 Alright, so welcome everyone, for those of you who don't know me, I am Amy Lin, I'm one of the Acornia faculty here. So I'll just be giving a little overview on Introduction to Acornia, kind of a little crash course, I'll be going over a lot of topics, so just let me know if there's any questions on anything. So I'll go over anatomy and physiology, basic slant lamp techniques, some common acute and chronic corneal diseases, and kind of special cases that one should know about in the burn unit. So cornea is an avascular, transparent structure as you all know, it does measure 11 to 12 millimeters horizontally, it's steeper in the center and then becomes less steep in the periphery, and that's termed a prolate cornea. That's a very, very high density of nerve endings, which is why any sort of abrasion or injury to the cornea is very, very painful. So this is the microscopic cross-section of the cornea, starting with epithelium, and then there's about four to five cell layers of stratified epithelium, and it sits on an epithelial basement membrane, and then beneath the epithelial basement membrane is what's termed Bowman's layer, or sometimes Bowman's membrane, which is a little bit of a confusing term, so Bowman's membrane is not the basement membrane of the corneal epithelium, just happens to be this avascular layer that separates epithelium from the stroma. So if you ever hear about Bowman's layer, Bowman's membrane, that's what that's referring to, it's right under the epithelial, and epithelial basement membrane. Stroma's consisting kind of the main bulk of the cornea, it consists of keratocytes that are arranged in a very regular pattern so that it can retain transparency, and the water content of the stroma also needs to be at a very specific percentage, 78%, so that it can't remain transparent. Then you get to the bottom of the stroma, you get decimates membrane and endothelium, decimates membrane is indeed the best basement membrane of the endothelium, and there are many protein channels, kind of TPA channels, within the endothelial layer, again to prevent excess water from hitting the stroma, and there's also tight junctions in between epithelial cells in the epithelium, again to prevent any fluid from ingressing into the stroma. The tear film consists of three layers, we got a top layer, which is the lipid layer, the aqueous layer, takes up the bulk of the tear film, and then a bottom mucin layer, so the lipid layer is formed by the mybomene glands, and that is responsible for maintaining or preventing evaporation of the tear film, like the oil slick tear film. Then the aqueous layer consists of the main lacrimal gland, and the accessory lacrimal glands of crows and wolf ring, and the accessory lacrimal glands are within kind of the tarsal conjuntiva, glands of crows are within the fornix, and wolf ring are just above the tarsal plate. Then the mucin layer is produced by the goblet cells, and the mucin layer is responsible for having the tear film actually stick to the ocular surface, so you'll see that there's these microbial eye on the epithelium that'll kind of stick to the mucins, and that is responsible for sticking the tear film to the ocular surface. Next I'll go over slip lamp techniques. So diffuse illumination is when you have your lip on the lower mag, and you just have it on not the brightest setting, and kind of a broad beam, and this allows you to see like the landscape of the cornea, just to kind of get an idea like is there going to be any one thing that I'll be concentrating my attention on, just getting a kind of a broad view. So you know in this picture here it shows that there's something going on here, so that maybe one should kind of pay attention to. Then focal illumination is kind of the next most common technique where you just kind of get the slip beam to a narrower beam, and you can mag up and kind of look at certain structures, or you can even kind of scan across the cornea, just to make sure you're not missing anything, and you can scan kind of x, y, and you can scan kind of deep and superficial. Then I'll talk about some techniques that are maybe a little less common. So specular reflection is a way to look at structures around light reflexes, and it's especially useful for looking at the endothelial surface. So what you do is you get your viewing arm about 60 degrees away from at an angle, and then you want to superimpose like you know that there's that that light reflex like off the light bulb that I don't know, as medical students, and maybe you and I for first learning how to use a slit lamp, like that was really distracting, like that was something like I wanted to concentrate on, but it's just like artifacts just like the light bulb reflection. You actually want to take that light bulb reflection and superimpose it on the actual, in this case like the endothelial light reflex, so you can see like these two are kind of becoming together, and you kind of focus maybe a little bit deeper, and you get this really bright light reflex, and you kind of look around the area of the bright light reflex to see the endothelial cells. Sclerotic scatter is a technique where you actually shine a really really bright beam at the limbus, and light kind of scatters into or diffuses into the cornea, and it can bounce off of some subtle abnormalities, in this case the corneal scar right here, and then retroillumination is a technique where you can see especially defects in the iris, you can also see abnormalities in the cornea and lens. You basically have the light going straight on into the pupil, and it bounces off the retina and kind of glows back, and so you can see iris defects very well, in this case it's showing diffuse iris transillumination defects, which may not have been really easily seen with just direct illumination. So these are kind of the basic techniques that one can use. Kind of skipping over to corneal stains, again this is kind of a potpourri of various exam techniques, so we all know about fluorescein. It can come in a solution, and it can come on strips, and fluorescein stains based with membrane, which you can see up here, so you can kind of highlight areas without epithelial cells, so you can show puncted epithelial erosions, you can show corneal abrasions, you can show corneal ulcers with epithelial defects. Rosebengal typically comes in strips, and the stains devitalize cells, some kind of dead cells, and it's really nice for highlighting, I mean not only, I mean I guess you could pick up staining on the cornea, but it acts actually really nice for staining defects on the contractiva. But the downside to rosebengal is it stings a lot, even with topical anesthetic, people can feel that it stings a lot. Lysamine green does the same as rosebengal, but it doesn't sting, so again lysamine green would stain the vital eye cells, and this typically comes in strips and less irritating, so this is kind of lysamine green staining of the punctate staining of the bulbar contractiva. Other miscellaneous exam tips, particular for maybe the med students and interns to know about, is you want to remove soft contact lenses prior to being stealing fluorescein, because fluorescein stains soft contact lenses forever, which is maybe not so great if you've got someone who's got their contact lenses for like a whole year. I mean nowadays people have contact lenses that are like daily disposable, so it's not that big of a deal, but that's something kind of a common rookie mistake that I think a lot of people do. You want to keep track of your topical anesthetic, like preparecane, tetracane, and fluorescein, which typically has topical anesthetic mixed in with it, because you can have people kind of stealing it from the ER or from the exam room if they've got like corneal abrasion, and you put in that drop and they're like, wow, this helps. You leave the room, if you leave the bottle out there they might just snag it, and that can lead to topical anesthetic abuse, which is not good for the surface of the eyes. Anyone with a red eye or corneal abrasion, you do want to flip the upper lid, because sometimes you can find things hiding under there that could be causing their issue. Okay, so next, switching gears to some common corneal and contractible issues. So conjunctivitis is kind of three major categories, bacterial, viral, and allergic. Typically the history will point you kind of in one direction or another. With bacterial they usually complain of tons of discharge, purulent discharge. With viral disease they'll complain of either having a recent cold or maybe being around someone with a cold, around someone with a red eye. Intimidate the viral, conjunctivitis will start in one eye and then very quickly go to the other eye, and with allergic to conjunctivitis itching is the main complaint. So there's a lot of itching, like they really want to get in and really rub their eyes and think about allergic conjunctivitis. And then you'll see these reactions on the tarsal, on the tarsal, contractival follicles and papillae. So follicles are kind of may point you more towards viral conjunctivitis, and follicles are actually clusters of lymphocytes, and the blood vessels will actually go around the follicles, so it's kind of relatively wider in the center. Whereas papillae are actually kind of you got these that's like basically dilatation of the blood vessels and they kind of sprout these capillaries around this dilated vessel and you get like edema around the capillaries. So papillae you'll actually notice they have red centers. You can see papillae that'll point you more to allergic conjunctivitis. Oftentimes you might get a mixed picture and then it's a little harder to kind of figure out if it's going to be viral allergic. So that's why kind of getting a good history can point you in the right direction. You can get giant papillae conjunctivitis, which you can see typically with people with reactions against their contact lenses. If you flip their lid, you'll see these are really large. Episcleritis is a benign transient inflammation of the ocular surface or every sclera. On history, and this is very important to kind of distinguish it from scleritis, is that there's minimal or no pain. And on exam, if you put in a drop of phenyl ephirin, the red area will blanch about five minutes after placing up an ephirin. Typically no workup is needed for every scleritis. However, if it is recurrent, then you do need to do a workup. So some of the systemic associations are exhaustor, collagen, vascular disease, gout, and syphilis. So you may want to kind of work up everything or maybe work up depending on any anything positive on their review of systems. Typically, episcleritis is self-limited. It can resolve on its own with just some artificial tears. However, however you consider high dose oral NSAIDs, my topical NSAIDs are steroids to maybe speed up the resolution. Whereas scleritis is very typically very tender and very painful. Classically, this is the type of pain that will wake someone up from sleep. And on exam, there's no blanching with phenyl ephirin or neosin ephirin. And there are a few types. There is non-necrotizing, necrotizing without inflammation or scleral malatial perforance, which is actually painless, and necrotizing with inflammation. And there's a significant association with systemic disease with any type of scleritis. So some of the systemic associations would be rheumatoid arthritis, lupus, ankylosing spondylitis or psoriasis, Crohn's disease, wagoners, syphilis and TB. And scleritis, you always want to work up. So even if it's the first time with scleritis, you always want to work it up. You can use history to guide testing. So here are again some of the common labs that you can look into, ANA rheumatoid factor, HLA B-27, looking for ankylosing spondylitis, looking for TB with BPD and quant gold and a chest x-ray, FTA, ABS and the Incas. If the labs are negative, you could consider VP testing later on. So going over the subtypes of scleritis, so with non-necrotizing scleritis, this is the least severe of the types. You have a very, very red or violacious hue. And there's a 50% association with systemic disease and 50% of the time it is bilateral. And scleritis, it's always going to be there unless you treat it. So if you leave it alone, it's just going to be there. Scleromalacia perforans is necrotizing scleritis without inflammation. So this is the one that's a little different from the other types of scleritis because it's painless. It looks like a white and quiet eye, but there's some thin sclera. It tends to be more common in the elderly and it's very commonly bilateral. 50% of the time this is for rheumatoid arthritis. So you can see in this picture down here, there's areas of the sclera which are very thin where you can be seeing the corroid of the UVS showing through. And scleral rupture is rare. This rarely needs surgical repair, but this does need to work up and definitely does need treatment with systemic pressure. Necrotizing scleritis with inflammation is also very painful, also most commonly bilateral. And this is the most destructive type of scleritis with vision loss in 40% of cases. Very high association with systemic vasculitis such as Wriganers, which I guess has a new name now. It's a new name. Polyangitis. I can't remember that. I'm going to call it Wriganers, but yes it's got the other name. And there's a very high mortality rate, 20% at five years. Contact lens abuse is a really common thing that's seen in the ER or triage clinic. Typically by history there's contact lens use of at least 12 hours a day. They're sleeping in their lenses or poor contact lens hygiene. Typically you've got bilateral red eyes. You'll see a vascular panis or basically neovascular use of the cornea because they've been wearing their contact lenses so long. They'll be punctate staining and sometimes you can see these really fine punctates of epithelial opacity. So these are not infectious, but rather kind of inflammatory reactions in the cornea. Treatment is discontinuing the contact lenses until everything resolves, using artificial tears. One could consider a mild steroid drop such as fluoromethalone or little predinal. I don't always give a steroid drop just because with contact lens abuse people they may not come back so you'd hate for them to maybe develop like an infectious keratitis. So I kind of use my gut feeling with dispensing steroid drops because I could lead to a corneal ulcer. So I'm in the most frequent risk factor seen with corneal ulcers is contact lenses whether with or without contact lens abuse. Other risk factors for a corneal ulcer include previous eye surgery, previous trauma, if they're a healthcare worker or a nursing home, if there is concurrent ocular surface disease, systemic immunosuppression and you do want to get a history with a degree of pain and duration. Kind of get a history of whether or any other eye drops were used or if they saw the optometrist and got put on something that's also important for the history. And there's kind of corneal ulcers can be mild, they can be very severe. The most common type are bacteria and that typically has a very quick onset. You can also get viral corneal ulcers, fungal and parasitic with the most common being acanthamoeba. So on exam you want to look at several things. The location meaning where in the cornea is a peripheral, is it central, is it superior, is it inferior. The shape of the corneal ulcer is like is it really round, is it really fluffy, is it kind of stellate. And then you want to use the ruler on the cilantro to kind of measure the size of it. See if you can get a sense of the depth, is it very superficial, is it all endothelial or is it panstromal. I get a sense of the density, is it really dense, is it like just really light, is it fluffy, is it associated with an inflammatory response like if is there a lot of haze surrounding the corneal ulcer. These are all important things to take note of. So then when do you culture corneal ulcer? You don't necessarily have to culture ulcers but you definitely want to culture. If they are large, large is kind of maybe anything above two or three millimeters. Vision threatening, so you might have a very small ulcer but if it's close to the visual axis that would be maybe one to culture. Definitely if there's a hypopia and definitely if they are post-op meaning like especially post-op corneal transplants. Because you can get a weird bacteria and fungal infections with post-op patients so I definitely want to culture those. There's a traditional culturing which I'll go over and then my next slide will be kind of how we all to do it now but the traditional culturing of corneal ulcer involves something called a chimera spatula which is this top instrument here so it's kind of a thin metal blunt instrument or you could use a calcium alginate swab which is kind of like a mini q-tip and you want to kind of get into the infiltrate and you want to spread a thin layer into culture plates and use a separate swab for each plate and you can do gram stain, you can spread it on blood agar which is good for growing aerobic bacteria. Chocolate agar is good for nyseria and hemophilus. Savory agar is good for fungi and thyroid glycolate broth is good for anaerobic bacteria. In the past year or so here at Moran we've switched to the e-swab which is really really easy it's it's just one swab so instead of having all these different plates and having like different culturing techniques you just swab one time. So it's a nylon tip swab with a flocked fiber arrangement which allows for an improved sample collection with increased capillary action and hydraulic liquid updates so it looks kind of like I guess like a small q-tip there's a little picture of it here but when you look at it under the slit lamp you can see all these little fibers that are kind of coming out and that really kind of improves collection from the ulcer and so you just do that you put that into you send it off to lab you still need to put it in the orders for aerobic bacteria anaerobic fungus or whatever else you want it doesn't do everything like I don't think it does viral culture but then when the e-swab is accepted by the lab they the lab people actually kind of spread it out onto the different culture media and it's been shown to be non-inferior to traditional collection methods with regards to culture positivity rates so it's nice it's easier and it's just as good as traditional plating. Initial treatment for acornia ulcer would depend on kind of how it looks so you can start with a fourth generation fluoroquinolone four times a day to q1 hour depending on the size, depth, density if it's more severe or more concerning or especially if they're like say post-corneal transplant and then I would start with fortified antibiotics which can be compounded at the marion or inpatient pharmacy, vancomycin and tobromycin usually for use like q1 hour to two hours. You can consider a cycloplegic agent such as cyclodial home atropine or atropine to decrease pain and also maybe cut down on the risk of sneaky eye formation from the pupil. We don't usually admit people with corneal ulcers here but you could consider admitting patients as an inpatient if they are homeless or if they're really really super questionable compliance then you might want to admit a patient. Okay next moving on to herpes simplex keratitis. The symptoms of HSV keratitis are you know it's kind of really non-specific redness, blurry vision, they could have mild irritation or they could have severe pain. The hallmark though is diminished corneal sensation so you want to check this prior to anesthetic. The way I do it is I just take like a q-tip and kind of whisk off the top of it and have and have them look straight ahead and kind of touch each side and ask them you know do you feel it more on one side or the other. Usually you'll see the reaction like on the side that might have decreased corneal sensation they're just kind of looking and you go over the other side and they're like whoa then you kind of know that they have decreased corneal sensation on one side. Types of HSV keratitis are epithelial and I'm going to start with epithelial and stromal. So epithelial, HSV keratitis, is it done right? I'm just seeing up here. It's kind of branching and it's got terminal end bulb so it's a little bulb of the bulby things at the end. Stromal keratitis, stromal HSV keratitis is the most common cause of infectious corneal blindness in the US. So you'll see some light opacity in the stroma. A type of stromal keratitis is discopharm which is stromal edema in a round distribution associated with curatic precipitants or KP's. It's also termed endothelianitis. Treatment of epithelial disease in most cases will actually resolve spontaneously but I typically do treat patients if they're coming in. This is Rosebangle-stained HSV dendrite. Traditionally you could use topical trifluoridine eight times a day but you want to discontinue it within let's say 10 to 14 days to avoid toxicity to the alkyl surface. There's been a newer drug called Zergam which is gang cyclotopical, gang cyclovir gel which you can use five times a day. I like using acyclovir and you could either do the kind of the traditional dose which is 400 milligrams five times a day an easier and maybe almost just as good of a dose that just 800 milligrams VID. You do not want to use any steroid for HSV dendritic keratitis. Some people do epithelial debreatment will actually take off the dendrite to shorten the course. There was many years ago the head study or the herpes eye disease study which looked at not dendritic keratitis but stromal and iridocyclitis and they were evaluating the efficacy of topical steroids. So then one arm which looked at topical steroids and stromal keratitis along with prophylactic dose of topical trifluoridine. They looked at oral acyclovir and treating stromal keratitis in patients on steroids and trifluoridine and then they also looked at HSV iridocyclitis looking at oral acyclovir in combination with topical steroids and trifluoridine. So the results showed that when you give topical steroids with a topical prophylactic antiviral it reduced the progression and shortened the duration of HSV stromal keratitis. They didn't show any additional benefit when you added oral acyclovir if they were already on steroids and trifluoridine and again this is for stromal keratitis and the HSV iridocyclitis arm that it showed a trend to benefit with oral acyclovir with topical steroids and antivirals but they didn't have as many patients in this category as they did in a stromal keratitis category. Here are some dosages of medications and the prevention of recurrent inflammatory disease so these are not the treatment doses prevention. So the acyclovir 400 milligrams twice a day, FAM, acyclovir 125 or 215 milligrams twice a day and Vali acyclovir 1000 milligrams. Late complications of HSV keratitis include a neurotrophic cornea so cornea that doesn't have normal sensation that can lead to chronic dryness and non healing epithelial defects there can be permanent scarring, neovascularization of the cornea, recurrent inflammation and corneal thinning. The sister to HSV is her disaster this is a reactivation of latent BCV and this will affect the eye when there's involvement of the ophthalmic division of cranial nerve 5. Classic sign is Hutchingson sign which is seen right there so there's involvement of the tip of the nose that means that the nasociliary nerve is involved and the nasociliary nerve innervates the conditivocornis, sclera, iris, chloride and eyelid skin so it's a strong predictor of ocular inflammation. Manifestations of disaster small commonly seen in the elderly although we are seeing it very commonly in younger patients now. There's a wide range of ocular involvement in severity it can be acute, it can be chronic, it can be relapsing and if there's epithelial involvement typically there's a pseudo dendrite which has a stuck-on appearance with no terminal end bulbs so a classic HSV dendrite will look kind of excavated whereas a zoster dendrite looks stuck on like it looks kind of elevated and you're not going to see those nice end bulbs and pseudo dendrites that you do with true dendrites. Stromal keratitis is common and like HSV you get decreased corneal sensation. So if the symptoms started in the previous 72 hours I want to start very high dose acyclovir so this is double the dose of HSV so 800 milligrams five times a day for 10 days and actually I think there is a role for a reduced dose long-term and we're actually very soon going to be starting Moran's going to be part of the ZEDS study our trial which is Zoster Eye Disease study so it's like heads but it says so I was looking at whether or not long-term valtrates or valicyclovir actually can reduce the incidents of recurrent Zoster Eye Disease. There may be a role for topical antivirals I typically don't use them I just go straight to the systemic antivirals definitely a role for topical steroids for anterior segment inflammation or keratitis and a lot of patients need a very very slow taper or even chronic use of topical steroids to prevent recurrence as well. Late complications of Zoster keratitis post-herpetic neuralgia which is a pain of the kind of nerves around the eye which can be very severe that's going to be treated with things like gabapentin, trisaclic antidepressants and lyrica. You get the same ocular complications with Zoster keratitis as HSV, get a neurotrophic cornea, again scarring, neovascularization, recurrent inflammation and corneal thinning. Any questions so far? Next talking about corneal trauma so again very commonly seen in the ER corneal abrasion and treatment is going to be with topical antibiotics to prevent an ulcer. I've seen and I don't agree with this but I see that like people kind of titrate the frequency of their antibiotic with the size of the corneal abrasion so like you know if it's a small corneal abrasion they'll put them on four times a day bigamoks and if it's like really large like this it's like q1 hour. I think it's just this is all preventative this is not an ulcer so I think regardless of the size of the corneal abrasion just blow up when alone four times a day so I mean. Consider a cycliclic agent just for pain control and then depending on the modality of the injury and how big the abrasion is you can consider the use of a bandage contact lens or a pressure patch to induce healing. The reason why I wouldn't always use a bandage contact lens would be if you've got someone who you think may not come back to get their bandage contact lens out you probably shouldn't put them in. If it was kind of a dirty kind of mechanism of action like tree branch scraping their eye maybe something that may have infectious organisms kind of floating around you also don't want to use a bandage contact lens. You do want to follow closely for an infiltrate follow for healing if there's no reason for there's no traumatic insult in the history could examine for exposure meaning maybe there's some leg ophthalmos or they may have something called recurrent erosion syndrome where they get these recurrent corneal abrasions because their epithelium is not healing over so you want to ask in the history like is this something that's been happening periodically. Corneal foreign body metallic being the most common if it's superficial I typically use a needle to remove it at the slit lamp you could also consider the use of a burr or a needle for a rust ring which is very very commonly seen after the foreign body is removed and then after that's allowed you treat it like an abrasion. It is common to have some surrounding sterile white kind of an infiltrate it's these are usually sterile they're not infectious so the use of a combination antibiotic in a steroid is okay if it's really deep don't pursue it and you definitely want to counsel patients on eye protection. Next corneal lacerations so so in the ER or at the slit lamp you want to determine if it's a partial or full thickness laceration full thickness would be a ruptured globe so you want to do a Seidel test where you run a fluorescein strip over the area and if you see like waterfall fluid that means there's an open globe. You can also look at the anterior chamber depth and see and if it's a shallow anterior chamber and let's say it's Seidel negative if it's shallow it could have been like a self-sealed wound and you can compare anterior chamber depths with the other eye to know what normal is for that patient. Obviously if there's peeking of the pupil or iris prolapse then you know there's an open globe. If it's a partial thickness laceration you can look for any foreign material remove or irrigate it. You do want to take patients to the OR for repair if it's full thickness on an urgent basis. Place a shield on the eye prior so that they're not rubbing it and no one else is kind of touching the eye. You might consider the IV antibiotics and you definitely want to make them NPO. Yes. Do you guys ever take patients to the OR with a deep partial thickness corneal laceration? Yeah. So what's kind of do you have like a cut off? It depends. I mean if it's like really superficial like it's kind of almost like a deep corneal abrasion probably just leave it alone. If it's like gaping then yeah you definitely want to take that back to the OR. Such of gears to common chronic eye disease so blepharitis is very common there's anterior and posterior with anterior blepharitis you'll see these colorates around eyelashes. Here lid scrubs are very effective for anterior blepharitis. Posterior blepharitis there's mybomian gland inspecations so you'll see these plugged mybomian glands there and warm compresses are effective for posterior blepharitis and some people can have a mixed picture of both kinds as well. Artificial tears are helpful because blepharitis does lead to dry eye symptoms. One can consider fish oil, doxycycline or minocycline orally, antibiotic ointment to the lashes. If you're seeing someone in like the ER and we don't need to start like the fish oil and doxycycline just artificial tears, tell them about warm compresses or lid scrubs might consider an antibiotic ointment to the lashes. Dry eyes, very very common here. They've got symptoms of tearing, dryness, redness, foreign body sensation, fluctuating vision that's a key one. Typically the symptoms are worse later in the day and typically worse with contact lens use. There are kind of a couple different etiologies in the traditional view of dry eye. There's evaporative which in which case there's usually concurrent mybomian gland plug-in. So again mybomian glands produce that lipid layer so if they don't have a lipid layer their tears are evaporating faster. Dementious tear secretion in my collagen vascular disease or sarcoid is also seen and it's typically associated with some component of inflammation in the eyes. So on exam you'll see interp, how people staining and you'll see a low tear film. You might see mucus floating around the tear film that's indicative of dry eye because when tears evaporate they leave behind the mucus. So if you see mucus that's a sign of dry eye and again you want to rule out infectious etiology if it's a lot of discharge. Low tear breakup time so this is looking at an evaporative etiology to dry eye. So what you do is you put fluorescein in each eye and turn it over to the cobalt blue and you basically tell patients to blink and then kind of have them open their eyes without blinking and you count seconds down until you start seeing kind of an area of where the tears kind of dry up so you can see these dark spots. So once you see a dark spot you stop your timer and so if that number is less than 10 seconds that's considered low tear breakup time so tears are evaporating really quick. You can also consider doing a Shermer's test. If I do it I don't do it very often but if I do it I'll do it with anesthetic and if it's less than 10 millimeters with anesthetic that's considered low. Lots of treatments for dry eye so you know starting with just really conservative things which would be taking frequent breaks when they're reading or at the computer just got to take a break close your eyes that can be helpful. I always tell people about humidifiers they're really helpful, preservative free artificial tears I recommend preservative free if they're going to use them more than four times a day just to prevent preservative toxicity to the ocular surface. Night time use of gel or ointment, restasis and Zidra which I don't only have time to go more into but they're both BID drops that do take some time to work so it's not really instantaneous. I used to be a big advocate of fish oil which not that it doesn't work but I think it works really well but there was a recent study it was called the dream study which looked at fish oil versus a placebo and they found that both the placebo and fish oil actually improve dry eye symptoms and their placebo happened to be olive oil so because of that you know I don't only tell people the fish oil doesn't work I think it works but it works just as good as olive oil so you don't want to take fish oil capsules just have some olive oil in your diet like at least a teaspoon is worth it's way cheaper and more yummier. Moisture chamber goggles if you think they're like have night time leg ophthalmos and puntle plugs and colors. Flucts dystrophy in a very common condition you'll see this is an autosomal dominant corneal dystrophy typically starts to appear clinically when someone's in their 40s to 50s and it's a progressive loss of endothelial cells that leads to corneal edema. It's usually asymptomatic and then what if and when it worsens there's going to be some blurriness in the morning that improves later in the day so what you see on pathology is you see this well the decimates membrane is abnormal so you see these little bumps here these are excrescent excrescences of decimates membrane and these are gutata which you'll see on a subsequent slide and then you see there's not very many endothelial cells here so the reason why this morning blurring with fuxtystrophy is that there's not very many endothelial cells and not going to be pumping the fluid out of the cornea very well and at night your eyes are closed all night there's more kind of more humid environment and so the endothelial cells aren't really going to keep up with keeping the cornea clear and so when they wake up they notice kind of a little bit of there's a little relative edema in their corneas and the patients notice it as blurry vision so on exam you'll see gutae or gutata which you'll see here so you can see them on retro illumination or i find they're easier to see if you turn up the light really bright and you have a narrow beam you're typically not going to see them if you have them on just the normal um light intensity so you got to turn up the light um you can in severe cases you'll see corneal edema and bullet um you could check up a chemistry it's um typically thicker in fuchs like greater than 600 microns um and you could do specular microscopy which will show a low endothelial cell count um so this is again showing gutata and these are pigmented so these um this is something that you'll see is that you might have actually pigmented gutata um so the way you distinguish gutata from carotid precipitates or kps the gutata will have like texture so i mean these are 2d images it's hard to see what's going on but they'll look like an orange peel like you'll see like texture and so if you see that it's gutata if the whatever you're looking at like the pigmented stuff is just flat along the endothelium that's going to be endopigment or kps so that's how you tell the difference um see treatment if they are asymptomatic do nothing if they've got blurry vision in the morning you could use have amuse hypertonic saline um which is sodium chloride 5% or mirror 128 um drops for ointment to decrease the corneal edema because that extra salt content will draw fluid out of the cornea and so you could tell people to use it more in the morning when they're having symptoms um you do there are special considerations in fuchs dystrophy with cataract surgery because the feco energy during surgery can cause more endothelial cell loss so you want to minimize that and there's certain techniques for doing that um if it's visually significant endothelial caretoflasty or corneal transplantation of the endothelial layer um is warranted and there's d-second d-mech which is beyond the scope of this talk um lastly i wanted to conclude with some special cases like things that you'll see in the burn unit which is not and not all hospitals have a burn unit so if you've never um been in one that does you do kind of kind of have to know what you're dealing with because there's very very severe conditions in the eyes that you'll see so you'll see thermal and chemical burns as well as stevens johnson syndrome or toxic epidermonic or lysis syndrome as well so with thermal and chemical burns um so thermal you're going to have flame blast injury or scalding liquids um you're not usually going to have um like globe involvement um because there's an eyelid reflex so usually they close their eyes and they just get it on their eyelids typically but you can have severe oculosurface burns as well uh chemical burns are you can be from solids the goods or gases and alkali agents usually penetrate deeper than acids so acids cause a coagulation necrosis so the cells die off and it prevents further penetration of that acid deeper in the eye whereas alkali agents cause spawnification of fatty acids that causes cellular disruption and it actually allows the chemical to go deeper into the eye um so on acute exam you want to irrigate um even if they've already well i guess if they've been irrigated in the ear you may not have to do it but if you're not sure if they were irrigated properly then i would go ahead and irrigate um you can check the pH on the pH strips um do a complete eye exam look at the eyelids i'll look for edema leg ophthalmosin lash loss if there is leg ophthalmosin you want to check the bell's reflex so here's a patient who has very severe burns as you can see and if you tell him to close his eyes there's still a large opening there so lots of leg ophthalmos luckily this patient has a good bell's reflex so he's heightened he's able to protect his cornea um look carefully at the at the contra type of cornea infornices looking for epithelial defects foreign bodies and the opacities we want to very importantly note the level of limbolechemia so limbolechemia is whiteness on the limbus and this means that there's loss of limbole stem cells and it means that there's actual poor poor prognosis so these are two eyes with chemical burns and the red eye actually has a better prognosis than this one let's see leg complications of burns um you can have persistent corneal epithelial defects typically if there's limbole stem cell deficiency associated corneal thinning corneal perforation and corneal nemasculization and the conjunctiva can lead to scarring or some blepharone and the eyelids there can be progressive scarring cicatricial ectropion or entropion um tracheosis and leg ophthalmos treatment for thermal and chemical burns um vitamin c oral doxycycline so the oral doxycycline can kind of prevent any further thinning of the cornea um lubricate the eyes really well with ointment um topical steroids if there's an epithelial defect um i highly consider topical steroids in the first couple weeks to reduce inflammation on the surface of the eye even if there is an epithelial defect um can consider bandage contact lenses even amniotic membrane in severe cases um if there's leg ophthalmos you want to have really aggressive lubrication like ointment q1 hour or um moisture chamber goggles um typically the eyelids do need to be repaired but often they need to wait um because if there's any sort of acute repair of the eyelids it's just gonna kind of open up again so typically they i mean maybe not the burn service they tend to be too aggressive i think maybe not here but um oculoplastics they tend to wait for a while before they repair the eyelids um and then here at moran we started um the use of inpatient scleral lenses for protection of the ocular surface so um so what's a scleral lens a scleral lens is a large diameter gas permeable contact lens which looks like this and it's typically used um as an outpatient basis um for patients with a lot of irregularity in their dreams high astigmatism where a traditional gas prim contact lens doesn't really help so much and this is nice because the scleral lens actually evolves over the whole cornea and it just touches the eye on the sclera and it's typically filled with like sterile vss or sterile saline um when it's used as an inpatient we're using it for exposure keratopathy with non-healing corneopathial defix or corneal thinning and scarring that's refractive to refractory to other treatments such as ointment and moisture chamber goggles um scleral lenses have a much much less risk of infection compared to bandage contact lenses um i believe we have a protocol somewhere on the box directory um so if any of the residents are on call and are on the consult service and you want to start a patient with scleral lenses run it by the fellows who run it by me because they probably don't know much about it so i definitely want to know if there's any patient who um scleral lenses on and so there's a whole kind of protocol of what you do um next talking about sjs intent so stevens johnson syndrome or um toxic epidermal necrolysis so this is a spectrum of rare potentially life threatening hypersensitivity conditions that's typically triggered by medications um and more infrequently triggered by infections where there is um sloughing of the skin and mucus membranes um this is a patient in the burn ICU and you notice like her face is really red it's not that there's blood on her face it's actually has no skin so there's that's why she looks this way definitive diagnosis is by skin biopsy and sjs involves um 10 to 30 percent of total body surface area whereas tens involves greater than 30 percent of total body surface area um the eyes are involved in the large percentage of cases 67 to 81 percent um and there could be a whole range of symptoms that you'll see there'll be congenitival inflammation uh pseudo membranes um on the torso congenitiva there'll be congenitival and cornea epithelial defects um and you also might see lid margins staining as well um the late complications of sjs are very very severe dry eyes because there's a loss of goblet cells and sjs um caritonization of the eyelid margin which can lead to chronic pain um and photosensitivity they'll be scarring of the congenitiva and cornea some blood form formation corneal opacities corneal thinning perforation and uvascularization so these are blinding complications um that can be seen chronically after the acute disease is gone um so treatment with sjs and tens um kind of the base level is lubrication and topical steroids um in more severe cases urgent membrane transplantation is needed over the entire ocular surface so bulbar and palpiboconge cornea and eyelid margins um and amniac membrane this is human amniac membrane that has a lot of growth factors and anti-inflammatory mediators to promote healing and reduce inflammation and this actually prevents the late complications so um if you've heard of amniac membrane for use in the eye i think this is the one actual indication for amniac membrane these are for a lot of other things it's not that's not indicated for anything else but this is probably the one like most important indication is for sjs tens um and a couple years ago um there was kind of a nomogram put out as far as that kind of can help practitioners decide whether or not to start amniac or to use amniac membrane so this kind of uh has a severity of mild to extremely severe ocular involvement and then um so if you look over towards severe and extremely severe so if there's at least one third of the lid margin uh staining on at least one lid that's considered severe um if there's any corneal epithelio defect more than puntate staining that is also considered severe if there is staining on the bulbar contantiva that's greater than one centimeter that would be considered severe so then um if you see any of that um medical therapy as well as urgent amniac membrane transplantation is indicated if there's anything less than the severe um just medical therapy and observation is indicated um here's some examples of chronic patients so up on the top these two pictures of the same patient this is showing um characterization of the lid margin um and you'll see a little kind of bumpiness along the lid margin there so this is someone who did not get uh amniac membrane transplantation um this is a girl who did um and you can't even tell if there's anything there it looks like a completely normal eye um this is a boy who got amniatic membrane late so if you um are going with amniatic membrane you want to do it urgently like pretty much ASAP they say within 10 days of the symptom onset so usually by a time they get to like admitted to the burn unit it's been at least a few days so the earlier transplantation is done the better the outcome so this boy has a lot of you can see tarso congenital scarring there's a lot of inflammation on the eye um there's even some scarring kind of coming in here so you want to prevent these um kind of late complicated complications and that is it in questions yes we're at amniatic membrane like the prokera or the desiccated one yeah so um so there's kind of two well there's two main types there's um um kind of the the frozen uh fresh frozen the amniatic membrane and then the dried so you definitely want to use the frozen the fresh frozen one that's made by bio tissue and then of that there's kind of different ways they package it like it can be in like rectangular pieces or it can be a prokera so prokera is an amniatic membrane that's attached to a plastic ring so you just put it on the eye so it's almost like a big contact lens oh yeah yeah um so um what I typically do is you want to drape the drape over the eyelashes and drape the tarso congenitiva with the pieces and then over the bulbar congenitiva you can put like a prokera prokera by seeing a patient and you see that there's a rest ring there but they're coming for something totally unrelated do you leave it oh yeah so if it's something that happened like not in the like recent history I would leave it and like you don't I mean typically they like if you read the books they say you have to remove like every single little bit of rest ring that would be ideal if you could do that like let's say if someone coming in with an acute issue with a rest ring um I mean remove as much as you can so there's always like a teeny teeny tiny bit left over that might be a little deep that could be okay to leave um but if anything major you want to definitely yeah so I guess this is something new we're doing some cornea questions and I looked at these questions that Sorav wrote they were really good they're really tricky two of them I just found in a book so first one I wrote I don't know if I necessarily talked about all these things in the questions but you know on tests they're not going to be based off blood disorders so it's good to know what people are kind of writing questions on um okay so which accessory lacrimal glands are located in the superior content tyrophonics we're not grading this so you can kind of think about it in your head glands of roofing glands of crows glands of mole glands of ice my voting glands are goblet cells um so over the answer unless someone wants more time to think the right answer is the accessory lacrimal glands of crows so of all the answer choices only the glands of cross and roofing are the accessory lacrimal glands which are equine glands the accessory lacrimal glands of wolf ring are located just above the superior border of the tarsus so it's actually a nice little mnemonic to remember at least where the glands of crows are so the crows ones are in the fornix which is like the corner of your of your congenitiva and crows it's like corner I don't know that's the only way I remember because otherwise I mean I have no mnemonic for wolf rings so if you remember crows is corner and it's in the fornix then wolf rings the other one so glands of mole are apocrine glands that are located at the base of the eyelashes and anterior to the mybomene glands and they secrete mucin, lysozyme, and immunoglobulins glands of zyces are sebaceous and holocrine glands on the margin of eyelid along eyelashes they can form styes mybomene glands are holocrine glands within tarsus and secrete lipids they can also form styes uh goblet cells are located in the fornices as well but they secrete to say secrete mucin okay so small non-central corneal ulcers may sometimes be treated with forest generation fluoroquinolones what is the mechanism of action of moxifoxicin which has gram positive, gram negative, and anaerobic coverage it's all basic science this wasn't in my lecture but so a inhibits bacterial DNA replication, b inhibits bacterial protein synthesis, c alters bacterial membrane vulnerabilities, d inhibits bacterial cell wall synthesis so if this was a test-asset situation you got to pick an answer you're the closest don't waffle you got to do it all right so the answer is inhibits bacterial DNA so moxifoxicin is a fluoroquinolone which functions by inhibiting topoisomerase and enzyme needed to separate bacterial DNA and thereby inhibits DNA replication penicillin inhibits formation of peptidoglycan crosslinks and bacterial cell walls these are like little bonus little tidbits gentamicin binds to the bacterial 30s ribosomal subunit and thereby interferes with protein synthesis polymixin binds to a negatively charged site in the lipopolysaccharide layer and thereby alters bacterial outer membrane permeability so this is a very OCAPs like question okay this is a better question I think that maybe less basic science a 70 year old woman presents with slowly progressive bilateral vision loss her ocular history is unrevealing a specular micrograph of her left eye is depicted what aspect of her history should be specifically addressed a clear early morning vision that worsens throughout the day b i rubbing c siblings with similar complaints or d improved vision in the summer months compared to winter months we use some extra time months yep so I didn't show you a specular micrograph in my talk but specular micro I mean I think I mentioned it but specular microscopy looks at the endothelial cell layer so this is a normal control where you can see nice endothelial cells they look all even they've got their hexagonal shape there's no dark spots where stuff is missing and this particular patient you can see that there's some endothelial cells but then there's all these like spots where there's no endothelial cells and other endothelial cells that are there there's they're not really all hexagonal those kind of different shapes and sizes so what condition is depicted here or what what's the disease yeah so fuchs corneal dystrophy so looking at the choice so knowing that it's fuchs it's like okay you got the answer like that's not the answer so you got to think some more so these are nice nice questions because you have to like think in like two or three steps so once you know that it's fuchs let's look at the choices to see what would be true at fuchs so a clear early morning vision that worsens throughout the day that's kind of the opposite of fuchs so fuchs there's blurry vision in the morning if a patient does have this clear early morning vision that worsens throughout the day you want to think about dry eye because dry eye gets worse later in the day b i rubbing so that has nothing to do with fuchs dystrophy that's a topic of a different talk so this is something that's seen with cure to conus see siblings with similar complaints so fuchs dystrophy is autosomal dominant so we think that siblings would probably have fuchs as well so they're gonna have similar complaints so c is the right answer d improved vision in the summer months compared to the winter months i think here in utah it's pretty dry all year round so all these matters if we were in florida um maybe it's more humid summer which would be the opposite so this is the incorrect answer regardless of where you live okay so let's see it did i go over all this um so specular my microscopy photographs didn't pick utah to variations in endothelial cell size which is polymegathism and variations in endothelial cell shape which is pleomorphism and these findings are most consistent with fuchs other etiologies can also present with similar findings including contact lens overuse surgical trauma inflammation and glaucoma um fuchs endothelial dystrophy has an autosomal dominant inheritance with high degree of penetrance and therefore other family members will be effective or be affected um patients often complain of blurry vision in the morning today um no system within the environment and yeah