 All right, I guess we'll get started. So topic is surgical treatment of ocular surface discolors. So we're talking about the ocular surface. It's not just the cornea. We're also including the lids and tarsal congenitiva as well as the bulbar congenitiva. And these are kind of the surgical procedures I'm going to go over, basically, anything to do with the ocular surface I'll try and mention. So congenitiva biopsy. Obviously, for a biopsy, anything, any sort of congenitival tumor, anything that's suspected to be CIN or pigmented lesions, congenitival biopsies are also helpful in diagnosing ocular secretarial pemphagoid. So you see linear staining of IgG against the base of membrane in OCP. So basically, my techniques for a biopsy are marking the borders, if it's not obvious. Typically, if it's not a pigmented lesion, I'll mark the borders because I'm going to inject lidocaine underneath the congenitiva. And that'll kind of obscure the margins of the lesion. With anything that's suspected to be congenitival melanoma, it's recommended that a very wide margin is used. The shields recommend a 4-millimeter margin, which is quite large. Sometimes if it's not possible, then you can go a little smaller than that. And they kind of advocate what's called a no-touch technique, basically not touching the actual lesion, if you're suspecting melanoma. And then I recommend cryotherapy of the cut congenitival edge if there's any sort of suspicious lesion, whether it be cancer or even like a CIN. And I use employed the double freeze thaw technique. So I'll show a little video. So basically, take the cryoprobe and go just on the conge edge. I'm not cryoing the sclera. This is the one. There's one cryoprobe that freezes in between when you're not pushing the pet petal down, so watch for that. And I basically just very lightly, barely get it to freeze. And then I take my foot off the petal and get it to thaw. And I have basically overlapping spots across the conge edge. So basically, until you see that ice ball and then I kind of take the foot off the petal. And so you get the idea. So I kind of march across. And then once I hit all the spots, I'll go back and do it again. So double freeze thaw just to make sure you don't to miss any spots along the congenitival. And this is to prevent any sort of recurrence if there's any sort of neoplastic cells along that cut congenitival edge. Next, talking about tarsorphy. So for really any sort of non-healing cornea epithelial defects that are recalcitrant to other treatments. So one may be surprised even if someone's been on vantage contact lenses for a while, not healing. Once they get a tarsorphy, they can heal really quickly. So it's something about just the patient's own tissue against their epithelial defect that can get them to heal. So consider it with ligophthalmos. You can make the tarsorphy temporary or permanent. You can make it medial. You can make it central. You can make it temporal, depending on whether or not you want any sort of opening for the patient. Typically, I'll put the tarsorphy in a temporal position just so they can still see a little bit and they can get their eye drops in. And there's different ways to do a tarsorphy. The most common is gonna be with a suture. This can be temporary or permanent. And with a permanent tarsorphy, you kind of debride off or cut off just the thin strip of the epithelium off the eyelid margin. So you can get the eyelid margins to fuse permanently. Other sorts of tarsorphy, there's glue tarsorphy, or basically take accrylate glue and glue their eyelashes together. It's not great, but I suppose if you've got someone who can't undergo a suture tarsorphy for whatever reason, it's a nice temporary fix. Botox tarsorphy is injected into the actual levator muscle to cause ptosis. And it's nice because then their eyelids aren't actually fused or sutured together so you can actually manually open up the eyelid really easily for examination, but obviously with Botox, it lasts about three months. So it's gonna be for people who need a little more long-term effect, but maybe not permanent. Next, teridium excision. So this is kind of a subset of congenitiva biopsies. So my indications for excising a teridium is, most obvious is gonna be any sort of teridium that's heading towards the visual axis or in the visual axis. Sometimes you can have a teridium that looks fairly small, but it's causing distorted vision because it can induce significant astigmatism. Or other times there may be a teridium that doesn't meet the above two criteria, but there is persistent discomfort or redness or inflammation that's not relieved by topical drops. So here's an example of a teridium. You can see here and it's inducing flattening in the area that the teridium is in on topography. So this may be visually significant. With excision, it's important to remove the underlying tenons layer to prevent recurrence. And when you remove the underlying tenons layer, the actual defect on the congenitiva after you remove the teridium, it actually kind of gets bigger because it relaxes. You wanna send the specimen to path to rule out any sort of dysplasia or neoplastic lesions. Sometimes you get surprised. As far as what to do after the teridium is off, they used to do, people used to do bare sclera. I mean, they just took the teridium off and that was it. There was a very high recurrence rate. It was about 50% recurrence with this technique. One could consider primary closure of the congenitiva with suture. I might only consider this with a really small teridium, really small congenitiva defect, but I typically will not be doing this for a teridium. These are the two most common techniques that are done to prevent recurrence. Congenitival autographed, which you could maybe term congenitival transplantation of the patient's own congenitiva or suturing or gluing down amniotic membrane. So congenitival autographed has the lowest rate of recurrence. It's been reported about 2% to 5% recurrence of terigia after congenitival autographed. And you basically take a free congenitival graph from the superior bulb or congenitiva. You then leave that superior congenitival defect open. And then you take that graphed and apply fibrin, gruel and or suture to the area where the teridium was excised. And it's important to seal the graph to the cut congenitival edge, again to prevent recurrence. Amniotic membrane is useful if the superior congenitiva is not available for a graft, such as scarring, if there's a TREB, or maybe a patient with significant glaucoma who might be getting a TREB, you probably might consider doing amniotic membrane. Sometimes you get a double-headed teridium, a nasal and a temporal one, so then I'll use a congenitival autographed on one of the teridium and amniotic membrane, not for the other. And again, you can apply it with fibrin glue or sutures. Mitomycin C I will use interoperatively if it's a recurrent teridium that's being removed. And this is to prevent further recurrence. So what I do is I soak sponges with mitomycin C and then tuck it underneath the congenitival edge, wait two minutes, take out the sponges, and then do a really copious rinse. There is a concern for complications, months to maybe even years later with scleral melts and infectious scleritis. So this is why I don't use mitomycin in all the cases of teridium excisions. When you use the, what's your indication for using the fibrin glue versus the suturing? So I do both, so I used to do suturing when fibrin glue didn't exist and it takes forever. So then fibrin glue is really, really easy. But then for billing purposes, I think you need to show that you sutured something. So I'll usually put two sutures, like two vicaral sutures at the limbus and then use to seal for the rest of fibrin glue. Next I'm gonna talk a little bit more extensively on limbal stem cell deficiencies and limbal stem cell transplants. So limbal stem cell deficiencies may be partial or they can be complete. And you'll see congenitivalization of the cornea, a thickened, vascularized irregular surface. There may be chronic inflammation, persistent epithelial defects, stroma ulceration, corneal scarring, and in some cases there could actually be corneal perforation with non-healing epithelial defects. So here's a good example of limbal stem cell deficiency of pretty much almost all of the limbus. There might be a little quadrant of relatively healthy limbus here, but this is all vascularized. You can see the blood vessels growing in and there's corneal scarring. Here's an even more extreme example with very prominent new vascularization and congenitivalization. You might see a little thinning of the cornea centrally. This is an example of stroma ulceration. So you've got 360 degrees of limbal stem cell deficiency, but then this is a non-healing epithelial defect. So with limbal stem cells, so these cells are defined by the capacity for unlimited or prolonged cell renewal to produce at least one type of highly differentiated progeny. And it's defined by their niche, which is kind of like their environment or their place. And it depends on the contact with the surrounding cells, extracellular matrix interactions and local growth factors. This is a major target of gene therapies and limbal stem cells are different than embryonic stem cells. Basically you've got the limbus separating the congenitival in the cornea and somewhere in the limbus you've got these corneal or limbal stem cells that cause kind of corneal differentiation and protects, it basically is a barrier for preventing the congenitiva from growing onto the cornea. This slide and basically just showing that this is a path slide, basically highlighting goblet cells taken from a biopsy of congenitiva that's kind of grown onto the cornea. So it does show that there is indeed congenitivalization of the cornea. There are basically six types of limbal stem cell deficiencies. It can be congenital, traumatic, iatrogenic, autoimmune, neoplastic or idiopathic. Congenital, the most common category is gonna be anoradia. So anoradia, I mean with the name, you think no iris, but in actuality they usually have some sort of iris, but also with that is pretty severe limbal stem cell deficiency. Other congenital conditions are ectodermal dysplasia, kid syndrome, keratitis ichthyosis deafness syndrome, and keratitis associated with multiple endocrine deficiencies. So these are gonna be more rare. Traumatic is also very common. Chemical and thermal injuries, contact lenses can actually induce limbal stem cell deficiency. If there's any sort of inflammation or infection that extends to the limbus, that could destroy limbal stem cells. It's also associated with neotrophic keratopathy and chronic bolus keratopathy. The prognosis of a chemical injury depends on the extent of the ocular surface involved and the amount of limbal ischemia that is seen acutely. And there is a classification scheme for this called the Roper-Hall classification, which basically grades limbal ischemia and kind of comes up with a prognosis. So you can see if there's a lot of limbal ischemia, there's a poor prognosis, and usually the cornea is very opaque and it's hard to see virus underneath. So here's an example of acid burn. There might be just a little bit of limbal ischemia, but it's not too bad because you actually can see some pinkness and some vessels. So if you see pink or if you see red, that's actually a good thing. That's a good prognosis. So this, if you kinda look back at this classification, I'd probably categorize it as a little grade two lesson that there are limbal ischemia. So still a good prognosis. And there is some haziness as seen in this picture here. Here is an example of chronic non-healing cornea ulcer post-alkali burn. Really not seeing limbal ischemia here. So this is also a good prognosis overall. Here's an example of an alkali burn with ischemia seen acutely. So this is a pretty large area. So this is very, very white. This is NACA. This is classic limbal ischemia. And then subacutely, this space just never really fills in with blood vessels. So everything else is fine out here. You see blood vessels kinda growing in here, but there's really nothing here. So this will pretend a poorer prognosis. This is an example of kinda more extensive limbal ischemia where you see limbal ischemia going all the way around and you can see that the cornea is very cloudy. And again, poor prognosis. You can get limbal stem cell deficiency from iatrogenic causes such as multiple limbal surgeries or cryotherapies to the limbis. Long-term topical medications, preservative can actually cause limbal stem cell deficiency. If there's any sort of anti-metabolite use such as 5FU or mitomycin either interoperatively or in topical form. And also radiation can induce limbal stem cell deficiency. Autoimmune causes include SJS and TEN syndrome, oculosecaterosalpinephagoid, any sort of chronic limbitis from atopic disease, vernal disease, or fluctenial disease, and also peripheral ulcerative keratitis including morins ulcer. Neoplastic, I put teridium on here. Technically could be considered neoplastic even though it's benign. And also CIN and something like screnous cell carcinoma and lastly idiopathic. So transplant, there's actually certain transplantation classifications that are done. So if you have a limbal stem cell deficiency and you wanna do a limbal stem cell transplant, it can be an autographed meaning from a patient's own tissue. So this could be harvested from the same or fellow eye. Usually it'd be from the fellow eye that is not affected or it can be an allograft which is harvested from a cadaveric tissue or from living related tissue. And usually kind of more HLA matched. And these are some of the abbreviations. There's lots of abbreviations used here in relations to the limbal stem cell transplant. So conjuntival limbal autographed. So this is from the patient's fellow eye. There's living related allograft from a living relative. Most common one that we'll see is a K-Lal keratolimbal allograft. This is from cadaveric tissue. These last two are not really used in the United States because these involve expanding limbal tissue outside of the eye and then putting it back in the eye. But I won't mention that later. So this is basically what we're doing. So the recipient has their limbus and kind of fibrovascular tissue removed. There is donor kind of peripheral corneal limbus that's harvested and that is sutured onto the recipient. So conjunctal limbal autographed. So again from patient's own tissue. So this is indicated in unilateral limbal stem cell deficiency and could be from chemical or thermal injuries, teridium, the source again, same eye or unaffected fellow eye. Up to six clock hours of the donor tissue can be safely harvested without risk to the healthy fellow eye. And the nice thing about this type of procedure is because it's the same if it's the patient's own tissue, there's not gonna be any risk of graft rejection and the patient doesn't need any systemic immunosuppression. Living related allografts indicate in bilateral limbal stem cell deficiency, the source is a living related donor with an optimal HLA match. And obviously the donor can't really have any other sort of risk factors for a limbal stem cell deficiency because it's not the patient's own tissue, systemic immunosuppression is still required. But because it's a living related donor, it kind of improves the prognosis for any future transplant, coronal transplant that's done down the line. So this is what's done. So this is the donor being harvested, patient also kind of has the peripheral cornea and a bit of scleral taken off as well as the fibrovascular tissue over the cornea and then the donor tissue is kind of sutured at 12 and six o'clock. So here's an example of donor tissue being harvested here. Curator limbal allografto-calow. So this is from Caterveric limbal stem cells. The peripheral cornea is the carrier for the limbal stem cells. Systemic immunosuppression is required and this may eliminate or delay the need for PK. If there's a lot of corneal neovascularization and there's a concern for extensive limbal stem cell deficiency, doing a limbal stem cell transplant prior to a corneal transplant can improve the prognosis of that corneal transplant by about 80%. So limbal stem cell transplants allow for healing of persistent epithelial defects, oculosurfstability and regression of neovascularization and then the chronic inflammation that is seen does subside. So here's the technique. So first the recipient, congenitiva, is marked off with coterie and this is gonna be the border for what is removed. So it's a couple millimeters back from the limbas. And then the fibrovascular panacea is removed along with that peripheral skirt of congenitiva right here. And then once everything is exposed, looks like this. And then the donor cornea is punched in the middle, usually about seven or seven and a half millimeters in the middle, so you got a donut. And then this tissue is split. And then the anterior part of that split is sutured. So here's another diagram, so seven and a half millimeter in the center and then about at least a millimeter of scleral tissue. And you actually need three halves just because when you manipulate things there's not quite enough tissue if you just have two halves so you need a little bit more from another eye. So you actually need two globes. And then when this split thickness is done we take kind of usually split it two thirds, one third and then this anterior one third is what gets sutured. You don't want to suture this whole bit of thickness because then it's way too bulky. So that's the reason for deep bulking and then the limbo stem cells are gonna be in this anterior one third anyway. And so then you can see kind of these three halves just to fit in the three pieces all around the patient's cornea and then this is sutured down with tenonylon. And this is showing a piece of tissue. I think this is not acutely post-op. This is acutely post-op, so it's pretty red. And I think in this case amniotic membrane was put over the whole thing as well. So all these pieces are sutured down and then amniotic membrane on top. So that's the K-LAL technique. I'm just gonna put a brief slide on this new technique for limbo stem cell transplant that's been talked about called slet simple limbo epithelial transplantation. I think what this was talked about in the Grand Rounds last year. But basically instead of doing that whole K-LAL procedure patients kind of cornea epithelium and fibrovascular tissue is removed and then you basically take small pieces of limbo tissue either from the patient's fellow eye or donor tissue, kind of cut them up into very small pieces, put them on the cornea. Before that you sandwich it between two layers of amniotic membrane. So you lay down amniotic membrane on the patient, then use fibring glue to glue down these little pieces of limbo tissue, kind of in the periphery, and then glue down or suture another piece of amniotic membrane on top. So this, I think long-term it hasn't really been studied too much. I have a feeling this may work for maybe partial limbo stem cell deficiency, maybe not for complete. But that remains to be seen. Okay, this is another, so the last kind of category of limbo stem cell transplants I'm gonna talk about is ones involving ex vivo stem cell expansion. So either taking the patient's own healthy limbis from a fellow eye and growing that in a lab on a sheet of amniotic membrane and then transplanting it back in or taking limbo stem cells from a category donor and growing that on a sheet of amniotic membrane. So we don't do this in the United States, but I think it's being done in Japan and maybe some other places in Asia. And if the patient's own tissue being used and those systemic immunosuppression is required, so then donor tissue is taken, it's grown onto a sheet of amniotic membrane and then sutured onto the recipient. And then this is showing after they expand the limbo epithelium on the amniotic membrane for three weeks, this number one is showing the limbo stem cells kind of on top of denuded, this is denuded amniotic membrane epithelium and then this is the actual amniotic membrane like the stroma. So it's showing that the human limbo stem cells are actually growing on top of amniotic membrane. So that's kind of cool. Postoperative management just overall for a limbo stem cell transplants, topical medications with steroids and cyclosporin, maximize lubrication, total occlusion. You might consider a torso for you to help with healing. This can be permanent or temporary. There may be a subsequent PK needed and then systemic immunosuppression is usually needed for about 12 to 18 months, maybe longer for younger patients. And these are some of the agents that are being used. Systemic steroids, cyclosporin or tachylimus and azathioprene or mycophenolate. Next is curator prosthesis which is also used for a limbo stem cell deficiency. It's kind of a surgery of last resort. Usually it's in a patient who's had multiple PK graft rejections and maybe they've even had a limbo stem cell transplant already. Problem with curator prosthesis is that there's resulting glaucoma which can be very hard to control. They often need a tube and they're at very high risk for infection as well. And this is basically what it is. It's got a front optic that patients look through and that gets threaded through a corneal graft that's been punched out in the middle. And then there's a back plate. This is the older version of the K-PRO which had a PMMA back plate with a locking ring. But there's a newer version that has their back plate made of titanium and there's not a locking ring. So here's some pictures. So this is of the older type of Boston curator prosthesis. So it's got PMMA in the back so that you can't really see the back plate as well. You can see those little holes here that are put there just to make sure there's enough nutrition that can transport in between. And then this is the newer titanium version which is a lot more apparent because it is made of titanium. But it's got the same type of holes in there. Switching gears to contactival flaps. So this is surgery that's done for things like a chronic sterile ulcer. A painful belay with poor visual potential might consider it for an unstable corneal wound such as progressive thinning. I don't really recommend it for active infection although some people have done it with success or if there's a cornea perforation. Can be a partial contactival flap meaning covering part of the cornea or a complete flap which is turned to Gundersen flap. You do need to remove the patient's corneal epithelium so that the contactiva can stick on top. So this is diagram of the Gundersen flap. So a superior contactival incision is made pretty far superiorly. You kind of dissect down. You got to do a 360 degree pyritomy and then you take the superior kind of large flap and bring it down over to cover the whole cornea. And the cornea needs to be denuded of epithelium and then kind of sew that down and then that stays permanently. So as you can tell it's gonna impact vision. So I typically will reserve this for patients with very low visual potential who need a contract. Mucous membrane grafting. This is for reconstruction of contactiva mucosa in inactive secretarial contactival disease from inactive SJS or OCP that's maybe not so late stage. And you can achieve better ocular surface lubrication by improving the tear film distribution and eyelid movement. Bucomucosa is usually used. So this is something that has to be combined with oculoplastics. This does not replace limbal stem cells however. Next, just wanna briefly touch on amniotic membrane transplant for severe Stevens-Johnson syndrome. And this is kind of the email I'd sent out last week regarding the protocol. So basically anyone with severe or extremely severe acute SJS will need an urgent amniotic membrane transplant. So the definition of severe is basically staining over at least a third of the lid margin on at least one lid. Any corneal epithelial defect that's more than punctate staining. If there's bulb or pebral contactival staining greater than one centimeter than urgent amniotic membrane is advised. And that's kind of the paper it was taken from. And it's usually better to do this sooner rather than later. So if it could be done within a week of the patient's eye symptoms, better prognosis there is. And the purpose for doing total amniotic membrane transplantation is to prevent kind of chronic scarring and inflammation that can occur with chronic SJS. There's various methods for putting on the amniotic membrane. This is the method we've been doing kind of more recently. So you take a large, the largest size you can get of amniotic membrane, which is five by five centimeters. And this is cryopreserved amniotic membrane. Take that square piece, split it in half. Then trim the patient's, all the lashes and suture an edge of the amniotic membrane just anterior to the lash line with a running 80 nylon. Then you tuck the amniotic membrane kind of over the lashes and tuck it into the fournesses and then take 6.0 proline and go through the eyelids and suture to bolsters. These are kind of some foam bolsters that I've used. I think here we've been using like IV tubing and using that those as bolsters. And then after that's done to all four lids, then a prokera is placed. And this is a prokera is amniotic membrane that's attached to a kind of a plastic ring and that gets put in. And then the amniotic membrane takes about a week or two to fully dissolve. And after it's dissolved, the proline can be removed, the 80 nylon can be removed, the prokera residual ring can be removed. And then the patients reassessed to see whether or not they need a repeat transplant. So if there's still epithelial defects, if there's still a lot of inflammation, then a repeat transplant might be indicated. But usually people do well with just one. Next, talking about superficial keratectomies. So this is a procedure where there's removal of the corneal epithelium, it may or may not include bowman's. There's no replacement tissue that is placed. So the indications are gonna be removal of any sort of superficial tissue. Technically peeling off a teridium off the cornea would be considered a superficial keratectomy or peeling off a Salisman nodule which usually sits on top of bowman's membrane. Epithelial basement membrane just refuse so basically if you're taking off the corneal epithelium, you might consider it for a very superficial scarring but this would only be involving kind of epithelium. Sometimes you get suspected corneal CIN which is like kind of a gray white sheet growing over the cornea. So if you suspect CIN, that epithelium needs to be sent to path. Taking out a retained superficial foreign body could be considered a superficial keratectomy. And there's a couple types. There's manual which is the most common type. So either scraping the epithelium off with the blade or peeling something off with forceps whether it be a teridium or Salisman nodule and also diamond burr polishing of underlying bowman's layer is considered part of superficial keratectomy. PTK is also maybe considered a subtype of superficial keratectomy. So this is using the eczema laser, same laser we use with BRK and Lasik to ablate tissue as a form of keratectomy. The Visix laser which is made by AMO has an actual PTK setting where you can set like a big broad beam and you kind of program how many pulses you want that big broad beam to go. Here at Moran we don't have the Visix but we've got the Alcon WaveLight EX500 laser so it can't give a full broad beams but what we do is we basically program it for PRK. So we're basically doing PRK but doing it for the purpose of removing anterior stromal irregularities. So what kinds of problems can you treat? You can treat granular dystrophy by just kind of smoothing out some of the anterior, those anterior crumbs. It's been done with in post-lasic striae and we're talking like striae that have been there for a while. Acutely, if there's striae, you wanna relift a flap and kind of take off that pithelium, get it to smooth out but let's say you've got striae that are chronic, could consider PTK to remove it. You can use it in certain scars. It's not good for anything deeper than a hundred microns in depth. It may not work as well in post-tropetic scars or traumatic scars. I think that's my last slide.