 A lot of kind of basic things about cornea. Just feel free to stop me at any time. So I'll go over the basics of corneal anatomy, pathophys, some basic slit lamp techniques, and really common corneal conditions that you'll see primarily on call and also in the clinic and then some special cases, most particularly with burn unit pathology, which you'll see here. So as you know, cornea is an avascular transparent tissue that measures about 11 to 12 millimeters horizontally. And it has a orientation that's called a prolate kind of configuration where it is actually steeper kind of in the center part of the cornea and less steep in the periphery, so it's termed prolate. If a cornea has undergone, say, myopic cornea or refractive surgery, it will become flatter in the center or steeper in the periphery, and that's termed an oblate cornea. And the cornea has a very high density of nerve endings, which is why, when there's any sort of injury, it's very, very painful. So this is a cross-section of the cornea. So the epithelium has about four to five cell layers thick of stratified squamous epithelium that's held together by tight junctions. And then there's a base of membrane to this epithelium, and then there's an unlabeled structure underneath that's called Bowman's layer. And this is an acellular structure, which is sometimes called Bowman's membrane, but it's not a true membrane. It's actually acellular. The bulk of the cornea is comprised of the stroma, which has several caratocytes, which have to be specifically arranged so that the cornea can remain transparent. And also it needs a very tightly regulated kind of concentration of water so that it also remains clear. The endothelium has an endothelial cell which pumps out fluid out of the cornea to keep it clear. And the basement membrane to the endothelium is decimates membrane. So this is a true basement membrane. Bowman's membrane isn't really a real membrane. All right, so next, the tear film also has layers. There's a top lipid layer. Then there's an aqueous layer and a bottom mucin layer. And the top lipid layer is produced by the mybomian glands and the eyelids. And this is responsible for preventing the tear layer from evaporating, so it's very important. And we'll talk about conditions where the mybomian glands can be affected. The aqueous layer comprises the main bulk of the tear film and is produced by the main lacrimal gland and also the accessory lacrimal glands of crows and wolf ring. The bottom layer is the mucin layer, which is produced by the conjunctival goblet cells. And it is very important to actually allow the tear film to stick to the oculose surface, because otherwise the tears would be made. They just fall off the oculose surface and they're not really hydrating the oculose surface. And the mucin layer is stuck down to the oculose surface, to the epithelial cells, as shown here. Again, this is kind of a potpourri of various topics in cornea, so we're going to switch gears to slit lamp exam. And here are the common techniques for examining the eye. So usually, when you first start out looking at an eye, you want to start with kind of a lower mag, not super intense light, kind of a broad beam of diffuse illumination. This is just to get an idea of is there anything there that I need to concentrate on. So just kind of get a broad overview. So then you can get down to slit lamp illumination, where we actually have the beam at a slit and at an angle. This allows you to see depth, and you can go on high mag to identify more subtle findings. So diffuse illumination and slit lamp illumination are, by far, the most common techniques that are used in the slit lamp examination. Specular reflection is most commonly used to examine really fine details around endothelium. So what's done is that you have the beam at a very high intensity at about a 60 degree angle. And then you kind of have to superimpose the light bulb reflex with the actual slit beam so they're together. And then you focus in, and you can kind of see reflections around the very bright light to look at endothelial cells. Sclerotic scatter is a method where you, again, have a very intense, bright beam at an angle. And you shine it right at the limbus. And you have it at such an angle that you can actually light up a little bit of the whole cornea. And so this picture is showing a light corneal scar here that's lit up by sclerotic scatter. So the scar isn't like, the beam isn't really on the scar. It's just kind of highlighted by light that's scattered from the limbus. Retrolimination is something that I use fairly commonly. Most commonly, I use it to look at iris defects. So this is showing some diffuse iris defects here. So it's a good way to look at to see whether or not you have a patent peripheral iridotomy. You can also see fine details in the lens and the cornea with retrolimination. And what you do is you have your beam kind of straight on into the eye, going into the pupil. And so what reflects back, you can see kind of reflected back here. Corneal stains, most commonly, by far, we use fluorescein. It comes in solution or strips. And this stains basement membrane as shown here. Rosebengal stains de-vitalized cells. And it's easy to see not only de-vitalized cells in the cornea, but also the congenitiva. Listenin' Green, I probably would use rather than Rosebengal. It does the same thing. It stains de-vitalized cells, de-vitalized cells. But it's much less irritating than Rosebengal. Rosebengal, people feel it actually stings even with topical anesthetic. Listenin' Green doesn't sting quite as much. And you can see the very, very green highlighting some congenitiva is staining here. Kind of this is, I'm sure you guys know this on call, but just to review some miscellaneous exam things, especially on call. So you want to remove soft contact lenses prior to instilling any fluorescein. So you always want to ask the patient just to be sure. You want to keep track of your properacane, tetrachane, and your fluorescein solutions because patients can steal them and leads to topical anesthetic abuse. Anyone with, especially like a unilateral red eye, you want to flip their upper lids. In fact, someone with corneal abrasion will flip. Sometimes you're surprised by what you find underneath. You might find a foreign body or some other cause of their corneal abrasion. So I'll go into some common corneal and congenitiva issues, both acute and chronic. So conductivitis is classified typically into three categories, bacterial, viral, and allergic. And there's various bumps that you'll see on the tarsal congenitiva with the various conditions. With bacterial congenitivitis, typically, you'll see a very purulent discharge. Follicles are shown here. These are actually clusters of lymphocytes where you see kind of the vascular, vascularity kind of surrounding a follicle. So you see the vascularity kind of on the periphery. And you'll see follicles typically in viral congenitivitis. And in viral congenitivitis, there's typically a history of either upper respiratory symptoms or sick contacts. And they'll typically have the symptoms in one eye and then it goes to both eyes. Papillae are shown here. So papillae are actually dilated capillaries, which kind of are in the middle of each bump, of each papillae. And then each capillary is surrounded by edema. So follicles, you see the vascularity in the periphery. In papillae, you'll see the vascularity in the center. And you'll see papillae typically with allergic congenitivitis. Oftentimes, you don't get a nice classification like this where you see all follicles and all papillae. It's common to see a mixture of both. So you don't always get this nice distinction, but if you do see kind of a bigger concentration of either the follicles or papillae, then that'll kind of clue you into what the diagnosis is. And this is an example of giant papillary congenitivitis, which is seen commonly as a reaction in contact lenses. So again, very important to flip the upper lids because you could find something like this. Next is episcleritis. So this is defined as a benign transient inflammation of the ocular surface in episclera. The history is that they'll have, patients will have a red eye, but there's not really much pain. It's pretty minimal if there is any pain. And on exam, when you put in some phenyl ephrin, it typically will blanch. I don't usually work up episcleritis patients unless they are recurrent. It can be associated with autoimmune conditions as well as other conditions here. So here are some systemic associations. Again, these are kind of single digit percentages of systemic associations with herpes zoster, cauldron vascular disease, gout and syphilis. So you can check lab work if needed. Episcleritis is typically self-limited so it can actually go away without any treatment. But you might consider some PO NSAIDs or some topical NSAIDs or steroids to maybe speed the resolution. Contrast, scleritis is something that's very different. So in scleritis, there is typically very intense pain. It is very, very tender. So you can also, you can push, if you're not sure if you have got scleritis or episcleritis, you can just kind of push on the globe through the lid and ask them if it's tender or not. And with scleritis, it's gonna be, they'll be jumping out of their seat if you do that. When you put in fennel efferent, there's typically no blanching scene. And there are a few types of scleritis here. You got non-necrotizing, necrotizing without inflammation or scleromalacia perforants, which is actually painless. It's the one type of scleritis which is painless. And then you have necrotizing scleritis as seen here is where there's severe thinning of the sclera. And this is typically seen in Wagoners, which is poly-antiitis. I can't remember the new name for it. And scleritis is a very, very high association with systemic disease. So yeah, here are the systemic associations, which are arthritis, lupus, and closing spondylitis, psoriasis, Crohn's, vascularities, syphilis TV is always on the differential. With scleritis, you always want to work it up, even if it's a first time episode of scleritis and you can use history to guide testing seen here. Occasionally, if the labs are negative, you could consider repeat testing in one year. With non-necrotizing scleritis is the least severe form. You'll see a violacious hue. And there is a 50% association with systemic disease and 50% of cases are bilateral. And this does not go away if you don't treat it. So it's gonna remain until it's actually treated. Sclera and malatia perforans, again, this is the type of scleritis that's without inflammation or it's actually painless. So you see a painless white, quiet eye within sclera, typically seen in the elderly. It's very typically bilaterally. 50% of these cases are actually for rheumatoid arthritis. Scleral rupture is rare and it rarely needs surgical repair, but there does need to be, obviously, systemic immunosuppression, which I'll talk about later, I think. Necrotizing scleritis with inflammation is painful. It's bilateral in most cases. This is the most destructive type with vision loss and 40%. High association with systemic vasculitis. And the mortality rate of this is high. It's actually 20% at five years. So it's really important to diagnose this so they can start treatment. Contact lens abuse, something that Joe very commonly see on call. You get a history where someone is wearing their contact lenses long periods of time during the day. Most commonly they're sleeping in their lenses. They've got poor hygiene. And this is, I'll talk about cornea ulcers, but this is not quite ulcer stage. You'll see these small, fine epithelial opacities that look like this. They'll typically be bilateral. There'll be some contractile injection. Treatment of this will be with artificial tears, having them stop their contact lenses until symptoms resolve. You could consider a mild steroid drop, but really important to get these patients in for follow-up in the clinic so that we can see that their symptoms have resolved and that it's not turning into an ulcer. Which leads me into the next topic of cornea ulcers. So this, the most frequent risk factor to a cornea ulcer is contact lens use. Other risk factors include previous eye injury, previous trauma. If they are a healthcare worker or a nursing home, concurrent ocular surface disease like severe dry eye. If they are immunosuppressed. And you do wanna get a history of the degree of their pain, the duration. If they've been using any other eye drops at all or if they've been seen by other practitioners and received any prescription drops. Bacterial etiologies are the most common and typically there's very quick onset. You'll also see cases of viral ulcers, fungal and also parasitic with a canthamoeba. So when you look at a cornea ulcer, there are different characteristics that you wanna look out for. You wanna look at the location. Is it central? Is it paracentral? Is it peripheral? Typically it's helpful to have a clock hour on there so that when you look at the ulcer later on you can find it again. Is it the shape? Is it round? Is it oval? Is it stellate? You wanna measure the size. You wanna assess the depth. Is it panstromal? Is it anterior? Meaning it's just kind of very superficial. Is it only deep or endothelial? And the density or consistency? Is it really dense? Is it super white and opaque? Or is it kind of light and feathery? And noticing kind of the borders of it is important as well. And I also like to know whether or not there's an associated inflammatory response. Like is the surrounding cornea very kind of hazy and kind of edematous? Or is the surrounding cornea very, very clear? And that gives you an idea of how much inflammation there is. So if there's a lot of haze around it, there's a lot of inflammation. If there's not really any haze, maybe this is an ulcer that's either very indolent or very concentrated or maybe it's kind of turning more into a scar. So when do you wanna culture a cornea ulcer? So if it's large, and I guess large is relative, but I'd say if you've got something at least two millimeters that would be considered large. Is it vision threatening? Is it in the central visual axis or close to it? Even if it's a small ulcer, I would culture. If any time there's a high popaeon, you do wanna culture. And any post-operative patient like a post-cataract or post-corneal transplant, you definitely wanna culture. So if in doubt, just culture. And there are different ways of culturing. Traditionally, when you read kind of in the textbooks about culturing, they use something called a chimera spatula or you can use something called a calcium alginate swab, which is like kind of a smaller Q-tip. You use this to scrape into the infiltrate and then you plate it out in a thin layer onto culture plates and you use a separate swab for each plate. And you can send off the cultures for Gramstain, blood agar, which is aerobic bacteria, chocolate agar, which is more in Nigeria than hemophilus, salvoids agar for fungi, phyoglycolate broth for anaerobic bacteria. Pages media is something we use here for acanthamoeba. So if you ever want to culture acanthamoeba, you do have to get this kind of separate thing called Pages Media, which comes in a tube. It does not have its own swab, so you have to kind of hunt down a separate swab. I've heard of people opening up the viral culture media just because that comes with a swab. So you can use that swab for the Pages Media. So kind of confusing. Typically nowadays, I don't use the traditional plates. I use something called the E-swab. And this is very easy because everything's kind of all in one and everything means kind of the non-viral, non-acanthamoeba. So the E-swab is a nylon tip swab which has kind of these kind of longer fibers which can improve sample collection because there's more kind of grabs onto the culture, whatever you're culturing a little better. And this is placed in a medium and a tube that looks like this. And then when you send it to the lab, you put it in your orders and the lab will actually aliquad it for culture. It is non-inferior to traditional collection methods with regards to culture positivity rate. I first started using these maybe three or four years ago and when I first started using it, I actually would culture the same patient twice, like once with traditional and once with the E-swab. And I found that the E-swab would actually have yield whereas the traditional plating may not have yield. So it might get a better yield with the E-swab. So how do you wanna treat a corneal ulcer? It's gonna depend on how bad it is. So typically I would start if it's not too severe just with a fourth generation fluoroquinolone. If it's tiny in peripheral, I might just go QID. If it's a little more severe, you'll go Q1 hour. Or if it's more large or severe, I would go with fortified antibiotics which can become hounded at the Moran Pharmacy and also our inpatient pharmacy. And it's an on formulary so you can just type in vancomycin and tobromycin and it'll come up as these concentrations. And you do wanna choose these and using these every Q1 to two hours. You can consider a psychoplegic agent and here are the most commonly used ones. CycleGill lasts about 12 hours. So use a TID, home atropine. Typically use BID and atropine 1% you can use once or twice a day. But atropine, I don't think people can find very much anymore so I'm usually using a CycleGill or jumping to atropine. With atropine, I always tell them, make sure you don't accidentally put it in your other eye because they're gonna be dilated for like seven to 10 days. So really important that you tell them to keep, I mean they always have to keep their drops in one eye, whatever eye it's supposed to be. But with atropine in particular, I've had patients accidentally put it in their good eye and then they're wondering why they're dilated. Any patient who may be homeless or has a questionable home life and may be not able to get in their drops to one hour, you might consider admitting as an inpatient. Herpes simplex keratitis is very common. Symptoms are kind of non-specific. It's redness, blurry vision, some irritation or you could have severe pain with it. There is diminished corneal sensation so you wanna check this prior to placing anesthetic. And I like to check corneal sensation by taking like a cotton swab and with clean hands you can kind of rip or kind of whisk off like a little top layer of it so you have a little wispy kind of edge. And then have the patient look straight ahead and touch both sides and ask them, does one side feel more irritating than the other or you can kind of see on their reaction like you're touching and they're not even blinking, you know they have decreased corneal sensation. So on exam there's various types of herpes simplex keratitis. There's epithelial disease where you see a dendrite here and classically you'll see terminal end bulbs at the end of each dendrite. Stromal HSV keratitis is actually the most common cause of infectious corneal blindness in the US. There's not really a specific characteristic look. It's just kind of more of some haziness and oftentimes it's kind of patchy as seen here. Discoform keratitis, you'll actually see corneal dema so it's affecting the endothelium. So classically you'll see stroma dema in a round distribution, it's kind of oval here and it's associated with keratic precipitates and it's also been termed endophiliaidis. So the treatment of epithelial disease, most cases actually resolve spontaneously. I don't typically have them go off without treatment. So you wanna use some kind of antiviral treatment. Classically, topical trifluoridine eight times a day. I've kind of shied away from this just because it can be quite toxic. You can use, again, gel five times a day. Unfortunately it tends to be quite expensive. So usually with oral treatment with either acyclovir or Valtrix you can achieve good penetration to the cornea. Classically with HSV the dose is 400 milligrams five times a day. I've seen people do 800 BID just to kind of consolidate things and make things easier. Typically you don't wanna use a steroid, any topical steroid with epithelial disease. You could consider epithelial debridement if it's not resolving with treatment. There's the head study, which is a study which looked at the use of topical trifluoridine and steroids and acyclovir. So the purpose of it was to evaluate the efficacy of treatment in HSV stromal keratitis and HSV eridocyclitis. So they looked at seeing whether or not topical steroids with topical trifluoridine was effective in stromal keratitis. If oral acyclovir with topical steroids and trifluoridine was effective and whether oral acyclovir with steroids and trifluoridine were effective in eridocyclitis. So the results showed that when you have HSV stromal keratitis, when you give topical steroids with topical trifluoridine, it actually reduced the progression and shortened the duration. There's no benefit of adding oral acyclovir when you have stromal keratitis and you're already treating with topicals, steroids and antiviral. Typically I do like adding oral acyclovir just because later on it kind of helps prophylax. There was a trend to suggest a benefit of oral acyclovir with topical steroids and trifluoridine in HSV eridocyclitis, but I don't think the head study had enough patients in this arm to really say for sure, but I think typically people do add oral antiviral treatment for this. So these are the doses of prophylactic doses for HSV keratitis, for acyclovir, famvir and valtrex. So with acyclovir, again the treatment dose was 400 milligrams five times a day and the prophylactic dose is 400 milligrams two times a day. Valtrex treatment dose would be one gram BID, prophylactic dose is one gram once a day. Late complications of HSV keratitis are neurotrophic cornea, you can have severe dry eye, you can have non-healing epithelial defects, you can have severe corneal scarring, neovascularization, recurrent inflammation and corneal thinning. And it's sister disease, shingles is very similar. Sozoster is a reactivation of latent VZV and when it's affecting the eye there is involvement of the ophthalmic division of cranial nerve five and the classic sign is Hutchingson sign where if there's involvement of a shingles rash at the tip of the nose that means the nasal ciliary nerve is involved and the nasal ciliary nerve innervates chronic type of cornea, scleral iris, chloride in the skin of both eyelids and so it's a very strong predictor of ocular inflammation if you see a positive Hutchingson sign. Shingles is most, or sozoster is more commonly in the elderly, although we are seeing it more and more in young patients. There's a wide range of ocular involvement in severity and maybe acute chronic overlapsing and you'll see a pseudodendrite. So unlike HSV where you see a very classic nice kind of pretty tree and with pseudodendrites and shingles kind of more of a stuck on appearance. There aren't any terminal end bulbs and you can't see stromal keratitis. Like HSV there's gonna be a decreased corneal sensation. So if the zoster symptoms started within the previous 72 hours you wanna start and actually I don't even wait, if it's even beyond 72 hours I would probably start this dose. So this is double the dose of HSV keratitis. So with zoster you wanna go to 800 milligrams five times a day for 10 days and we think that there is a role for reduced dose long term which is the topic of a clinical trial that's going on right now called the ZEDS trial which we are a site. There may be a role for a topical antiviral treatment and topical steroids are highly, highly recommended for anti-segment inflammation and keratitis and oftentimes you need a very slow taper of topical steroids or even chronic use to prevent recurrent inflammation. And with shingles you see post-herpetic neuralgia which is kind of severe pain even after all the kind of the signs of zoster have gone and this pain can be very severe and can be treated with gabapentin tricyclic antidepressants and lyrica. So I will always refer patients out to see their primary cure doctor and maybe also a pain specialist to help manage these symptoms. You get the same late complications in zoster as you do with HSV. So neurotrophic cornea, scarring, neovascularization, recurrent inflammation and corneal thinning. Next, corneal trauma. So the most common type of corneal trauma that you'll see is a corneal abrasion. I'll treat with a fluoroquinolone four times a day. I don't change my treatment based on the size of the corneal abrasion per se as far as the antibiotics go. So don't do like fluoroquinolones queue an hour when it's really just abrasion. No infiltrate based on the size. Like if it's a total corneal epithelial defect or a tiny one, I just do fluoroquinolone four times a day. You can consider a cycloplegic agent for pain control. You can also consider a banded contact lens or a pressure patch. And you wanna follow closely for any infiltrates that can develop down the line. If there's no trauma history, you don't wanna examine for exposure. Is there any like ophthalmos or is there something under the lid that might be scratching? So you wanna examine for other causes for a corneal abrasion. Corneal foreign bodies are very common. Oh, question. Yeah, would you, you would always use it for gender? I mean, I guess you could use like a polytrim. Is that what you're thinking of? Yeah, yeah, just like if it's like a ground source versus say like a burn or something. I usually like the fluoroquinolones. Yeah, I usually do. If it's the only times I don't because if there's allergy, if there's like an insurance kind of cost issue, I'll go with polytrim. I typically do fluoroquinolones. Corneal foreign bodies, metals most common. If it's superficial, you can remove these with a 27 or 30 gauge needle. You can consider using a burr as well. Afterwards, you treat it like an abrasion but it is common to have like this kind of a white, almost looks like an infiltrate that's usually sterile kind of in the spot where the foreign body was. So if there is a little bit of a kind of a white appearance there, you can use a combination antibiotic and steroid but you want to follow these patients to make sure they're not developing infection. If it's really deep, you don't want to pursue that. And you always want to counsel patients on eye protection. Corneal lacerations. So you want to determine very importantly if it's partial or full thickness like is this eruptor globe or not eruptor globe. So you can use a Seidel test to tell that. You can look at the anterior chamber depth. Like if it's shallow, that's a clue that there is a full thickness situation going on. And if you're not sure about the depth, like what's normal for this eye, look at the patient's other eye. And so if the other eye is kind of the same AC depth as the affected eye, feel good. If the other eye is a lot deeper then there's probably a full thickness laceration going on. Obviously there's peaking of the pupil or iris prolapse and that's a very obvious sign of full thickness laceration. If there's a partial thickness laceration you want to remove or irrigate any out, any foreign body material. Depending on how deep it is, obviously if it's full thickness that needs to be prepared in the OR. If it's partial and superficial, you can leave them alone. They're a little deeper. You probably still want to take them back to the OR for suturing. You want to place a shield on the eye prior to going back to the OR. You could consider IV antibiotics, but more importantly, you want to make sure the patient is NPO. So if you get a call from a community ER that there's a patient coming in with a rupture globe, you want to tell them, make sure they're NPO. Okay, so moving on to chronic diseases, blepharitis. There's anterior and posterior types. With anterior, you'll see colorates around the eyelashes. And so when I see this, lid scrubs are very effective. If it's posterior, you'll see mybomian gland insipidation or blockage and warm compresses are effective for this. And artificial tears are going to be the mainstream of treatment in addition to warm compresses. You can also consider official oil, oral official oil, oral doxycycline or minocycline in an antibiotic ointment to the lashes. Dry eyes oftentimes is, there is concurrent blepharitis or mybomian gland dysfunction. The symptoms of this are gonna be tearing, dryness, redness, foreign body sensation. If there's fluctuating vision during the day, that's a hint that this is dry eye. Classically, there's an evaporative etiology where mybomian glands get clogged and so that lipid layer is not really present and the tears are evaporating very quickly. You can also have diminished tear secretion as seen with sarcoidosis and collagen vascular diseases and there's a high association of dry eyes with oculosurface inflammation. So clinically, you'll see interpalpable staining. This is showing rose bangle staining. There'll be a low tear film. Oftentimes, you'll see mucus floating around in the tear film that's a sign that there's dry eye. And you'll see a low tear break up time. So the way you do this test of tear break up time is you put in a drop of fluorosine, you get in up to the slit lamp, put on the cool bulb blue light and you tell them, you kind of time it and you can even time it in your head. Ask them to stare and not blink. And so you count in your head how many seconds go by before you start seeing a break up of the tear film which is seen as a dark spot on the cool bulb blue light. And if that break up time is less than 10 seconds, that is a low tear break up time. If it's greater than 10 seconds, it's normal. You can also do a Shermers test. I typically have abandoned Shermers just because you can see if there is dry eye based on other exam findings. But if you do a Shermers test, I do use it with anesthetic. And if you, so you put the filter paper strips in and then you wait five minutes and if it is less than 10 millimeters then that is a low Shermers finding. Treatment, various treatments ranging from just taking breaks when you're reading on the computer, humidifier, artificial tears, gel or ointment at night. You can consider topical anti-inflammatory treatment with restasis or Zidra, but these do take time to work. Oral fish oil or olive oil can be effective and you can consider moisture chamber goggles if there's a component of nighttime lack of thalamus. I'll typically suggest gel and ointment and humidifier for those cases. And you can also consider punctal plugs and cotterie down the road. Lots more to say about these conditions I'm just kind of breezing through, so. There'll be hopefully more lectures in the future about these. With Fuchs dystrophy there is, this is an autosomal dominant corneal dystrophy that appears typically around age 40 to 50s. And Fuchs dystrophy is a progressive loss of endothelial cells which leads to corneal edema. And it is asymptomatic in mild cases and later on there is morning blurry vision that improves later in the day. The reason why you get that particular symptom is that there's basically edema in the morning. So eyes are closed all night. There's kind of a more kind of humid environment and there's more, those endothelial cells are just, there's not enough of them to pump out all the fluid. And so when they wake up, they are looking through maybe just a little bit of a cloudy cornea. And this is a pathologic slide showing that there's few endothelial cells here. And then you see these little bumps in decimates membrane and these are the gutata that you'll see in Fuchs dystrophy. So gutae or gutata are the first sign. You'll see these little bumps. It looks almost like a kind of an orange peel appearance on the endothelium. And then later on you'll see corneal bulae and edema. And there's two ways you can see these gutata. It's hard to find, especially when you're kind of medical student or just kind of beginning in your residency. And the easiest way is that you have to turn the beam on to the higher intensity. You're not gonna see gutata on the the kind of lower intensity beam. So higher intensity, put it at a slip beam, focus on the endothelium and you'll see kind of this appearance here. This is retro illumination. So you can put the beam on retro illumination and that can also highlight gutata. Typically in more, say moderate to advanced Fuchs dystrophy, you'll have a thick cornea that will be greater than six to three microns. And you can do specular microscopy, which is a way to image the corneal endothelium and there'll be a lower than normal corneal endothelial cell count. So treatment, if they're asymptomatic, I do nothing, but I'll mention that they have this condition and that they will need some routine eye exams to monitor. If they start getting blurry vision in the morning, I recommend the use of hypertonic saline, which is mirror 128, and this hypertonic saline can decrease corneal edema. And since patients will have these symptoms more in the morning, I tell them to kind of use more of this in the morning. There are special considerations in cataract surgery. You wanna protect the endothelium as much as possible. You wanna decrease facial time, kind of coat the endothelium. So there's things that you wanna watch out for with cataract surgery. If the fuchs dystrophy is visually significant, then endothelial caretoplasty is recommended. So lastly, I wanna go over kind of special cases that you'll see in the burn unit. So you'll see thermal chemical burns, as well as SJS 10s. So with thermal burns, I mean, it's kind of obvious what the causes are. Usually the globe is not involved because of the eyelid reflex. You're gonna close your eyes. So usually there's more eyelid involvement with thermal burns, which can be quite extensive. Chemical burns can be from any form, solids, liquids or gases. Alkaline agents will usually penetrate deeper than acids. The reason for this is that acids actually cause a coagulation of the crosis that prevents deeper progression of that acid. Alkaline agents cause a pontification of fatty acids which actually caused cellular disruption and allows that acolyte agent to penetrate deeper into the tissues. So acutely, definitely wanna irrigate. You can check the pH. I think there was, someone was asking me the other day about pH paper. I don't, did you guys ever find it? Forget who it was, who else asked me. It's somewhere, hopefully. And I've had like kind of defective pH paper that showed like a very base number regardless of what was added. So you can always check it on your own eye if you're not sure. So to test if it's actually working. You wanna do a complete eye exam. Look at the eyelids. Look for edema and legophthalmos and lash loss. You wanna check to see if there's a good bell's reflex, if there is legophthalmos. So this is a patient with very extensive facial burns, but thankfully he has a good bell's reflex even though he has a lot of legophthalmos. You wanna look at the contantive acornia and fortices, assess the epidefacts, clean out many foreign bodies. We can see if there's any opacities. And then most importantly with chemical burns, you wanna note the level of limbo ischemia. And limbo ischemia means that there's a loss of limbo stem cells and portenza, poor prognosis. So here are two pictures of two different eyes. One with this limbo blanching, one that looks very red. And so the eye that actually looks very red and beefy has a better prognosis than the one that's not red. There are several late complications to ocular burns. You can get persistent corneal epithelial defects because of the most stem cell deficiency. You can get corneal thinium perforation, corneal neovascularization. On the contantiva, you can see scarring and some blepharone formation. On the eyelids, there can be progressive scarring, cicatricial ectropion, truchiasis, and ligophthalmos. So the treatment, vitamin C and doxycycline can be effective. The doxycycline actually has, oral doxycycline has an anti-inflammatory effect. The eyelids do need to be lubricated. And you can use it with remycin ointment. Use a topical fluoroquinolone if there isn't any corneal epithelial defect. And if there is, I actually highly consider using a topical steroid, especially in the first couple of weeks after a burn to reduce inflammation. If there is a persistent epithelial defect, you can consider bench contact lenses, amniotic membrane, either sutured or non-sutured, such as a prokera. If there is lagophthalmos, then you wanna do very aggressive lubrication like ointment Q1 hour, moisture chamber goggles around the clock. You wanna get ocular plastics involved. Unfortunately, you can't really go in surgically acutely because there's oftentimes a lot of scarring that occurs late. So if there is lagophthalmos, often the patients do need a wait a while before they can get their eyelids treated. So in severe cases, consider the inpatient use of scleral lenses, which we'll talk about. So scleral lenses for inpatient use, so we use this for exposure keratopathy with recurrent or non-healing epithelial defects, or if there is corneal thinning with scarring that are refractory to other treatments, there is a much less risk of infection with scleral lenses than with soft bandage contact lenses. We do have a protocol here. I think it's on the box resident folder, correct? So let me know personally if you're thinking about using scleral lenses. I feel like it got used maybe only once or twice though, maybe once last year. It doesn't come up very often. Oh yeah, two years ago. So maybe none last year, maybe not. Okay, so hopefully the scleral lenses are somewhere, I don't know if they're in the resident room, hopefully they're somewhere safe. So sounds like we need to ask Tina if make sure they're still around. Because there's a whole protocol about what you need to do to take care of the scleral lenses. Next, we're gonna switch gears to Stevens-Johnson syndrome slash toxic epidermal necrolysis. So this is a rare potentially life-threatening hypersensitivity condition that's triggered by medications or infections. There is sloughing of the skin and mucous membranes and the definitive diagnosis is by skin biopsy, which is done inpatient. SGS involves typically 10 to 30% of total body surface area, whereas TENS involves greater than 30%. And this is a patient who actually looks this way, it's not that her face is red, she actually has no skin. So there's no epithelium here. That's why they have this look. So it's very, very severe. I mean, they're in the burn unit because it's almost like they have burns because they have their skin has left off. There is a high association of ocular involvement in SJS. You see contantival inflammation, pseudo membranes, contantival and corneal epithelial defects. Late complications are severe. There is severe dry eyes because of a loss of goblet cells and often my blooming glands. There is keratinization of the eyelid margin. There is scarring of the contantiva corneas and blepharone, corneal opacities, corneal thinning and perforation and corneal new vascularization. The treatment will be lubrication and topical steroids. And then you wanna consider amniotic membrane transplantation over the bulbar and palpibral contantiva cornea and over the eyelid margins if there is significant inflammation and sloughing. And this amniotic membrane is human amniotic membrane. It is harvested from women who have undergone C-sections and have elected to donate to their placentas. And so the amniotic membrane contains growth factors, anti-inflammatory mediators to promote healing and reduce inflammation. And it also prevents these very late complications. So there's a new grading system for when to do amniotic membrane transplantation based on the exam. So notice that it is classified into mild, moderate, severe and extremely severe. You wanna look at the lid margin. If there is staining of less than one-third of the lid margin, you can just do medical and close observation. Anything bigger than that, you wanna consider amniotic membrane transplantation in addition to the medical therapy. If there's any corneal epithelial defect, that would be considered severe. If there's staining on the bulbar and palpubocondentiva of greater than one centimeter that is considered severe. So basically let us know about any SJS patients that are out there. Here are some pictures of SJS patients. This is a picture showing severe care organization. So this is stained with fluorescein, but as you can imagine, this can cause chronic and sometimes even debilitating pain and irritation. And this is just showing that there's kind of a little irregularity of the lid margin there. And so when you pull it back, you'll see this. This is a patient who had a really good result. She had a young patient with SJS who underwent amniotic membrane transplant and I think it was about a month later. Can't tell that anything even really happened. So she looks great. This is another patient who I think had very late amniotic membrane transplantation with chronic scarring and inflammation. So there's a lot of scarring of the palpubocondentiva, a lot of chronic inflammation of the congenitiva in general. I think he had some corneal neovascularization as well. So that is it. Any questions on anything? Well, we're always around. We've got some great corneal fellows this year and it can also always help as well. So I think that's about it.