LASIK Flap Complications

Hello, welcome to the Isre Ears, we're off the Malzian OCADS Board of View Podcasts. We're your host Ben Young. And Amanda Redfern. Each week we take a high-yield topic and talk about the why and the how. Amanda, what are we reviewing this week? So I wanted to review Lasik Flap Interface complications, or otherwise known as DLK and things that look like DLK or diffuse lamellar caratitis. Yeah, I think this is hopefully really useful for a lot of residents to review because I know in all my training scenarios that I went through, there wasn't like a really heavy refractive component. So as a result, I really didn't see much refractive complications. But you know, we got to know it for the boards, it didn't real life and everything. So hopefully this is useful to our average resident. Yeah, I can honestly say I've never seen any of this, but I know it exists. And I did think about it a lot when I got Lasik. Ah, oh, well there you go. I actually didn't know you had Lasik. Thanks for reviewing it by information. Yeah, you don't know if it's gonna work less as anymore. I mean, I'm a very keen the student clinical observer that holy crap. Ah, I just, you were thinking about it the whole time. Okay, let's start with, let's start with the most, I think the one that will require the most discussion in terms of flap interface complications from Lasik, which is diffuse lamellar caratitis, or as we'll call from here on DLK. What is that? So DLK is a non-specific sterile inflammatory response to a variety of insults that will happen when you're doing Lasik. So that could be mechanical insults or toxic insults from the chemicals that we put on the eye or anything that might be left behind, like little fibers from the surgical sponges or whatever. Basically, anything that irritates the anterior stroma can trigger a white blood cell accumulation or response to that irritant. DLK is associated with many different risk factors or events that can happen during Lasik. Do you want to review some of those? Yeah, so if you have an epidefect during your, like the initial procedure or an enhancement, that's a risk factor. It can also happen after the initial Lasik, if you had something like a corneal abrasion or even infectious caratitis can trigger an episode, it can come an episode of DLK as well. For some reason femtophlapse have a higher incidence of DLK. I honestly don't know why, but. Yeah, it doesn't make sense to me either. You think it would be kind of cleaner, but maybe something about the micro-explosions that occurred during femtophlapse? I would just be speculating why. Basically, the general principle, though, besides the femtophlapse, is anything foreign that touches the flap interface. It can trigger it. So it could be mybomian glancing resins, like during the procedure, for material from the micro-curitome, the iodine that we use, the marking ink, etc. There's not supposed to be stuff in the flap interface. So all that can trigger an immune response, like Amanda was saying. How would a patient know that they've had something like this? So they may have no idea that they have DLK in the beginning, because it can be asymptomatic if it's really mild, but they may become aware of it if it is progressing to a later stage. In those cases, they'll have decreased vision. And that leads me to the four stages of DLK. Yeah, this is something that I think could be asked on. Like, it's one of the more high-yield things to remember for ocaps and boards. So let's go through it. Four stages. Stage one is just peripheral faint white blood cells. That kind of has a granular appearance to it. Stage two is when those white blood cells start making it in a scattered pattern centrally. So starts from the outside, then comes to the central part. Stage three is when it's not just scattered white blood cells, but they're dense in the visual axis. They will generally have some visual changes at this point. And the stage four is when they have scarring or even stromal melting from the robust white blood cell reaction. So peripheral then does kind of faint or scattered central effect than a dense central effect. And then the scarring is like the last stage of it. And I think some people describe this as like a sansusahara kind of appearance. Is that right? That is what I remember too. Yeah, so if you see that, I think it's more of a clinical term that you might hear like your faculty talking about. That sansusahara keyword is, you know, it looks kind of sandy in the stromal interface. I don't know if they would actually use that term in your ocaps. From the pictures I've seen, I encourage everyone to look at pictures of this. You know, it's a decent description that kind of sandy appearance. Okay, what do you do though when you find it? What do you do with these stages? So it's easy to remember stage one and stage two. These are not as critical because they may or may not be visually significant. But again, that's the peripheral infiltration versus a little bit of scattered central infiltration for stage two. And you're just going to frequently use topical steroids and just really try to get that inflammation down. It gets more complicated when we get to stage three and four where things are getting a lot more visually critical. So for stage three, you're going to lift that flap, irrigate, and then directly place steroids and NSAIDs in that bed to get that inflammation down. And then following that procedure, you're going to be treating them with intensive topical steroids. Some surgeons might even start oral steroids at this point. Stage four is very, very similar. And honestly in stage four, it's pretty severe. So you're just hoping for any improvement. But like we said, stage four includes like melting and scarring. So it's not a great prognosis. You're going to try anyway by lifting the flap, irrigating, direct placement of steroids and NSAIDs, intensive topical steroids, afterwards and oral steroids. Now, here comes the big catch. If you're not responding at all to steroids, especially if you have the earlier stages, and it's been about seven to ten days, you need to start considering other things that are mimicking this appearance of DLK. Such as infectious carotitis, which I think is our next topic. And that's a good general point, Amanda. If you're treating someone with steroids, if they're not improving, and I think this is a decent rule. Like in a lot like if I have someone with simple interior UVitis, I'm treating them for a week, is how long I get them to respond to steroids, and are not, you need to like rethink your diagnosis. And then definitely in this case, because infectious ideologies are on our differential. You know, obviously we don't want to see someone who has an issue with their lactic flap and miss that it's actually infectious, as opposed to an immune reaction like in DLK. Can you kind of describe to us Amanda, what, how would a patient present if they had infectious carotitis? So like with many eye infections, they're typically going to be symptomatic with eye pain and decreased vision. They can also have eye redness and photofolio. So that's not really a surprise. The most common infectious organism is going to be grand positive bacteria, so staff are strapped. But the thing to also consider is that you could have an atypical micro bacterium. And in that case, what are you using in your stains or cultures to determine if it is a micro bacterium? Yeah, you can do an AFB stain, SFAS basil stain, or use low-instein gentsan medium to culture it. Good job. Yeah, totally knew that off the top of my head. I mean, the big thing is if your suspicious for it, do the stain because that's going to come up way sooner than the the culture. But it doesn't hurt to do both because obviously you don't have 100% sensitivity when you're doing a stain. So doing the culture doesn't hurt. But the answer is faster with the stain. Yeah, micro bacteria are like the worst when it comes to surgical infections. Do you see that like you're thinking of something? Yeah, this is like, I don't want to share my PTSD with everyone. Let's talk about treatment. Here, if you suspect it, it's a bacteria in its sort of enclosed space, like a lacy-clap interface. So initially what you want to do is you want to lift that flap, culture of the interface while you're there, irrigate the heck out of antibiotics, and then do topical treatment afterwards. Forth generation, fluoroquinalones are usually the choice, though PCAC notes for us that monotherapy may not be enough with these kinds of infections. But what if that doesn't work? Amanda, do you know, is there anything else I can be done? So this is actually really scary sounding. But if it doesn't work, then you may need to amputate the flap to improve the penetration of your antimicrobials. That's going to be one heck of a conversation with a patient. Yeah, if you're a resident on call, I probably wouldn't go for that right away. Yeah, these are things you staff with, surgeons and all that. But that's an option. It shows up on your boards. Okay, we've talked about infectious keratitis and the fuselomelic keratitis. They kind of sound similar-ish, and it's critical because in one you treat with steroids, the other one's true with antibiotics. How do we differentiate between them? Amanda, should we go through it? Do you want to be DLK or IK? I'll do the IK once. Let's talk about onset. So DLK roughly, one is that usually start. So DLK is usually within the first 24 hours, whereas IK. - Yeah, as IK is usually a couple days postup with like basically any infection, right? It usually takes two or three days for it to inoculate and grow and become a problem just like in Dalflamitis and all these other ones. Keep in mind, it could be a week or more later too, especially with atypical micro bacteria, harder to grow, so it takes longer for them to become clinically apparent. - In terms of appearance, DLK will begin in the flat periphery and then will work its way inward. So you'll see more intensity of the specs or the white blood cells in the periphery unless so in the center until it gets to later stages. - Yeah, and IK, it can really occur anywhere under the flap wherever the infection pops up because I'm sure there are some white cells that we're seeing, but some of it's the infection too. Remember in DLK, it starts typically with some periphery and comes towards center because white blood cells come from the liberal periphery and then migrate in, but in IK, doesn't, you know, the infection is where the infection is. - That's a great point. In terms of layers, the DLK will be primarily in confined to that interface. So you wanna do a really good slit lamp exam and get that cross section of the cornea to see where the inflammation is within, well within the thickness of the cornea. - Yeah, yeah for sure. - But it should be pretty clear right on slit lamp exam. And an IK would start, you know, you know, at the interface, but it can go above, it can go below, it can go beyond the flap edge, you know, it won't follow the rules. It would just probably start within the interface, but you know, you may not be able to tell on your exam. What about the AC, Amanda? Do you typically get like a robust AC inflammation with DLK? - So there should be minimal to no anterior chamber reaction in DLK. - Right, any infectious curatitis, any like cornea ulcer, you can get, you know, a mild to moderate AC reaction. - And then in terms of flat melts, either one can give you a flat melt. - Yeah, don't use that to differentiate between the two. So, you know, I think in terms of kind of relating this to other ideas within ophthalmology, I kind of think of DLK is really similar to TAS, toxic anterior segments syndrome, which happens usually it's similar within the first 24 hours or so after cataract surgery. And we think it's a similar mechanism, you know, surgical debris or, you know, something maybe contaminated that was used during the cataract surgery, causes a robust inflammatory response that's treated well by steroids. And it starts early on, like, you know, it should be, you know, like the day one visit, you should be able to see that reaction. And it's also you always had to try to figure out and differentiate it from endopathy mitis from cataract surgery. So I would view DLK and IK's analogous to TAS toxic anterior segments syndrome. And, you know, cataract surgery associated in dolphin mitis, that helps you kind of conceptualize and bend these separately. But okay, I think those are like kind of the big ones. What other conditions should we know about that can happen with the flap interface Amanda? - So a highly testable one and maybe less obvious, but can be sometimes mistaken for DLK is pressure induced stromal carotopathy or otherwise known as PISC, at least from this point on in this podcast. - Yeah, it's a fun one to say, PISC. - I know, for some reason, are you a Spider-Man fan? - Yeah. - It reminds me of PISC and he has like the big belly. - Yeah, Wilson FisC, yeah. Yeah, that's actually a great, wow, I love it. Well, let's go into why the big belly thing can, if you don't know, Wilson FisC is also known as the Kingpin. I know it at our Academy of Spider-Man and Daredevil, typically though he is a prominent in the Marvel Universe. Anyways, we can, he's so cool. - Yeah, highly recommend the Vincent Denoffrio version. But, - Oh, God, she's so good. - Right, okay, getting back to PISC. So this usually presents about 10 to 14 days after surgery. And it comes from having elevated post-op IOP from prolonged steroids, pleading to all this pressure and a formation of a fluid cleft at that flap interface. And that fluid cleft can give you some corneal haze. Hence the big belly of FisC. - Yeah, yeah, he gives it, yeah, that belly. And I think a key, because this is really just like quote, "Stereo to News" glaucoma. You know what I think, I don't know if you've done an episode on it, but it's a common thing I can happen with any steroids. But the key is that when you take to pressure, especially with aplination, it may be artificially low because that kind of, like if you could applinate the stroma without the flap being there, then you would probably get the accurate pressure. But because of that kind of belly formation, where you have fluid between the flap and the stroma, it makes it seem artificially low. Like you're like checking the pressure like a water bag is both of the actual eye. So it may be confusing, you know why they might have some pain or you know worse vision. You may be thinking of DLK or something. When if you do a good exam and see that there's a fluid build up, you'll know it's PISC instead. So Amanda, are there better ways to measure besides aplination to try to get around this problem? - Yes, this is one case where actually tone-off head is recommended over-applination. - Yeah. - Probably the only time I could think of that, they recommend that you should be tone-offending or even using a no-mo, sorry, new-mo-tanometer. And you want to check the pressure both centrally and peripherally. So you're not being tricked by that artifact. But these methods are less prone to the artificial lowering effect than aplination is. - Yeah, I bet an eye care worked to, in terms of like checking peripherally, 'cause I find with an eye care, it's easier to check peripherally. But I don't think it's in our textbook. So yeah, if you're on call, you could think about using that, I think. And then what do we do? - No one's out to be needing on call. - Oh, I guess you would if they're calling after hours and you're seeing them in clinic. - Yeah. - I'm thinking about the ED, I'm like, I'm not using an ED slip lab to applitate. - Yeah, that's how you cause eye care, right? (laughing) All the milieu of the ED environments right on the surface surgical eyeball. Okay, we found it, we like, oh yeah, centrally it's pressure-stand, but peripherally it's like 50. What do you do now, Amanda? This is the key, as opposed to DLK, where you're using lots of steroids, you want to rapidly stop steroids as safely as you can in these patients, because you want to bring down that pressure-induced glaucoma or IOP elevation. And then as you're waiting for that pressure to come down, you're using glaucoma drops to help lower the IOP. - Yeah, you know, treat it like a steroid-induced glaucoma, basically. - Yeah. - Cool, okay, so that's a PISC. What else can happen to the interface? - Epithelial in growth. - Oh, epithelial in growth. Before we go more into this, I do want to make a small distinction for residents where, like I was really confused with this, like, especially in early residency, that epithelial in growth is, we're going to talk about as we're first to like, lacy flap interface, but there's a separate thing that most people term epithelial down growth, but like in some texts they also call it epithelial in growth, where the epithelium gets inside the eye and it can cause glaucoma and grow and like, proliferate inside the eye and do kinds of all kinds of crazy things, but that's distinct from what we're about to talk about, which is epithelial cells getting under the flap interface and not inside the eye. I wish that we were clearer and like more texts and literature that down growth. I prefer the term down growth, meaning it goes into the eye, like, you know, usually through like a surgical wound and your cornella pithelium starts, or work, I guess, can you tell epithelium, can start growing into the eye and then proliferating and causing all kinds of problems, but that's not what we're talking about now. - That's a great distinction, thank you Ben. - Yeah, no, yeah, I just, I remember being like super confused by that as a resident, like, how are these the same? Like, what's going on? So that's a distinction. How often does this happen though with lacyk Amanda? - Not very often, it's less than 3% of eyes, and it doesn't have to be visually significant or anything super intense. So it may also not go notice for a while. - Yeah, are there risk factors for it happening? - Why indeed there are. The big one is having an epithelial defect at the time of the procedure. And I think the theory behind this is that when you have an epithelial defecting, you have local swelling around that area, that interface between the flap and the stroma where it's trying to reconnect is not well aligned because you have one side of that joint being swollen and not one to one. - Yeah, and then it's probably the, you know, the level, the epithelial stem cells is a march and the limbis into the center, probably just crawl under that interface when it's not well opposed. How would patients know they have it? - So they can be asymptomatic and just never know unless you point it out to them. Or if it's really bad, they can have severe vision loss. So it is a spectrum. - Yeah, I mean, and the vision loss can come from things like just a regular astigmatism. You know, if you have like this kind of sheet of cells and like one, usually it's not like 360 around. It's, you know, one quadrant or so of the, of the cornea. I can give them some of regular astigmatism. If it does cross a visual axis, it can blur their vision just by having this kind of like light gray you know, the sheet coming across the cornel interface. Or it can cause flat melting actually, you know, when it's like very severe. So what do we do about it? Well, nothing if it's not bad. If it's just isolatedness of epiphalial cells in the periphery that aren't really advancing or affecting the vision, you just leave it be. If you are starting to have complications from it like been listed, then you could lift the flap, scrape the epi from the underside of the flap, and then the stromal bed as well because you really just want to get all those cells off and then reposition the flap. If it does recur, you can keep doing that procedure over and over again. It doesn't sound like that would be a fun experience for anyone involved. Things that you could do though for the recurrence that might be different from just lifting and cleaning and repositioning the flap would be maybe suturing or gluing at that edge to really make sure things are well-opposed and sticking together and in position to heal. Some people even treat the that stromal bed with alcohol to really get rid of any remaining epiphalial cells. And there's some people who yag these. That sounds really difficult and scary. I don't think we'll talk too much about it, but it's like reported. Yeah, it was reported in just early cases, not like these terribly complex ones where you're definitely going to be lifting. Yeah, so it's an option out there. So that's epithelial end growth as it relates to lacyc flaps. The last thing we'll talk about is just interface debris. This is kind of along the same spectrum as deal K. I think. If stuff gets into the interface, maybe it's like post-op, floppy hissens or something like that, then they can get inflammation from that. So those kinds of things are going to be like lint or non-descript particles, even tiny metal particles from like the blade, which is just mind blowing to me. But anyway, any of that stuff can actually wind up in the interface. And it's not actually necessarily going to cause an inflammatory reaction like we see in DLK sometimes or oftentimes it's well tolerated. Yeah, blood and things you have to know about, you know, you're cutting things. You can get blood during a surgery. All amount of blood is like usually not a problem. We'll just kind of go away over time. But a lot of blood has inflammatory cells within it and can trigger that response. So if you have a lot of blood, usually the advice is to try to make sure you get it out and get that hemostasis at the time of the lacyc procedure. You know, we see a similar thing, not to relate everything to right now, but you know, if you leave a lot of blood on like a retinal tear, then it can cause a progflammatory response and cause, you know, a profited vitro retinopathy in that area too, because blood has, you know, all these like, you know, all the inflammatory cytokines are in the blood, right? So it can cause those issues. So you tend to not want to leave a ton of blood on your surfaces when you're doing surgery. Pro tip. Pro tip. Pro tip. Cool. I think that's it. Yeah. Should we do a quick review? Yeah. So first thing, DLK and inflammatory reaction to lacyc at the interface in four stages where one and two are peripheral versus central. Just scattered white blood cells and you treat those with steroids, where it's three and four, you definitely got to go back in there and clean things up and treat aggressively with anti-inflammatories. Yeah. Don't forget about an infectious carotitis that can cause, that's usually caused by staff for other grand positive organisms. We had to keep a typical micro bacteria in mind, which we detect with a acid fast stain or low-antine gentsome culture. And in that case, you always treat and blossom with antibiotics. Yes. And DLK will be more apparent early on in the course, usually within the first 24 hours, whereas IK bacteria takes time to brew, so you're thinking about it a few days out. Yeah. Pisc or pressure-induced thermal care top of the, it's really just dirt-induced glaucoma in the setting of lacyc, but you'll have artifacts with low pressures because it builds up a fluid cleft in your lacyc flap interface. You get to check around it using usually tone-up pen or even a new emitting with denominator to figure out what the pressure situation is. And then epithelial in-growth is just in-growth of epithelial cells at that flap interface. It can be very mild or it can be pretty profound, in which case you're going to also go in and lift that flap and do some cleanup. Last, you can get debris in your interface. Be careful if you have a patient with some inflammatory reaction and has a lacyc flap. You can be lint or random particles that end up in there. And that's all we have for this week. If you like what you heard, you can a rating review on iTunes or wherever you found us is really helpful for our podcast. And we appreciate your support as we have come back to trying to do regular episodes. Thanks for your time. Bye. [Music]