 Okay, I guess I'll go ahead and get started. So today I'm talking about ocular surface disorders. And these are the topics I'll be covering, so it's off of BCSC, although I'll be spending a lot more time on blepharitis and dry eye than the rest. So starting with blepharitis, basically two main types, anterior and posterior. Anterior is going to be lash line, so you have colorates around the eyelashes. Another name for anterior blepharitis is seborrheic blepharitis. And then posterior is going to be posterior to the lashes, which is myblomien glands. And so you have myblomien gland plugging or insipidation. And rosacea is a common cause of posterior blepharitis. Anterior blepharitis, you often see it in combination with posterior blepharitis. Symptoms, eyelid, redness, burning, and foreign body sensation. Treatment is going to be eyelid hygiene, worm romances, and lid scrubs. If there's an inflammatory component, you could consider a brief course of topical steroids, and then a topical antibiotic, such as orythromycin or abacitracin, would be warranted as well. With posterior blepharitis, more commonly known as myblomien gland dysfunction. What happens is that the myblomien glands are responsible for producing the lipid layer in the tears. And so when you have plugging of the myblomien glands and the tears are going to be evaporating faster than normal. And rosacea is a risk factor to this. And actually, if you have severe blepharitis, it can lead to corneal inflammation or even an ulcerative keratitis. So myblomien gland dysfunction results in tear film instability, like I talked about. So you can measure that increased evaporation by looking at the tear breakup time. And you do that by putting a drop of flow receding in the eye and turning on the cobalt blue light on the slit lamp. And then after the patient blinks, you start counting. Once you start seeing a black kind of space appear in the tear film, that's when you stop counting. And if that number is less than 10 seconds, that's going to be increased or that's going to be decreased tear breakup time or increased evaporation. Symptoms, burning sensation, foreign body sensation, redness of the eyelids, also recurrent tralasia. And the signs will be myblomien gland plugging, as you can see in this picture. And you also may see some telangiectasias at the eyelid margin. And with chronic blepharitis, you can see actually metaplasia of the myblomien gland orifices with keratin. This is kind of a new way to measure the quality of the myblomien glands. And it's a scan called lipoview. And it's an interferometer that actually measures the thickness of the lipid component of the tears. And it can assess the quality and the quantity of the lipids being released from the myblomien glands. And you can get a lipoview, too, I guess, is their updated version. And you can actually see, it's really cool to see all the lipids kind of in the myblomien glands, get my mouse back on the left. You've got normal myblomien glands, and you can see all those oils there. On the right, you can see myblomien gland drop out. And you can see that there's not as many lipids in the myblomien glands in the lids there. So traditional management, you all may know, include warm compresses. Lid scrubs, I don't really emphasize in people with a big posterior or myblomien gland dysfunction component. I think it's more helpful if you've got scruff and colorettes around the lashes. But I don't really recommend lid scrubs for those with just truly posterior blepharitis. Just because the lid scrubs, I don't think it really gets back there to like unclog myblomien glands. So warm compresses is a big thing because warm can unclog those oil glands. You can still consider topical antibiotic wait-min at bedtime. You can also consider low dose tetracycline class antibiotics, such as doxycycline or minocycline low doses. I typically do 50 BID for blepharitis. If you've got someone who's really sensitive to medication or really skinny and small, you can go with a lower dose, like even just 20 milligrams a day. It works better on an empty stomach. And I do tell everyone that when I start doxy or minocycline that women are more prone to get yeast infections. There can be skin photosensitivity and GI upset. It is contraindicated in children under 10 and pregnant women. If you have a child with blepharitis, you can consider erythromycin orally. And there are several new treatments that are out there for blepharitis with varying amounts of success. Tea tree oil is an entity that's used for eradication of the demodex mite, which is seen up there. Which is believed to be a common cause of blepharitis. And with demodex you actually see some cylindrical dandruff at the base of the lashes. So it's a little bit different than what I'd shown previously with anti-blepharitis. So you see like a little kind of clearish cylinder at the base and if you see that, it's thought to be due to the demodex mite. If blepharitis is due to demodex, it's often refractory to conventional blepharitis treatments. And this can be treated with in-office 50% tea tree oil and daily lit hygiene with tea tree oil, shampoo or wipes. The problem with tea tree oil, I think it works, but it really stings a lot. So you need to have someone who is willing to kind of go through the burning that you feel with tea tree oil. So I don't actually recommend it unless someone really wants to try it. It does eradicate after four weeks and usually there's no repeat treatment needed for a whole year. There is a newer product which I think may be hopefully better than tea tree oil called Avenova, which just got I think released a couple of years ago. So Avenova is a product that contains neutrox, which is hypochlorous acid 0.01%. So it's a very, very dilute acid available by prescription. It's a non-stinging spray and you use it BID. And it actually kills demodex and 99.99% of other microorganisms and it gets rid of debris and inflammatory markers. So this may be a better option than tea tree oil because it doesn't sting. The next is an in-office treatment called Blefx. So Blefx is basically like, if you imagine, it's kind of like an electric toothbrush. At the very end of the tip here you've got a soft cotton brush and it spins. And so you dip this into some sort of mild soap like a baby shampoo mixture or you can deep dip it even into tea tree oil and you numb the eyes and you basically run it along the lashes and I put my booming glands in the office and then you rinse and that basically works like a really, really good lid scrub. So this is done in-office. Patients still need to perform at home lid hygiene but their lid hygiene may be more effective after Blefx because this is like a deep cleaning and then they still need to maintain their routine at home. This may need to be repeated about every three to six months. Lipaflow is another in-office treatment. So this is a 12 minute thermal lid massage to open up blocked myomian glands. Topical anaesthetic is needed. And the way it works is that there's actually a heat component that kind of rests on the inner part of the Tarsal Conjunctiva and so it uses heat and massage to kind of open up the myomian glands. The effects of one treatment can last about 12 months. The problem is that it doesn't work in everybody. 20% of patients may not see an improvement in their symptoms and I'm told that you need to really have good patient selection because it's not for everybody. Patients do need to have some open myomian glands for it to work. So if they're all clogged, it really doesn't work. And they also need to have complete blinks. So if they don't have good blinking then the lipaflow is not as effective. It's really expensive. It's like $800, $2,000 for, oh I don't know if that's one treatment or multiple treatments, but it's not for everybody because of the expense. Thermaflow is another modality, not much literature is out there, but this is also another in-office treatment of lids with pressure and heat, but the difference here is that there's no inner component of heat and the pressure is actually applied by the practitioner. So it's not like an automatic thing that you just like set and forget you have to be there. Still 12 minutes, you don't need a topical anesthetic because it's just external. And I'm not sure how much this one costs, but it's three to four treatments that are needed about two weeks apart. Intense pulse light or IPL is another in-office treatment. This uses a laser light to heat the lower mybomian glands and that closes down the telangiectatic blood vessels and you can only do it on the lower eyelids. It uses a different wavelength than IPL for facial acne. You need about three to four sessions within a four month period. The effects are supposed to last about a year, but this is another really expensive treatment. Then there's mybomian gland probing, which I think was kind of maybe in favor a few years ago and I thought it died off, but then I just recently saw a study which was looking at this. So maybe people are still doing this. But this is an in-office treatment that you use a small steel probe to open up the mymobian glands and it's thought to work by like kind of opening up fibrotic membranes covering the mymobian glands and you do this right at the slant. And it's available in different lengths and you do it under topical anesthesia. The effects of the treatment can last at least six months, but there is a concern that by like physically, mechanically shoving something in the mybomian glands that could cause more trauma and cause more inflammation. So this is not something that I typically do. Okay, so next we're gonna talk about dry eye. So the traditional definition of dry eye was that dry eye is a disorder of the tear film due to tear deficiency or excessive evaporation which causes damage to the interpupubular ocular surface and is associated with ocular discomfort. It sounds very reasonable. However, in the past several years, we've noted that dry eye is a lot more complicated than just tear deficiency and excessive evaporation. So there's a newer dry eye definition that came out which says that dry eye is a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface. So I've highlighted an underlying inflammation because that's thought to be very, very important in dry eye and it's actually gonna be a newer definition of dry eye coming out later this year by the international dry eye workshop. So the tear film is composed of three main layers. The lipid layer which I mentioned earlier which is produced by the mybomian glands. You've got the water or aqueous layer that's produced by the main and accessory lacrimal glands and then you've got the bottom mucin layer which is produced by the goblet cells and that mucin layer is responsible for sticking the tear film to the ocular surface. And traditionally, there's two main types of dry eye, aqueous deficient and evaporative and it's still useful to think about dry eye and these two definitions even though it's a little bit outdated it's still nice to kind of separate it into these two types. So with aqueous deficient etiologies you could have lacrimal gland insufficiency and this can be primary or secondary. The most common causes of primary lacrimal gland insufficiency are gonna be Shogun syndrome and also age-related or postmenopausal. Secondary causes would be lacrimal gland infiltration such as by lymphoma, sarcoid or viral infection. You can get lacrimal duct obstruction so scarring of the ductal orifices of the main and accessory lacrimal glands. You'll see this in chemical and thermal burns, Stevens-Johnson syndrome, membranous conjunctivitis and oculocytritional pinfogoid. And there's reflex hyposecretion so this occurs when there's a problem or a blockage of the sensory nerves and that there's no feedback to the brain to kind of produce a basal amount of tears. So you'll see this with LASIK, you'll see it in contact lens where HSV and Zoster can also cause it as well as diabetes. So any sort of situation which could almost lead to like a neurotrophic keratitis causes a sensory block. You can also have a motor block to the lacrimal gland itself and that is caused by cranial nerve seven damage which damages the secret of motor fibers of a lacrimal gland and anticholinergic medications. Next evaporative etiology. So the main one is gonna be mybomian gland disease which we talked about earlier. Musin deficiency is kind of included under evaporative and you'll see this in chemical burns, Stevens-Johnson syndrome and vitamin A deficiency. Also any sort of situation that can lead to an exposure keratopathy such as lag ophthalmos, exophthalmos, poor eyelid apposition can lead to increased evaporation. Also if there's infrequent blinking such as in Parkinson's or a sedated patient. Topical drug preservative is another common cause of evaporative dry eye and also contact lens wear. So you notice contact lens wear was present as an aqueous deficient etiology under sensory block and also evaporative. So contact lens wear can kind of cause both components of dry eye evaporative and aqueous deficient. So as we know dry eye does have many inflammatory mediators. There's increased HLA class two antigen expression in the conjunctival epithelium, increased CD4 T cell infiltration, also increased protease and MMP9 activity which I'll talk about later on and increased pro-inflammatory cytokine activity such as TNF alpha and interleukin one beta. And actually it's a lot more complicated than this. This is just a few of the inflammatory mediators. It's been found that there's probably hundreds of mediators out there in dry eye. So as you know these are all the dry eye symptoms. So they can feel dry, they can tear, people can feel like a burning sensation, foreign body sensation itching, blurry vision, classic symptom is blurry vision that fluctuates or changes with blinking. So if patients kind of note that their vision fluctuates it's gonna be dry eye. Typically it's worse later in the day because your eyes have been open all day. Worse when they're outside or if it's windy and also worse when reading at the computer or watching TV because people blink less often when concentrating. Physical exam, so you wanna look at the eyelids. We talked about blepharitis and my booming gland dysfunction earlier. Look for any eyelid, malposition. Look for something like entropion or ectropion because that can cause tearing. Also look for trichiasis or dyschiasis because that's another cause of tearing. Then you wanna inspect the tear film. So as you look at patients you'll get a sense of how what's normal tear film or what's a high tear film, what's low tear film. If you see low tear film, it's gonna be dry eye and you might see some mucus floating around in the tear film. That's also another indication for dry eye. A high tear film is actually epiphora. So that's suggestive of dysfunctional tear drainage. So that's tearing, like actual over tearing and not reflux tearing from dry eye. And we talked about tear breakup time earlier. You wanna look at the ocular surface to look at any congenitival inflammation. Look for corneal filaments, which are indicative of very severe dry eye. Tarsal congenitiva, congenitiva scarring and some blepharot. I mean, you'll see this in really severe causes of dry eye such as Steven Johnson. And there are various stains. So fluorescein is by far the most common stain that you use in it. So fluorescein stains basement membrane. Rose, Bengal, Anglicium, and Green stain divide a lot of cells. And you can see rose, Bengal, staining on the cornea here. And you can see Lysum and Green staining on the congenitiva here. So the nice thing about rose, Bengal, and Lysum and Green is they're a little more sensitive. You can see more of it, especially on the congenitiva as far as staining. And Lysum and Green is used more often than rose, Bengal, because it's less irritating. So even with anesthetic, people can still have stinging with rose, Bengal. Shermer's testing is another traditional test for dry eye where basically filter paper strips are used to measure basal and sometimes reflex, reflex secretion over five minutes. There's a modification of it where a topical anesthetic is used to measure basal secretion only. And so this is measured over a five minute period. And then you check and take up a filter paper strips and check and see how much of the tears have gone up the tear strip. And so less than five millimeter length of tears is moderate to severe dry eye, five to 10 is mild to moderate and greater than 10 millimeters is normal. There's another modification called Shermer's 2 which actually you stick something up their nose to induce some reflex tearing. I don't know anyone who does that, but that's out there in the literature. The do so the dry eye workshop has a dry eye severity grading scheme from one to four. So basically level one dry eye is gonna be your mild dry eye. So they may not have seen, you may not see any signs clinically and patients just have mild symptoms all the way up to grade four, which is severe constant debilitating symptoms with very market clinical signs. So that's kind of the whole spectrum of the disease. There are a couple of new point of service tests for dry eye. There's tear lab, which measures tear osmolarity and inflammatory dry, which measures MMP nine. So tear osmolarity refers to the concentrating of electrolytes and tears. So the higher the number, the more concentrated tears are. So dry eye disease is associated with elevated tear osmolarity. And elevated tear osmolarity is a contributing factor in cellular damage and upregulation of inflammation. And it correlates more closely to dry eye symptoms than some of the older dry eye tests. And it can also be diagnostic in the absence of symptoms. So this may be important in someone who's about to have refractive or cataract surgery, which can increase dry eye. And so if they have an elevated tear osmolarity before surgery and they may not have symptoms, you might want to tell them, look, you may have, you may be more prone to have some dry eye symptoms after surgery. Tear, so with tear lab, what it does is that you have to sample the tear film. And it takes about 20 seconds to do that. And so you just take the tip to the lateral canthal area to take the measure of the tears. And dry eye is diagnosed as there's elevated osmolarity greater than 308, or if there's variability between the eyes of greater than eight, or if there's variability on repeat measurements, then it's diagnostic of dry eye. And this test is a sensitivity of 88% and specificity of 75%. And this is a scale that's used. So anything that's above about 300 or 305 is mild dry eye and higher the number, the more severe dry eye. So next I'll talk about MMP9, which stands for matrix metalloproteinase nine. So this is an inflammatory marker and it's elevated in the presence of elevated tear osmolarity. And so higher levels of MMP9 in the tears actually correlate with moderate to severe symptoms on that report of the international dry eye workshop. But it's a little bit nonspecific because MMP9 is also elevated in allergy and it's elevated in infection. So it's not that specific. But in the right clinical setting, it's very useful. So there is an MMP9 test called inflammatory dry eye and it was shown in the FDA study that this test had 85% sensitivity and 94% specificity. And it's similar to the adenoplus test which detects adenovirus, which is similar to a pregnancy test. So it looks exactly like that. It takes 10 minutes to process the result and the brighter, there's basically two kind of stripes that you look at. So the brighter the red positive stripe, the more MMP9 is present. So this is what it looks like. So you kind of assemble the kit and you touch the inferior Tarsal Conjunctiva to collect tears. Then you run the test and after 10 minutes, you'll be able to read the results. So if you see a pink positive stripe, it means positive. And the more bright that pink stripe is, the more MMP9 there is. So it's kind of nice that if you just have like a tiny little bit of red, technically positive, but you know that maybe there's not as much MMP9 whereas if it's like really bright and positive, then you know that there's a lot. There are some limitations to the tear lab and inflammatory tests. They must be done prior to exam, prior to any drops. So there has to be some indication, maybe based on symptoms to do the test. And the patient actually can't put in any drops within two hours prior to testing because that can interfere with the result. So these tests are helpful for diagnosing dry eye in earlier stages. So kind of mentioned earlier, it's good for people who may not have symptoms, but it's also helpful for patients with symptoms, but they may not have slit length findings. And this is a nice test to kind of show that they actually do have dry eye. We talked about dry eye prior to cataract surgery and refractive surgery. So it's actually important to treat any dry eye present because that can affect pre-operative measurements. And it's important for pre and post-operative treatment. If you have positivity on this test, you might think about starting some anti-inflammatory therapy sooner and I'll talk about what those therapies are. It can give the provider and the patient objective data and it can be used to gauge the efficacy of treatment. So you could have a positive test and then give them treatment later on, repeat the testing and see if anything is better. So I'm gonna start with kind of basic non-prescription dry eye treatments and we'll kind of work our way up. So some basic things that are cheap include just taking frequent breaks while reading at the computer, drinking more water. People ask about that. I think it's only helpful if someone's dehydrated for it to work for dry eye. There's only a limit to how much water you can drink. Limiting contact lens wear or changing to a high decay and contact lenses can be helpful for dry eye. Increasing humidity in some way, shape or form. So that could be limiting heaters fans or AC, adding humidifier, using moisture chamber goggles which you can wear, these are helpful to wear at night. And then there's actually moisture chamber goggles which kind of look more stylish like sporty sunglasses that have like a little rim around the edge that kind of sucks onto around the eye that acts as a moisture chamber. Moving to a humid environment because we live in such a dry climate is also helpful. Tier supplementation. I don't recommend any vasoconstrictors, nothing that's good to get the red out or good for dry eye. Increased viscosity coats the cornea better so the thicker drops can coat the cornea better but the downside is that they cause blur. If patients are saying like they have a lot of irritation when they first wake up in the morning, they might have nighttime lag ophthalmos so then I would recommend a lubricating gel ointment at bedtime. And if patients are using their bottle tears more than four or five times a day, I'd tell them to switch to preservative free because the bottle drops have preservative in it which can actually irritate the eyes a lot more if they use it a ton. So I tell them to switch to preservative free if they're using them a lot. Okay, so next I'm going to talk about omega-3 fatty acids. So they are necessary for the lacrymal gland to make tears and they can also decrease systemic inflammatory activity, decreasing interleukin 1 and TNF alpha. So there's two I guess main classes of omega-3 fatty acids. There's fish oil which is comprised of EPA and DHA which are kind of listed up there and there's also flaxseed oil which is alpha linoleic acid. And there was a study done several years ago, the women's health study which kind of first showed that omega-3s may be helpful for dry eye. So this was looking at a whole lot of other systemic diseases. So this was not looking at eyes at all but looking at, they looked at almost 40,000 female health professionals, most of them age 45 to 84 and they completed a dietary questionnaire. They also have some self reports of clinically diagnosed dry eye cases and when they adjusted for demographics, whether or not they were on home therapy and total fat intake, they found that those who had a higher ratio of omega-6 to omega-3 fatty acid intake actually had a higher incidence of dry eye syndrome and tuna consumption was inversely related to dry eye symptom, dry eye disease. So there really wasn't any much done as far as studies kind of proving that omega-3s were helpful for dry eye until just recently in this month's cornea journal. So this was a study which was a multi-center perspective double masked randomized trial which looked at placebo versus fish oil and the amount they used was kind of listed up there. They've got 1680 milligrams of EPA and 560 milligrams of DHA. So that comes out to be almost 2200 milligrams of fish oil daily. And this was the brand that they used, physician recommended nutraceuticals. And they found that by 12 weeks there was a statistically significant improvement in tear ulcer molarity. Tear breakup time was statistically increased. There was a reduction in MMP9 positivity and there was improvement in OSDI scores. So OSDI is a dry eye questionnaire which has 12 questions and they found that there was an improvement in scores so symptoms based on fish oil treatment. So this is actually a nice kind of scientific way to prove that fish oil does work. So about two to three grams a day of omega-3 is recommended. For fish oil there's a couple different formulations, ethyl ester and triglyceride formulations. Ethyl ester is what's used most commonly. It's kind of used for, makes it easier to process the fish oil in factories whereas triglyceride is a more natural form. And it's thought that maybe the triglyceride form may be a little easier, better absorbed by the body. So fish oil comes in usually capsules and you can also buy flaxseed oil capsules. However, it's not as effective as fish oil. There's kind of been other studies which have shown that flaxseed oil is, I mean, yes, it's helpful but you need to take like four times at the amount as you would in fish oil to have the same result. So because of that reason, I don't really recommend flaxseed oil. I mean, someone's already taking it. I say that's fine but I usually don't recommend it just because it doesn't work quite as well. But if you have someone who's a strict vegetarian then flaxseed oil is fine. You can buy flaxseed oil capsules or you could buy like whole bottles which you can find in like whole foods. Just bottles of flaxseed oil. It's important if they're using the bottles that they don't cook it because heat can actually cause it to not work anymore as far as effectiveness. Oil has about 2.5 grams per teaspoon. People on really strict diets do have to know that there's just a few extra calories. There's like 10 extra calories per gram of fish or flaxseed oil. Okay, so that's all about Omega-3s. Next I'm gonna talk about prescription anti-inflammatory therapy. So topical cyclosporin 0.05% or stasis is an anti-inflammatory topical treatment used twice a day and this prevents T cell activation. So the vehicle, so the non-active component to the fish or to the stasis is a castor oil and glycerin-based emulsion which decreases evaporative tear loss with minimal blur and it's also designed to make the cyclosporin more soluble. It does take a while for the topical cyclosporin to actually work at least three months. So I will sometimes consider the use of concomitant use of topical steroids for six weeks while the stasis is working and the topical steroids can maybe eliminate the sting that some people get with the stasis. It's really not effective against buffaritis but it's actually helpful in people who have allergies as well because there's a anti-inflammatory component which can help calm down allergies. Like I said, it takes at least three months to become effective and then when people start googling, they Google cyclosporin and they may be alarmed by what they find because, as you know, it's a chemotherapy agent. So there was a study which looked at rostasis-instilled BID for 12 months in dry eye patients and then they checked their blood and they did not find any, no cyclosporin was actually detectable within less than 0.1 nanograms per ML and they took samples at different times of the day and they couldn't find a cyclosporin, so that's good. They can reassure patients that it's not transmitted or it's not, yeah, transmitted systemically and there's actually been no systemic side effects from rostasis. Just about a couple months ago, there's a new competitor to rostasis called Lefitograst or Zidra and this blocks the binding of lymphocyte function associated antigen one or LFA one to interleukin adhesion, oh, I put that wrong. I can't one, basically. So, antisoactivation is also influenced by this binding and Lefitograst was shown to significantly improve inferior corneal staining from baseline to three months and then they also found that it significantly improves the eye dryness score, so meaning patient reported symptoms after three months but then they kind of did a subsequent study which showed that the corneal staining did not improve in this subsequent study. The most common side effects were stinging, blurred vision, change in taste and there's also no systemic toxicity scene. So, my personal experience with both of these medications, I have no financial interest in either of the companies that make it, so I actually take rostasis and the nice thing about the rostasis is that, so both of these are packaged in preservative free vials and the rostasis has like a lot of drops in each vial. So, I actually tell patients that it's okay to reuse the vial over one use and you can actually use it technically over a 24 hour period, which is three doses and so if they're buying like 60 vials which is technically a one month supply because you use it BID, they can make that one month supply last three months if they reuse the vial and so the company knows that this pretty much everyone tells, all physicians tell patients this and so they kind of, they know it's not like part of their technical like instructions but they say it's okay to do that. In practice, there's about eight drops so you could use it for four doses. So, rostasis for me took literally four months to become effective but since then it's been really effective and there's some low grade stinging that lasted a few minutes initially but that resolved or got better over time. And so I'll tell patients this, that this is possible, it's gonna take a while, it might sting, for most people it's tolerable, it'll get better. Zidra, the jury's still out because it just came out as far as how effective it is but the downside to Zidra is you can literally only get two, maybe about two and a half drops out of each vial so it's literally each vial is for one time use. So, a one month supply of Zidra is only gonna last one month which may be financially like three times as expensive as rostasis potentially. So the stinging, so I tried it for a few days so the stinging varied from like the first time I put it in it was like a lot of stinging and then sometimes it was less and then the next time it'd be more so I wasn't really sure why but the stinging didn't last very long, it was like 30 seconds but then I did have that dysguzia or that kind of strange taste in the mouth and for me it lasted like 30 to 60 minutes which was a long time to have a really nasty, bitter taste in your mouth. So, I mean I didn't use it long enough to know if it was effective but these are just kind of some things I'll be telling patients about Zidra. Okay, so next I'll talk about punctal occlusion and the most common methods are with collagen which is dissolvable, seen at the bottom and silicone which is seen at the top. There are a kind of punctal plug called smart plugs which are, they actually sit within the cannulaiculus so you put them in and then you can't tell if they're in or not and the problem is that they don't dissolve. So there's been several studies or not studies, case reports which have where the smart plugs kind of got infected or if there was a problem and they needed to be taken out and so you have to like consult oculoplastics to get in there to like remove these things so I don't recommend the smart plugs. I don't think we have them here so I don't think you have to worry about that. I usually occlude the lower puncta first because about 60% of the tear outflow will go through the lower puncta and if the patient still need more occlusion then you might consider the upper puncta. Could consider punctal cottery which is a more permanent solution but I always try plugs first and I'll recommend punctal cottery if the plugs aren't staying in and if the patients think that they had improvement in their symptoms while the plugs were in and punctal occlusion has better results after starting anti-inflammatory treatment because if you, the thought is if you plugs in before starting any anti-inflammatory treatment all those pro-inflammatory mediators are now just gonna sit on the ocular surface longer because of the plugs. So if you start anti-inflammatory treatment first and then go to plugs I think that's a more logical way to go about things. Next I'll talk about floppy eyelid syndrome. So you'll see this as extensive lid laxity and it's more than just the lid laxity that you'll see in really elderly patients because this is a situation where just pulling up their eyelid, their upper eyelid completely averts that. So you can't do that in normal people. So if you do that and they're lid averts and you can look into their upper pharynx like they've got floppy eyelid syndrome. Symptoms will be the symptoms of dry eye. So eye irritation, redness and discharge. It responds poorly to lubrication and topical steroids and it's a bit tough to treat. But there's a high association with obstructive sleep apnea. So I tell patients who I see floppy eyelid syndrome I won't ask them if they have sleep apnea or if they don't know they have sleep apnea and do they snore and pretty much almost always those are like, oh yeah, I wear a seat pad to bed or I don't know what sleep apnea does and their wife says, oh yeah, you snore all the time. So it's like, okay, you got to see your primary care doctor, get a sleep study because there's a high association of obstructive sleep apnea with major cardiovascular events like heart attack and stroke. So I think you could potentially save someone's life by just telling them they have floppy eyelid syndrome or diagnosing it. Floppy eyelid syndrome is also associated with careticonis and Down syndrome. Even though it responds poorly to lubrication, it's kind of the only treatment you can do. Nighttime ointment as much, you're using as much topical lubrication as possible. You could consider horizontal eyelids shortening for this as well. Next is superior limbic careticonjunctivitis or SLK. The signs of this are gonna be inflammation and staining of the upper tarsal and bulbar congenitiva. So it's kind of the opposite to dry eye. Usually dry eye you'll see inferior corneal staining and SLK you'll see everything superiorly and you might see some filaments at the superior limbis and superior cornea. It's thought that the etiology of this could be possibly from excess superior congenitiva, kind of laxity leading to friction on the superior oculosurface. But the symptoms will kind of be non-specific. It's gonna sound like dry eye. They'll have foreign body sensation, burning sensation, itching and dryness. And there can be an association of SLK with thyroid disease. So you wanna check thyroid function tests. You could consider testing for autoimmune disease as well. The treatment initially is gonna be with aggressive topical lubrication, punctal plugs, topical steroid or cyclosporine or other anti-inflammatory treatments. A bandage contact lens can be helpful. People have used topical silver nitrate to kind of apply to the superior congenitiva to try and decrease some of that friction. And another kind of more drastic method that works is recessing the superior congenitiva or resecting it or applying cottery to the superior congenitiva. Next is recurrent corneal erosion, which will present with severe pain upon awakening or severe pain when they kind of wake up in the middle of the night. And predisposing factors for this will be epithelial basement membrane dystrophy or mapped up fingerprint dystrophy which is shown at the bottom there. Or prior traumatic corneal abrasion. So the treatment, again, is with aggressive lubrication, plugs, topical steroid or rostasis. Bandage contact lenses can also be helpful. You could recommend hypertonic saline or mirror 128 once the epideffect has healed because what that does is it tries to tack the epithelium down so it doesn't slough off. But if that doesn't work, then they're looking at some sort of procedure. So epithelial debridement or superficial keratectomy is the other name for it. Basically kind of scraping off that abnormal epithelium and then putting in a bandage contact lens and hope that the epithelium that heals over heals over more smoothly. During the procedure, you could also consider doing some diamond burr polishing to kind of polish down Bowman's membrane or you could do anterior stomomicropuncture which is basically taking a needle and kind of making little dock marks into Bowman's that act as little kind of irregular areas for the epithelium to kind of stick into once epithelium is kind of healing over. You can't do anterior stomomicropuncture over the visual axis, however, because it causes little scars so you don't want that in the visual axis. PTK or phototherapeutic keratectomy is another possible treatment for it. So this is basically like PRK, so refractive surgery, but you're not doing it to achieve a particular refractive result. You're applying the laser just to kind of take off epithelium and kind of roughen up the Bowman's layer. Topical anesthetic abuse is a commonly overlooked and misdiagnosed entity and this leads to a neurotrophic keratitis because they can't feel anything. When they can't feel anything, you know, their epithelial defects are not gonna close and they're gonna have chronic inflammation that may have sterile ulcer. So topical anesthetic abuse is in the differential diagnosis of any chronic keratitis that doesn't go away. So the signs include a persistent epithelial defect. They may have a ton of inflammation like corneal ulcer or a hypopion. They could have a ring infiltrate and the corneal thinning can actually lead to perforation and it's gonna be difficult to elucidate this in the history because patients usually aren't gonna be very forthcoming about saying they've been using this drop all the time but risk factors include care on the emergency room either or you know, they may have stolen a bottle of the topical anesthetic. So if you're on call kind of just anywhere where you're examining a patient, you wanna keep track of your bottles of tetrachine and propera kinks. You don't want patients to just walk off with it because you put that magic drop in and they're like, ooh, I wanna have that at home. They may just take your bottle. Some emergency room doctors even now are kind of giving them bottles of propera kink which is really bad. If the patient's in the healthcare field and has ready access to topical anesthetics or if they have a close family member who can like get the stuff for them, those are risk factors. So it's really hard to figure it out but with anyone who just isn't healing with the normal treatments, you wanna suspect anesthetic abuse. And this is what it can look like. It could have like a small infiltrator. You could have like a really big ring infiltrate with tons of information. You could have kind of a gray white looking kind of ulcer there so it doesn't have any sort of classic appearance. Okay, so next I'll talk about corneal delens. So a corneal delen is a saucer like excavation of the peripheral cornea near the limbis and it's associated with some sort of adjacent elevated thing. So this could be a contantival growth, a limbal growth. It could be commosis, chronic commosis. It could be a bleb. So what happens is that the cornea that's adjacent to this elevated thing just doesn't get proper, the tears don't really flow across that area because the tears are kind of flowing on the top of whatever is elevated. So it might be a big bleb and it doesn't get down into the cornea, this little area of cornea right next to it. And so any area of the cornea that doesn't get proper moisture is gonna thin. Okay, so that's what I just talked about. So here are some pictures of delens. So on the left is a delen that's actually associated with an elevated or a demidus graft host junction. So that graft host junction is very elevated, that adjacent area of the cornea is not getting tear film coverage and so it starts to thin. On the right is a delen from contantival swelling surrounding a sclera buckle. So it's really elevated and that cornea is just not getting enough moisture. So the treatment is gonna be very aggressive, lubrication or ointment, you could consider a tarsorphy and if it's possible at all to remove or solve the problem with whatever's elevating the contantiva next to the cornea, that should be done. Next is limbal stem cell deficiency. So corneal stem cells are located around the limbus and they're responsible for renewing the oculosurface with new epithelial cells. The limbus also acts as a barrier against corneal new vascularization from the emission of contantival cells and about 25 to 33% of stem cells are needed for normal resurfacing of the cornea. So if you have limbal stem cells absent, this could be from a few different reasons or this can result in a few different things. It can, you can lose your ability to have effective wound healing. We'll start to get super superficial corneal new vascularization and you can have a irregular corneal surface from abnormal corneal epithelium. So this is what limbal stem cell deficiency looks like. On the left is stem cell deficiency from mitomycin that was used during a Trab and you'll see just this, you know, you don't really see any vessels here but you notice that there's a lot of kind of abnormal worlds of abnormal epithelium. On the right is severe limbal stem cell deficiency. So you got vessels kind of coming from the congenitiva over the cornea into the visual axis and this is from corneal neovascularization and epithelial dysplasia from just chronic soft contact lens wear. So people sleeping in their lenses all the time or even people just total abusing their contact lenses. You can have limbal stem cell deficiency. So there's several causes of limbal stem cell deficiency. Primary include aniridia or pex-6 gene mutations, a condition called scleroconia and there's another condition called keratitis ichthyosis deafness or kid syndrome. So these are more rare causes but the secondary causes of limbal stem cell deficiency are gonna be a lot more common. So this will include thermal chemical burns that will damage the limbal stem cells. I talked about contact lens wear, radiation to the eye can damage limbal stem cells. Eye surgery, so if you have enough damage to the limbal stem cells all around the cornea that can lead to a stem cell deficiency. Mucous membrane, Pemphagoid and Stevens-Johnson syndrome can lead to scarring and damage of the stem cells. A teritium is actually a very localized limbal stem cell deficiency. So it means that right in that area where the teritium is and when it's growing onto the cornea, there's a loss of limbal stem cells right there. Topical medications such as palocarpine, anti-metabolites, antibiotics and beta blockers can lead to a limbal stem cell deficiency. So the treatment, so if it's mild and due to local factors such as contact lenses or drops, you can try and discontinue them. You could consider debriding abnormal epithelium but this is only gonna work if there's enough normal limbal stem cells to repopulate the whole surface. You could consider a scleral contact lens because that actually doesn't touch the cornea or the limbus. Surgically, if you've got a teritium, you just take out the teritium and you could use a congenitival autographed. If you have someone who has a unilateral chemical or thermal burn, you could actually do a limbal autograph from the patient's fellow eye. So you harvest a section of limbal stem cells from the fellow eye, so normal eye and put that on the burned eye. If there is bilateral disease, you can do a limbal allograft from an HLA matched living donor or eye bank eye and do needs a systemic immunosuppression for this. Or you could do a cure to prosthesis which is an artificial cornea. I think that's my last slide, yeah. So any questions on anything? Well, thanks for coming.