Lecture: Mastering OCT & Visual Fields for Diagnosis & Management of Glaucoma Progression

>> Dr. Kherani: I am Irfan Kherani, I’m one of the ophthalmologists at the University of Toronto, and I practice at the University health network, the Kensington and Trillium Health Partners, and Laser Vision Centers. It’s my distinct honor and privilege to present today: Mastering OCT & Visual Fields for Diagnosis & Management of Glaucoma Progression.
These are my disclosures, none of which are specifically relevant to today’s presentation. I have spoken for one of the technology providers for OCTs and visual fields, Zeiss. What are our objectives here? First, we want to develop a systemic approach to OCT and visual field interpretation. And this is really gonna be the portion of the talk that take up the majority of our time together today. Second, we will attempt to differentiate true glaucoma from imaging artifacts as well as what’s more exciting, glaucoma suspects. And learn to correlate structural and functional findings with confidence. When are they true changes? When are they untrue changes? And recognize pitfalls that lead to over or under diagnoses. And apply OCT and findings to real-world management decisions. Rapid fire cases to get us utilizing these OCT and visual field findings. So, we’ll start off with an opening case just to get us started. Here we have a 58-year-old AI-generated male who has no family history of glaucoma and no history of trauma or eye surgery. He comes in for a regular ongoing checkup for screening of eye disease. He has no visual complaints. These are his optic nerves that we can see here which do look, you know, slightly on the larger side. These are Optos-based images, so they are not true color. But there certainly appears to be perhaps some tilting on the left-hand side. We can appreciate maybe an enlarged vertical disc ratio with some apparent thinning, more so on the nasal side, but potentially on the temporal side as well. And have on the right-hand side a disc ratio and an enlarged nerve. Which could be consistent with glaucoma. Here we have an OCT of the optic nerve. This is an automated OCT that helps to look at disc ratio from the rim, and we are looking at an enlarged disc to cup ratio. We are going through this, but around this area here, we have what’s called the circular tomogram, which cuts through the peripapillary area of the optic nerve in an attempt to get a better assessment of the peripapillary retinal nerve fiber layer. Here is the patient’s visual field, both on the left and the right-hand sides in the patient’s view. And there appears to be some small, scattered, non-specific changes. We do see some reduction slight on the top area, non-specific and not following any sort of specific pattern. So, my question to the group here is: Does this patient have glaucoma? Yes or no? Now the answer is I’m gonna give you is I’ll give you an answer in about 45 minutes as we get through things here, okay? Start off with the first section, analyzing and getting a better sense of the difficult diagnostics that we have in glaucoma. So, technology in our world right now improves faster than interpretation. And here I really want us to look specifically at this graph that I’m highlighting here. Technology increases at a very, very fast rate, especially in the world of eye disease, we’re really fortunate that we have lots of technology. And as technology becomes more and more a part of our everyday world which it really has in many cases from a glaucoma side of things, it can associated with massive increases in amount of data. With the increase in amount of data available for assessment, we have to learn how to interpret that data. Learn what is good data, learn what is bad data, and because of that, there are — there is an associated human adaptation to that data which unfortunately tends to grow at a slightly slower rate than the technology itself. So, when we take the difference between that rate of change of technology and that human adaptability, what we clearly see is an area for improvement. And that is my understanding as to why a lot of you are here with us today. To look at that difference between the available technology and how we adapt to that technology to really optimize things moving forward. So, it’s a great opportunity for us to optimize our learning. In the world of OCTs, we’ve seen an incredibly large and growing amount of information. We started off with, you know, slower OCTs that focused entirely on the macula. And didn’t really differentiate the specific layers to the degree that we would want. Then we started exploring the retinal nerve fiber layer, kind of looking more in the glaucoma realm of OCTs. Then OCTs started to look and subdivide the various areas of the macula into what we would call the more neuro retinal side of things. So the retinal nerve fiber layer from the more external or outer segment of the retina, more consistent with retinal pathology. And then we started exploring nerve fiber and OCTs of the anterior segment. And so, it isn’t an area that we’re specifically gonna focus on today, but I definitely encourage all of you to make sure you have a good background in anterior segment OCT imaging as they can very much help us to diagnose angle disc glaucoma. One of the most under-diagnosed types of glaucoma that does account for up to 80% of glaucomaous pathology and vision loss. And what else makes things complicated? There are artifacts. Artifacts, artifacts, artifacts. So, with every good imaging technology, we have to know how to use that imaging. And so in the world of glaucoma, there is — I mean, as there are in any other area, an incredibly large amount of artifacts. And some of which we’re gonna chat on today. But again, I focused more on really developing an approach to analyzing OCTs and visual fields together, rather than specifically looking at the many, many different types of artifacts that exist in the optic nerve and visual field world. Now finally, the October and the visual field do not always agree. And so, we often talk about structure function, and what we will talk a bit about today, which is structure-structure correlation. And sometimes they don’t correlate. And my encouragement to all of you today, when the OCT and the visual field don’t correlate perfectly, it’s often an opportunity for us to re-think our diagnosis. Now that doesn’t mean that glaucoma is not present. It may mean that it is truly glaucoma and we have to reinterpret the data in a more correct fashion. Or it can mean there is — as well as a number of other things going in at the same time. Or it could mean there’s whole other pathology to consider. And my encouragement today from this point is outer retinal pathology generally relates to retinal disease, and inner retinal pathology tends to relate to optic nerve disease, of which, of course, glaucoma is one of them. And finally, progression detection can be very difficult. So, I’ve shown you a picture here of a clear area of progression, especially on the visual field, with a potential associated estimated retinal nerve ganglion cell loss. And what we’ve — and here, you know, it can be fairly consistent that there is progression of the glaucoma. However, often our cases are not this simple. OCTs have what we call a test/re-test variability that could suggest progression when it may not be there. But it could also have visual fields that, of course, by nature are subjective. So, making the assessment of whether or not there’s true progression can be very, very challenging. Fortunately, however, glaucoma typically follows a predictable structure-function pattern. Meaning generally speaking, and again, there are many, many, many exceptions to this rule with all of our patients, where there is clear retinal nerve fiber layer loss that is followed by optic nerve loss. When we look at it directly from an on — appearance, looking at vertical cup-to-disc ratio, which then follows visual field loss. Now what I want to bring to your attention here is we know that retinal nerve fiber layer loss proceeds visual fields. However, what’s often very challenging in these situations is that the retinal nerve fiber loss tends to be fairly consistent and regular. We don’t want to wait for visual field loss to occur. As at that point in time we have lost, you know, upwards to 60 to 80% of our optic nerve — our optic nerve thickness. And we don’t want those relational ganglion cells to die off and wait for visual field progression. We want to use the technology that’s variable to help us diagnose our glaucoma early and intervene early to prevent things from getting worse. So, to be clear, even though we know that retinal nerve fiber loss in general proceeds visual field loss, we don’t want to wait until there’s visual field loss to intervene. Because at that point in time, in many cases, it is often too late to have a, you know, the most meaningful impact that we can have on our patients. Now, we always step back to the question of how do we truly diagnosis glaucoma? We have so many sources of data. We have on our clinical exam, we have obviously their intraocular pressure. And even their intraocular pressure can be based on the Goldmann tonometry, based on indentation that’s more digital like the tonal pen, for example. It could be rebound tonometry like with the eye care, we have many, many different types of tonometry, all of which gives slightly different readings with different irregularities. We have Puget Sound dispersion syndrome. And, of course, we always have the optic nerve head appearance, which was the classical sign for glaucomaous damage. Do we diagnose glaucoma really based entirely on our clinical exam? The answer is often that’s our only option. If we don’t have access to testing with OCTs, which fortunately with a lot of the modern technologies becoming increasingly available and increasingly less expensive, sometimes we do have to base our diagnosis of glaucoma on the clinical exam. However, my hope today is that we can appreciate the value of OCTs and visual fields in order to help make those distinctions a little bit easier. In diagnostic testing, now, we have the retinal nerve fiber layer as well as the ganglion cell layer. And often we ask the questions, if we do have access to this testing, do we base our diagnosis off of the OCT of the retinal nerve fiber layer or the ganglion cell layer? And, you know, I will explain to you my kind of — my thoughts here. However, there isn’t a clear consensus quite yet in our glaucoma space. What about our visual fields? Do we need a visual field area of loss or some sort of scotoma in order to diagnosis the glaucoma? Or do we have to really refer back even further to our truest definition of glaucoma, a progressive optic neuropathy. Do we need to see that progression in order to make the diagnoses? And again, you have to make that answer to yourself. In my practice, if an optic nerve is acting like an optic nerve that is glaucomaous, I’m fairly comfortable making that diagnose independent of progression. But in its truest definition, glaucoma is a progressive optic neuropathy. So, there’s a couple of mantras that I would like to kind of relate to you today as we learn more about OCTs and visual fields. And that is: We generally speaking use the OCT to diagnose glaucoma. And we use the visual fields to stage glaucoma. Now again, this isn’t a perfect world where our optic nerves follow classical patterns, which is not always the case. And often we must depend on the visual field to make that diagnose. But in a perfect world with perfect testing, we want to use the optic nerve itself, and ideally the retinal nerve fiber layer to a greater extent than the ganglion cell layer to diagnosis the glaucoma. And then use the visual field to stage the glaucoma. Now there are many different staging tools for the glaucoma. And here I’ve presented the Hodapp-Parish staging, what I use on a day to day basis. It gives a bit of a framework. In general, early defects are considered less than 6 decibels, moderate, 6 to 12, and severe, greater than 12 decibels. However, you can automatically move to the moderate or severe or advanced categories if there is a point of a scotoma within the central 5 degrees. Why include moderate and advanced? It’s because if we’ve lost that area of visual field, that central part or early central part of our visual field is the most important part of our visual field. So, any progression can cause significant functional decline for our patients. So, we want to be more aggressive about our management at the very beginning, especially if they’re presenting with pericentral visual field defects as in the case of many of our normal tension glaucoma patients. So, first glaucoma mantra: OCT to diagnosis, and visual field to stage. Our glaucoma mantra number two is: Progression can be any of them. Here I’ve shown optic nerve head, vertical cup-to-disc ratio progression, I’ve showed OCT progression and visual field progression. And making the case for progression, progression in any of these is a sign of progression. In my practice, in the surgical realm, I like to see increased pressures or structural progression, that’s on the OCT in order to recommend, or what I often recommend, minimally invasive glaucoma surgery. And if we’re really stepping up to larger glaucoma filtering surgery, whether that be minimally invasive blood surgery or traditional surgery, trabeculectomies or tube shunt surgery, I want to have either very, very high pressures or progression on the visual field. Again, our second glaucoma mantra: Progression can be either structural or functional. So, let’s move on to section II: OCTs in particular. Now this is where we’re going to spend the majority of our time today. We’re gonna talk about a five-step OCT framework. And within those five steps there are many subcategories that we’re gonna go through. But really it’s the five steps that I want to take you home with today. And we will review at the end of the presentation. The first one, step 1, confirm your quality. What we want to see here is our signal strength, and ideally, and this would be really on all of our OCT technologies that we have, we want to see a signal strength of ideally 8 out of 10 or above. Now, of course, if there’s other media opacities or difficulties, that signal strength needs to be lowered. If you have consistent readings, it’s probably okay. But in general, looking for a signal strength of greater than 8 out of 10. Motion artifact. If we look at this optic nerve, it’s very wonky, going up and down in different areas. And most artifacts can present in many different ways. This is one type of motion artifact of how it presents on an optic nerve held, you see up and down appearance where the OCT machine has a significant difficulty actually assessing the different areas or the segmentation. So, this is motion artifact. Related to motion artifact really can be secondary to many, many things including myopia, very thin nerves, other pathology or even a device that has a bit of dust on it can be these segmentation errors. I’ve included here a breakdown of a very good segmentation of the retinal nerve fiber layer using the circle tonogram. However, there are many different ways that they segment the maculas, the area of the retina, but I want us to always check and make sure that we look at segmentation when we’re analyzing our OCTs in order to ensure that there’s correct segmentation. As you can imagine, if things aren’t segmented correctly, the retinal nerve fiber we’re using to make our decision processes can be artificially increased in thickness or artificially decreased in thickness. And we definitely don’t want to make clinical decisions based on incorrect data. Next we have centering. So, our tonogram is a defined area around the optic nerve. And four, if that is not centered on the optic nerve, the normative databases that we refer to will not be clear. So, for example, in this case I’ve developed I’ve shown here, we have an inferotemporal decentralization of the tomogram. And appears that the superior area is artificially increased in thickness, and the inferior area is artificially decreased in thickness. We have an artificial increase our nasal RNFL and an artificial — sorry, other way around. We have an artificial thinning of our nasal retinal nerve fiber layer and an artificial thickening of our temporal RNF field here. And finally, a bit of a media opacity. Now media opacity, very often when it’s pronounced, so things like cataract or corneal pathology, or anything that’s in the vitreous, when you have a significant media opacity that’s limiting the assessment of the optic nerve, more often than not, you simply don’t get a good view. Everyone if you dilate the patient or you work your way through, you cannot get a clear view of the optic nerve and as a result you really don’t get any valuable information that you can interpret. What’s more common, however, is if you have a relative amount of media opacity, say a moderate or a moderate to advanced cataract or moderate corneal pathology, often the RNFL and the thickness of the values of the numbers that you have on your OCT can be reduced. And this is a result of the light rays entering the eye, bouncing off of the different areas of the optic nerve itself, and coming back to the reader and because of the media opacity, they slow down, which artificially informs the machine that the retinal nerve fiber layer is artificially thin. This is the one area, where if you, for example, proceed with cataract or corneal surgery to improve media opacity or the challenges, you might get an increase in your macular thickness after surgery to remove that media opacity. Now we don’t really want to assume that the media opacity is the cause of retinal nerve fiber layer, but in general, it’s a generalized thinning of the RNFL or the macular areas and not necessarily focal disease. Keep in check if you have media opacity, your results may not be present, or may be artificially thin. Step two: Disc anatomy. We want to look at the disc itself. In many patients, we have very large discs. This is a printout of one of my patients. We can see that the disc area is grayed out, and has a squared millimeters, 2.8 on the right-hand side and 2.6 on the left-hand side. These are large optic nerves. In the past, we used vertical cup-to-disc ratios to help diagnose glaucoma. Yes, use the vertical cup-to-disc ratio in understanding the size of the optic nerve. Not every disc ratio has optic nerve loss in terms of thinning. Here we have an example of a large optic nerve, and here we have an example of a very, very small — now, in the case of the large one, back here, we have clearly preserved superior and inferior peaks of the retinal nerve fiber layer on the circumstance hallucination Tomogram oar the plot, we will talk about afterwards.
and here the itty bitty, 1.54 — but again there’s a lot of artifact in this automatic interpretation that is much more difficult to assess whether or not these are glaucomaous or just congenitally small optic nerves. There’s some suggestion that they could be — and the second case, tilting of optic nerves. As our reference, where do we want do look at disc anatomy? I want us to focus on the thickness circular tomogram on the top portion rather than the numbers and the colors situated down below. One of my main in my fellowship really focused a lot on ensuring that we look at the RNFL thickness itself rather than that information down below. And the example here is we want to treat ourselves as radiologists where we interpret imaging rather than stockbrokers that look at the numbers going up and down. So, here in our picture, we can see what we call a temporal insertion of the RNFL. There’s two humps that we can clearly see on the optic nerve head, which is largely normal, just temporally inserted, not in the classic area. Now you may ask: How does that work? So I’ve shown a picture here where we have a tilted optic nerve. Instead of entering the eye head-on, it’s tilted lightly. And when it’s tilted, we get this atypical insertion of the optic nerve. Almost as if you didn’t take an on-of the optic nerve. Which is often the case. Here is a temporal insertion of the optic nerve that accounts for that movement of what we would normally see in the superior quadrant moving closer to the temporal quadrant. This explains our temporal insertion. Here I’ve given an example of a nasal insertion. Rather than the two humps following in the generalized green area, we can see those on the TSNIT plot, again right in the middle of the sheet, that’s moving closely inward, nasal insertion. Nasal insertion of the optic nerve in this picture, and temporal insertion in this picture, the movement out on the TSNIT plot, or the nasal one where it moves inward. And finally, a bit about peri-pupillary atrophy. These are the most challenging to interpret from an OCT standpoint. Because the circular Tomogram goes through the and we don’t have data to directly interpret. There is no direct retinal nerve fiber layer, it often comes across as zero which is incorrect. We have to adjust the imaging we do, or compare patients back to themselves. Rather than the normative database, looking for the progressive nerve disease to see whether or not there’s been true changes. Now often why these patients become even more difficult is that they often have secondary retinal pathologies. So, whether or not that’s macular pathology or peripheral pathology that’s with secondary retinal detachments or not, that can lead to generalized loss of the nerve itself as well as centralized loss on the plaque, especially our nasal RNFL. So, again, our peripapillary are very, very challenging. And everyone who has difficulty with this, including myself, to read over the systemic reviews of the patients with myopic nerves because they are challenging. Move on to step three, really focus on the RNFL. And here I want to encourage you: Do not depend on average RNFL thickness values. I want you to look for focal disease. So, glaucoma typically affects the supra-nasal or the superior RNFL and the inferior RNFL. So, in glaucoma we look for loss of the mountains where we have these two humps. And as those humps decrease. We are not looking for valleys. We don’t want those valleys that are in the nasal, direct nasal area and the direct temporal area when we have loss of the nasal or temporal direct RNFL, direct where the humps are, that’s not typically glaucoma. Again, glaucoma is not consistent for everyone. But in general, look for focal disease in the superior or supra temporal or inferior or infratemporal. Again, try not to depend on average thickness, look for focal disease. However, it is known in the literature that average RNFL and progression of RNFL is the most sensitive measure for RNFL loss, but with increased sensitivity, you get decreased specificity. always look at the TSNIT plots and the RNFL plots rather than the average numbers. Green is not always perfect and red is not always bad. Here I’m going to bring you to the area that I want you to focus on, which is the TSNIT spot. Stands for temporal superior nasal inferior temporal. What we’re looking for is the loss of the superior and inferior humps. In this picture here, we can see that the left eye is very well preserved than the right eye where we have significant loss of the superior RNFL and the inferior RNFL. You want to pay special attention to what we call the double hump sign. Here we can also see a double hump, what we call a split bundle. Where we can see that, especially that superior RNFL kind of has two humps, and it’s okay for there to be two humps. All that means, there’s generally some sort of vascular supply that is in between those two humps that is not blocking a generalized hump. Some you’ll find, the double hump sign goes into the red zone. That’s okay. That’s a vessel going through the superior portion of the optic nerve that’s breaking up that area of RNFL thickness into two separate bundles. We have what’s called the split bundle. If it’s into the red zone, that’s what we call a split bundle artifact. Finally, I want to look at asymmetry. Now asymmetry is a double edged sword on the RNFL. On the one hand, it can clearly indicate where a patient may have been in an earlier portion of their life where they had had glaucomaous disease before the progression. As is often the case, and we are aware, vertical cup asymmetry is a risk factor for glaucoma. However, always think that patient that has that very significant amount of asymmetry, make sure you’re not missing anything else. Our primary open angle glaucomas typically don’t have as a significant amount of asymmetry as some of our secondary types of glaucomas. In that case, I include the primary enclosure, and the secondary, pigment dispersion and others. Those are more likely to have asymmetric disease rather than classic open angle glaucoma disease. Look for asymmetry, but always use it as an opportunity to rethink your diagnosis. Step four, let’s look at the macula. For the longest period of time, the glaucoma world focused only on the retinal nerve fiber layer. Over the last 10 years, seeing increasing usage of the ganglion cell complex on some machines and the ganglion cell layer combined, which is on other processes here. I’ve shown an example here of a macular cube looking at the ganglion cell layer using one machine here. And what we find is significant change on the macular pathology specifically at the ganglion cell layer. Now, what you’ll find right in the center here is a demarcation at the horizontal. And that demarcation of the horizontal that gives a very sharp line, that’s not, you know, fairly normal in all parts of the body, but when we see something that’s this striking of a change, it’s a sign that we call the horizontal raphe sign. As we’re aware, glaucoma typically respects the horizontal meridian. Given that the way the nerves travel on the retina to the optic nerve. And for that reason, there’s often a sharp demarcation, called the horizontal raphe sign, shown in both cases here or what I like to colloquially the Pac-Man sign. When we have the inferior temporal quadrant involved, that’s known as the macular vulnerability zone. The macular vulnerability zone here. Just gonna check back for one quick second. I wanted to quickly elucidate why we get this macular vulnerability zone as well as the inferotemporal quadrant that’s often affected earliest. This was explored by Dr. Don Hood from New York University. He’s done an incredible amount much research in this area. I encourage everyone to listen to his OCT assessment lectures that he has online. Or even read up on some of his papers. And here this area, again, the inferotemporal quadrant is called the macular vulnerability zone, and it’s particularly susceptible in the glaucoma space. I want to always, always look in this area here. The macular vulnerability zone is associated with central or pericentral visual field defects. That’s an increase of why we want to look at a 10.2 visual field or focus on the inner area or the central area of the visual field. And finally, we do know that the RNFL and ultimately bottoms out. Once you’ve lost pretty much all of your retinal layer and have the tissue, you can bottom out at 40 to 45 microns. What we have found in the more recent literature, the ganglion continues to thin. Even when you have a bottoming out effect of the retinal nerve fiber layer, may still have nerve tissue on the ganglion cell layer to follow progression. We hope patients don’t end up in this area. We want to treat them and look at the progression rather than getting this far. Finally, look at progression. We talk about physiologic, stable glaucomaous and unstable glaucomaous, as well as what we call test and re-test variabilities. So, in the same way as many parts of our body, there is generalized OCT RNFL progression per year. I told you I don’t want you to look at the average near-term numbers. But if it’s progressing at less than 0.5 microns per year, that could be consistent with a healthy physiologic rate of progression. Typically around 1 micron per here, anywhere between 0.5 and 1, that’s probably the only area I would accept in my practice and not necessarily call it progression. Progressive glaucoma is anything greater than 1 micron a year. If you’re losing more than 1 micron a year in general, that could be concerns for progression. Now what I want to caution all of us here is that simply by testing the patient every year and looking for that 1 micron change is not sufficient. Because of test/re-test variability. If you test the patient today and 5 minutes later, may have a different RNFL thickness as measured even using exactly the same machine. For that reason, follow our patients every 3, 6, and hopefully not 12 months in order to for a consistent area of progression with multiple readings. We cannot use just one reading to assess for progression relative to a previous one. I do want to look at what’s considered a statistically significant RNFL change. To do with test/re-test variability. And can only definitively say there’s true fro aggression with 4 RNFL change, whether it’s a statistically significant change. Okay? We talked a bit about asymmetry, any difference between 9 to 12 microns would be consistent with a significant amount of asymmetry that we have to understand and assess for glaucoma in that one eye. Finally, for step five, progression. So, this last area here, I’m gonna show you some visual field progression here. Here we can clearly see visual field, OCT, and both of the RNFL and the ganglion cell layer here with progression. I’m gonna defer specific progression conversations until our second area where we’re gonna look at visual fields. So, with that, let’s move on to section III, which is ours visual fields. Like step one when we look at OCTs, we want to confirm our quality. So, the first thing is we want to look at our reliability in the disease. With a reliability indices we’re looking at the fixation target. We’re looking at fixation losses, which I’m gonna show right here. Again at the top of this Humphrey visual field looking for the fixation target if it’s in the center or where our technicians — and the fixation losses, again, shine a light directly on to the optic nerve and if the patient is able to identify, that’s our natural blind spot. False positives and negatives, anything greater than 20% are an unreliable field. False negatives are a little bit more okay. And the reason I say that is the more visual field that we’ve lost, the more likely we are to have false negatives or to question whether or not we’re seeing parts of the visual field. Whether or not a patient, if they’re not able to see things, it could be a sense that they may not just not be sure if they’re seeing things. So, false negatives, a little bit more fluid, but false positives, really anything greater than about 20% is really concerning for an unreliable visual field. Test duration, you can see that the patient took 2 minutes and 38 seconds to complete this visual field, which is well within the normal range. But I want you to look as we talked about the fixation on the bottom left. On the bottom left of the visual field, we can see the eye tracker movements, the landscape-like appearance on the bottom. The patient was pretty good for the first half of the visual field, but in the second half, they did have a couple of areas or periods of time, they lost their association, but were able to come back. And finally with the trigger happy patients, every time they hear a sound, they click that they did see the stimuli, these patients, again, are a little bit more unreliable. And what’s challenging in these situations, and I’ve had them in my own practice, you believed a trigger happy patient’s visual field, go for surgery or recommend a certain lens and then repeat the visual field and get a much better visual field and find out they have advanced visual field loss. Also be conscious of the trigger happy patient. Step two, generalized depression. We know that glaucoma can be associated with internalized depression. Even in early cases when there is overall RNFL loss. It’s not normal or classic, we want to question things. It is potentially present. General depression, especially on the deviation maps on the bottom left are likely or can be associated with media opacities, cataract, if they’re on pilocarpine, that can increase the generalized depression, and you can see a significant change in fields starting patients on pilocarpine. And wept to make sure they have their required reading add when taking visual fields. And this is again when we’re looking at the total deviations. Glaucoma classically does not result in generalized depression, but if it does, you need to get an assessment to see to make sure we’re not missing anything. So, here in the glaucoma side of things, this step three. Pattern recognition. So, our classic glaucomaous patterns of visual field loss include the most common one — nasal step I’ve shown here on the right eye. We get an arcuate. I show a superior and inferior arcuate, the classic tunnel syndrome pathology. More common in glaucoma patients. At the visual field, only a mean loss of .65 decibels, but a very significant superior pericentral visual field defects. Looking at the numbering, minus 33, just above the superior margin on the right-hand side here. Familiar, we would probably call this patient an advanced patient even though they haven’t lost much visual field and likely associated with macular vulnerabilities that we noted on the OCT. And finally, we talk about horizontal respecting visual field defects. So, again, we hear, see a kind of arcuate change that doesn’t go necessarily to the side or the peripheral part or the mid-peripheral part of the visual field, but see more of a mid-central area of visual field loss and a horizontal respecting visual field loss here. Finally, sorry, step four — sorry, second to last one — looking for structure-function correlation. And look to RNFL to ganglion, we have the inferior RNFL correlate with the inferior ganglion cell layer. And structure to structure, RNFL to GCC to correlate with the visual field. From this combined printout from the Zeiss machines by flipping the OCT of the RNFL, they can superimpose on the OCT assessments to look for structure-function correlation, which is clearly shown here more on the left-hand side — sorry, than on the right-hand side. Here I focused again on that specific area right in the middle. Helping to flip the RNFL data of the OCT in order to assess that correlation. Finally, on the progression analysis, we want to look at progression of either the visual field index or the mean deviation. We want tone sure that we have a good baseline. So, for example, if the patient’s undergone surgery, reset the baselines. We want to utilize as much as possible our glaucoma hemifield assessments, our progression analyses, as well as our trend analyses. If one of one reading that’s completely out of the blue relative to previous, repeat the visual field. Sometimes patients are having a difficult day, and benefit from a repeat visual field. That’s often the case with OCTs as well, if you have one reading that doesn’t make sense, if you repeat it, you’ll not necessarily recover, but get a better test. Always look at the draw data itself to see if there was an error with the draw data. And to end up, rapid fire cases. First we had a patient that has this RNFL with this visual field on both sides, and we can clearly see that the humps of the RNFL thickness on the TSNIT not, even though they’re marked red in the average readings, what we’re actually seeing is a temporal insertion of the optic nerve. And for this patient, I would call them a glaucoma suspect, by virtue of being atypical, but not diagnosis with true glaucoma. Given the slight change, repeat that, to see if it was an eyelid artifact. Well-preserved tissue, just temporally inserted, this could be a moderate myopic patient. What we have here, we have a very, very thick RNFL specifically in the inferotemporal area, but really in the supra temporal area. When I see this type of change, everything is green and super-normal, white on this designation, this is a situation where I want to make sure I’m not missing any optic nerve head edema. Again, likely not consistent on a patient that hasn’t been in both eyes in terms of an inflammatory condition. Do a secondary workup for a an optic nerve head to see if there’s a lumpy, bumpy appearance. Completing an ultrasound of the optic nerve, and if we needed to, jumping up to angiogram, but hopefully that wouldn’t necessarily need to be taken. Again, when we see an atypical thing, we want to question things. But we also see preserved artifact, but it’s kind of too preserved RNFL. Next we have a patient that has a very large optic nerve head, again in both eyes. We can see maybe some enlarged blind spots, slightly. But maybe to a little bit degree here. This nerve tissue, even though the optic nerves are large, and maybe diagnosed with glaucoma in a previous world without the imaging, this patient, again, can be considered a glaucoma suspect just by virtue of the fact that they have enlarged disc to cup ratios, but not necessarily significant nerve thinning. Now one thing we could also consider is following this patient with repeated testing to see if there’s any progressive nature. Because if there is progressive nature, this could be what we call green disease — there’s not necessarily loss of the nerve tissue. But going from an area of thickening, an area that was artificially thick, or an area that was thicker and became a little bit smaller, that could be consistent with early glaucomaous loss. Next here we’re gonna look first at some nerve — we see some clear loss of the superior and inferior nerves, and with see clear loss of our superior and inferior ganglion cell layers. But interestingly, a little bit of an element of the horizontal Pac-Man sign, to me this patient clearly has glaucomaous loss. And bring up the visual fields, very advanced disease, very little peripheral and mid-peripheral fields left. Take into account for sure that this patient likely has advanced disease. Our next patient, asymmetry. On our RNFL analysis, seeing loss of the superior and inferior RNFLs, again, looking at our TSNIT plot. More so on the left-hand side. The right-hand side looks largely normal. And correlate with the ganglion cell layer, more pronounced raphe’s sign. But more like the inferior RNFL, we are seeing a bit more of a change in the superior ganglion cell layer, which is a vulnerability zone, just not the knack layout vulnerability zone. And as we look on our testing here on the left-hand side, we do see more pericentral visual field defects, again, consistent with that inferior visual field and superior pericentral visual — sorry, superior RNFL thinning and GCC thinning. Our final patient here, look at a bit of an analysis for progression. So, on the right-hand side we can see a visual field that’s largely stable, both as well as, you know, some stability on the average RNFL. However, on our other side, we are seeing what looks like could be some signs of superior thinning of the RNFL on subsequent tests. And likely consistent with progression. So, again, progression can be OCT or visual field, we generally don’t want to wait necessarily for significant visual field progression. Again, once we lose it, we can’t necessarily get it back and so do we want to intervene little bit more. Just in closing, we have our case we showed before. I showed enlarged optic nerve, enlarged vertical cup-to-disc ratios. Does this patient have glaucoma. Better assessments with the circular tomogram. And there seems to be a large I preserved inferior retinal nerve fiber bundles, probably call this patient a glaucoma suspect. Again, watch this patient and ensure that he or she is not progressing. In summary, our OCT analysis, we want to confirm quality, confirm our disc anatomy, assess the RNFL, then assess the macular ganglion cell layer and as well as look for progression. And specific on OCT. And summary of visual field analysis, looking at confirming quality, generalized depression. We want to assess for pattern recognition of our main visual field loss of main visual fields that we typically see in glaucoma. Assess the structure-function correlation and finally assess for progression relative to the OCT of the RNFL and the OCT of the ganglion cell layer. With that, I will open up for some questions. Thank you again for all coming into today’s presentation. And I’ll stop sharing my screen there and look at our questions area here in the last few minutes that we have. All right. So, we’ll go through things here. So, once a patient receives advanced glaucoma and then the OCT hits the floor effect where the RNFL, what specific visual field protocols and analysis do I rely on? I typically rely on the visual field of the 10-2, specifically at the central visual field. And I’m starting to use more and more the ganglion cell layer as the RNFL. Can visual field 10.2 detect early glaucoma? Absolutely. The visual field 10.2 gives the pericentral visual field defects, we’re finding more and more common in the patients. Given that association with the macular vulnerability zone that we looked at earlier. How to diagnose pre-perimetric glaucoma. Really the best way to diagnosis this is kind of more about that mantra. We’re looking at the OCT to help make that initial diagnosis. And again, if it’s a classic pattern, you probably can make that initial diagnosis, however, if not, then you’re looking for optic nerve head progressive thinning on the — on the glaucoma, on the RNFL hopefully in advance of the visual field loss. All right. How do we know the normal values of the parameter seen on OCT? So most of the OCTs — so the normative databases that were typically created in the past by the larger companies, including Zeiss and Heidelberg, based on a small group of normal databases, largely localized to Caucasian European populations. And now they’re incorporating a large number of more international parable populations to create larger normative databases. This is an area of great deep exploration. And really I think artificial intelligence is going to play an important role as we assess what’s truly normative in the database moving forward. Clinicians recognize when it’s due to poor image acquisition than true disease? Very, very difficult. And my best answer here is actually repeat the testing. Especially on the OCT, takes just a second or two. Repeat both or repeat at least the OCT. And then you can assess to see if that same acquisition artifact you have was resolved. Repeating the testing is very, very helpful. All right. Can retinal ganglion cell loss despite achieving target IOPs? Yes, it’s both the retinal ganglion cells and the nerve fiber. Both layers do continue to have a slow rate of progression, even in a controlled situation. For that, we want to make sure we look at our kind of physiologic rate of progression versus our pathologic rate of progression. In progressive cases, test more often to ensure that we have that data. There was a question here about the OCT assessments online of the doctor who had provided the information on the macular vulnerability zone, that was Dr. Donald Hood based out of New York University. Hood analysis and association with visual fields, we just spoke about that. So, there’s a question here about what visual field methodology should we use? And so I pretty much switched all of my patients on their initial and follow-up assessments to what we call the 24.2 faster. This is based upon the Humphries. They have correlation on the top and the Heidelbergs. And the reason I use this faster, number one, it is a little bit faster given it’s the fastest algorithm. But what’s most important is it actually includes the central visual field areas. And so for a lot of my patients that are finding are presenting early with pericentral visual field defects that we weren’t looking for them in the past with the peripheral and mid-peripheral visual fields. Utilizing the 10-2 or specifically using the 24-2C, that means central, includes a number of central points that can help us diagnose that early pericentral visual field change from the very get go. So, there’s a question about what evidence supports using macular ganglion cell analysis over peripapillary RNFL in the early glaucoma. The evidence is still under development and being used. So, if a patient that shows a clear, horizontal raphe sign, with not necessarily a clear loss, I will call that patients a very, very early case of glaucoma, and regular follow-up. I see signs where the ganglion cell could proceed to the — do we know that the ganglion proceeds the RNFL? We don’t know that quite for sure. But that’s where the evidence is heading. Great question, next one here, on whether or not there’s a value for OCT angiography. In my practice, we complete optic nerve head angiography on all of our patients are and it tells me it plays a large role in the addition make something unfortunately not. Part of the reason, there’s a lot of artifact in OCT angiography, especially in the papillary area. But what we are finding is it is providing a ton of information with areas of potential loss. So, I think as more information for OCT angiography comes from a research standpoint, we’ll have a much better sense of exactly what role it’s going to play in the future. I think it’s going to play a large role, we have to figure out what that is. But my thought is it elucidates of the pathology that drives normal tension glaucoma. Is there a setback in OCT visual assessment based on age? So really good question. Because a lot of our normative databases do not include children. Really below the age of 18, and actually a lot of them are — they don’t include patients below the age of 35. For that reason, often you have to follow and assess patients relative to themselves to see if they’re progressing or changing, but as I had mentioned earlier before, we’re really heading into a good space where a lot of the major companies are starting to utilize larger normative databases that include children as well as people of different ethnic origins. All right. Is the GCA the ultimate floor effect? There is, but it’s less pronounced than the RNFL. Next question, which is more dependable between RNFL and ganglion cell loss. RNFL cell loss. Ganglion cell loss can be found earlier, but also very, very sensitive to other macular retinal pathologies. There can be artificial thickening of the ganglion cell layer, diabetic disease, diabetic macular edema, for example, all can have a large impact on the ganglion cell layer and have a much smaller impact, really not much at all, on the retinal nerve fiber layer. Definitely for sure the ganglion cell layer and the macular assessment are much more sensitive to artifact than the ganglion cell layer. Can you look at progression through OCT? You can, as long as you’re using the circular tomogram that goes around the nerve layer itself. Screening — the question is, if you’re trying to screen for baseline, do you want to use the 24-2 or the 30-2? I generally err on the 24-2C because it includes both peripheral and central points. For patients with myopia, you have a bunch of different options for how you can assess and follow them, if they’re mildly myopic, use the normative databases. However, if they have a significant amount of myopia, you have to follow them relative to themselves. Use the visual fields because the OCTs are hard to interpret. And if they have lost from the myopia, have to follow on intraocular pressure. That’s challenging for glaucoma patients that are highly myopic. However, often they’re our only options. How can we differentiate between a physiologic enlarged optic disc relative a glaucoma disc with a cup-to-disc ratio? Look the at TSNIT plot and the inferior and superior thinning of the retinal nerve fiber layer itself. The next question is can we have a situation where the RNFL is normal and the ganglion cell layer is abnormal? Yes, theoretically, our parents that are have been requester very early may show signs of the horizontal raphe sign and have a completely preserved RNFL. All right. So with temporal — there was a request to just review the temporal and nasal insertion. Normally our optic nerves enter the eye head-on, however, if they’re tilted in either direction, cause the outward or inward changing of the TSNIT plot on our nerve print outs. All right. Question here is classical teaching holds that we should complete gonioscopy annually for patients, especially with ongoing checks, I would endorse that. With the advent of anterior OCT, we are able to catch disease better than our gonioscopy. And when we teach our residents and fellows, including myself, we’re often not as good as gonioscopy as we ought to be. Gonioscopy is still considered the gold standard for the angle closure, but completing OCTs at the same time can help keep us honest. Next question is OCT needed for follow-up once we have diagnosed glaucoma? Or is only perimetry sufficient? Definitely, definitely, definitely complete both, because as we talked about, the OCT can change and you can lose up to 80% of your optic nerve head function before we actually have any significant visual field loss. So, definitely look for progression on the optic nerve head itself, including the RNFL. All right. Just looking through the next round of questions. If a patient has known — is that reassuring for asymmetry? Probably not necessarily. You want to follow the patient regularly to ensure that it’s not progressing. As we get to the end here, find if there’s any other kind of new questions… we’re getting a lot of good repeats. Imaging in patients with no visual field defects, but thinned out RNFL. If your RNFL is not that classic superior temporal and inferior temporal loss, brain imaging is relatively low. Especially if it’s asymmetric, affecting one eye and not the other, make sure we’re not missing optic nerve neoplasm, including –. The next question is how does the signal strength of a machine take into account the interpretation of the OCT and the visual field? The signal strength is not really a huge portion of the visual field. In that case, looking for the reliability indices. But they can artificially thin the OCT itself or you just won’t get a reading at all. Question is: How often should we be seeing our glaucoma suspects? I generally recommend every year. It looks like we’re seeing — those are pretty much all the new questions. So, with that, I want to thank you so, so much for coming to today’s presentation. And thank you to Orbis and Cybersight for the invitation to present. I really appreciate that opportunity. And again, if you ever wanted to reach out, please be in touch.