During this live webinar, we will discuss how to evaluate and diagnose Keratoconus clinically using clinical history and signs at examination. Confirmatory investigations will also be discussed along with current therapeutic options. The webinar will conclude with an algorithmic approach to Keratoconus.
Lecturer: Dr. Sheraz Daya, Ophthalmologist, Centre for Sight, UK
Well, good morning and welcome to Cybersight. I see we have a lot of participants. That’s good good to see. My talk. My name is Sheraz Daya, Medical Director Center for sight and my specialty, is cornea and the anterior segment and refractive surgery. I’m going to be speaking to you today about keratoconus. Now, for many of you in the audience, I expect you know all this, a good portion of it, but I, I’m almost certain you’ll you’ll learn something new.
Anyway, it’s a very long talk isn’t going to be coming a lot of material. I’ll be going very, very quickly. So just to start, I mean, I like to start with fundamentals. Whenever I give a talk, I’m going to talk about the cornea. So the cornea you need to understand, what the anatomy of the cornea is. It consists of the epithelium, which you can see very clearly at the top here, but about six layers can can remodels and goes up to 12 layers of all. There’s Bowman’s layer, which is right behind the epithelium, and then the bulk of the cornea the stroma and then you’ve got decimate’s membrane and the endothelium. If you notice, the cornea architecture is a lot more compact anteriorly coalescing to Bowman’s there, and a lot more a lot less compact posteriorly. The columns is arranged in such a fashion that the corneal tissue is transparent.
So this is the anterior stromal structure here, you can see a crisscross lamellar pattern and as you go on posteriorly it becomes a more loosely arranged silk layer, but it’s that loose arrangement is of significance in conditions like keratoconus. Now the textbooks will say that keratoconus is a progressive non inflammatory thinning disorder of the cornea, leading to altered shape and adversely affecting visual performance. The reality is it is actually inflammatory. It is not non inflammatory, just because the eye is not red doesn’t mean there’s no low grade inflammation taking place.
So, there’s a variety of hectasia that results from the cornea thinning out. keratoconus is the most common. It can occur centrally or inferiorly. Then this pellucid marginal degeneration, which is another thin hectatic disorder, and that occurs at the margin towards the margin of the cornea in the periphery, and keratoglobus involves the whole cornea.
What are the facts about keratoconus, varies a lot in terms of prevalence. In countries in the Middle East, the number of cases is about one in 200. And it increases to about 1800 in some parts of the world. There’s a strong association with atopy, people rubbing their eyes, and Damien Gardner, a good friend and an expert in this area has a great video on YouTube showing what happens to the eye when when patients rub their eyes. So patients must not rub their eyes. Why did they rub their eyes while they they eyes get inflamed. Remember said to you about inflammation being a contributing factor not straight from high rubbing, but actually the cytokines influences the elasticity of the cornea. So there’s definite rationale for reducing inflammation when you see it. And treating chronic conjunctivitis quite aggressively with mast cell stabilizers and steroids and even cyclosporine topically if necessary. It is an asymmetric condition.
The onset is usually during puberty and the hallmarks are progressive myopia. So optometrists will see these patients first, and then eventually develop irregular astigmatism, Corneal thinning and cone deformation. And as I said, the association with atopy, eye rubbing, down syndrome and Marfan Syndrome as well.
So what is the pathogenesis? Why does this all began, a lot of people homing in on just one area, the genetics, that doesn’t make any sense because there are other things that take place. Genetics might identify areas of collage abnormalities. However, there are other issues. As I said, there’s the inflammatory cytokines that may be present. So in this this table, courtesy of Jesus Mereyo, from Oviedo in Spain, is divided up into Atopy, contact lens related, hormonal, systemic conditions. And then the mechanisms here, they don’t remember all this stuff. Just suffice it to say it’s a multifactorial condition, a lot of causes there. But as everything in life, the common things are common, eye robbing, allergies.
And with any degeneration, it’s an it’s an imbalance. Typically, the body regenerates itself otherwise we wouldn’t be standing still we just be crumbling. So as we as we degenerate, as things get degraded, we have healing mechanisms regenerates us, When that balance gets upset and there’s more degradation than there is regeneration, then you get disease. And that’s essentially what happens with the cornea. So we’re not getting re healing of the corneal stroma. And it just thins out. And it gets worse because you’ve got aggravating factors that contribute to degradation.
So how does one make the diagnosis, clinically is a big one, especially in developing countries. There’s topography that can be used, corneal hysteresis, a bit more sophisticated looks at the elasticity of the cornea, and its ability to be deformed. And then there’s epithelial mapping as well. So let’s go through each one of these. Clinical is vital, we are all doctors, we want to examine patients, and we have to use the slit lamp to the best that we can. Patients will will come in because they’ve got problems with the vision and why is that? Their myopia is increasing and the astigmatism is increasing. So optometrist need to be warned, if you see this happening, think keratoconus, especially if you see them rubbing in the rubbing their eyes in the waiting room or otherwise.
Retinoscopy is very, very useful. I find that amazing when it comes to looking at patients, corneas, you’ll see in a an extreme case because you get this droplet type appears. But you might see actually see scissoring. So when you see scissoring, you know that astigmatism bit irregular, is going the wrong direction. At the very extreme, you’ll see Munson sign. This is a patient with hydrops bad keratoconus and Munson signs were the lid because because the cone is so ectatic, the lid is being pushed away from the globe as Munson sign.
In Rizzuti’s sign, which is where you shine a light in the periphery of the cornea where this pointer is, and you see an angle of light at the other side. And that’s a sort of a optical phenomenon from the keratoconus and the ectasia. But they’re more common signs that you need to look for, of course, keratoconus causes central thinning, so you look for that. And because there’s stresses on Bowman’s layer and lacquer cracks, you can find this apical scarring because those are the cracks have to heal. And you can see that in this in this image over here the apical scarring, sometimes the scarring can be caused by contact lenses that are on the eye too. And then when there’s you get stress factors in the posterior cornea and you see what’s called vogt’s striae, they’re vertical lines if you indent the cornea with a Q tip or your finger on right back with by the lid. You can you can make those striae disappeare.
So there’s a stress lines on the descemet’s membrane, so you can understand when the when the keratoconus gets extreme, those restaurants can result in a tear in decimates membrane, you get what’s called hydrops. A fleischer ring is an iron line. And it’s an iron line because it’s deposition of tears at the base of the keratoconus and I’ll show you all the signs in a moment. So here we go. So this is the fleischer ring I don’t know if you can see it on your screens there. But there’s a fleischer ring at the top here that, this keratoconus is so extreme the there’s no fleischer ring, it’s actually out in the periphery. If it was if it’s present at all, and we’re using cobalt blue, why do we use cobalt blue because iron which is brown absorbs the light. Probably better with with using a green filter because green light will be absorbed by by the airline. That’s another fleischer ring right there with arrows.
So this is vogt’s striae, I don’t know if you can see them. They’re very, very fine lines, right in the center there. And as I say if you push on the corneal Limbus, you can make those go away. This is the extreme,when the cornea stretch so far, you wind up gettinga tear in descemet’s membrane, and then you get swelling in the cornea. Now, we know from doing surgery, we can tear descemet’s membrane and they don’t get any swelling. So what’s the difference? Why is it that keratoconus patients who have a tear and decimate membrane get swelling? Well, the reason for that is actually getting decimate’s membrane detachment as you can see here on this OCT. So descemet’s membrane separated away from from the cornea tears and it separates. Because it separates it gets corneal swelling. Now the traditional way of taking care of this has been give the patient Cyclopedic, steroids and wait and wait and wait until it goes away. And winds up often with the scar in the center or in the area. Hopefully it doesn’t involve the visual axis. And sometimes if cornea gets flatter and patients see better. But that’s they’re in pain for quite a long time and they can’t see.
If they’ve got a decimates detachment. Well, it’s very simple. We do DMEKs and DSAEKs, you could inject air into the anterior chamber under pressure and push decimate membrane back up again. You have to be careful the pressure doesn’t go up too high. That actually does work and reduces the healing time by about by about four or five months.
This is pellucid marginal degeneration, you can see the thinning of the cornea in the periphery. So the central cornea is fine, but the Peripheral Cornea is very, very thin. As pellucid, meaning clear marginal towards the periphery degeneration.
This is keratoglobus. This is a patient of mine from Israel, who could have this condition, was diagnosed as keratoconus when he was a small child at the age of four or five. I have been seeing over the years and you can see his cornea there, is paper thin from Limbus to Limbus. And not only is it thin, he’s got megalo cornea, has corneal diameter was 17 and a half millimeters, in normal eye is about 11 to 12 Five. So this is 17 millimeter cornea. And in this case, I did a lamellar graft which was quite challenging. And I still see him now 15 years later, and he’s doing very, very well. So, those are the clinical signs and that’s what you need to be looking for.
But how can you diagnose keratoconus perhaps earlier? Well, they get their steep cornea and their steepennig is inferior. So if you have corneal topography or even a fleischer ring, you can see this is these are the rings here. This is the astigmatism is oval shaped, and the rings are closer together in the inferior portion of the cornea, compared to the superior portion. This tells us is that rate of change in inferior is much higher. They’ve got inferior steepening. Now with topography you can see this quite clearly. This is the sagittal keratometry map of the cornea that shows inferior steepening. What we’re looking for in in corneal tomography where you’re looking at the anterior elevation, posterior elevation, Corneal Pachymetry here, this is anterior elevation, yep, posterior elevation, all these three coincide. And that also is a good hallmark of keratoconus.
And then the grades of keratoconus, you know, there’s a mild keratoconus. This is clearly subclinical, it’s got inferior steepening the top, the bowtie is not symmetric. So this could be the start of keratoconus, it goes on to mild keratoconus, which looks a bit like this. So, that area of steepening should be in the center is inferior, and that get increases with time and then it becomes severe. So, these are different grading systems. There’s the ABCD, Belen which is, which I think is a good one and one that you can consider. I’m not really one for for grading systems. They’re very useful for research. And I like the terms subclinical, mild, moderate, severe. Anyway, that’s me.
So what sort of three dimensional topography systems do we have? The orbscan was was one of the earliest read any back from 1995, 1996. It’s now going by the wayside. It’s scanning slit beams across the cornea. Scheimpflug cameras are extremely useful. There are many of them out there right now. There are some that have become the gold standard. Then now we’re moving to ICT based corneal tomography with devices like the cassia 2, the MS 39, Antereon from Heidelberg, our great supporters of Orbis and also Optopol, and there are more coming.
So this the ORB scan video, and this doesn’t work, but scans slit beams right across, takes the images and takes the video images and maps out where the sets are, and figures out mathematically, what the anterior and posterior elevation is, as and is a procedure to measure the power map.
This is Scheimpflug imaging on the Pentacam. And you can see the cornea here, it goes in a circle around the the cornea. So it actually gives you a lot more central information. And it’s two integrated cameras, 55 Scheimpflug images in one second, in one scan, which takes less than two seconds. And this is sort of topography that we’re looking at the quad map that ORB scan came up with. The great thing about this as a device is, you can take a look. And you can see how change takes place. So this is a patient who had keratoconus. This is pre collagen cross linking, which I’ll talk about in a moment. And this is post op. And you can see the difference it looks quite similar. If you look at it qualitatively. If you look if you look at the numbers, then you can see there’s a difference but, the systems can do this for us by subtracting one against from the other and you can see that this is this cornea has flattened centrally with that blue area.
There’s ultrasound, digital topography, which can is also useful in in looking at this but it also looks at at epithelial thickness mapping, which we know is important nowadays for diagnosing keratoconus early where the point that epithelium is really good at remodeling the cornea and it gets thicker in the periphery and thin at the apex. So axial thickness map is extremely useful. We use it all the time now for screening patients with refractive surgery because we don’t want to do anybody who’s got early keratoconus or any keratoconus, for that matter.
Corneal biomechanics. This is it. Ultimately you want to know how elastic the cornea is and what better way to do it than to actually prod on it, push on it. And we do that with air. And how the cornea recovers tells us quite a bit. And so what we’re looking at is hysteresis. This is the applanation pressure, this is the, the amount of deformation and and how the cornea recovers. And the difference is hysteresis. If the hysteresis is, is too low. It’s very elastic. This is all been visually imaged on the corvus from Oculus and you’ll see the the image above is keratoconus versus a normal. If you look at that, keratoconus, you’ll see it wobbles and deforms a lot more. So it oscillates. And that’s an elastic cornea. This is courtesy of Renato, Ambrosia from Brazil, did a lot of work on this in this area. So again, going back to the diagnosis of keratoconus, so, you’ve got all these gadgets. But clinical is really really important, if you have oblique or against the rule of astigmatism, which has been increasing scissoring on retinoscopy. Those are very, very useful pointers for keratoconus and if you want to actually measure it with 3d tomography probably is the gold standard. And hysteresis is useful. We all had to have a biomechanical measures of corneas to make the diagnosis of keratoconus.
So what are the treatment options for keratoconus? Well, traditionally, it has been spectacles, followed by contact lenses, they start up with soft lenses. Then they go totoric. And then they find they can’t see with those and they go to gas permeable lenses, then eventually they graduate to Sclera Lenses for those that can fit them. Now those are not available, it’s a specialty fit. And then when they can’t tolerate lenses anymore, they want have a corneal transplant. That’s what used to happen. He used to be a full thickness graft, a penetrating keratoplasty. We gradually moved to ilamellar keratoplasties, but a lot has happened in the intervening years. And what has happened? Well, things have changed now.
One of the the biggest changes to the management keratoconus has been the advent of collagen cross linking. We’ve been doing that this since 2004. And it really has changed the course for a lot of patients with keratoconus. The important thing is to diagnose people early and stop them progressing and Collagen Crosslinking can do that. It can sometimes be combined with with PRK. I don’t often do that. But it can it can regularize the cornea as well. There are people who will do this and they’ll try and play in extreme cases, it doesn’t work in extreme cases, mild cases, fine.
Intercolonial rings ever come along the intacts, Ferrara rings, Keraringss, the Myoing and now Kara natural which I’ll be talking about or Cares, ccorneal allografts, the rings made from corneal tissue, intrastromal corneal rings. There’s a toric phakic lenses can be used in patients who have good spectacle correction and don’t want to wear spectacles. And then there’s finally this corneal transplantation.
So let’s talk about keratoconus a little bit, about crosslinking. Crosslinking uses riboflavin a large molecule it unfortunately doesn’t penetrate the epithelial tight junctions. So you’re gonna have a way of breaking down the epithelium. And there are some measures to remove those tight junctions using say tetracaine and certain riboflavin solutions. Lot of work has been has been done on epithelial removal, which is the Dresden method. And they’re not necessarily the protocol, which is 30 minutes or three milliwatts of ultraviolet light, but you need to get that epithelium off or you need to disrupt it. We have been using a disruptive method and that’s worked quite well but it takes quite a long time for riboflavin to penetrate. When the riboflavin penetrates the cornea and we check to make sure it’s in the cornea look all looks yellow, then we can go ahead and collagen crosslink.
So how does it work? It’s really as we get older. Ever wonder why people get wrinkles as they get older. But actually that’s Collagen Crosslinking taking place, it’s an aging process whether the collagen becomes a lot more rigid and it got more rigid, because it’s crosslinking within the actual lamellar fibers. It can occur in people with chronic hyperglycemia from diabetes mellitus disease, their tisue gets crosslinked.
And it’s been used in the past to strengthen collagen as valves, say for for cardiac surgery where they do valve replacements and now we have it for the cornea where we crosslink the cornea to make it stronger. So essentially it’s riboflavin penetration of the cornea, ultraviolet exposure is formation free radicals and this is an oxidation reaction, which develops cross things within the collagen. Now this what all the images look like. So you’ve got more more crosslinking, that takes place as a result of the light exposure with the riboflovin. Actually is probably within the collagen molecule itself, as opposed to adjacent molecules, they are too far adjacent bits of collagen because they’re too far away from each other. But suffice it to say, you get a lot more collogen rigidity. And this is a cornea, thiick cornea has been treated with crosslinking. And this is one that is not as a control.
This is the epithelial disruptive method is a little device that we use to break up the epithelium and to make a lot of pot marks in it. We use this in children because they can’t really tolerate having the epithelium marked, it is really painful. Their pain receptors are far more sensitive than adults. And it’s kind of a mean thing to be doing. I think collagen crosslink is probably the most uncomfortable thing we do in our as a procedure. So that’s what it looks like looks like a medieval garat or multiple garats. And we use that in the corneass to break up the epithelium and then we use riboflavin. Once the riboflavin penetrates, it usually takes about 45 minutes, we check penetration in slit lamp, because we give them pilocarpine to shrink the pupil to make the make the pupil smaller, to make sure there’s less light going through. If it does go through, usually it’s absorbed by all the riboflavin. And then we go ahead and use ultraviolet light on the cornea. And we typically, we used to use three milli watts for 30 minutes. Now it’s nine milliwatts for 10 minutes, and there are rapid cross linking methods have been developed. There’s a great device that’s been developed by Farhad and Nikki Hafezi, called EMAGine, where you can do crossing again at the slit lamp, we have the device and it’ll have a transepithelial protocol, is a bit more sophisticated than the traditional cross linking devices. I don’t think it’s it’s a huge, huge rocket science. It’s not that that precise, but there are ways to enhance cross linking. And they’ve done a really good job with that particular device and I have no financial interest in any of these things.
We looked at our results in these patients, pain is a big problem. 61% of our patients got a demarcation line, which I’ll show in a moment. And we always worry about ultraviolet light going through to the retina. And this illustrates that the amount of light that gets transmitted in a thick cornea, which is impregnated with riboflavin is very, very low. And this is a demarcation line, I don’t know if you can see this video on your screens. But you see there’s a line that’s quite deep in this particular case, probably about three to 400 microns. And that’s that’s reassuring when we see that in the first month. And that tells us that something happened in that cornea, in terms of, of crosslinking. And, and you can see that here with this OCT, is a demarcation line there. And that’s probably because there’s something’s happening that collagen and it’s not transmitting light as clearly, eventually will. And maybe it’s a disruption of the relationship between dichos immunoglobulins extracellular matrix and collagen fibers. And when you get a disruption, you get a reduction in clarity, in other words, a bit of translucency in opacification. So that’s causing crosslinking very good and it’s actually changed the course of keratoconus to the point where keratoconus is no longer the number one reason for doing a transplant.
Now, the number one reason in the UK for transplant is Fuchs endothelial dystrophy. So these are intracorneal rings in text and the video here that you’re seeing, and how do they work how to how do these plastic rings work. But what they do is they shorten the arc length, so you in doing so they flatten the central cornea, by putting rings in raising up the periphery, it’s elastic dome, you end up flattening the center. And the closer you are to the center, the more flattened you’re going to get. So the Kerarings and Ferara rings at five millimeters will have far more effect because they’re much more central. There are two ways to put rings in. One is conventional with a with a device where you can make a tunnel with a device, you use a diamond blade to go down to say 400 microns, and then you use this ring on a what looks a bit like a trephine. You insert that and you and you dial that hopefully won’t go through. But you get down it and you and you create a channel. Much more elegant way is to use a femtosecond laser. It’s quick and it’s a lot more precise. And you can also change channel diameters to suit. There are different rings will do different effects and have different nomograms for different types of cones.
This is a ferara ring which is very clever. It’s shaped like a prism. So light comes in and it gets and it comes right out again. That’s the goal. This was to reduce the edge effect of the rays. It reduces it quite considerably, but doesn’t get rid of it completely. Patients are very good at tolerating this thing. So they might get like halos or edge effects to begin with over time, the brain shuts it down from your adaptation, you can see the actual shadowing, where light is not been transmitted in this particular cornea here, this is the Ferara in place. So that light comes in and goes straight out again.
What are the indications? Well, if their spectacle or contact lens intolerance of the keratometry is up to 62, diopters, 62 and above is going to be a bit extreme and is less likely to to work, they must have a clear visual axis, they can’t have a scar. If there’s a scar and you put a ring in, the vector forces would change the dynamics there. And you could wind up having a really irregular cornea afterwards. And the pachymetry ideally should be 400 microns in the center.
So this is a video of INTACtS going in with a femtosecond laser. So there’s a laser docking onto the eye and creating the tunnel. This is in real time on a slow laser and 30 kilohertz laser and that’s incision there. And once that’s accomplished, where we can make sure that before the bubbles go away we’re marking up with a channel should be, so we begin channel and move the rings in those directions. This is a little hook that goes in to to identify the posterior level and is that sort of like a pocketing hook. And once we’ve identified that, then we go ahead and we insert the INTACTS ring. And this is quite a tight channel, I like take channels and it can be kind of tough to get those rings in. So we’re putting the spear ring in first. And one of the things that does happen is when you put one ring in, the cornea deforms a little bit and putting in second ring can be a little bit challenging at times. Now here we are putting the second ring in. Keep the area moist with antibiotic.
These are solid PMMA rings, and they have a habit of causing trouble at times they can extrude sometimes they can intrude, they can go into into the anterior chamber, I’ve seen that we used to put a suture in I didn’t do that anymore because it becomes a focus for infection. Here we put a contact lens on and we take that contact lens out within a couple of days. They use a lot of antibiotics afterwards. And this is these are OC T’s and these are images of INTACS in the eye instead of hexagonal cross section. So what are the complications that can occur from INTACS and and fairings they get infections are usually often at the site or where they might extrude. They can extrude as I as I mentioned, they can perforate into the eye. Certainly during the procedure, you can get channeled deposits, and sometimes they don’t work. So these are this is a ring in place with a bit of an infiltrate here. This is a proper infiltrate at the side of the incision.
These rings have kept the incision open. And they could have done with being pushed in a little bit more. And this is the extrusion patient complaint a foreign body sensation seen by the optician who didn’t know what was going on. And they came to see us and sure enough, there’s right there. The index was extruding the cornea melted above and that index had to be removed. These are channel deposits. These occur more often with mechanical creation of channels, I suppose to femtosecond laser channels, these rings are certainly dissented. And you can see that these deposits are present, they do no harm, except if they were to increase to the point where they start going into the visual axis, you might want to consider removing them before that happens.
Overall, the rings are extremely good. They improve contact lens tolerance and they improve best practice with corrected visual acuity. There’s a reduction in its vertical mean case and astigmatism. And we have found from comparing mechanical insulation versus femtosecond. That foam second is better. This is the new new thing. And this Sunday we’ll be doing a lot of I did a case today, a patient with 10 drops of astigmatism with with central keratoconus and right after surgery. She’s we checked it she’s only got three diopters left. And already a vision map from from six over 120 to 618. Straight after surgery. Very, very effective.
And what’s the difference? It is actually corneal tissue that we use. And we were very grateful to it in college and to Susanne Jacobs, who came up with this concept to use cornea the cornea is kind of a selfish issue. It only likes itself. You will plastic in there, it gets up to mischief. You put cornea in there, it integrates and this is the Karen natural product is a pre cut product from it’s from a vision gift. So you don’t have to do anything you can keep it on the shelf. Whenever you have a patient you can use it but is corneal tissue and it’s a cellular. It has been tested In terms of safety test checks, so it’s like a corneal graft, except it has no cells in it. And it is like a corneal graft, safe to use.
There are different nomograms used by different groups. This is just to show you a patient who has sort of keranatural, it’s space filling and reinforcing. So this is a patient with keratoconus, you can see the refraction here is minus 4.75 minus six, giving an acuity of 6/12, which is not bad. And it can take, you can see that the area of of deformation is here, this, this area here is quite extreme and the choma, and this patient will be on the other side. So what we want to do is fill in the space and move that cone into the center. And this is the treatment to Keranatural graft, which we’ve created a tunnel the same way you saw with intact space and much bigger tunnel. And this is kind of a ragged bit of tissue.
The quality of tissue has improved dramatically in the last while, but the one I did today was superb, but doesn’t really matter. It’s tissue that needs to go into the, into the right space. I’m just trying to identify which side is up, which is the anterior side. If you’re lifting up the coin and inserting it, and it’s soft tissue, it’s not like an intact, which is hard, but you can drive it forward. This takes a bit of doing and ideally you’d have two incisions. So we now use a femtosecond laser can create two incisions, you can actually create two incisions manually if you only have a laser like interlace, it creates one incision. And you’re using a hook. You see it looks a bit clumsy. And this is a it’s been edited, I will admit. But just to illustrate this, you’re all the videos you see, sometimes it really, really smooth, but life is not like that. So yeah, I want to get that, that ring all the way around to here.
So it’s a bit of pushing and shoving. As I wish I had another incision to get in place. So here we are, it’s in place and pushing it across. It’s kind of Constantina there, which is a bit of a problem. So what I need to do is overdo it and put it back again. In this case, it looks like I left it that way, as they didn’t make any difference. The volume filling was accomplished. And this is the what it looked like, on this patient afterwards. You can see the choma that this was like afterwards. This is pre op, post op. So quite a huge change in in corneal topography.
This is a another patient that’s got a ring in place, this is preop here in the middle. Postop on the left hand side. And this is difference map showing the amount of flattening of the cone, which I’m sure you’ll agree is very impressive. This is a pitch for the milderr cone. And again, we put the ring in here. And you can see that the there’s flattening in the center. And this is what it looks like on high resolution OCT. You can see the keronatural here. The cornea has been indented as well, posteriorly but the anterior surface is what we really most concerned about. And that actually looks pretty good in terms of corneal shape. So that’s rings, plastic rings, the INTACS kerarings, Ferarings, and now cornea. And as far as I’m concerned cornea probably is the way to go for the majority of these sorts of cases.
What about cornea transplants? So we’ve gone through the gamut of treatments. What about transplants for keratoconus? keratoconus, I gotta say that when when patients have graft for keratoconus, you know, in most cases the endothelial is normal. So, there’s absolutely no reason to change the whole cornea. It’s not as though it’s less safe surgery. And you put these patients at risk of rejection. So why don’t, why doesn’t everybody do anterior lamellar keratoplasties. Well the it is a little bit more difficult to perform this kind of surgery. So there’s technical skill required you could perforate, it’s good to do some of the courses into practice. But really it’s a you’ll do your patients have phenomenal level of service if you do lamella r grafts. So let me see if I can convince you.
This is penetrating keratoplasty. What are the hazards of doing a penetrating keratoplasty. Severe explosive hemorrhage This is a patient who didn’t have a graft for keratoconus they had a graft for other things is the only eye, was 16 years old, is my patient and they had an exulsive choroidal hemorrhage. So that was only eye, that can happen. What is the incidence of choroidal hemorrhage in PK, which you believe is between point five and 1%. So between one and two how 100 cases and one in 100 cases. So just be aware penetrating keratoplasty is not without its troubles, you can get rejection and failure. So the mean survival for a corneal graft is between 17 and 20 years for somebody gets a graft in the, say even 30 years old. By 50, they’re going to have to have another one.
But who wants to do that? And the if that’s the regraft, the chance of surviving regraft goes down, and they can also get Glaucoma, 19 to 30% of patients will get glaucoma, hope I’m convincing you. Penetrating characterized, if you can avoid it is better. Do lamellar graft if you can and they always get cataract and endophthalmitis, because you go Open Sky situation. It’s prone to risk. And this is a study that we did when I was in director of the Queen Victoria Hospital and we took a look at our outcomes a three year grafts versus the UK national outcomes. Our material was actually part of that UK transplant data. So it’s a bit skewed in their favor. But you’ve noticed in keratoconus, the survival rate in the UK was was nearly 93% in three years. What about the 7% that failed. In our case, only one patient had a rejection, that was a Down Syndrome patient in a nursing home, there was a neglected, had an intumescent cataract. And that’s why it failed, not from rejection.
And the regraft rate, the regaft survival. So if you have to take a graft that’s rejected and you have to re graft them, the National survival at three years is only 57%. Our survival 67%, better and statistically significant, using cyclosporine and close vigilance and so on. But this doesn’t have to happen. If you do lamellar graft, this patients tissue is their own. It’ll never reject. They may reject their anterior cornea, it’s easy to treat. So how can you do a deep anterior lamellar keratoplasty, that’s a topic for another day. But just there was there are several techniques you can use. The big bubble technique of Anwar is a great one to master but it cannot be done in your hydrops or corneal scars that go down to decimate membrane. Visco dissection advocated by shigge Shimamura from Japan is another way of accomplishing the same thing.
There’s a pre decimates method, which I use a lot because I get really extreme keratoconus and it’s a recognition of Melles, a good paper I mentioned it in the moment. And then that you can also use a femtosecond laser for those of us that habit. So this is an anterior lamellar keratoplasty using Melles method, modified Melles’s method, here I am injecting air into the anterior chamber through long paracentesis, the trephine is used to go to about 75% depth. And I’m pretty satisfied with that. And then I use a lamellar dissector to push away some of the stroma till I can see descemet’s membrane, but I’m also using that spatula to look for a black line, that black line is double the thickness of stroma between the instrument and descemet’s membrane.
And we also find that when we go deep in the stroma, remember I said at the beginning of this lecture, posterior stroma is not less compact, well, you if you find it difficult to dissect. That’s what you’re for sure you’re too anterior, the cornea. If it is easy to dissect, as you can see me dissecting here, you are probably in the right place, quite deep in that cornea. So I’m just removing all that I’m dissecting that cornea.
This is a video from back 20 years ago. So you see we do this for a long time, remove that anterior stroma. So we got a little bit of lamellar tissue left behind, but that’s okay. It’s an another tissue with descemet’s membrane and endothelium, the patient’s endothelium. Remove that and actually that’s quite a good dissection very little stroma there. And I’ve removed, now removing the corneal tissue and then we go ahead and suture in a graft where we taken descemet’s membrane off and here I’m using combined technique 12 and 12, Twelve interrupted sutures and 12 running and not boring you with the suturing this has been edited out and you’ll see it at the end here, the sutures are in and the good thing with this is we can adjust for the astigmatism with a chamber formed and using a procedure type ring or even as the back of a safety pin. You can take a look to see what the mires are like to make sure that the astigmatism is correct. So this is a much better technique, lamellar graft in for patients who have keratoconus. Here we’re just checking the mires to make sure they’re secured.
With a femtosecond laser, there’s something that we developed with a laser, where we have a configuration where it’s like a tongue and groove This is how tires of cars are treaded. They treaded so that the the treads go inwards, so when you put pressure on them, they go in. If you were to go the other way they would pop out and they would you dethread tyres. So the same principles are used in doing these kinds of grafts. So this is using a femtosecond laser to create the donor. So here we’re going through our pre op checks making sure the donor is correct and so on.
We use an artificial anterior chamber using air to inflate the cornea to the right sort of pressure. We are now putting on the artificial chamber. This is a disposable device, you can use a non disposable device but because this is donor tissue, we worry about transmission through instrumentation, we will use disposable instruments where we can. So I’m locking in that graft, it has to be good enough rim, taking off the epithelium here after air has been injected. So that cornea is pretty cloudy now. And then we go ahead and we use the laser. This is interlace to create the donor and the donor in a geometric fashion using sort of the sag square technique. So here we go and make sure that everything’s fine, you’ll see my view in a moment.
This is what it looks like on the anterior chamber, and off we go, with a cut. So what we’re doing is we’re cutting the cylinder going up from inside the eye up, and then across from the outside in, and then from the outside up to the anterior surface of the cornea. So this is all real time. So it takes a bit of more time than maybe cutting a LASIK flap or making tunnels for rings. But then we’re getting a lot more cutting going on. And then we go ahead and cut the superior bit. We need to make your team care because now that Cornea is penetrated, the graft can fly off if we’re not careful. And this is what we do on the recipient. So this is gonna be the big bubble technique because no scarring, is suitable for it we put a ring on.
And again, same this is speeded up now. So the same thing that we did on the on the donor, we do on the host except we didn’t go all the way through we go down to about 400 to 450 microns in the periphery. So you can see that’s a geometric cut. I’m going to make a long paracentesis in a moment and pushing your decemets’ membrane here. This is speeded up video I don’t operate this quickly. And this is a Fogla trockar, from Rajesh Fogla from India. A very useful instrument is the Fogla cannula to create that big bubble, see the bubble there. And you see that the air inside the anterior chamber has become softer, tissue is going off to one side.
So now we are removing this in two layers. I’m taking the top fixed trim off. The bubble is still in there, you can see the sausage shape in the periphery and we do what’s called the brave slash to cut the remaining stroma and inject viscoelastic. And you’ll see that bubble move across. And now I’m going to remove that tissue, you’ll see that there’s a nice shiny decimate’s membrane there that’s left behind, the bubble still in the eye. And this probably will provide patients with the best clarity when it comes to a deep anterior lamellar keratoplasty. So the big bubble technique of Anwar is a superb technique for the sort of precision. Here I am removing descemets’ membrane, which sometimes is tedious but the graft on marks. And off we go, we switch to the graft in place. And that’s it with a 24 bite running in this particular situation.
And this is what this is about. There’s another patient but this is what it looks like. It’s six weeks. And you can see the configuration of the graft is this you can see the true tongue here. The imagination and the Zag square on OCT, they heal very quickly in usually about nine months in a young person, we can take the sutures out. So that’s grafting for keratoconus. And so I’ve gone through the gamut of the different procedures that we can use on different patients or different patients depending on the how bad the keratoconus is.
There was a Delphi panel on which I was a participant to look at global consensus on keratoconus and ectatic diseases and how to manage it. And there were three different groups, there was how do you diagnose keratoconus? And by the way, that’s a very good paper to get from from cornea, the journal cornea. There’s one group that dealt with diagnosis of keratoconus, another group dealt with non surgical management. And then the third group dealt with surgical management. And that’s the group that I was part of, thats quite a few years ago, probably about eight, nine years ago. And it came, it resulted in publication and this is the algorithm that they came up with. So just to illustrate it for you. So if you have keratoconus, you advise patients that you’ve you know, from the diagnosis criteria that they’ve put together, you advise patients to stop rubbing their eyes, and you tweak their allergies with whatever drops that are required. And I would say that, you know, any patient with keratoconus, you’d really just treat them with anti allergy drops, any whiff of it any inflammation treat it. Consider crosslinking if they are young and the consensus is if they’re 21 or younger. Don’t wait for the keratoconus to get worse, it’s going to get worse, crosslink them anyway. If you if it says crosslinking, you are suitable or not suitable if their corneas are very, very thin, so something to consider.
And then if their vision is, is good with glasses, they can stay with glasses, or they can consider contact lenses if they wish not to glasses, then they need a trial of hard contact lenses, or scleral lenses. If it’s satisfactory, you can leave them with those. If it’s unsatisfactory or they cant wear contact lenses, then they move to surgery. And you can continue to consider intracorneal rings, nowadays will be Kera natural, and then again, they go back into glasses or contact lenses. If rings are not satisfactory, or they’re not suitable, then unfortunately, we have to move towards corneal transplantation. And a deep anterior lamellar keratoplasty is the preferred option, even if they’ve had previous hydrops.
So I’m going to summarize that one more time. My way. This is what I teach everybody. keratoconus I want to know is it stable? if it is, just keep them on glasses and contact lenses. And that’s fine. If they have good vision, you might want to consider toric aphakic lenses like ICL in these patients, and that’s between you and them, it’s a very good option in those cases. They can’t, If they’re not a good vision, contact lenses, hard lenses, or Scleral Lenses. You can now consider intracornial rings to put them back into spectacles, or even contact lenses. If they’re progressive or less than 21 years of age, they can have collagen cross linking if they suitable and we do that on every patient walks into the door and often do bilateral cross linking, because what happens is they get one eye done and it’s so painful, they don’t come back for the other eye. So I urge them to have both eyes done at the same time. And we watch them closely to make sure that they heal properly and so on. So the if they are not sitting for crosslinking and few are not, they will have contact lenses. And in time they might have to have a lamellar keratoplasty.
And now I’m happy to answer questions. There’s quite a few in the q&a. So let’s start with the first one. What is your frank opinion of the no rub no cone hypothesis of keratoconus etiology? I’ve already said that EYE rubbing is a big problem that should answer your question. they will get if they rub their eyes the keratoconus can start and increase. I do believe that that cuticles can occur in elastic corneas without rubbing, but not as often, they usually are rubbing their eyes. Either way, keratoconus is keratoconus and you need to tell patients that they’ve got to stop rubbing their eyes.
What is the final treatment options for advanced keratoconus? I hope I answered that in my presentation.
What do you think about Athens protocol? Athens protocol, this is doing a PRK. As I mentioned, I have done PRK in some of these patients and very very mild cases. What I actually do is I use PRK, I know what the epithelial thicknesses is in the centre, I will do enough, PTK on the surface to eliminate a bit of a cone, and then use riboflavin. And you know that there’s a lot of data out there. All the patients who come to see me after the so called Athens protocol are ones that are got problems and require corneal transplants. And some of the cases I’ve seen have not been very good. Maybe they’ve been treated when they shouldn’t have been treated. So it’s up to yourself. I like to look after patients and I’ll be careful with them. So I don’t do any topographic linked PRK and crosslinking, I know some people do, it’s been advocated even by the giants like Farhad Hafezi. Again, I do I take a lot of keratoconus, I have done for 35 years. I don’t do that because I think thinning out the cornea anymore than we have to, is not such a great idea.
What is the earliest finding of keratoconus in clinical exam, I think I went through that already.
Are all facrefarctive procedures off limits for keratoconus? Well, Corneal refractive surgery is off limits. So I would I would avoid this at all costs. We’ve already talked about topographic linked topography to to change corneal shape at the same time, it’s crosslinking of crosslinking and then do PRK. You know, for me, crosslinking is the most important thing in these patients, get them stable. Sometimes my immediate question to these patients, in fact, a lot of times the vision improves. The topography doesn’t change that much, but their vision improves. They might not need any topographic linked PRK and so on, so give them a chance to crosslink first. So yes, all corneal procedures are probably often amiss. However, if a patient sees well, the spectacles, you could consider toric ICLs. They are a great option in these patients.
The reliability of an OCT scan to detect keratoconus? I’m not sure what that means. Maybe you’ve got topography, and you’ve got to thickness mapping from your ICT that should really help you to detect the keratoconus. So I hope that sort of answers it. We’re moving towards OCT mapping, and it depends what device you use, and they’re all going to be all converging and doing the same sort of thing.
How do you define keratoconuskeratoconus suspect and subclinical keratoconus, but basically the same, we’re talking about the same thing really. If you see inferior steepening in the absence of contact lens and contact lens warpage. You need to worry about those patients. I think you’ll look at other parameters that we’ve already discussed. In terms of, epithelial thickness mapping, you can look at the progression of corneal thickness across the cornea. That’s a whole other talk. And that’s more related to selection of patients for laser eye surgery, as opposed to keratoconus, but you do but they do go together, you want to make sure you don’t do anybody who might develop keratoconus in the future. So keratoconus suspect, or subclinical keratoconus have formed fruste keratoconus. Here’s another one to add to the mix. Something to consider. For me, it’s all much the same thing.
If you have additional risk factors, early signs, without having an advanced disease, do you recommend observation? Or can we look up to preventive treatment? It depends on age and if you have somebody who’s got progressive change, then they need crosslinking? Does that make sense? We are going to get patients who come to you because they got a problem, they can’t see. And if refraction is changing, the astigmatism is changing and you pick up the retinoscopy, they got scissoring you believe they’ve got keratoconus, then crosslink them, you’re doing them a favor. Observation is, to me is a nonsense, especially in the young people. If they’re in their 30s 40s. We don’t know if they’re progressing or not, then you could you could consider observing them, get some history, what was their refraction two years ago, five years ago, or before that and see what’s changed in the meantime, then consider. Remember, this is you being a doctor, approaching your patient, clinically, you’ve got to treat that patient individually and customize treatment for that patient.
What is the most sensitive for the diagnosis of keratoconus? Well, I don’t think this is competition. Okay. You can use procedural imaging, you can use three dimensional tomography, which is very sensitive physics of the posterior cornea, you can look at the center screen here, you can look at that I think posterior posterior elevation mapping is very useful. And at full thickness mapping is also very useful. So you can if you’re if you ask Dan Weinstein the question, he will tell you it’s ultrasound by using the arc scan. If anybody wants to bother with it, you could diagnose code comes with a three dimensional tomography. And the gold standard is probably a Scheimpflug at the moment, but OCTis taking over. But you know, even a procedure can help you and and and guide you. So I wouldn’t wait away, I wouldn’t make this a big deal. I hope I’ve answered that question.
How much time can you wait to do the procedure the patients with hydrops? Well usually when patient has hydrops and only procedure would probably consider doing that is going to be a lamellar graft. I usually wait six months before I do a lamellar graft in these patients and I don’t do a big bubble technique, I do Melles, modified Melles technique to get as deep as possible. And I keep the area where the hydrops occurred, to the last before I take the cornea off.
In case of observation, how often do you recommend observation appointments with studies? Take your pick, I told you I you know, I like to look at history, I might probably do it in six months, if I just had no information and the patient will say 45 years old, and I just didn’t believe that they were progressing. I would wait six months and then do a difference map using pentacam or on one of the OCT type methods we have a mall over here, three different OCTs and and also some mapping devices and we will use them and measure.
What is the earliest age of keratoconus onset and children. It can be very young. We treated patients as young as five years old, six years old. I now send them to somebody else because there are all sorts of issues with treating children. But we’ve crosslink these kids and I saw somebody I did when he was seven is now almost 20, Is at university and he’s driving a car. And his corneas are not progressed, which is really, really good to see. He still has keratoconus, but it stayed the same. And that’s very gratifying to see that because he was heading to a corneal transplant.
Can topography guided PRK followed by collagen cross linking and the same setting be done for comfort. I think I’ve already answered that question. So I’m not gonna go over that again.
How often do you see superior keratoconus? I don’t think I’ve ever seen superior keratoconus. And maybe something else that’s going on as opposed to superior keratoconus.
The impact of intrastromal rings and crossing patients with keratoconus, What’s the question? The rates of corneal transplant reduces. Yes, it does. We what we tryingto do is, is get patients rehabilitated, so they can wear contact lenses or glasses. And if the rings fail, then we go ahead and they graduate to corneal transplants. So I already said that using these these other methods Collagen Crosslinking intracorneal rings, our rate of transplantation has decreased dramatically, certainly in the UK.
What about genetic testing for keratoconus? Yeah, I think this useful? I’m not sure how much is going to guide me though, because some of those genetic markers, maybe genetic markers for allergy too. We still, there’s a lot of work that needs to be done in this area. Because it is not just genetics. As I mentioned in my opening slides, it’s multifactorial. So it can help you. But then, you know, the question is what if it tells you it’s, there’s moderate risk, or there’s evidence of risk. Is that going to influence anything? It my influence you, whether you’re going to do laser eye surgery, but this is this is a topic of keratoconus, not laser eye surgery. We were talking about diagnosing keratoconus and treating keratoconus, that actual condition.
Is this important to treat this disease? earlier? Yes. Yes, yes, please treat it as early as possible. So, if you find, we make a diagnosis of keratoconus, please crosslink that patient you’ll get lots of blessings. That patient you’ll probably avoid putting that patients through a corneal transplant. And for those of you in developing countries, you don’t have access to corneal tissue as easily, or rings or femtosecond lasers, but cross linking is well within reach. And I would do it, I would I would do it without hesitation.
What is your experience or opinion ortho K lenses? In regards to energy and time? No experience? Maybe you can tell us, I have no idea. We don’t come across too many patients who have had ortho K in this country. And I don’t think orthoK has been used for keratoconus. So, I have no experience in that. And it’s not something that we would advocate without good data. One of the problems with with keratoconus is you had a thin epithelium, the other issue with OrthoK is, it makes the epithelium even thinner. So you might even put them at risk of infection.
What’s you preferred technique for crosslinking in regards to energy and time? We’re typically using, nine milli watts for nine minutes, in the majority of cases.
How to manage if the corneal thickness suddenly decreases after crosslinkig? you don’t manage. Yeah, we expect that it always does decrease and then increases with time. And there’s nothing to be too alarmed about. We measured all these things in the early days. And yes, we were bothered by it. But not anymore. It does thicken up in time.
What iss your opinion about transepithelial corneal crosslinking I don’t have any experience with it. We do need agents that can they can enable riboflavin to penetrate. I know this one ones coming up from the EmaGine group from Switzerland. And looking forward to seeing that. And we do know that we can break tight junctions from using drops. We can also break tight junctions from just lasering the touch the surface of the cornea keeping the epithelium intact even. So those are options you can consider and then there’s trans epithelial. The corneal disruption technique that we developed, you could try that, the contact lens comes out within 48 hours and the heal very, very quickly but we reserve that for children.
Do you recommend cross linking for keratoconus with best corrected visual acuity of 20/20 in an adolescent? Yes, I don’t see any reason why not, if they’ve got an established diagnosis keratoconus, I will cross link an adolescent. Because otherwise, wha are we going to wait for? you to wait for them to become 20/30, 20/40 and then do them, make them worse. Now you want to treat them as quickly as possible.
What is the ideal moment to start with rigid contact lenses? Well basically as I said earlier on, when they can’t wear glasses any more, then you gotta go to contact lenses. If they can’t tolerate contact lenses, then you can consider corneal rings.
When would you consider crosslinking? Right away. If they have keratoconus at an early age, they’re going to progress. Treat them.
Is there any age criteria for calling crosslinking? So for me in my books up to the age of 21, I think there’s general consensus, we will treat patients automatically. They walk through the door with keratoconus between them. Above that you could do the observation bit. But if you have a history of change, so it’s good to get the history from the optometrist, has the efraction been changing. If it changed in the last year, you can make the assumption that’s continued to get worse. Go ahead and cross think.
How is the directory that so that’s age criteria? How is the abbreviation? So abreaction? I’m not sure what this question is a brief abbreviation? I’m sorry. I don’t know what the question is. Maybe you could could type it again, this might be a spelling error.
Does the intracorneal ring effect keratoconus progression? No, it does not. We have that before we had crosslinking. We’re using rings. And those patients, some of them did progress to further thinning in the center of their cornea and they required corneal transplants. So I don’t believe it stops it. But crosslinking does, if you crosslink and then put rings in. You probably arrest keratoconus. So what is it that arrests the keratoconus, probably the crosslinking more than the rings.
I keep getting asked this question about diagnostics. And you know, I work for a lot of the industry, I don’t have any favorite devices. All these devices that measure in three dimensions are useful. It was scanning slits from Orbscan, not as accurate for the posterior cornea. Scheimpflug came along, very accurate for anterior and posterior cornea. And now we have OCT, which is even more accurate. However, they all do the job. So I’m not going to get into a discussion about which is better. This is not a competition.
Until what age, Is it recommended to do these types of surgical procedures for keratoconus. Well, as I’ve said, up to the age of 21, I’ve said this many times now, I will treat everybody. After that, I might watch them if I believe that they’ve stopped for whatever reason, and if they stopped rubbing their eyes.
Anatomical changes especially with keratoconus resulting in less accurate IOL power calculations, what considerations should be there. This is a whole topic on its own. There are no formulas for lens calculations for keratoconus, it is an art form, figuring out what lens calculations are. That’s not what this topic is about. If you don’t mind, I believe we can leave that for another time, on what I do and what others do in terms of measuring lens power in patients with keratoconus.
After some time removal ring, or not any? I don’t know if there’s a question. We do not remove the rings unless there’s an indication. So if somebody has to have cataract, we’ll keep the ring in and we measure the keratometry. I don’t see any reason if there’s a complication or if the rings are not doing their job or the extruded are going through a problem, then we take them out. Hope that answers that question.
How can I determine size of Keranaturals? I gave you a very simplistic overview of Keronatural, that requires a whole kind of mini course in itself. And there’s an art form and how we treat these patients. So I think we need to leave that for another time. And maybe that can be a whole discussion in itself.
How does Keronatural work exactly? As I said in my talk, it fills in space and changes the anterior shape of the cornea. So it fills in areas where the cornea is depressed. Outside the visual axis. We lift the cornea up and push the cone into the center and it flattens it.
Have you heard about intracameral riboflavin for keratoconus? intracameral No, I haven’t. And I don’t know if that’s such a great idea. I’ve heard about intra corneal, where someone when they make a flap I think was it was, Kenoloplus who came up with this idea. I didn’t think it was a great idea because you’re weakening the cornea by splitting the cornea but he did use a femtosecond laserto create a flap, inject riboflavin and it would absorb very quickly and then you go into crosslinking. Many ways to skin a cat but not intracameral, I have not heard of it. And I have never done it.
Is there any risk of keratoconus recurrence after PKP? Well, everybody talks about inferior steepening after a penetrating keratoplasty. Please, please don’t do a penetrating keratoplasty in these patients. If you come across a patient that’s had a penetrating keratoplasty and they’ve got inferior steepening, in all probability is that residual cone, that’s the residual cornea that steepening. If that’s the case, you might want to crosslink the periphery. And that’s what I do in all these patients. And sometimes if the astigmatism is really bad, then I do a sort of tucking wedge resection, topic for another day. This is this is really advanced cornea that we’re talking about.
Corneal layers, five or six, what does it matter? You can count as many as you like.
Even though DLK is much better in keratoconus, vision rehabilitation, there will be cases that you cannot do DLK. Yes, that’s fine. But indications of doing a PKP rather than the Okay. Well, if I’ve got a big scar that goes from front to back, involving descemet’s membrane right in the center, then I might do a penetrating keratoplasty. But how many penetrating keratoplasties have I done in patients with keratoconus and I get extreme cases. I can’t think of any actually, for the last before I left the health service, probably 18 years, 17 years. I did one patient, one eye. And what I did was actually didn’t, its not a keratoconus. And I switched his graft and asymmetrical so I push the scar and the lamella graft out of the way. And that worked quite well. So there are jazzy things we can do. But you know, if there’s this scar is in the center, then it makes sense to do a penetrating keratoplasty.
In your experience, what is the percentage that decreases in rejection grafts, cecause compared to PKP. There is no, there is no significant rejection in anterior lamellar keratoplasty. If there’s any kind of rejection, sub epithelial rejection, or epithelial rejection in the first year, put lots of steroids. I’ve seen two cases. And I do a lot of these, two cases of stromal rejection. That can be quite tough. You’re getting recorded and get quite a Dimittis, treatment and a lot of steroids IV and otherwise, and eventually cleans up again, their vision is just never as good. But it clears up. You wont see rejection like penetrating keratoplasty.
And how long will lamellar grafts lasts? For the patient’s lifetime, whereas in a PK, it will eventually poop out in about 70 to 20 years. 20 years is the mean.
Steroid regime post crosslinking. I don’t use any. I only use antibiotics for a week. And that’s it. Why not? Because I don’t want, I want it’s an inflammatory reaction. I want that Collagen Crosslinking. And there’s no studies either way. So I don’t use the steroids unless they’re really very photophobic afterwards.
What mechanical factors are currently believed to play a significant role in the progression of keratoconus? Well, right eye rubbing is the biggest biomechanical factor. I can’t think of any others. Sleeping maybe on the eye is not a good idea. So if they are sleeping on their, on their face, you might want to put them in shields.
In the realm of cutting edge ocular therapies, could you highlight any emerging approaches that aim to holistically address the multifaceted challenges posed by advanced keratoconus? Advanced keratoconus is advanced keratoconus and I can’t think of holistic approaches besides doing a lamellar transplant in somebody with very advanced keratoconus. I have given you the gamut of what we do in the allopathic side. holistically, I’m not an expert. There’s all this energy testing and crystals and all sorts of stuff. That’s beyond me. That’s more California. So if you don’t mind, I’m gonna go on to the next question.
Can you explain more why keratoconus is not inflammatory? I said it is inflammatory. One line, keratoconus is a result of inflammation and you got it the textbook say otherwise? The textbooks are wrong. They all copy each other. keratoconus is an inflammatory condition. I think there was a recent paper written by somebody that actually states the fact. So please read that article.
How pratical and frutiful was it to have iintracorneal ring segments after crosslinking? What about rigidity? I think that I’ve already discussed these things. We put rings in they work. Comparatively, things are a little bit of difference here and there. You know, I really can’t get into that. There have been people who who’ve done those studies, crosslink first, crosslink afterwards and so on. You know, the goal is to reshape the cornea and to get patients to restore their vision. So consider that when doing whatever procedures you’re going to choose to do. Again, there’s no competition here. Our goal is to look after patients and get them to see as well as possible.
Can KMax be used as an indicator for severity progression? It is used as a indicator but you need to look at everything, you need to look at the other factors too. And what’s really useful is subtraction and mapping. If you can see posterior elevation. An increase in posterior elevation, that is really probably more of a hallmark than all the other parameters but it’s good to look at all the parameters for keratoconus. k max, people, it is interesting how we as doctors sometimes can get a little bit lazy and just look at one parameter and use that. You are doctors, you’re thinking individuals, you’ve got a brain, you’ve got a subconscious mind that processes information for you, look at all the data and come up with a collective analysis I suppose to one thing.
Does it mean if patient is greater than 21 years, you should establish progression before CXL? Yeah, that would be ideal. And usually, I have come across too many that come to see me because usually they’ve been told by the opticians they’re progressing. If I’ve got new information, then I might watch them.
What will be the cutoff Pachymetry value? Well, you can use 400. But if you’ve got certainly thinner corneas you can use hypotonic riboflavin, to thicken up the cornea.
Can we repeat crosslinking? If yes, after how many months? Well, why would you repeat crosslinking if it worked, you will only know if it’s not worked after maybe a year or two. So that I have repeated crosslinking in five to seven years in some patients. And more often than not, they started rubbing their eyes again. And they will tell you that they can’t help themselves. And I tell them that crossing them again but there’s no guarantee the crossing is going to work, if they don’t stop rubbing their eyes. So you can crosslink them again but you don’t know after months after years. And if you if you find that it does not work.
So I think you’re asking you about genetic testing and and treatment genetically, that nothing has been done. There’s nothing we haven’t got clear. genetic tests for keratoconus, Avellino, the company has looked at this and keeps looking at it and they do have some some reliable data. But you don’t have a single gene, so multiple genes, and that’s a big topic. But again, remember I said to you keratoconus is multifactorial, the many reasons for it.
How do you manage hyperopic keratoconus emerge hyperopic keratoconus? I haven’t seen it too often. I’ve seen mixed astigmatism. I will treat them the same way as I treat any keratoconus, crosslinking first, and then so on.
How are toric lenses going to help as astigmatism is irregular? Well, that’s something that I mean we were toric lenses will help if they are glass permeable. I think you mean contact lenses, I hope you mean contact lenses. If somebody has good spectacle vision with a toric spectacle correction, the chances are they will get an improvement if they have a toric ICL. So that’s what we’re talking about ICL. So I hope that answers that question. But it depends on spectacle correction. If it’s contact lenses, of course, toric lenses are going to help in keratoconus because you’re creating a whole new anterior surface.
I can do cross linking for less than 400 microns. Yes, of course you can. Congratulations. Just make sure that the cornea is thick enough when you when you use ultraviolet light. Well, that’s people are questioning whether it’s necessary or not. I think the jury’s still out, you can go ahead with it, the worry was it would damage the endothelial layer. What I do in cornea is that as I’ve already mentioned, that are thinner than 400 is I use hypotonic riboflavin and I’m checking the corneal thickness before I go and debate. some people put a contact lens on and then exposed to ultraviolet light. Other people use a bit of cornea, there are many ways to do it.
Please tell us about the ideal contact lens. I think the there’s all contact lens questions. I’m not a contact lens specialist. I think it may be a good idea for Cybersight to have a contact lens practitioner talk about contact lens fittings in keratoconus. So we’ll try and recruit somebody to do that for you. Please let us know about your interest in this area. And we’ll arrange that.
Does age matters through the treatment process. Yes, the younger they are, the more chance they’re going to have progression. So something to consider. I think we’ve been through that. That’s why we treat younger patients more aggressively.
How much progression consider progressive. Good question. How should we do tomography in keratoconus to see the progression. So as I mentioned that already, what we need to do is look at the three dimensional tomography and subtract your previous results. Your current results from the previous results, see if there is any progression, especially in the posterior elevation mapping, Because that if that’s ectasia, right? You get thinning of that anterior and posterior or protrusion, anterior and posterior and thinning, the combination of the three and it has to be significant. So There are no numbers. Everyone wants numbers from me. There are no exact specific numbers here. You’ve got to take a look at every patient. They may have a little bit of protrusion in eccentric area, you need to know whether it’s real or not. You can check them again repeat the test.
What method of IOP measurement do you prefer? We use the tonopen. And we we look at corneal thickness we try and we can use a tonopen peripherally where the cornea is thicker. That usually is helpful.
How do you treat if glaucoma develops but we treat glaucoma like we always treat glaucoma. We just have to be sure a good question about the measuring their their pressures and making sure that the pressures are real and corrected for corneal thickness. I’m not going to get into Epi epi off where we’ve already discussed that.
Can you please explain more why keratoconus is not inflammatory. Again, I got this question again. keratoconus is inflammatory. Okay, it is inflammatory. Oral use of riboflavin can be useful treatment, no evidence to suggest that it does. You’ve got to have a certain level of, you need the combination of riboflavin in the cornea and ultraviolet light of a certain level of exposure, a certain frequency and a certain level of affluence to for crosslinking to take place. So riboflavin orally is not really going to do it
What about crosslinking a thin cornea? I’m not sure what the question is. So I can’t answer it. I’m sorry. As regards the question of ortho K, is it not at all recommended? I don’t have any expertise in the area. And I think that it would be unwise because they have thin epithelium in that area. And you’re going to be putting a contact lens on forcefully pushing that area down, you could erode a thin, if they only have one cell layer. And you erode that you put them at risk of a contact lens with an epithelial defect, it could get an infection.
Which is better to use in crosslinking, isotonic, or hypertonic way, but riboflavin it really depends on how thick the cornea is. isotonic is what we usually use most of the time. But we do check the cornea. And before we go ahead and expose the cornea to ultraviolet light, to make sure it’s of sufficient thickness before we proceed. I hope that answer that question will use hypotonic if the cornea is thin, so what I do is I take off the epithelium, measure the cornea and decide whether I’m going to use hypertonic of the cornea is less than 400. Or isotonic, if it’s at about 400. What’s preferable and the last question here what’s preferable crosslinking and intercalary ring at the same time for different sessions. As I said before, sometimes when we do crosslinking patients improve on their own thing division gets better the the best bet correct division improves, even though the two are probably does improve. Maybe it’s because the refractive index of the cornea changes as possible. So they may not need rings. So I’d rather do crosslinking first. And if they need a ring, then I go ahead and do the ring. Hope that answers that question for you.
Well, that was a marathon. It was a bit about 70 questions there. At there are no further questions, I think I answered them all. I’m going to call it a day, 20 minutes over time. Well, I thank you all for your attention. I think we certainly generated a flurry of interest there. It’d be great to get some feedback. I know this particular seminar will be posted on the Cybersight website and it’s a reference point for you to come back and and go to I hope I’m sorry, I’ve been a bit dismissive for some of the questions I didn’t I didn’t quite answer, understand some of them. And some of them will repetitive so apologies to those who feel they’re not answering the questions. I hope you find this session useful. I’ll try and do some other sessions on cornea for you and other things. Be great to get some suggestions from you as to what you’d like us to talk about.