 no matter how minor is going to cause a lot of pain. There's just a lot of nerve endings in the cornea. And this is the kind of the cross-sectional path slide of the cornea. So we'll start at the top with the epithelium. So the epithelium is four to five cell layers thick composed of stratified squamous epithelial cells. And there are tight junctions between the epithelial cells which prevent tear fluid from getting into the struma. And the bottom layer of the epithelial cells rests on an epithelial basement membrane. This is not to be confused with an acellular layer called bowman's layer, which is not labeled here or sometimes termed bowman's membrane, which is this kind of avascular light pinkish area right under the epithelium. So bowman's membrane is not a true membrane, so bowman's layer is kind of a better way to term it. And it is not to the basement membrane of the epithelium. So underneath bowman's layer is the stroma, which is comprising the bulk of the corneal thickness. Stroma, the stroma is composed of keratocytes, which must be arranged in a specific configuration to allow for transparency of the cornea. And another factor that's very important for transparency besides the specific arrangement of the keratocytes is actually the amount of hydration of the stroma. So the stroma needs to be at 78% water content to maintain its transparency. And it's maintained by not only the tight junctions at the epithelial layer that I discussed, but also barriers at the endothelium as well as a functioning endothelial pump, which pumps out excess fluid. Once we get down to the bottom, you've got a decimates membrane and endothelium. And so the endothelium is one mono cell layer thick, and the basement membrane of the endothelium is indeed decimates membrane. So next we're going to talk about layers of the tear film. And there are three layers to this. So see kind of starting from the bottom up. The bottom layer is the mucin layer, which is produced by the goblet cells. And the mucin layer is important because it actually what it's what makes the tear film actually stick to the surface, kind of the ocular surface. So these mucins kind of stick to microvillae of the epithelial cells. So very important maintaining a good tear film. The bulk of the tear film is composed of the aqueous layer, or the water layer. This is produced by the main lacomal gland, but also there are scattered accessory lacomal glands of crows and wolf ring. The accessory lacomal glands of wolf ring are in the kind of underneath the palpebra conch, kind of around the margin of the tarsal plate. And the ones of crows are in the cornices. So I remember this by crows is in the corner, corner with a K, so corner of the condentiva, which is condentiva formancies. Okay, at the very top is the lipid layer, which is produced by myomian glands. And the lipid layer is important because it prevents or slows down the evaporation of the tear film. So if you have a very poor lipid layer, your tear film is going to evaporate more quickly and also lead to dry eyes. So I'll be I'll be talking about all this later on in this talk when I talk more about dry eye. So next, I'm going to go into some slit lamp techniques. This is really basic, but we'll kind of go over a few techniques, probably the two most common techniques that I use probably 99% of the time are going to be diffuse illumination and slit lamp illumination. So with diffuse illumination, you're starting at a low mag, kind of a broad beam, low light intensity, and this is just to get an overview to see what's going on. See if there's anything kind of remotely obvious that you might want to concentrate on later on. And then the slit lamp illumination is when you have the beam at an angle and at a slit and you can use it to examine the anterior segment at all the different layers. Some of the other techniques here I use a lot less often. Specular reflection is a technique that's used to examine the tissues that are around the normal light reflexes, especially the posterior corneal surface. So what you do is you have your kind of a very small intense beam, a slit beam at a 60 degree angle from the viewing arm, and you want to superimpose the posterior corneal light reflex, which is here, with the very bright and a slit lamp light bulb reflex, which we usually were ignoring. But in this case, you want to superimpose those two reflexes so that they are going to be together. So you kind of superimpose them together and then you move the joystick forward just a little bit so you can look at the posterior corneal surface. And if you're on high mag, you can actually see some of the kind of subtle things that you can see around the endothelium. Another technique is sclerotic scatter. So what you do here is you have a very, very intense high kind of high intensity beam right on the limbus. And what happens is that the light from the sclera actually scatters and reflects kind of all over the cornea and you can actually highlight subtle corneal superficial corneal abnormality. So in this case, this picture is showing kind of a light corneal scar that's highlighted by sclerotic scatter. So the light isn't on the scar, but it's kind of lit up with light coming from the sclera. One technique that I use sometimes is retro illumination. So this is where you have the light beam kind of shining directly into the pupil. Light actually bounces off the retina and it shines back. You can see abnormalities not of the cornea, not only of the cornea and lens, but it's really good at picking up iris defects. So in this case, we're seeing diffuse kind of iris trans illumination defects. This is a good technique to finding out whether or not you have a patent PI for iridotomy. Sometimes you can see a iridotomy on slit lamp exam, but you're not able to tell if it's actually open or not. So retro illumination is a nice way because you'll see a bright red reflex coming back. And stop me anytime. I mean, if anyone ever has any questions on anything. So corneal staining. So most common stain that's used is fluorescein. You can find it in a solution or in strips. And this stains exposed basement numbering. So you can highlight corneal epithelial defects. You can also highlight punctated epithelial erosions, which we see in dry eye, which is shown here. Some other stains are rose bengal and listening greens. So rose bengal stains debitalized cells. It also can highlight kind of staining patterns that are similar to what you can see with fluorescein and dry eye, but probably stains even more. You can highlight, they can highlight debitalized cells even on the congenitiva a bit better. However, rose bengal stings a lot even with topical anesthetics. So listening green is a nice alternative, which also stains debitalized cells, but it's less irritating than rose bengal. And this is a very, very intense dark green. So in this case, you can see some dryness on the bulbar contractiva. Let's see what other exam tips to know about when you're starting off. You want to remove soft contact lenses prior to placing fluorescein because fluorescein will stain contacts forever, doesn't damage it, but it's just going to be bright orange forever. So you want to make sure you take those out prior. You want to keep track of your tetra cane and your bottles of fluorescein because you worry about tetra cane abuse, especially in patients with corneal ulcers or corneal abrasions because they'll notice as soon as you put in those drops, everything feels a lot better. So they may not, they're not going to know that it's bad to keep putting in topical anesthetic. So keep track of that. So I always keep mine in my pocket and not really have it out on the counter. Anyone with an abrasion that's not easily explainable or anyone with red eyes, you want to flip an evert upper lids to look for foreign bodies. Sometimes you're surprised by what you find under there. So make sure you always do that. All right, next, common corneal contractival issues. So I'm going to go over all these issues here. These are kind of bread and butter. The acute category are things you're going to see on call. Chronically, no one might see some of these on call, but I typically will see a lot of these in my clinic. So here are kind of the three classic categories of conjunctivitis, bacterial, viral, and allergic. Oftentimes the history will actually point you to one of these categories. So with bacterial conjunctivitis, the classic thing is there'll be a very purulent discharge seen here. With viral conjunctivitis by history, there's usually a respiratory symptoms, maybe some sick contacts. They'll have some tearing, some discharge that'll start in one eye. You have some redness, and then it goes to the other eye within a couple of days. With allergic conjunctivitis, it's class, it's typically in both eyes, pretty symmetrically, and itching is going to be a big hallmark with allergic conjunctivitis. So on exam, looking at the palpipoconjunctiva, we can look at conjunctival reactions. So follicles are typically seen in viral conjunctivitis, and a follicle is a cluster of lymphocytes, and there are vessels, but they tend to be kind of more in the periphery of the follicle, less so often right in the center. And let's see what else. Papillae, in contrast, are vascular changes within the palpipoconjunctiva. So with papillae, you actually have a dilated vessel that kind of sprouts some spoke-like capillaries all around, and that whole thing is surrounded by edema. So with papillae, it's very vascular, that's kind of the hallmark of papillae. So that's one way to kind of tell the difference. Sometimes you have a mix, actually oftentimes you'll have a mix of both papillae and follicles, so you may not have, you know, such a classic appearance, but those are kind of the ways you distinguish papillae and follicles. Papillae are most classically seen in allergic conjunctivitis, but you can also see it with bacterial conjunctivitis as well. Giant papillae conjunctivitis is seen here, so you have these really large bumps on the congenitiva, especially when you flip over the upper lid, and this is seen, classically seen as a reaction to consequences. Next, episcleritis, so this is a benign transient inflammation of the episclera, which is right underneath the congenitiva. So by history, patients will complain of redness, really minimal or no pain. Typically, it's going to be kind of a sectoral pattern like here. On exam, classically, this redness will blanch after placement of phenyl ephrin. So about five minutes later, this will all kind of blanch out to be very, very light in color or even white. Typically, I don't work up episcleritis unless it's recurrent. There are some, a few systemic associations associated with herpes zoster, collagen vascular disease, gallatin syphilis. So if it is recurrent, here's some of the lab work that can be checked. Typically, this is self-limited. It actually can get better on its own without any treatment. You can consider high dose oral NSAIDs or topical NSAIDs or steroids to really speed up the recovery. Next is scleritis, which is typically very tender, very painful, very red. There's no blanching with any phenyl ephrin with scleritis. There are three types. There's non-necrotizing, which is probably the most common type. There is a type that's painless, that's necrotizing without inflammation in terms of their own Malaysia preference, as well as a necrotizing type with inflammation. And scleritis has a very significant association with systemic disease. So here's some of these systemic associations, rheumatoid arthritis, lupus, and closing spondylitis, psoriasis, Crohn's, vasculitis, esculitides, and always syphilis and TB. So this scleritis, as opposed to episcleritis, you always want to work up scleritis. And you can use some of history and review systems to guide testing, kind of as shown here. Sometimes the lab work will be negative, and if that's the case, you want to consider repeat testing. The other thing about scleritis is that it's typically going to be there until it's treated. So it's not going to get better on its own. So non-necrotizing scleritis, this is kind of the most common one that we'll see. It is also the least severe version of scleritis, classically a very violacious hue, a very bright red. There's a 50% association with systemic disease, 50% of the cases are bilateral. And like I said, this is going to be remaining there until treatment is given, which I'll go over later on. Next type of scleritis is scleromalacia perforans or necrotizing scleritis without inflammation. This is a painless white-white eye within sclera. Typically you'll see it in elderly patients, very commonly bilateral. 50% of these cases are from rheumatoid arthritis. So you can see these thinned areas of sclera with some of the uveal tissue kind of showing through. Scleromupture is thankfully rare and it rarely needs surgical repair. But again, medical treatment is warranted. Necrotizing scleritis with inflammation. So this is the last kind of subtype of scleritis. This is very painful, bilateral in most cases. And this is the most destructive form of scleritis. There's vision loss in 40% of cases. High association with systemic vasculitis such as weganers or it's new name, granulomatosis with polyangiitis. And there's actually a really high immortality rate, 20% at five years. So you can see that there is kind of very severe thinning of the sclera. This can lead to sclera perforation. So this is one that you will want to basically work with the pneumatologist on treatment. So I guess I didn't really go into treatment, but it's going to be systemic immunosuppression for scleritis. So oral steroids, maybe working with rheumatology to work with other nonsteroidal systemic treatments. Next, contact lens abuse. Very common. So typically by history, patients will have greater than 12 hours a day of wear, commonly sleeping in their lenses, poor contact lens hygiene. And this is going to be bilateral in most cases. There's a lot of redness of the contenteva here. You'll see a vascular panacea, which is a sign of chronic long many, many hours compounded of contact lens use. You'll see some punctate staining on the cornea. And you can see these fine epithelial or sub epithelial opacities here. So treatment is artificial tears, stopping the contact lenses until symptoms resolve. You can also consider a mild topical steroid drop, such as FNL or modem acts. Next, cornea ulcer. The most frequent risk factor is again, contact lenses. But there are other sort of other kind of risk factors as well, previous eye surgery, trauma, being a healthcare worker in a nursing home exposed to a lot of bacteria, concurrent ocular surface disease, meaning very, very severe dry eye can also predispose one ulcers. If one has a systemic immunosuppression. And by history, you want to get from the patient their degree of pain, how long they've been experiencing symptoms, any other eye drops that they've used, or maybe they see care at a care doctor or an optometrist or treatment with any other drops. Bacterial etiology is the most common etiology is typically a very quick onset. But you can also get viral cornea ulcers, fungal and parasitic. So here's kind of a whole range of different what the cornea ulcers can look like. So on exam, you want to carefully look at the ulcer and be able to describe it. So location, is it peripheral? Is it superior? Is it inferior? Kind of where is it at? What's the shape? Is it round? Is it linear? Is it stellate? Is it fluffy size of it? So you can kind of measure that with a slip lamp. The depth, is it a sort of facial cornea ulcer? Is it endothelial? Is it panstromal? And you can tell with the slip lamp exactly how deep it goes. And kind of the density and consistency is a very like opaque, very dense ulcer. Is it kind of light? Can you still kind of see through it? Consistency? Is it kind of fluffy? Have feathery edges? Also look and see if there's an associated inflammatory response, meaning are there periodic precipitates? Is there a lot of haziness around the actual borders of the cornea ulcer? Kind of in the stroma, you can sometimes see a lot of haziness. So kind of note all that, but that all in the exam. So when do you want to culture? You don't have to culture all cornea ulcers, but you definitely want to consider it in some of these instances. So I want to culture if it's large and large, you know, probably anything over two millimeters, I might consider large. Is it vision threatening? Meaning is it close to the visual axis? So this one could be a vision threatening one. So maybe this is more into culture, even if it's a small one. Is there an associated hypopoean? Definitely want to culture that. And anyone who's had previous eye surgery, especially a cornea transplant, want to culture. So this is an example of a large, obvious large cornea ulcer. Maybe there's a hypopoean kind of starting there. So this is definitely one to culture. And this is also one to culture. So how do you culture? So in the books, the Canora spatula, which is shown here is the classic way of culturing, which we don't really use too often. But if you do happen to find one, you could have to sterilize it and use it to scrape into the infiltrate and kind of culture it over different culture plates. You can also use a calcium alginate swab, which is almost communicative, kind of do the same thing. And you can send the cultures for her Gramstain classically. And again, I'm going to go into a new newer method that we've been using to culture. But classically, we do culture on different plates. So there's blood agar for aerobic bacteria, chocolate agar for myseria and hemophilus, severed agar for fungus, thiopolecate broth for anaerobic bacteria. Page's media is something that you do have to still get for if you want to culture Acanthamoeba. So there's a separate swab for that. And there's also a separate media for viral cultures. It kind of comes in a pink test tube looking thing that comes with it. It's on swab for culturing herpes viruses. However, we have something called e-swab, which is really nice because it really simplifies culturing. So you don't have to go around finding all these different plates. So the e-swab looks like this. It's a little bit of a Q-tip look. And it's got, so it's a nylon tips swab and it's got kind of these fine little fibers within the swab that allows for improved sample collection by increased capillary action and liquid uptake. And so the e-swab comes with this container here, which is a modified amy's medium, which is then aliquoted in the lab for culture. It has been found to be non-inferior to traditional collection methods with regards to culture positivity rate. So you can run, so off of one swab you can run aerobic cultures, anaerobic cultures, and fungal cultures. So again, don't have to go hunting around for different plates. But like I said, if you want to get Acanthamoeba or fungus, or sorry, Acanthamoeba or viral cultures, you do have to get separate media for those. Stop me if there's any questions on anything. Okay, so you've got an ulcer, you've cultured it, how do you want to treat it? So it depends. It's going to depend on how bad it is. So generally, you might consider starting off with fourth generation full of quinolones, such as Vigilmox four times a day or up to every hour. But it is going to depend on how bad it is. If it's a pretty large ulcer, I would go to fortified antibiotics. So whenever we mentioned fortified antibiotics for me, that usually means Vank and Tobra. You can order them right in Epic. They're a compounded either at Moran or also in patient pharmacy if you have someone over the main hospital. These are the concentrations here. Vancomycin is 25 milligrams per ml. Tobromycin is 15 milligrams per ml. And having that placed in Q1 to Q2 hours. You might consider also adding a cycloplegic agent such as cyclogeochromatropine or atropine to kind of prevent iris spasm. And I kind of describe to patients it's going to take the edge off of some of the pain. Definitely not going to significantly get rid of pain, but it helps a little bit. I like it because if there's a big inflammatory response, like if there's a lot of cells in the EC or a hypopia, you're going to decrease the chance of getting CineTI if you add a cycloplegic agent in. If you have a patient who's homeless, maybe some questionable compliance issues, you want to consider admitting as an inpatient for treatment. Okay, so moving off of that kind of more bacteria or ulcers, we're going to move to herpes. So herpes simplex keratitis, something that has seen very commonly. Patient symptoms are going to be kind of vague. They're not going to really point to any specific one thing. They're going to complain of redness and blurry vision. And they could either have mild irritation or they could have severe pain. So it kind of runs whole gamut. They will have diminished corneal sensation on exam. So you want to check that prior to anesthetic, placing a topical anesthetic. And what I do is I take kind of one of those sterile q-tips and kind of pinch off the edge of it so that it kind of strands off into a very fine fiber and use that little fine strand to kind of touch the corneal surface on each eye and ask the patient, you know, do you feel it more in one eye versus the other? Or is it pretty equal? And usually people will tell you like if they have diminished sensation that they'll feel it less in one eye. Let's see. Types of herpes simplex keratitis. There's epithelial and you'll see a dendrite here and kind of a branching lesion that's superficial that stains. And you'll see kind of terminal end bulbs at the end of each little branch. So kind of have a little bulb at the end. That's classic for herpes simplex keratitis. Stromal keratitis is going to be the most common cause of herpes simplex keratitis and it's actually the most common cause of infectious corneal blindness in the U.S. A subtype of that is dyskoform, which, yeah, it's kind of a very blurry picture, but dyskoform type is stromal edema that's an around distribution that's associated with keratic precipitates. So it's kind of more posterior in the cornea. Another term that's thrown around is endothelitis. So it's kind of more at the endothelium or focused on the endothelium with dyskoform keratitis. So treatment of epithelial disease. Cases will actually can resolve spontaneously, but I usually will treat patients with HSV keratitis. Treatment will dramatically shorten the disease course. Kind of in the past, the only antiviral, topical antiviral that was available was trifluoridine, which is veroptic. However, I rarely prescribe this nowadays because it's pretty toxic to the ocular surface. If I'm going to prescribe something topical, it's going to be zirgan, which is topical gang sycovir five times a day. Downside of zirgan is it's sometimes very expensive, not covered by insurance. That's okay because we can go with something oral, such as acycovir. The classic dosage is 400 milligrams five times a day. You could do kind of a variation of that 800 milligrams twice a day just to make it easier for patients. And you can also do Valtrex. Classically, do not want to give any topical steroid with endothelitis keratitis because that could actually worsen it. Some people actually debris, you can actually debride off a dendrite with like a Q2 surface. That's something that could be considered. I don't typically do that. I might consider it if I have someone who's not responding very well to treatment to a traditional treatment. A few decades ago, there was the herpes eye disease study or head study, which is kind of one of those big landmarks, trials. And the purpose of this was to evaluate the efficacy of different treatments on HSV keratitis. They had three arms. One arm looking at HSV stromal keratitis, and they were looking at whether topical steroids along with myoptic, topical, bioptic was helpful. Second arm was also again looking at stromal keratitis, seeing if oral acyclovir was helpful and patients already on topical steroids and topical bioptic. Last arm was looking at HSV erotocyclitis, again looking at steroids and bioptic and seeing whether or not the addition of oral acyclovir was helpful. Here are the results. With the first arm, they did find that topical steroids given with trifluoridine reduced the progression of and shorten the duration of stromal keratitis. I'll give steroids for stromal keratitis. They didn't see an additional benefit of adding oral antivirals in patients already on topical steroids and topical antiviral. However, what I usually do is I'll either with if I've got stromal keratitis, I usually do like oral antivirals such as acyclovir and or Valtrex in addition to steroids. If I'm giving someone Zergan, say I may or may not give the oral, but I usually do. There was a trend to the benefit of oral acyclovir in patients with HSV erotocyclitis who are already on topical steroids and topical antiviral. However, the weakness of the study was I didn't have a ton of patients with HSV erotocyclitis. I think most clinicians will actually will give oral acyclovir with HSV erotocyclitis. Let's see, with HSV disease, I talked about the doses for acyclovir in the treatment, which is the 400 milligrams five times a day. But if someone is taking prophylactic dose, it's going to be lower than the treatment dose. So can be acyclovir 400 milligrams twice a day. Here are some of the alternatives you can do Valtrex once a day or FAMVIR, which I don't use quite as often. There's a dosage there. HSV late complications are many. Number one is going to be a neurotrophic cornea, meaning a cornea that doesn't have proper sensation. That's going to lead to dryness. It can also lead to non-healing epithelial defects. You can get corneal scarring, neovascularization, recurrent inflammation, and corneal thinning. Switching gears to a related condition, herpes zoster. So this is a reactivation of latent varicellular zoster, and there is involvement of the atomic division of cranial nerve 5, so the V1 distribution. Classically, you have Hutchinson sign, which is a rash going all the way down to the tip of the nose. And the involvement of the tip of the nose means that the nasal ciliary nerve is involved. The nasal ciliary nerve innervates the conventival cornea, sclera, iris, chloride, and skin of both eyelids, and it's a strong predictor of ocular inflammation. Zoster manifestations are going to be more common in elderly, but nowadays we're seeing this in plenty of younger patients, so it's not just something that we'll see in older patients. A very wide range of ocular involvement in severity. It could be an anterior segment, it could be a posterior segment, both. It can be acute, chronic, or relapsing. You can get kind of a dendrite appearance just like you can with simplex, except the dendrites look a bit different, so they have an iterma stuck on appearance. So with simplex dendrites, they're kind of excavated, like it's almost like there's a divot in the dendrite, but the pseudo dendrite, it looks more stuck on. So with these 2D pictures, you can't tell that, but you'll see it kind of looks almost like a blob on the cornea, like it's a little bit elevated in zoster, and the dendrites are not quite as well formed. You don't have terminal end bulbs, like there's no nice kind of ending to the dendrite. It's kind of a little bit branchy, but not quite as, I guess, pretty that you'll see with a simplex keratitis. It can lead to stromal keratitis, and like simplex, you're going to have decreased corneal sensation. So, classically, if the symptoms started more kind of more recently, start a cycle of your 800 milligrams five times a day for 10 days. I will start this nowadays, even if symptoms started kind of no more, maybe earlier than 72 hours prior, and there may be a role for reduced dose long term, which is kind of the topic of a big multi-center study, the ZEDS trials, zoster eye disease study, that's looking at whether kind of low dose valtrex for one year after kind of acute symptoms can reduce the incidence of recurrent disease. There may be a role of topical antivirals as well. Definitely want to use topical steroids, and you often need a very slow taper, and I've got many patients who need to be on chronic topical steroids just to prevent any. Dr. Lin. Let's see, late complications of simplex post-herpetic neurologia, where there's continued severe pain, even after the inflammation in the eye is gone. I'll typically refer these patients off to their primary care doctor or neurologist for something like epipentin, or tricyclic antidepressants or Lyrica. As far as eye complications, long-term complications, it's the same as HSV. So this is the same list that I had before, neurotrophic cornea, scarring, new vascularization, recurrent inflammation, corneal thinning. So it can be pretty devastating. This is an example of someone with scarring, new vascularization, corneal thinning in spots. This looks like maybe it does medicine also and cause very severe complications. Next, again, this is a potpourri of lots of topics. So next, we're going to switch gears to corneal trauma. So corneobrasion, something you'll see very commonly, you put in the fluorescein in a patient who has a lot of pain and you see a big VD effect. So treatment of it, typically chloroquine alone four times a day is fine. You can also consider a psychoplegic agent just again, or taking the edge off of pain. You can consider a bandage contact lens or a pressure patch. If there's any concern for infection or if the abrasion happened in the setting of someone whose contact lens wear, I worry about infection. So I may not place a bandage contact lens in those cases. You could consider even a pressure patch on the eye to help the eye heal. A patient would have to kind of take it off once a day, put an ointment and either you have to see the patient to put the patch on or they need a very good kind of person who lives with them or you can take care of them to put the pressure patch on in a correct fashion. You want to closely follow these patients, make sure they don't get infection. If there's not really a clear reason why there's an abrasion, such as there wasn't really any trauma or any known foreign body that flew in, kind of look at the eye exam for exposure. So meaning, you know, make sure the eye, there's no lag ophthalmos, make sure the eye can actually close. You can also avert the upper lid to look for foreign bodies that could have caused that abrasion. So corneal foreign bodies are very common and here's what they always look like. Metal is the most common. You pretty much will get a rust ring that will start to set in pretty frequently. So they're typically pretty superficial. You can remove it with a 27 or 30 gauge needle and you could consider a burr to kind of burr out the rust ring or you could, I like using a needle actually for removing the rust ring but you know both ways are fine. Afterwards there's like a little crater in the cornea so you want to treat it like a corneal abrasion. However, sometimes you can see like a surrounding white, it's like a white infiltrate that's usually sterile. So in those cases, I'll add a little bit of a steroid like a combination antibiotic steroid such as Maxitrol. If it's really deep, you don't want to pursue it, kind of send them to you know me or one of the other cornea specialists to have a look and you always want to counsel a patient on eye protection so they don't get this again. This patient's lucky it's not in the visual axis but if you imagine if this removed a few millimeters over, this would be very visually significant. See other traumas, corneal laceration. So you want to determine if it's a partial or full thickness laceration. So do the Seidel test, see if you have evidence of leakage. Another test you can do is to kind of check the anterior chamber depth and kind of comparing it with the other eye. So if you've got like a full chamber, probably a full thickness penetration, if you've got a shallow chamber, kind of compare with the other eye and if it looks equally shallow, you're probably okay but if the other eye looks a lot deeper then again you kind of get concerned about a full thickness perforation. Obviously if there's peaking with the pupil, iris prolapse, we've got a full thickness perforation. If it's partial thickness, and if you see any foreign material there, you can try and irrigate it out or remove it with Juul's forceps at the slit lamp but if it's something more complicated than what you can do at the slit lamp, you want to take them to the OR. Definitely want to take them to the OR if it's a full thickness maceration. So you want to place a shield on the eye prior just so no one else or no one else or the patient you know will be able to bump their eye. You might consider IV antibiotics and making them MPO in preparation for surgery. Okay so we've gone through some acute eye diseases. We're going to go into some common chronic ones. Blufferitis, super common. I feel like the vast majority of patients have some form of blufferitis. Anterior blufferitis is seen here so that you'll see colorates around the eyelashes. For these cases, lid scrubs are very effective. More commonly, a lot more commonly than anterior is posterior blufferitis where you'll see plugged up oil mybomian glands on mybomian gland insubstitiation which we see here. Warm compresses are going to be very effective for posterior blufferitis. Other treatments, artificial tears, you can also consider oral fish oil, oral doxycycline or minocycline. You kind of use it for not for its antibiotic properties but it's actually got the positive side effect of opening up plugged up mybomian glands. So low dose doxy or minocycline can be helpful. I use 50 milligrams POV ID as my standard dosage. You can also consider like an antibiotic ointment such as erythromycinol into the lashes at bedtime. Related to blufferitis is dry eyes. So symptoms typically can include a whole range of symptoms including tearing or dryness, redness, foreign body sensation, fluctuating vision during the day, having symptoms worse later in the day, worse symptoms with their contact lenses. And there's usually a combination of both evaporative etiologies along with diminished tear secretions. So the evaporative etiology is going to be a lot more common so you'll often see concurrent blufferitis such as mybomian gland plugging. And again when the mybomian glands are plugged you don't have a proper lipid layer for the tear film. Tears are going to evaporate more rapidly. You could also have diminished tear secretion or kind of diminished aqueous layer of the tear film. And you'll see this with autoimmune diseases, sarcoid and collagen vascular disease. And you typically see inflammation associated with dry eyes meaning some redness, inflammation of the congenitiva. On exam you'll see inter-palpibule staining. So this is some rosebangle staining that you'll see the inter-palpibule space. You'll see a low tear film. You can see mucus in the tear film. So mucus and tear film represents dried up tears. So that's a sign of dry eye. And there's also a low tear breakup time. So the way you measure pure tear breakup time is I put a fluorescein drop in each eye. I get the light onto the cobalt blue and I'll ask the patient to kind of close their eyes and then open their eyes and stare. And you can start counting seconds off. And once you start seeing these dark patches, that's actually an evaporated or a broken up tear film. So you stop counting whenever you see one of those kind of patches of black. And if that number that you get when you stop counting is less than 10 seconds, that's a low tear breakup time. So again kind of pointing to an evaporative etiology to their dry eye. I don't do Schermer's testing really at all. I might do it if someone is really asking me to or for research purposes. But it's not a great marker to dry eye. I feel like there's a lot of all these other things that you can do with the slit lamp are going to be pretty indicative of dry eye. But classically there'll be a low Schermer's test. So the Schermer's test is where you put kind of little strips of filter paper hanging off the eyelids. We measure how much of the filter paper gets soaked with the patient's own tears over a five minute period. So five minutes pass with anesthetic in their eyes and they're soaking less than 10 millimeters on the filter paper than that is an abnormal test. Treatment, there's tons of treatments. So I kind of start usually with the non-prescription and non-invasive treatments first. So something as simple as telling patients to take frequent breaks from reading on the computer. So I just tell them, hey, every 20 minutes or so just close your eyes real tight for like 20 seconds. That can help me moisturize everything. A humidifier is really helpful. Artificial tears, of course. Bottle to artificial tears. I tell people not to use them more than four times a day because the preservative can actually start to cause toxicity. So switching a preservative free if they're using drops more than four times a day is something that I recommend. Gel or ointment at night. This is something I'll recommend if someone is waking up with dry eye symptoms. That kind of tells me that their eyes are maybe not closed all the way while they're sleeping. It's a nighttime like ophthalmos. So for those patients, I'll tell them to put in something thicker at night. You know, if they're doing all the above and they're still having dry eye, then you can go prescription route. There's now three prescription drops available on the market now. Restasis, Zydra and now Sequa. For all of these, they do take a little bit of time to work. Restasis takes the longest time, three to four months. Zydra and Sequa maybe about a month to start working and they're all twice a day drops. Taking oral fish oil or even having olive oil in your diet can be helpful for dry eye. Moisture chamber goggles at bedtime can be helpful again if they're having a lot of AM symptoms and then punctal plugs and cottery and lots of other treatments for dry eye even beyond this list, which will be the topic of future literature. So lastly, talking about Fuchs dystrophy. So Fuchs dystrophy, very common. It's an autosomal dominant corneal dystrophy. You actually don't see signs of it until patient is usually in their 40s or 50s, even though it's an inherited condition. And what Fuchs dystrophy is, is a progressive loss of endothelial cells that leads to corneal edema. So again, endothelial cells are in a monolayer kind of all along here. And in this case, you see there's very few. You don't have like a whole bunch in a row like I had in that, I don't know, one of the first slides. There's just only a few endothelial cells. And you also see these bumps in decimates membrane here. So these are excrescences of decimates membrane. And you'll see this clinically as butata. So patients will typically be completely asymptomatic if you're catching them early on exams. So if I see that, I tell them, hey, you've got this condition called Fuchs dystrophy. You're not having any symptoms from it. You know, we'll watch it. You may need treatment later on. Once patients start getting symptoms, they'll start off with having actually morning blurry vision like right after they wake up, that improves later in the day. And the reason why that happens is during the night, you know, your eyes are closed, and there's more fluid kind of around the cornea. And because there's not a great endothelial pump here, the cornea starts to get more edematous. And so when they first open their eyes, they're looking through a little bit more of an edematous cornea, and they can notice some blurred vision. During the course of the day, or maybe an hour or two later, depending on how severe the disease is, they'll notice that their vision's improving because they're literally the corneas drying out just from their iris being opened. So that's the mechanism of the AM blur that improves later. So on Slitlamp, you'll see butte or gutata, these little dots. So it kind of looks like, I'll describe it more like of an orange peel look to the endothelium. So again, this represents the excrescences of decimates membrane. And to see gutata, you have to have kind of the highest intensity like beam. If you just have it on the low intensity beam, you're going to miss like 75% of gutata. So have it on the high beam, focus on the endothelium with a slip beam, and you'll be able to see them more easily. And it takes time to, you know, when you're first starting out interns, first-year residents, it's going to be really hard to see your first, even 50 cases of foodststrophy. But you know, if you keep looking for it, you'll start to see it. In more severe cases, you'll see corneal edema, and that can even lead to bullay, which are kind of blisters on kind of underneath the corneal epithelium. With the edema of the cornea, you'll get a thicker corneal thickness, which is measured with pachymetry. So you might have a cornea that's over 600 microns. I don't do pachymetry, typically in foodstrophy, because again, I kind of base my exam on the slit lamp. And so whether or not a patient has a 550 thick cornea or a 650 thick cornea, it doesn't really matter. What matters to me is what the patient's seeing, what their vision is, and what I'm seeing on exam as far as what I'm going to do next as far as treatment. And same with specular microscopy. So if you do a specular microscopy on patient with Fuchs, what this does is it measures the endothelial cells. So it counts endothelial cells within a small area of the endothelium. And if it's lower, again, it's going to be indicative of Fuchs dystrophy. But again, this is not something I'm doing on all my patients, but it's useful for research doing specular counts. So treatment. So if they're completely asymptomatic, there's really nothing to do except just tell the patient about it, tell them they should come in once a year for exams. If they're having blurred vision in the morning, you can tell patients to put in hypertonic saline or Muro 128. And you want to make sure they get the 5% concentration, not the, I think 2.5 is the other one you can get. I never, ever recommend 2.5. It's always 5%. And you can get it in drop ointment form. I typically do drops just because it's easier to put in. And it's more useful in the morning. So tell patients, use the Muro in the morning when you wake up. That's going to kind of try and that hypertonic saline will kind of draw out some of the excess fluid or edema in the cornea and try to decrease the cornea edema faster. So in mild cases of Fuchs, this will actually work really well. If it's more severe, it's not going to do too much. So it's a nice treatment because I tell people it's literally just concentrated saline. It is going to sting a little bit when it goes in because it's kind of a higher salt content, but you know, it's not really like a prescription. You can get it over the counter. So it's a nice, a nice way to have people maybe help with their vision faster in the morning. If someone has Fuchs dystrophy and they need cataract surgery, there are some things you want to know about making sure that during surgery you protect the endothelium as much as possible because they're going to be more prone to get corneal edema after surgery. If the Fuchs dystrophy is more visually significant, then you want to consider endothelial teratoplasty. Okay, next, special cases in the burn units. So I think this is my last topic. So we're talking about thermal and chemical burns, as well as Stevens-Johnson syndrome. Let's check the time here. Okay, eight minutes. We can do it. Thermal burns are from flame or blast injury, scalding liquids. People are usually not involved because you've got an eyelid reflex or the eyelids are going to close and also you get a bell's reflex as well, but you can have extensive eyelid involvement with thermal burns. Chemical burns can be from any number of agents. Alkaline agents can usually penetrate deeper than acids. The mechanism of that is that usually acids cause a coagulation necrosis, so it prevents further penetration of the acid further down deep into the tissue, whereas alkali agents cause a saponification of fatty acids, which cause cellular disruption and it allows the chemical to actually reach the deeper tissues. So that's why usually alkali agents are worse than acids. However, there are a few strong acids that can be really bad on the eye, but typically it's going to be alkali injuries. So acutely on exam, when you're consulted in the ER or when they're up in the burn unit, hopefully they'll have already irrigated the patient. So if not irrigate, get the pH, make sure it's seven. Do a complete eye exam if you can. And look at the eyelids, look at the edema, look at leg ophthalmos, look at lash loss. Very importantly, you want to check the bell's reflex if there is leg ophthalmos. So here's a patient who, you know, this is him looking straight ahead, very severe burns, as you can see. And then when you ask him to close your eyes, you still see that there's globe there. So this is severe leg ophthalmos, but there's a good bell's reflex. So he's at least protecting his. Look at the conjunctiva cornealophornis, looking at epidefix, foreign bodies, and these sort of acidities. With chemical burns, you want to note the level of limbo ischemia, noting how white the eye is. So that whiteness actually represents a loss of limbo stem cells, which is a actually poorer prognosis than the side that's very red. Eye that's very red is actually good. That means it's good vasculature all around. Hopefully they can heal this large epidefact and maybe this little easy inflammation that's on the eye. Whereas this eye with a very white appearance has lots of vasculature. So they're going to not heal their cornea as well. Late complications on the cornea, persistent corneal epithelial defects, you can even lead to corneal thinning and perforation. Neurovascularization and limbo stem cell deficiency are common. The conjunctiva others can be scarring or some blepharone formation on the eyelids. They'll be progressive scarring, secretarial tropion, tracheosis, and mycoplasmos. So treatment, oral vitamin C and doxycycline. Doxycycline to kind of help with counteracting any sort of corneal thinning that may be going on because it's got an anti-inflammatory effect. To the eyelids, some over through mycinolemia is good. Topical steroids if there's a corneal epithelial defect. I'm sorry, you have fluoroquinolone. Or consider a topical steroid in the first one to two weeks to reduce inflammation. My consider a bandage contact lens or amniotic membrane. If there's a lack of thymos, you want to have very aggressive lubrication like ointment Q1 hour, moisture chamber goggles. Consider eyelid repair, but oftentimes you don't want to go into repair things acutely because things are going to change. So often you need to wait a while before they can get their eyelids repaired. So you want to consider scleral lens as an inpatient, which so scleral lens is a large diameter gas permit contact lens. And so this can be considered in anyone with exposure and non-healing corneal epithelial defects, even despite a frequent ointment and moisture chamber goggles. The scleral lens has a much less infection risk compared to a soft bandage contact lens. We actually have a whole protocol unboxed and we have scleral lenses which are hidden somewhere in the resident room. Hopefully seniors know where they are. So consider this and let me know if you are considering putting this in a patient. They can be really, really helpful. So definitely know that that's something that you can do if you are being consulted on a patient. Lastly, SJS and toxic epidermal necolysis syndrome. So this is a rare, potentially life-threatening hypersensitivity spectrum of conditions that's triggered by medications or infections. There's slipping of the skin and nupus membranes. The only way to diagnose it definitively is by skin biopsy. So that's typically done in a burn unit. So SJS involves 10 to 30% of total body surface area. TENS involves greater than 30%. And patients look like this. I mean, this is a patient with literally no skin. There's no epithelial layer to this patient's skin. That's why it's red. It's not just red because of blood coming from somewhere else. This is red because you're looking at dermis. So very severe. Eyes are involved in the majority of cases. There can be inflammation, pseudomembranes, epithelial defects, a lot of late complications listed here, severe tri-caretinization, eyelid margins, scarring, symboferon, corneal opacities, thinning perforation, and neopascularization. So lots of really horrible complications are possible. However, there is treatment. So with everyone, with SJS TENS, with ocular involvement, de-liberation of the steroids, and then consider urgent surgery with amniotic membrane transplantation, which covers kind of the whole ocular surface, bulbaric and palparybocontin-plavocornia, and the eyelid margins. And there are indications for this in the next slide. But amniotic membrane contains both factors in anti-inflammatory mediators to prevent healing and reduce inflammation, and it prevents late complications. So it's kind of the only thing that's been found to really prevent those horrible complications I had mentioned in the last previous slide. So this is a table that helps us determine when to do amniotic membrane transplantation. So anyone with severe or very severe disease, which is defined as staining, or at least a third of a lid margin on at least one lid, any corneal epithelial defect, more than one state staining, staining of the conjunctiva are greater than one centimeter. So if there's any one of these, you want to do urgent amniotic membrane transplantation. So here are some pictures of what some of these complications look like. So this is a picture of lid margin characterization. So you can tell there's not, I mean, this is not a picture of patients whole eye, but patients whole eye actually looks pretty good. There's not really too much in the way of some blepharone formation. But this patient has really, really severe pain, night sensitivity constantly because of lid margin characterization. And you really have to pull the lid down to see it. Because this is the same patient, I think, with just looking at the slimmap without pulling the lid down. You just might see a hint of it with an irregular lid margin, but you don't really see it unless you pull the eyelid out like this. This is a young patient who, her disease was kind of mild to moderate, kind of was kind of borderline for needing amniotic membrane. But it was done, you can see a little suture of one of the sutures that was placed for the amniotic membrane. But her lid margin looks great. No characterization. I mean, besides that little suture that's there, you can't even tell that anything really happened to this patient's eyes. So this is a great result. Here's a patient who had amniotic membrane transplant done a bit late, maybe more than two weeks after presentation. And so that was a bit too late. This young patient has had severe inflammation, severe scarring. You might get a sense of some of the lid margin curatization. So really important to do amniotic membrane transplant kind of sooner or rather than later in SJS. And that is it. Any questions on anything thus far? Hey, Dr. Lin, since the sequelin restasis, you know, are both like the spore. And if someone doesn't respond to restasis, do you not try sequa? Is it so reasonable to give sequa a try on this kind of thing? That's a good question. I mean, I would say usually no, but I have had actually a couple patients that I've tried sequa on where restasis didn't work and they had a good response to sequa. So I wouldn't say it's a definite rule out if someone didn't respond to restasis. You can still try it. Any other questions? All right. Well, let me know if you have any questions on anything else, cornea-related. I look forward to kind of seeing you all with this new year. And that's about it. I guess have a great Monday, everyone. Thanks, Dr. Lin. Welcome. Thank you. Bye. Bye.