 Are we ready? So good morning. My name is, for those who don't know me, my name is Luis Santiago Cabana, one of the cornea and refractive surgery fellows here at the Morana Center. I have two kind of quick presentations today. The number one is basically the LASIK enhancement, the PRK on flap versus flap relief. And the other one is an interesting case presentation that I just recently saw at Dr. Marcifar's clinic. So if you have any questions, you can stop me and I will kindly answer the questions for you. So LASIK is the most common corneal refractive surgery that is performed today. It has some advantages over surface evaluation, aka PRK or LASIK, EK LASIK, including quicker visual rehabilitation, minimal post-operative discomfort, and the ability to correct higher degrees of myopia without the complication of corneal haze that is seen in PRK and surface evaluation. For every refractive surgeon, LASIK enhancement is a reality. It has been reported to be as high as 5.5% to 27.5% in reported series. And some of the risk factor for enhancement after LASIK include high preparative myopia, a high hyperopia, or a hyperopia more than one diopter, preparatively, and a stigmatism of more than one diopter, preparatively, age. It's been reported that patients about 45 or 50 years old, they are an increased risk for undercorrection or overcorrection depending on the aggressiveness of the surgeon. And sex and room temperature and humidity has been reported, but those three are basically controversial. Other factors that are associated with the enhancement rate include the surgeon nomogram, the different surgeon nomograms may affect the rate of enhancement that is seen on the different series on the literature. The criteria of every surgeon also affects the enhancement rate. It all depends on how high or low the threshold for enhancement is for each and every refractive surgeon. And laser technologies has improved significantly the past 15 years, 20 years. Wavefront technology and the use of larger oblations have decreased the rate of enhancements compared to the beginning of laser correction surgery in the late 90s. Refractive regression is one of the main indications for laser enhancement is basically the regression of the treatment applied to the patient. There are different theories behind the myopic regression including epithelial hyperplasia, nuclear sclerosis, making the patient more nearsighted, changing corneal biomechanics, corneal stippling, increasing actual length, and stroma remodeling. Again, these are theories behind the pathophysiology of myopic regression. So basically, when we have a patient that needs an enhancement, there are two popular surgical approaches performed by refractive surgeon. Number one is lifting the flap, the previous LASIK flap, and the other one is performing surface ablation or PRK on the flap. But which one is better? We're gonna review the advantages and disadvantages of each technique and then I'm gonna give you our suggestion of how to proceed with the case of LASIK enhancement. So PRK on the flap has some advantages. Number one is the easy surgical technique. The surgical technique is basically the same as in a PRK, as a primary PRK. The only thing that you need to be cautious is basically avoid any trauma to the LASIK flap that the patient already had. It works better for patients with thin corneas. As you may know, PRK removed or less tissue compared to LASIK, decreased risk of ectasia compared to LASIK, it is better for a patient with post-LASIK dry eyes and it's also better for patients with previous flap complications and it has been reported that the PRK can actually reduce flap-related higher order aberrations and micro-stree A. And obviously, since we're not lifting the flap or making any new flap, we avoid any flap complications. The disadvantages of PRK on the flap include, and this is a more worrisome haze, it's been reported to be more common or more likely to develop haze after PRK on a previous patient with LASIK compared to primary PRK. There's one, all report, basically the first one reporting the rate of haze in patients with PRK enhancement over LASIK flap that actually recommends to not perform PRK enhancement in patients with LASIK. But that all report basically, they didn't use any mitomycin C, which is an agent that we actually use to decrease the rate of haze in PRK patients mitomycing the haze actually, it's caused by activated keratocytes in the cornea and the mitomycin basically controls that activation. And also, in order to prevent the haze after PRK, we need to use prolonged use of steroids, of topical steroids and the complications that are related to them are well known including the possibility of intraocular pressure spikes. Another thing, another complication that may happen, especially with poor surgical technique is basically an inadvertent flap lift or dislocation. So that's something that every surgeon needs to be cautious about. And the possibility of the pain and possibility of visual acuity fluctuation, which are seen also in primary PRKs. So these are two pictures of post-PRK haze. You can see the opacity on the visual axis in the top picture here and in here too. Another picture of more significant haze in a post-PRK patient. You can see here two, the haze in the visual axis and this is a more dramatic photo of a patient with a PRK haze. Sometimes if the PRK doesn't improve after prolonged use of steroids and after giving enough time for the eye to heal, superficial carotectomy or even PTK is needed to improve this patient's visual acuity. So what about flap lift? The advantage of flap lift on laser enhancement include an accurate and predictable outcome. The enhancement or ablation is gonna be done in the same plane as a primary laser treatment which in theory will decrease any higher order aberrations and it causes minimal discomfort and a quicker visual rehabilitation. But what about the disadvantages of flap lift? Number one is a more difficult procedure to perform, it can be difficult to lift the flap especially on flaps performed with femtosecond laser technology and the more time, the more far away are we from the primary laser procedure, the more difficult the lifting of the flap is. And this difficulty with a flap lift can cause an epithelial disruption that may end up with one of the worrisome or the main complication after flap lift in patient with a laser enhancement which is the epithelial ingrow which is basically the growing of epithelial cells in the interface of the laser flag and the corneal stroma it has to be shown to be as high as 32% in different series. So this is mainly the reason why some of the people who have fractal surgeries do not perform flap lift on the laser enhancement. Also post-lasic dry eye is another possible condition that may be exacerbated by a flap lift enhancement. Flap complications including diffuse lamellar keratitis, infectious keratitis, folds in the flap that may cause irregular stigmatism, displacement of the flap, flap edge necrosis and a condition or a symptom that is called interstitial fluid syndrome which is basically accumulation of fluid in the interface between the corneal stroma and the laser flap mainly caused by increase in intracular pressure secondary to a steroid response. And there's always a possibility of developing post-lasic atasia in patients after flap lift enhancement. So these are a couple of pictures from complications for flap lifting in patient with laser enhancement. The number one is, and the upper two are basically post-lasic dry eye. You can see the epithelial apathy that is seen on the laser flap here and this here with the fluorescence staining. Over here is a DLK grade II DLK. You can see basically some inflammatory cells in the reticular pattern on the visual axis. The centrotoxic keratopathy is a condition that has been described. It's basically a denser pacification of the flap lift, of the laser flap and corneal stroma seeing in patients after laser enhancement or primary laser which basically starts as a DLK but then progresses to a more dense of pacification of the cornea causing hyperopic shift. The cause of it is unknown. In the beginning, the theory was that inflammation caused this kind of presentation but actually it has been suggested that the inflammation has no role in patients with centrotoxic keratopathy and actually it heals by itself, improved by itself without any intervention. So these patients usually you need to see them more closely for basically to follow up on the improvement of it. Another cases of flap complication include flap edge necrosis you can see here, the edge of the flap here, the necrosis of the flap here on the edge and the interstitial fluid syndrome. You can see here that there is a little bit of liquid accumulated in between the laser flap and the corneal stroma and again this is secondary to an increasing trochlear pressure, usually secondary to steroid response. Epithelial ingroth, again this is the most worrisome complication after laser enhancement with flap lift. You can see here some epithelial nests underneath basically in the interfacing between the laser flap and the corneal stroma and this is a more advanced case of epithelial ingroth. You can see some nests here inferiorly and paracentrally here too. This is a higher modification of epithelial ingroth. You can see clearly here the epithelial nests underneath the flap. More dramatic photo of epithelial ingroth at the top two and this is basically how the patient looks after we perform removal of epithelial ingroth for vitroless significant epithelial ingroth after laser enhancement. I have a little clip of how the surgery for epithelial ingroth vitroless significant epithelial ingroth is performed. This is a case demonstrating the treatment of multiple epithelial ingroth status post-lasic. We first basically mark the flap edge of the previous lasik carefully with the Sinski hook. We basically delineate and start lifting the flap. I'm sorry. I don't know what I touched. Probably. I was just trying to increase the volume. So this is the, where's the volume? That's the first one. So if you want it up. So this is a little break. What's been our break of epithelial ingroth? That's a good question. Do you? Thank you. So let's continue with the clip. So again, we delineate the flap edge with a Sinski hook and then we lift the flap using two flat forceps, using work so we can scrape the stromal side of the flap to remove the epithelial cells there. And we do also the same thing on the stromal bed. The same process is used to remove epithelial from the stromal bed. Epithelium is removed from the stroma there. Then after that we can use a beaver blade to try to get, to remove all the epithelial cells on the stroma of the cornea and carefully on the stroma of the flap. Same thing can be done on the flap. Again, be very cautious and delicately because we don't want to rip that flap off. A very moist Maricel sponge is then used to remove the epithelial. And then we reposition the flap back in place. The stromal bed is dehydrated. Flap is carefully put back into position. Moist Maricel sponge is then used to massage the flap. So with this sponge we basically decreased the chances of developing any stray or micro, or micro-straying on the flap. And after removing the epithelium at the edge of both the flap and the cornea we basically put some stitches in there. To decrease the chance of developing recurrent epithelial ingrown, one thing that you will see in a second is basically that we don't bury the nuts to basically decrease the chance also of developing recurrent epithelial ingrown. And after that we put a bandage contouring on it to basically decrease the number one, the pain or the discomfort from the nuts. And second to again avoid developing any recurrent epithelial ingrown. Xymar and Predforte are placed on the surface of the eye. Then on island. And after a soft contact lens is placed, the case is concluded. A couple of weeks after the procedure, you can see here the nuts are still there. And then the pin. Have you seen the sutures induce your regular stigmatism or they're not in long enough generally? They are usually not long enough there. Notice you're all on one side. Doesn't that run the risk that you're going to slip up? You're going to slide the flap up. So these are also another possible complications. This is basically seen in almost all basic cases. Microstria, you can see the stria here. These are not visually significant, but if they are big enough, they can cause irregular stigmatism. So again, after seeing all the pros and cons of both of the procedures, we suggest that in a patient, depending on the criteria of the surgeon and laser enhancement, if the primary laser surgery was performed less than one to two years, the decision can be made whether or not to go with PRK on the flap or flap lift based on the greater complications that can happen after each of the procedures. But definitely in patients over two years, we strongly recommend to perform a PRK on the flap, mainly because of the high chance or rate of developing epithelial ingrowne after lacy flap lift for enhancement. So this is the end of the first presentation. Anybody has a comment, question, doubt? Okay, so these are my references. Now we're going to continue with the case presentation, the man with the bilateral corneal edema. This is the case of a 76 year old male patient with a history of hypertension and Parkinson's disease who was seen for follow-up of Dr. Moshifar's clinic for left corneal scar. Patient has a history of a previous episode of central corneal ulcer that healed and resulting in scar and thinning in the visual axis on the left eye. But the thing is that the patient during that visit refer a chronic decrease in vision in both eyes. So his past medical history, a patient has a history of Parkinson's disease, hypertension, he uses a verbal medication, aspirin, carbidopa, levodopa for his Parkinson's, amantadine, and a couple of medications for depression and psychiatric illnesses. And he has a surgical history of bilateral faker misification and intraocular lens. On the slip line examination on the 17th of January, the patient was found to have a best corrected visual acuity of count fingers on the right eye and hand motions on the left eye. It is worth to mention that the right eye on the previous visit about two to three months before the presentation on the 17th was 2030 corrected. The left eye has been on the count fingers hand motion range mainly because of the central corneal thinning and corneal scar. So basically his eye went, especially his right eye went from 2030 to count fingers. The pressure of the eyes are both normal. Patient has evidence of may bone and gland disease on the lids, scolera and congenitiva quiet. The cornea on both eyes showed three plus decimate folds with one plus trauma edema. And there was no evidence of gutata or any sign of inflammation or infection on both eyes. The left eye, although the central cornea was thin and scar, there was evidence of decimate folds too without evidence of gutata. The tear chamber was quiet on both eyes and the rest of the examination was normal. The patient has Parkinson disease so it was a little bit difficult for us to take a picture of the patient. This is not a picture of the same patient. The patient is on a wheelchair. So this is a representative illustration of the patient's right eye. You can see basically the decimate folds on the cornea and the increased trauma edema. So when we talk about cornea edema, we need to know that cornea on the field maintains the cornea clarity through mainly two functions, basically number one, it acts as a barrier for the aqueous to come into the cornea. Number two provides a metabolic pump to maintain the cornea hydration in about 70%. And increased permeability and insufficient pump sites occur when we have endothelial cell count of less than five hundred cells per millimeter square. The pathophysiology of acute cornea edema, it's basically a secondary to an altered barrier effect of the endothelial or the epithelial in chronic cornea edema, we see more of an inadequate endothelial pump. The causes of cornea edema include for acute cases, trauma, inflammation, hypoxia, especially as it may be seen on patients with anterior ischemic syndrome after multiple muscle surgery, high drops from rupture of decimate and increasing tracheal pressure. Under chronic side, trauma can cause chronic cornea edema along with toxins. These trophies can also cause chronic cornea edema as it's seen in fuchs, posterior perimorphous dystrophy and eye syndrome, post cataract surgery, retain less fragment, can also present with chronic cornea edema. Hypotenin also can present with chronic cornea edema. So basically we have a patient with a subacute chronic bilateral cornea edema, secondary to endothelial dysfunction. We didn't see or we didn't find any gutta around the patient. There's no history of trauma. It's a bilateral condition. There are no signs of inflammation. Could this be a secondary to a toxin? Could this be a secondary to any medication? Does anybody has a possible explanation for this patient presentation? You got it. Was that? There's another possibility. There is a condition known as guttallus could necessarily have a lot of guttallus. That's true. But only corneal attendants can see that. So yeah. Amantadine has been shown to cause an endothelial toxicity resulting in corneal edema. This is the first report that we have on amantadine. It was done by Dr. Blanchard from Oregon. Basically describe a patient, a female patient, 64 years old, developing acute corneal edema following amantadine use. And in this case, it was completely reversible after cessation of the medication. Same thing here, Dr. Jiang described cases of amantadine-induced corneal edema or corneal endothelial dysfunction found that actually after cessation of the medication due to prolonged chronic corneal edema, it wasn't possible for the cornea to get clear and some of the cases needed corneal transplantation and other case report of patient with corneal endothelial dysfunction following amantadine toxicity that actually resolved completely with amantadine cessation. And what happened to our patient, basically in the 17, we sent a letter to the neurologist to consider stopping amantadine. And the patient was starting on pred forte and mural four times a day. Two weeks after the initial evaluation, the neurologist discontinued the amantadine about a week before the visit. The vision was still count fingers on both eyes without any resolution or improvement in the corneal edema. A possibility of decimus stripping, automatic endothelial cartoplasma was discussed with the patient and the patient's wife. And we continue on pred forte and mural. We decided to see the patient again in about a month. A month after the presentation, the best corrective visual acuity of the right eye, which is the best, his best eye was 2040, basically back to normal. The left eye continued with count finger vision, mainly secondary to the corneal thinning scar from the initial corneal ulcer. The corneal edema resolved completely on the right eye. We decided to do a tapering of the pred forte and basically put the patient on mural ones. So after basically the take home message about this presentation, this patient is basically, if we see a patient developing bilateral corneal edema on a chronic side, nothing on the, on the slid-down examination shows into inflammation and the corneal dystrophy, we need to check and the review the medication list because sometimes we can see or we can find medication that can actually cause endothelial toxicity. Even in children, there are a couple of reports of children developing corneal endothelial toxicity. Again, secondary to man to the use. So it is very, very important for every patient that present with bilateral corneal edema to basically review the medications. Any question? That one, sir? Yeah, sir, is there any evidence that the topical steroid and the mural was anything to that? There's, there's some reports basically that there's, there may be an inflammatory component behind the development of corneal edema secondary to mentoring. We don't know the exactly cause of how the mechanism of a mentoring in these corneal and the field dysfunction happened, but there are reports of improvement, slight improvement after, especially pre-40 with patient with a mentoring corneal edema, but yeah, after the session of the mentoring, the natural catalyst to improve depending on how chronic the corneal edema is and if there's the development of scarring on the corneal hormone. Any other question? Thank you.