, I don't know, invasive, but it seemed to work. Okay, it'll come back if they continue to leave things untreated. Alright, I give you a little better picture because I just have a really good picture of this. I thought it was a good picture. So this is a patient that I actually saw when I was fourth year, they showed up in my community clinic. And they had, they had lost vision over the last week. What was their claim? True or false? Completely false, right? No chance. No chance that you could have lost vision over the last week. I mean, I mean, maybe like right here, like you were looking down and had your, I don't know, but no chance of that. Okay, so what's happening here? What is this called? You have blood vessels on the surface of the cornea, you got blood vessels in the stroma of the cornea. It's kind of deeper, you can't really appreciate the depth of it. Some of these are superficial, but it's kind of full thickness in the cornea. So blood vessels in the deep cornea, I think I heard it. Inner, somebody say it? No, it's in the Okay, it could be that. But this is interstitial keratitis is what they're trying to get at, just kind of deeper, deeper blood vessels kind of growing in the cornea. You'll also get them up on the surface too, even if you have that deep vessel kind of growing. Okay, so patient presents with the following condition. What is not a cause of this condition? Good. So thyroid eye disease can cause chronic eye irritation, right? It's usually just going to cause kind of a kind of like a marginal neobascularization that's right at the edge of the cornea. But interstitial keratitis can be caused by so you're thinking something that causes infection or really bad inflammation of the ocular surface. So a chemical burn can do it. I actually have a patient that's like, it's one of the most challenging cases that I've ever had to deal with, who drank, fell asleep, was like passed out on a heating pad. And so he fell asleep on a heating pad on his face somehow. I don't know why he had it on his face. But he burned his eye. So it was like a thermal keratitis and it caused interstitial keratitis, the deep vascularity of the cornea. Syphilis can also do it. So thyroid eye disease is the one that does not do this. Okay, so interstitial keratitis, the one that they love to get at is this syphilis congenital is most likely bilateral. If it's unilateral, then it's more of an acquired syphilis later in life. You have this Hutchinson's triad with congenital syphilis where you get the teeth abnormalities and deafness as well. Tuberculosis, HSV, Lyme, these things are always something that you should have in your differential when you've got theobascularization of the cornea. And then you have this Kogan's sort of triad as well, maybe quad, what do they call it? We have vertigo today just hearing loss, so it's involving the eighth cranial nerve. Other less common causes, you have to kind of think about all these things, but it's usually something that you don't really come up with a diagnosis on and you treat them for a viral keratitis just to cover them and then how are you going to treat that? How are you going to get rid of that? So they might present this to you and say what are the treatment options for this? Steroids to start off just to see if you can kind of calm down that inflammation scarring, but I think it eventually requires a PK. Yeah, so you have different options before that that you could try. So steroids is kind of the mainstay is to try to just calm down any active inflammation. Active inflammation is what drives new blood vessels to grow and so you can probably get some of this stuff to regress that's kind of on the edges. These big vessels are probably not going to regress with topical steroids, so what could you do to these big vessels? So you can burn them, so what are the methods of burning a vessel? There's a couple of different ones. So you can do pottery, right? Is there anything else? You could do some in clinic. I do that in the OR, but you could do it in clinic. You can do some with a laser, so you can use an argon laser to actually ablate them and that again may not work on a big vessel but it would probably work on knees. You could ablate those vessels. Okay, what else could you do in clinic? Are there medicines that you could use? Maybe. What did you say? Well, that's a temporary thing. Like maybe you put them on lumefi, alfagan, some to kind of close them off. What about what causes, how do we treat neobascularization in other parts of the eye? Anti-veget, right? So you could do, so a vasin is actually kind of approved for this. You could do subconju vasin kind of in this area, which is what I ended up doing on my thermal burn guy and it worked okay. It didn't work perfectly but it regressed the vessels pretty well. So you might do a series of three over the course of three months and see if you can get it to regress. They typically come back. It's not like, I don't feel like it's like the retina issues where you can actually get it to go quiescent over time but maybe you can't eventually. So you've brought up an interesting one, is mitomycin C, which you could potentially do that topically to kind of help it. But there was a guy just recently who actually took a cannula or a needle and injected mitomycin C into the vessels. Like he actually cannulated the vessels and injected it and it actually made it pretty much completely go away on a case that looked pretty similar to this. Not published yet, not really widely agreed upon it, that's okay. Because if you inject mitomycin to the stroma the cornea probably melted but he claims he got right into the vessel. So kind of an interesting one. There's other sort of vascular surgeons that will actually go in and sclerose vessels by injecting like a soap or something. So you could put like a, I think it's called like saponification of vessels. So you could potentially do that. But these are tricky because you may end up needing a PK. What's the problem with a PK in this setting though? So the vessels are going to be right at the edge of the graft. So it's probably going to regrow but rejection right? Super high risk of rejection in that setting. So you'd want to try to calm these down, get them to be as ghost vessels as you can before you go in and do a surgery. All right, what do you got? This right here. We put a picture on OCAPS for this. It's really bad. Looks like a white iris too. So really light iris. Should the limbis ever look like this? You should never have pigment on the cornea, right? Yes. That's a reflection. Okay good. Okay so the patient has the following finding. That's what I think that's the exact picture from OCAPS. That's crazy. You went and found it. I remember having a picture that looked pretty much like that. Okay so the patient has the following finding. So the PSC cataracts, they have hypertension, they have splutter hemorrhages, they have decreased the riloplasma. Increase the riloplasma. So what's the disease? Wilson's. Okay so Wilson's disease. I want you to come to the bedside and see if they have the Kaiser flight. I've tried. So they actually do have decreased the riloplasma, increased copper. So it was that one. And they have this sunflower cataract. So it's copper deposition in. That's a maze memory. Okay that's kind of the key. And then the treatments they'll sometimes get into and it actually does go away with adequate treatment. That's another item that might show up on the test. If you have a Kaiser flight sharing it's not just in Wilson's disease. There's actually some other really weird things that can cause it to. But it all has to do with that suruloplasma that kind of binds to copper. Okay uh I forgot my picture. But I don't think you need to know. You're not going to remove any else, right? So patient at this lesion removal kind of line would be present on the corning exam. Okay so fly string is in what? We said this fly string, like the Kaiser fly string. So this one's different. So the keratoconus. So that's a that's a round iron deposition in just kind of around the apex of the cornea, right? So it's going to be displaced a little inferior with keratoconus. Okay a stocker line is a teridium, right? I have a really good picture of this and maybe that's I might have fallen asleep trying to find it. But and then what's a ferry line? That's the bleb. So I always think of a ferry being water and in blebs we're kind of dealing with water trying to move it around. And then the Hudson stolly line is just like I just think of like a Russian with like this straight line or something I don't know that just like it's just just above the lid. It's where the tear film kind of just deposits a little bit of iron. So it's like a a millimeter or two above that lower lid margin. Okay did everybody have good breakfast? Maybe. I almost did when I saw this. Seen this before. Disaster. It's one of our own patients at the Moran. Okay so V1's Oster. So what makes you think this is Oster not something else? Like because what are you gonna use on this to kind of determine I mean I'm just a test to say this looks like Zoster compared to other issues with it. It doesn't cross midline. So yeah the biggest key is if you draw a line right up the nose there's nothing coming across. Okay and then the other thing is that if you take it and you kind of say okay V1 is typically sort of out here at the lateral canthus and goes up this way sometimes you'll be a little bit crossover in that lower lid but you're typically not getting much lower lid involvement right. So lower lid actually looks reasonable and it's mostly just this upper lid right on the forehead. I had a patient one time that came in for she had supposedly been splashed by a chemical at work and she was trying to get disability from her work because she was suing them and she said that somebody had like sprayed a chemical on her and she developed a rash and the rash was on one side of her face like you look up at her she's like I got stuff in my scalp all over it it was literally just like inner hair one side face one side nothing over here nothing up here so you have Zoster this is not a chemical injury it's Zoster because it's that dermatomal thing okay so that's the key to it. I had a patient yesterday presented with V2 Zoster just like right here. So what are you worried about with Zoster? There's a lot of things but can you give me the rundown of what they're going to test you on what things they're going to be worried about on an exam? So clearly the cornea is involved here right? I don't know if it's involved because the lid sucks or if it's actually infected but the cornea is hammered. So intracular involvement too right so you could potentially get a UBI this or R in the retina so you're having to dilate them and try to get a look back there. So you're going to deal with all the eye issues okay so what else? I mean you want to worry like think about their just like systemic immune status as well that they're immunocompromised. So is this a disseminated thing? Are they altered in your clinic or are they having a hard time like understanding what's going on? Do they seem like they're they've got it going on and centrally like CNS involvement right? Okay you're going to check their pressure for sure what if they're saying things just sound muffled to me? Yeah so you can get the Ramsey Hunt syndrome where they've actually got cramps or eight involvement which my patient yesterday I was she was like I'm having like I feel like it's muffled. I said to her how's your hearing those muffled. Have they done anything about that? What are you going to do for that? So they'll actually test hearing so they'll actually do hearing tests to kind of see what the frequency of their hearing is doing and they can kind of follow that over time but you're going to treat it with what the thing is steroids for that part of it. So she was on Valtrex on an appropriate dose of Valtrex. She'd just been diagnosed like two days before I saw her. She had a prodrome of symptoms which is sometimes really challenging to figure out. So I've actually missed it. I had a patient that came in that was like complaining of swelling in her cheek and it just felt like tight. She didn't have any lymph nodes that were positive. I wasn't sure what's going on. So when I was a fellow she came in the next week with just raging disaster and this patient presented the same thing. She went to insta care. She had a swollen cheek kind of around her ear just felt funny and then like two days later broke out in a disaster. So you've got to watch out for the hearing part of it along with it. So okay so what's the optimal treatment for this patient? They only have eye involvement or something else. Nothing right just watch them see how it goes. Surgery of the bereavement maybe this is like a necrotizing fasciitis again that midline idea right? Try to try to look for that midline to get that out. So obviously we're doing oral maltreks and then kind of a little threshold to use oral steroids or something like this probably with how bad it is once they've kind of got appropriate coverage of the antivirals. So maybe like three four days into it. Other considerations long term with the disaster? Neurotrophic. Yep so neurotrophic pain is probably or neuropathic pain whatever you want to call it. It's probably the it's probably the biggest long-term consequence of having zoster no matter where it is and and how do you prevent it or what's the idea if you do something you might be able to minimize the risk of it or I mean GABA I know. It's really getting an antiviral started in the first five days is kind of what they think. So and then you may treat it with like a GABA pen. Let's keep out the detection for zoster attention. What do you do? I don't know if it does it for eyes. Oh I don't know. Could be. I'm not sure on that one. Okay so this is kind of a weird one where they'll have they'll come in with the a dendrite antiviral pain. It's kind of a weird thing. HSV usually causes pain compared to zoster. So zoster has asymptomatic dendrites. It's kind of the way to think of it. So they don't even know they have them. Their vision might be slightly blurry. But the the treatment for zoster keratitis is essentially on the steroids. Okay we're trying to figure out if if chronic antivirals help but we don't know because we don't have a good enough study on it yet. I tend to keep my patients on it for a little bit longer than the two or three week course that's kind of recommended. And then you've got all these other things that you have to think about here. Is it random there's seven or facial paralysis Ramsey, huh? Well confused now. Which ones that I thought that was the hearing one? Occidental one. I think. Eight's the vestibular nerve, right? Yeah. Sorry, the vestibular. Seven is facial. I forgot that. Seven is facial paralysis. And I think that is Ramsey, huh? So you got to watch out for eight involvement too. Okay, so this is kind of the treatment that you have to come up with. So it's either you're kind of going high doses here. So 800 milligrams, five times a day. Fambier 500, three times a day or Valtrex one gram TID. It's kind of full treatment dose. And if you can get that started within the first three to five days, then you lower the risk of their chronic pain afterwards. Which can be really debilitating that. Okay, so trying to figure out dendrites and appearances between that dendrite versus pseudo dendrite. So this is trying to say, okay, is this HSV versus VZV. So the dendrites and HSV just look clean. That's kind of the way that I would think of them. It just looks like a perfect branching lesion, like this one up here. You get the base that stains well, forcing the edges with Rose Van Gaal. That's what this is trying to get out here. Whereas a pseudo dendrite is just like blunt ends. So it just doesn't look, it just kind of looks fuzzy on the edges. And you tend to get a little bit more of the geographic ulcerations on this too. So it may not be a perfect pseudo dendrite. And then not really great stain on them. And then steroids here, you're not going to treat it. Here you are going to treat it with steroids. So, and I'm usually pretty chicken about this. So I don't start the steroid initially on first presentation. So I might wait a week to get it going. All right, another blurry picture. But I think this is actually a pretty good photo picture. I think you can tell what's going on here. So somebody describe this to me. It's a ring infiltrate, hypopion, the eye is very injected. Okay, good. So lots of conjection, hypopion. You got that flat whitening that's a hypopion layer out of things inside the eye. And then a ring. So it's dense around the edges, a little clearer in the center. Okay. So what do you think? 26 year old contact lens wear, 10 out of 10 pain. What treatment is most likely to lead to success? So we're going to get the pool cleaner going. Core hexadine. So corneal scraping. Maybe. Is corneal scraping a treatment for Akanthamoeba? Absolutely. Yeah. If it's epithelial. So you can actually cure somebody of Akanthamoeba if they present with epithelial Akanthamoeba only by scraping them. But it can be, it's really challenging to diagnose someone there at that point because there's nothing that's kind of leading you to say that's what it is outside of what can you get to kind of help you know. It's confocal, right? That's the only thing that's going to really help you know this is epithelial Akanthamoeba this deeper stuff. There's no way you're going to get that out by scraping. Okay. You're not going to be able to debulk it. So don't even, don't even try. You do have to try to scrape it maybe to get a diagnosis. Kind of get deep in there and see if you can scrape it. What about this? What's wrong with the PK? They actively have it probably recur. Yeah. So if you look at this, like where is there Akanthamoeba? Who knows, right? It could be anywhere. But what, what if, what if it's out in the sclera? What if you've actually got infiltrated into the sclera? It's across the limbis. Then what are you dealing with? You're probably dealing with the death of the eye. It's pretty much impossible to treat. You may have to go on to like radiation or cross-linking of it with collagen to try to, try to kill it. Like it's just, once it gets into the sclera you're pretty much, pretty much host. So here you could argue that you could do a PK to debulk it, but you're kind of huge risk of it reoccurring in the PK, which isn't the end of the world because sometimes that gets you a little bit ahead of the game because you're probably going to have to do a PK anyway. But these can be really challenging cases. But yeah, it's going to be chlorhexidine. It's kind of your main treatment. And then you've got other, other medications like PHMB, Roline. There's oral medications. Sometimes you put them on like IV medications as well to kind of help with it. So if you look at all the different sort of issues with Akanthamoeba it's really, it's a trophozoite. It has these epithelial cysts, which this is where you can actually cure it if you can get this, if you can get, get it out at that point. As soon as it gets into the deeper kind of ring-shaped infiltrate, then you're probably ending up with a PK because it's hard to get it to completely clear. Convocals are really your best treatment. You can get it to grow on this fancy line here that's always on OCAPS, this non-nutrien agar with E. coli overlay. They're double-walled cysts, which is what you're looking for on the Akanthamoeba foal. So if it's superficial, theoretically, you can de-bride it and it will go away. Again, it's rare because you have to have a really low suspicion for it. High suspicion. High suspicion for it, but you probably have a low suspicion for it. Again, you're usually using chlorhexidine and HMV. Rolling is something that you can technically get from outside the U.S. It's becoming harder and harder to get it to come in, but you used to be able to just get it on Amazon. If you look at the bottle on rolling, it just says for minor eye infections, which is fantastic because we use it for the worst eye infection that we get in the U.S. And then there's all these other treatments that you can use as well that seem to have some sort of benefit. So this is a patient that I saw at the Marin with a really tricky clinical course. I thought she had, she actually presented with an endothelial plaque on her cornea, high-risk contact lens wear, but it just looked like an endothelitis. So I treated her like it was a viral keratitis, kind of got a little better and then a week later presented with this really dense hypovion. And I was like, that shouldn't happen. So I kind of took a step back and was like, what could be causing this? She had almost like a little mild infiltrate in her cornea. So I started her on broad-spectrum antibiotics and she came back and she was worse and her pain was always like 10 out of 10. And she didn't really have a lot of epidefacts. So it was like just really confusing. Did this confocal on her and then so it kind of sealed it. It presented like a viral keratitis and then ended up being a canthamoeba. So these are the cysts that you'll see in the cornea. What's this? What is this linear thing in the cornea? And there, yeah. So this did, this should be actually pretty clear. This is actually a good picture, but it's not very clear because it has pareneritis. So that nerve will kind of look like it's just not crisp. Have you ever seen pictures of corneal nerves? They just look really thin and crisp. So this one's got pareneritis. And for whatever reason these a canthamoeba cysts will tend to like line up. So you'll kind of get a marching out kind of lining up on the confocal. So amoeba cysts there. You can get these subbomans cysts which is what these are. And then pareneritis. Okay. So I've probably managed like four patients with a canthamoeba in four years. So it's not terribly common, but they're awful. So she ended up patient that presented for me ended up with a PK and then a repeat PK. And she showed up as a nurse in the OR one day at Marin and was doing fantastic. Love and life. But okay. Does she have a good reason to have an eye infection? So she was kind of an interesting one. She did wear contacts, but she was actually pretty good at her contacts. She was she wasn't really sleeping in them. She was a nurse of the Huntsman, I think at the time. But she took a trip to Mexico and she was swimming in them some and she was showering with them in. And so I think we think it was just the water source in Mexico. There she go. So that was the other hard thing is it was like you don't have a great reason to have a contact lens keratitis. All right. What do we think here? Keratoconus. Good. So that's kind of what you have to jump to. It's like I see a picture it's keratoconus. Okay. So then you take a step back and you say they can ask me a trillion different things about keratoconus. Keratoconus is a disease that you just have to know front to back, back to front, up and down. You've got to know everything about it. Okay. Those big ones you just have to know everything about it so that they don't fool you. So 28 year old with increasing caretometry readings. What's the recommended treatment? So what are where they trying to get out here? Stabilize it. It's progressing, right? Progressive, unstable keratoconus. There's an FDA approved treatment for that now and is it intact? Is it a PK? No, it's collagen cross linking. So they want you to cross link these patients with unstable keratoconus. So all of these are treatments for it and even this in some cases if they've got that floppy eyelid problem. What if they're not progressing? So if they're not progressing you can cross link them at least currently because you have to prove progression for it to be FDA approved. But some people argue that you should cross link anybody who presents with keratoconus. But yeah, they're not progressing you just follow them closely until they do. You can do in tax for non-progressive keratoconus. You can do PKs for non-progressive keratoconus. There's kind of two different ways that I manage keratoconus. One is vision. Okay. You got the vision pathway. How do we get your vision better? Glasses, contacts kind of in tax potentially. And then the second pathway is how do we keep it for progressing? And some people think that if you put them in hard contact lenses it's kind of like this suspender that you're putting on the cornea to kind of help it. It doesn't work. So the only treatment for progressive keratoconus is cross linking. If it gets too bad that you can't cross link them then you're looking at a PK or a Dalker some sort of a cornea transplant. Okay. If you ever do for someone who has progressed so bad that you need to do a PK do you do a PK and then just like do cross linking? Because you recur in the graph a lot of times. Yeah. I mean it's been looked at. It doesn't work as well as you think it would because you're trying to secure that kind of graph host junction with the cross linking is kind of the idea because that's where it usually recurs is kind of in that lower portion. But it doesn't seem to be that effective so you still can get progression but potentially yeah absolutely that'd be the way you do it. So we try to create a pretty good scar inferiorly with Kariacona scraps. So you try to be long sutures and then you try to really tuck that cornea down so a shallow pass through the donor deep pass through the host to kind of keep it keep it low so you're not getting donor elevation. And then I usually I try to keep those sutures in longer if I can to try to help help a scar down because that's the area where it's going to protrude the most. Okay so Kariaconas is typically bilateral. You have all these systemic things so that's why they're going to they're going to hammer you on these systemic things. Down syndrome patients are really common other connective tissue diseases like aero standalone smart fans. There's tons of ocular associations with it. It's this inferior steepening with abicle thinning. You got the fly shearing the boat straight. You got prominent corneal nerves. I mean there's just tons and tons of stuff to that are testable on this. So that one was this sign here months in sign. And then hydrops is another one that though they'll try to get you to do something risky on. So when somebody presents with hydrops you're not you're not treating them with pk initially and it's not an infection. So that's the hard thing to kind of figure out. So they have an infection as it's hydrops. They have a history of Kariaconas. It's most likely hydrops and then you just kind of watch it. It's mostly just supportive care initially. Some people will put an air bubble in the anterior chamber. Because what is hydrops? Decimates membrane is actually ruptured from the stress of that corneal kind of protruding forward. And so if you can put an air bubble in there you can potentially replace decimates membrane quicker. So it seems to help. I don't like to do it in somebody's faking because you're probably going to push a cataract forward unnecessarily. And I usually just watch them. And they'll usually this is where you'll end up with an apical scar is after they've had hydrops. With Kariaconas. That last one apical or aqueous suppressants. It doesn't show up on that. I don't know why that one. Aqueous suppressants possible to counterlare. Why do you do aqueous suppressants? The idea is just if you have high fluid in the eye pressure in the eye you're going to get more fluid rushing into the corneal all the time. So the idea is if you lower intracutal pressure there's maybe that less of that dry for it to push into the into the stroma. But I usually don't I usually just cycle pleasure for pain. Maybe use a topical steroid muro. That kind of stuff. Okay, so you've got the kind of the different findings here. So that's a bad apical scar. These are hopstriae. No. They're vertical boatstriae. That's Monson's sign and then the Kaiser. Or sorry, the Pleasure Ring is what that's trying to show but that's pretty hard to see. All right. You love cornea for these because they're really easy if you can recognize the picture. Because you've got a memorized. So what is it? So granular stromal dystrophy, right? So you've got these little salt granules, sugar granules wherever you want to look at. They're centrally located. Spare the limbis. There's intervening clear spaces. Okay. Which thing would be positive on pathology of penetrating carotoplasty? Granular gets her man. Granular has what substance? Highland. Stains width. Monson trichrome. Okay, good. So you've got to have this down. There's usually three or four questions related to it on test because it's just so easy to test. So we won't spend a lot of time on it here but. So you've got macular. I just wanted to show you the pictures. So there's another picture of macular dystrophy with the Highland material of Monson trichrome stain. So the difference between macular. Or sorry, I just said that completely wrong. This is macular. So that one is that it extends limbis to limbis. Yeah, it's a little bit broader involvement. And there's not really, there's clouding in between them. So that's kind of the key is that there's clouding between the spots. Whereas with granular, it's super clear between the spots is kind of the idea. So it just kind of looks mushy with macular. Macular is mushy. So macular has what? Sorry. Merlin Monroe. Mutual. Quality sector. Really. Possessive. Possessive. All. Option blue. Always, really always. Right, let's get started. Yeah, option blue. Sorry, confusion though. So there's the granular. And the stain for it. Okay, and then lattice. So lattice you're just thinking linear lines like cracks in the cornea. And there's lots of associated, all right, I hated lattice because they could test you on tons of different stuff with lattice. I felt like, oh, it's lattice. And then it's like, I don't know what you're asking me because it's a little bit of a trickier one because there's all these little like different types here that can be involved. All right, so what does this patient have? So you can see these little dudes, these plateaus here on what membrane? Desiree's membrane. What's kind of missing? Back here. Okay, so there's not a lot of endothelium. There's a few. So the endothelium can't grow over the top of the gutata. So they're kind of stuck in between here. And then this is actually some pigment granules in between. So you can sometimes get a little pigment deposition in Fuchs dystrophy. What do this patient have? What surgery? It's not a path slide. They have some surgery. Yeah, PK, right? There's stroma here. So they've had a PK. Which is not how we treat this anymore, right? How do we treat Fuchs now with the surgery? DSEC or DMEC? DSEC or DMEC. So a DSEC is essentially going to be probably about this thick this on here. So it's about 60 microns thick of some stroma. Whereas a DMEC is what layer? It's only decimase and endothelium. So it's going to be super thin. Okay. So this patient presents with a following complaint. Constant burning. Blurry vision in the morning. Blurry vision with reading. Blurry vision late in the day. Morning, right? That's super high stress on the corneas when the eyes closed. Creates this fluid filled cornea in the mornings. So it takes them a while to kind of wake up and get that fluid pumping out. How can you help it along? What are some things that you can do to treat that? If they're just presenting with morning blurriness. So Muro. So this hypertonic saline on the surface draws fluid out from the front. Okay, how else? You can use a hairdryer. Ouch. A hairdryer in front of you for a couple minutes. That'll help kind of dehydrate it too. So Fuchs is another one of those that you just have to know everything about it because it's just such a very, it's very common and highly testable. So it does cluster in families. It's probably autosomal dominant but we don't really know. But you definitely see it clustering in families and it seems to have that little kind of I forgot what that's called the lead bias where you like younger people have a worse. What's that called? Anticipation. Doesn't sound right but we'll take it. Trying to put it to repeats. Yeah. So polymegetism can sometimes be the way that it presents where you've got large cells or pleomorphism where the cells are actually different shape. So sometimes you can get what's called guttodalus spooks. In that condition they might see that decimates membranes just a little bit thicker on the path slide. Or endothelial cell counts you might be able to tell that there's there's weird shapes to the cells and stuff. Okay what is this? So anytime you see something white growing on the surface of the cornea what should you think of? You should think of cancer right on that spectrum. Squamous cell all the way to potentially a mild tritium. Right? Tritium to squamous cell. So once you get into an abnormal tritium you call it a CIN. And so this is a picture of a type of CIN. So you can almost get like a little papillomal with it these kind of fine little vessels that are kind of growing around here too. Another appearance, same thing right? White plaque on the cornea leukoplakia. You're thinking CIN to squamous cell. Another one, same thing. CIN to squamous cell. We call it ocular surface neoplasia because we don't know what it is. CIN is technically a pathologic diagnosis. Squamous cell is too so what about this one? It looks like a pretty regular tritium. I probably would send this to the pathologist just because of that spot right there. It looks kind of funny. So I usually don't send tritia to acrimanulus but if they have something funny about them they've got like some gelatinous kind of something going on or the surface seems a little leathery where they've got white spots on it. They don't send it. Another one, same thing right? So typically we might actually try to debulk some of these with the topical interferon especially one that looks like this that's really angry blood vessels around it that's going to bleed like crazy. Those are huge and so I might try topical interferon to see if we can dump this away. Same thing just lots of different pictures of the same thing. Same thing. Yes, no probably not. I think it's probably just a pinguiculate but there's there's a couple little spots here that it's like well maybe that's something I don't know I'm not going to do anything about this other than watch it. It's in the slide deck so somebody took a picture of it but it looks like a pinguiculate to me. What about this one? A little more subtle you might actually gloss over this one because it's not that angry looking but you got this little teeny tiny patch right there again something I'd probably just watch or potentially treat with topical interferon if you can get insurance coverage. Same thing? No. All right what's this? Dermoid. All right so this one looks kind of scary because it's like right at that pupil margin even though it's a 2D image it probably looks pretty it looks pretty deep to me I don't I don't really like this. How are you going to treat it? First step not the last think of the first step Oh we'll head treat the amblyopia treat the astigmatism amblyopia that's the first step but you're probably in a kid you're probably going to go after this because this one's going to be pretty debilitating there's another one there Dermoid so they love to have these weird associations like with golden hars where they have these pre-illicular skin tabs tags and other stuff go on but it's mainly it's this corneal astigmatism so you're going to excise it but these are usually pretty deep so you're not probably not going to get rid of all of it and you always have to have a graft ready just in case it gets too deep you're trying to just shave it off so that it's sort of playing out with the rest of the cornea but like a shaved dissection is what they call it but sometimes you have to do a little mellar implant by a transplant really crappy picture what do you think they're trying to show you you almost have to guess sometimes what you think they're trying to show you you have this yellow area up here dermalipoma so this is a corastoma you have the hammer tomas corastomas that will sometimes come up on the test you have to kind of remember those but it's mostly just kind of watching something like this or treating it with excision the other thing that can kind of look like this is if you have orbital fat prolapse where you've got fat kind of coming up from behind the septum there and then this one kind of all these kind of dermoid type things this is a dermoid system you remember they're always in a suture frontosalumatic suture is the most common one so these you would either leave them alone or excise them I think if it's causing too much distortion of the lid or if there's some sort of cosmetic reason to remove them so we're out of time 7.59 just ways to think about cornea they just jump a lot is this sort of the format of the op-camp questions? sometimes so I was surprised because I thought I thought it would be more like op-toe questions where you've got this long question stem and then you got a you're kind of logically kind of stepping through this question but I think they're more like this it's more like churn really what? the churn he has ever used churn so they're more questions that are literally like like short stemmed so it's literally like one, two, three lines with a picture okay so they're like kind of a multiple choice or a couple of paragraphs which is really nice the hard thing was is it's like I need in a lot of cases you're like I need more information to be able to decide but you just have to kind of go for your best guess