This lecture will discuss the pertinent risk factors, clinical signs and diagnostic tests used to accurately diagnose glaucoma. Clinical exam including tonometry, pachymetry, gonioscopy, and optic nerve evaluation will be reviewed. Pearls for reviewing OCT and visual fields will also be presented. Artifacts and physiologic variability will be stressed.
Lecturer: Dr. Jody R. Piltz-Seymour, Clinical Professor, Perelman School of Medicine, University of Pennsylvania, USA
DR PILTZ-SEYMOUR: Good morning! Good afternoon, good evening. From Philadelphia, USA. It’s such a pleasure to be here today, and I’m honored to have people from every continent today. I’m gonna talk to you this morning a little bit about basic signs of glaucoma, like: Does my patient have glaucoma? How do you really assess that? I’ve noticed a lot of times when I get cases from Cybersight, it’s really a question of: Is this really glaucoma? And it’s sometimes very, very hard to figure out. So here are a couple of questions. And we’ll just poll the audience. Which of the following is associated with a decreased risk for glaucoma? Low blood pressure, Asian ancestry, thick cornea, or disc hemorrhage? Place choose an answer, and we’ll review this at the end of the talk. Okay, let’s go on to the next question. When checking IOP with a Goldmann applanation tonometer, the mires should: Be as thick as possible, directly align, the inner edges should align, or the outer edges should align? And we’ll go on to the next question. It is important to perform gonioscopy in myopes, in hyperopes, in eyes with shallow chambers, in anyone diagnosed with glaucoma, in eyes with high IOP, all of the above? Good. And question four: Glaucomatous visual field defects typically have the following characteristics: Respect vertical meridian, cluster in the arcuate pattern, spare the paracentral area, are easily distinguished from defects that develop after a branch retinal vein occlusion? Did we want to show results now, or just at the end, the comparison? Okay, sounds great. And question five: Features of glaucomatous optic nerves include notching, saucerization, disc hemorrhage, peripapillary atrophy, generalized rim loss, or all of the above? Okay. So… Let’s just talk a little bit about what glaucoma is. Glaucoma is a group of diseases that cause damage to the nerve of the eye. It is a heterogeneous group. It’s usually associated with high pressure in the eye, but not always. In glaucoma, there’s progressive damage to the nerve fibers of the optic nerve, which causes a specific pattern of damage called cupping, and this is associated with defects in the visual field and defects in visual function. Glaucoma is very, very common, and with our aging population, it is going to increase. In 2013, there were 64 million cases of glaucoma worldwide, two thirds primary open-angle glaucoma, and one third primary angle closure glaucoma. For populations between the ages of 40 and 80, the global prevalence of glaucoma is about 3.5%. Open-angle glaucoma is highest in Africa, with a prevalence of 4.2%, and primary angle closure glaucoma is highest in Asia, with a 1.1% prevalence. But our population is increasing greatly, and it’s increasing — we’re gonna also have older patients. And the greatest increase in population is going to be seen in Asia, so the burden of primary angle closure glaucoma is going to increase. And we can see here with the population 65 and older in 2000, versus what is predicted in 2050. So in 2010, 64 million people with glaucoma and 7.4 million with blindness in both eyes, worldwide. In 2020, 76 million people with glaucoma, and 11 million anticipated to have blindness in both eyes, and in 2040, 112 million people with glaucoma. Glaucoma is very underdiagnosed. In the US, half the cases of glaucoma go undiagnosed, and worldwide, this burden is even greater. So why is glaucoma so difficult to diagnose? Well, one: It’s asymptomatic. People do not know they have glaucoma, until it is end stage. Failure to have routine eye exams. The best way to diagnose glaucoma is with a routine eye exam, and many people, if not most people, don’t have routine eye exams. And then there’s a great variability in what is normal. It’s not great to diagnose glaucoma by high intraocular pressure. At any point, up to half of patients with glaucoma will have an intraocular pressure within the normal range. There’s also ocular hypertension, where most people with high eye pressure will not have glaucoma, and normal tension glaucoma, where you’ll have glaucoma with pressures that are always in the normal range or typically in the normal range. There’s also a great deal of variability in the appearance of optic nerves, and visual fields are difficult to interpret. So in general there’s asymptomatic, failure to have routine exams, and there’s great overlap in what’s normal and what’s pathologic. So we see two optic nerves here. One has a small cup and one has a large cup, and these are both normal optic nerves. And then this optic nerve is an extreme example, but this is actually a very tiny optic nerve, where we have documented that the disc used to have no cup, and so this is actually glaucomatous cupping, because this disc used to have no cup, and now it has a cup to disc ratio of approximately 0.2 or 0.3, and beta peripapillary atrophy. And we’ll talk about how you tell the difference between this being glaucoma and this not being glaucoma. So how do we approach this problem of diagnosing glaucoma? We need to assess risk factors, measure pressure, do gonioscopy, evaluate the optic nerve, and if possible, the nerve fiber layer, with OCT if available, and assess visual fields if possible. Risk factors from the ocular hypertension treatment study and the European prevention trial include older age, thinner corneas, higher IOP, increased vertical cup to disc ratio, and higher pattern standard deviation. And pattern standard deviation is a measure of localized visual field loss. One thing to keep in mind is that thinner corneas are much more common in people from Africa and African ancestry. Thinner corneas. Other risk factors are race. We’ve already heard that primary open-angle glaucoma is increased in people of African ancestry, angle closure, people of Asian ancestry. If people have a history of glaucoma in their family, particularly first-degree relatives and especially siblings in the same age cohort, that’s an increased risk. So the best person to screen for glaucoma are family members of known cases. Ocular anomalies, trauma, vasospastic syndrome, people with cold hands, cold feet, migraine headaches. Hypertension is interesting, because you can get long-term glaucoma problems from prolonged hypertension, when people develop atherosclerosis, but you can also get it from medication, because low blood pressure is a risk factor for progressive glaucoma, especially in people with advanced disease. So we want to avoid low blood pressure and hypermedication of hypertension. Steroid use and sleep apnea are risk factors, people in inverted postures a lot, people that have external eye pressure on their eyes during sleep. If you press on your eye even with a pillow, you can greatly increase the pressure, and people who play wind instruments. It’s the Valsalva maneuver that can increase pressure. If you’re practicing for six hours a day, that can be significant. So intraocular pressure is a causative risk factor. As I mentioned, 50% of primary open-angle glaucoma patients will not have elevated pressures if you’re just doing a single measurement, and the majority of people with intraocular hypertension will not go on to develop glaucoma. So it’s important to assess treatment of glaucoma, rather than diagnosing glaucoma. We’ve learned from the ocular hypertension treatment study that corneal thickness greatly impacts the accuracy of our intraocular pressure readings. So patients with thick corneas have falsely high IOP, and patients with thin cornea have falsely low pressure. Normal is about 550, maybe even a little thinner. Normal tension glaucoma patients tend to have thin corneas. Ocular hypertension tend to have thicker corneas. And I mentioned African-Americans and people of African ancestry tend to have thinner corneas. So it’s very important to get an accurate pressure measurement. You need proper thickness of the mires. Not too thick, not too thin. The one pictured on this diagram is perfect. You want to align them with the inner edges overlapping, just as in that picture. Very often, we’ll see an ocular pulse, and you’ll see the mires move, and you want the central part of that pulse to align, as you see in that picture. If patients have high astigmatism, you need to check in two meridians. You’ll see that because they may have widely oval mires or very sharp, steep mires. They won’t be this nice curve. They may be much steeper, or more splayed. And also, it’s very important not to have the lids touching the tonometer. If the upper lid sits on the tonometer, the pressure will read falsely low. And you don’t want to press on the globe at all, because that will raise pressure. Also, if you have handles on your slit lamp, avoid having the patient grip those handles. If they grip really tight, that’s a way to raise intraocular pressure. And we used to use that in research to raise intraocular pressure. So have your patient relax, encourage them to breathe, don’t ask them to open really wide, because that can raise intraocular pressure. If people are wearing neckties, have them loosen their necktie, so they don’t have tightness and closure of venous return, and if patients are obese and they’re straining to get into the slit lamp, use a handheld technique. It’s great to get multiple readings. It’s great to also get diurnal checks. And this does not have to be a formal diurnal tension curve, where people sit in the office all day and have their pressure checked. It can be just a morning visit one day, and an evening visit the next time. And if you can, you can use alternate instruments, rather than Goldmann. If you have a TonoPen available, this is a picture of an iCare on the right. There’s non-contact, pneumonia tonometers, other tonometers as well. But Goldmann is the gold standard. And as I mentioned, IOP is more important in the management of glaucoma rather than the diagnosis. So those are the issues with pressures. And then you want to examine the patient, to look for signs of secondary glaucoma. Are there old KP? Krukenberg’s spindle? Iris transillumination, as you see in the top photograph, or exfoliation as in the bottom photograph? Signs of trauma such as angle recession, phacodonesis, or chronic mydriasis? Unfortunately, gonioscopy is not performed commonly. Many studies have shown it is done uncommonly, but it’s impossible to diagnose open-angle glaucoma if you don’t know that the patient has open-angles. Anyone with any refractive error can have narrow angles. And subacute and chronic angle closure glaucoma are more common than acute, and they’re frequently missed or misdiagnosed because people have not examined the angles. I recall a number of years ago having a physician, a pediatrician, come in with angle closure, and he was a -8 myope with plateau iris syndrome. So gonioscopy should be performed on every patient. Not every visit, but definitely when you’re evaluating whether or not they have glaucoma. Learn a recording system. I tend to use the Spaeth system, because it gives me so much information, but you need to record how steep the approach is, is it a curved, a steep, a regular, or a backward bowing approach. This is not the nomenclature they use anymore, in that slide. It’s been updated. And you want to see what the deepest angle structure is. You can record that in words. You don’t have to use the Spaeth system. But it’s very good to have a recording system that gives multiple points of information about the angles. I think it works best to learn your landmarks with a Goldmann lens, if you’re inexperienced. But have a 4 mirror gonio lens available. The ones that don’t need a coupling solution, and you can do compressive gonioscopy. If you’re having trouble seeing the angle, have the patient look towards the mirror. So first perform your gonioscopy in bright light, to identify all the landmarks you can. But then recheck it in dim illumination. So that you can — when the pupil dilates, you can see if the angle closes. That’s what we see here. Here it looks widely open in bright, but when the light goes dim, the iris bulges back. And recheck with and without compression. Here’s a UBM, showing a light. You can see it’s quite narrow and plateau-like. This is what it looks like in the light, but in the dark it completely closed on the bright side. And remember, a gonio lens is a simple mirror. We use a lot of lenses that flip up and down and back and forth, but a gonio is a simple mirror. What you see on the top is on the top on the opposite side, not criss-crossed. So there are some problems that can happen with gonioscopy. Sometimes it’s very hard to see the angle, when the trabecular meshwork is lightly pigmented. We can mistake Sampaolesi’s line for the trabecular meshwork. That’s the pigmented Sampaolesi’s line that’s usually seen inferiorly. We need to discern PAS, peripheral anterior synechiae, from iris processes. So I hope these pictures are showing well, because they look a little bit pixelated on my computer now, but this is an angle that has a very lightly TM — you can sort of see a little bit of variation in pigment there, and the one on the bottom is a closed-angle. It’s hard. And here is with and without compression. Is this a Sampaolesi’s line, or is this trabecular meshwork? And using a wedge of light can really help with lightly pigmented angles and distinguishing Sampaolesi’s line from trabecular meshwork. You take a really thin beam of light, and you shine it, and you should be able to see an anterior and posterior beam of your cornea, and where those two beams meet is Schwalbe’s line. And so your angle should be between that, where that meets between the Schwalbe’s line and the iris. So if your Schwalbe’s line, where those two beams meet, is at the iris, that is a closed-angle. And here we see what looks like trabecular meshwork, but when you press, is actually a Sampaolesi’s line, and there’s TM down below. Iris processes look like little threads coming up. Versus PAS, which are more tented or broad-based. So you can learn a lot from gonioscopy. Aside from just: Is the angle narrow. You can see if there’s a recession, if there’s pigment dispersion or prior pigment dispersion, are there PAS, is there plateau iris, is there bumpy peripheral iris, that may indicate an iris cyst? But you can only diagnose and you can only make these assumptions if you actually do gonioscopy. So again, you can’t diagnose open-angle glaucoma if you haven’t looked at the angle. And chronic angle closure glaucoma looks exactly the same as open-angle glaucoma, unless you see the angle. So we just know with chronic angle closure glaucoma patients are often misdiagnosed as open-angle glaucoma, and then they get to the point where their glaucoma just gets terrible, and they often need surgery, because chronic angle closure often needs surgery, but if you catch them early and do iridotomies, you can often prevent this whole cascade from intermittent to chronic angle closure glaucoma. So please do gonioscopy. Now we’re gonna move on to the optic nerve head. This lecture is a little bit of everything. It’s going to cover a lot of information in a short time, and then in the future we can do other discussions just on the optic nerve, which we’ve done before. And it should be on file. Or just on visual fields, just on gonioscopy and angle closure. But right now I’m trying to give a quick comprehensive overview. So just as there’s a problem with gonioscopy for not doing it and not looking at the angle, the number one cause for the undertreatment of glaucoma is the inadequate assessment of the optic nerve. So if you wait for a patient to have high pressure, to bother looking at the optic nerve, you’re going to miss so much. Every patient we should take a good look at the optic nerve with very critical eyes. And I like to have a bit of a system. So I like SHIP, which is size. We look at the size of the optic disc. Not the size of the cupping, necessarily. The size of the optic disc, hemorrhages in the optic nerve, ISNT rule, which is the rim thickness, and parapapillary atrophy. And then as a bonus, we could try to look at the retinal nerve fiber layer. So what is normal? The rim tissue is composed of ganglion cells, glial tissue, and blood vessels. And axons pass through the pores of the lamina cribrosa to form the optic nerve. It’s usually vertically oval, follows the ISNT rule, which we’ll go over, where the rim thickness should be greatest inferiorly, then superiorly, then nasally, and then temporally. And in most people, the cup to disc ratio is less than 0.5. I think one of the most important things to take away from this lecture is to look at the size of the optic nerve. The size of the optic nerve varies greatly between patients. And people with small optic nerves have a small scleral canal. All those neurons need — all the optic nerve fibers need to pass through this small scleral canal, and it’s very, very tight. And those patients should have a small cup. People with big optic nerves have large scleral canals. All the nerve fibers have plenty of room to get through the scleral opening, and they hug around the edge, and they can have a big — the patients with big discs can have big cups, because there’s lots of room for those nerve fibers to just hang around the rim. And then the rest of people that have medium sized optic nerves should have medium sized cups. So the first thing to do when you’re assessing the optic nerve is to get a feeling for whether the optic nerve is small, average, or large. Because that will help you determine the significance of the cup that you’re seeing. As I mentioned, there’s great variation in the size of the optic nerves. Here’s a small optic disc. And here’s a large optic disc. And both of those nerves are normal. So how can we measure the optic nerve? I think the easiest way is with a direct ophthalmoscope. The direct ophthalmoscope, if you use the middle sized spot, or if you have a very old one that has two sized spots, use the smaller one. It’s the 5-degree spot. When you shine it in the eye of a patient that has a refractive error between +8 and -8 diopters, so most people, it will shine a circle of constant diameter, 1.5 millimeters in the back of the eye. And you can measure your optic nerve size versus the size of that light spot. So most optic nerves are about 1.8 millimeters square — I’m sorry, it’s 1.5 millimeter circle, or 1.8 millimeter square. And that circle should be just a little bit smaller than the average optic nerve. So you use your light, see the optic nerve. If the optic nerve is the same size as that circle or smaller, you have a small optic nerve. If that spot of light sits as a teeny circle in the middle of your optic nerve, you know that it’s a very large optic nerve. You can also use your fundus lens, and use the height beam height on slit lamps. Not every slit lamp has the measurement of the light beam height. But with a 90-diopter lens or superfield lens, it should be the vertical diameter of the optic nerve — should be about 1.4 millimeters. If it’s greater than 1.6, it’s a large nerve. If it’s smaller than 1.2, it’s a small nerve. And there are different measurements for other lenses. If you have a 60 diopter lens, for instance. So again, here we have a small optic nerve, with a small cup. But this optic nerve is actually pathologic. Because it has changed over time. And large nerves with large cups. And here we can see that small optic nerve, and then if we put that light beam, that’s about how it would look. So that’s a small optic nerve. And here’s that same light beam and that large optic nerve. I say that it swallows the light beam. And here’s that tricky one that I showed you before. This is an extreme example. So if you just saw the disc on this side, most of us would not appreciate that that’s glaucomatous. But we have followed that patient before, and that patient had very high pressures, and was lost to follow-up, and went from this to this. And we can see the cupping has increased, and peripapillary atrophy is sometimes an early sign of glaucoma in small optic nerves. So always look in a small optic nerve for whether or not there’s peripapillary atrophy. And again, the large optic nerves can have a large cup. And then if you have cup-disc asymmetry, always look for disc size asymmetry, and this is a case of disc size asymmetry. Most people are pretty symmetric in their disc sizes, but this can certainly happen. So the risk of not recognizing disc size — so in small discs, you are going to miss glaucoma. In large discs, you are gonna misdiagnose people with glaucoma who don’t have glaucoma. And the same thing for asymmetric discs. So that’s the first part of disc size, which I just can’t say enough important things about. Disc hemorrhages are very, very important also. They are like a little red flag to tell you that this patient is certainly at risk for glaucoma. In the 13-year follow-up for the ocular hypertension treatment study, the cumulative index of developing primary open-angle glaucoma was 26% in people that had disc hemorrhages and only 13% in eyes without disc hemorrhages. So a 2.6fold increased risk of developing glaucoma in people with risk hemorrhages. It sometimes can be subtle. Disc hemorrhages can be subtle. And so what I recommend, when you’re examining the nerve, at one point say: And now I’m going to look for disc hemorrhages. Because if you just glance at the nerve, you can sometimes miss a subtle disc hemorrhage, because your brain will sort of pick it up as just a blood vessel. So make a concerted, direct, conscious effort to look for disc hemorrhage. And here we can see a small disc that has a small cup. Looks like a pretty good-looking disc. And here it has a disc hemorrhage, and we can already see it’s developing a notch in that area, where the disc hemorrhage has occurred. So disc hemorrhages typically occur at the edge of a notch, or on healthy rim tissue. They do not occur in the notch. You actually need the rim tissue. And they’re like a little axe that’s picking away at your optic nerve. So the ISNT rule, as I mentioned, looks at the rim thickness. So now we’re getting into the cup. And people always like to talk about the cup, but the cup is the empty space. So I like to talk about the rim. How much rim tissue is left. If you have less rim tissue, certainly your cup is going to be large, but the normal, healthy optic nerve has the thickest rim inferiorly. The next thickest rim superiorly. Then nasally. And the thinnest rim is generally temporally. So really look mostly at your inferior and superior rim. That’s where the nerve fiber bundles come in. That’s why those rims are thickest. And those are the areas that are most prone to glaucoma damage. Then the beta zone peripapillary atrophy is that atrophy around the edge of the optic disc that develops in glaucoma. It is not pathognomonic for glaucoma. You can see this in other disorders. But it does correspond with areas of damage and loss of nerve fiber. It is the atrophy of the RPE and the choriocapillaris. You can see sometimes large choroidal vessels underneath, and in darkly pigmented people, that area can pigment. Retinal nerve fiber layer is very hard to see, diffuse loss of retinal nerve fiber layer, but sometimes you can. Especially more darkly pigmented people, you can see local focal loss of the nerve fiber layer. So in this patient, in both direct examination with regular photography, and certainly with the ophthalmoscope or your lens at the slit lamp, and red-free photography, focalized nerve fiber layer jumps out inferiorly, and this defect superiorly, in those perfect arcuate areas. So let’s look at this optic nerve. Is this normal or is this glaucoma? So let’s look at the size. Some moderate size. Let’s look at the hemorrhage. Yep, there’s a hemorrhage down here. Now we can see how subtle that hemorrhage can be. Let’s look at the rim. What does our inferior rim look like, and is it our thickest rim? It gets pretty thin down here. So there’s inferior rim thinning, and possibly even superior rim thinning, because this rim looks — the nasal rim looks just as wide as the superior. Now, let me preface this. Not every optic nerve perfectly follows the ISNT rule, so you just have to get a sense of it, but there does look to be inferior rim thinning here. There’s no significant peripapillary atrophy. And if we look here, we can see a bit of a retinal nerve fiber layer defect. So here it’s gonna look more orange. Because the nerve fibers run on top of the retina, and sort of smudge the whole appearance of the retina. That’s why your blood vessels sometimes have a little bit of a smudgy appearance. But where there’s a nerve fiber layer loss, that nerve fiber layer is off the top of the retina, and you can see more of the orange of the deeper choroid, you can see the retinal vessels crisper, because they’re not being blurred by the overlying nerve fiber layer. So this is glaucoma. Let’s look at a couple of slides here. Let’s look at the size. So that top optic nerve — a little bit on the small side. And the bottom optic nerve is a little bit on the large side. How about here? The top one is a little bit — is pretty average. The bottom one is maybe a little bit on the small side, but pretty average. So that size… There we go. And then what about hemorrhage here? No, I don’t really see any hemorrhages. What about the ISNT rule? Let’s start on this side. Here we can see the rim edge comes all the way down to here. So this rim, the inferior rim, which should be thickest, is thinnest. And up here we can see somewhat thicker rim. There’s peripapillary atrophy. Here the rim again is not quite as thin on this side, where there’s a notch. Look at this blood vessel. It goes down and then pops back up. That’s a notch. The blood vessels are very important in looking for notching and thinning, because they’ll dip down, and then pop over the edge of a rim. So we can see the edge of the rim is right here, which is also very suspicious. So we have average size nerves. No disc hemorrhage. But certainly problems with our rim tissue, our ISNT rule. We have thinning of our rim on the left eye more than the right, but on both sides, and peripapillary atrophy on both sides. So that’s suspicious for glaucoma. Just gonna take a quick look at the questions and see if there’s anything. You know what? I think we’re gonna wait for the end for the questions, because we have a lot to cover. So that’s the quick assessment of the optic nerve. So again, most important is first assess size, then look for your hemorrhages, your ISNT rule, and your peripapillary atrophy. Visual fields. Visual fields help us defect glaucoma defects and determine progression. So we use visual fields to determine if the visual field is reliable, and then we need — before we even assess the defects, we need to know if they’re reliable and consistent. And then is the visual field abnormal, and then is that abnormality — that specific abnormality — reproducible? Anyone can have a mistake or an abnormality on one visual field. We need to know if it’s reproducible. And then is the defect that we’re seeing from glaucoma? And we’ll just go through this. So is it reliable? There are many reliability indices. But the most important is your false positives. Your false positives are assessed by patients — have a measurable threshold. They actually press the button and see a light. Forgive me. That’s a mistake. So false positives are when the machine makes a clicking sound and the patient presses the button when no light is shown. So if someone is just pressing the button when there is no light, this is the best measure of a poorly performed test. False negatives occur when there is a measurable threshold one time, and then they go back and test that same spot again, and the patient doesn’t see it. So false negatives can sometimes increase just from glaucoma, because there’s more inconsistency in the visual field. So you can have elevated false negatives and still have a reliable field, and in fact, the newest versions of the Humphrey visual field test have removed false negatives. So really mainly look at your false positives. Because if your false positives are high, the patient is just clicking away, and that’s not a reliable field. Fixation losses are when they shine a light and measure where the blind spot is, and later in the test, the patients will see that spot where they shouldn’t. So a fixation loss means the patient can be looking at the light, but it can also mean that they tilt their head, which will shift where their blind spot is. So again, fixation losses can be a measure of inconsistency, but it also can just be a mistake. So again… Oops, sorry. The most important measures of reliability are your false positives, and if you have an eye tracker, you can see if the patient is looking around a lot. So false positives, and if there’s an eye tracker available, those are the two most important things to look for. Are the visual fields consistent? You want to make sure that you’re comparing the same exam type. On a Humphrey, this is a SITA standard. It may be different than a SITA fast, or a SITA faster, which is available now. You want to make sure you’re comparing the same stimulus size. You can’t compare a size 3 stimulus, which is the standard, to a size 5, which is what we use when people have diminished field or diminished acuity. The field size can be 24-2, which is the standard, but sometimes we do a 10-2, which is a central visual field. And pupil size. This used to be very important, when we used a lot of pilocarpine, years ago. But if your pupil size is less than 2.5, it’s going to affect the field. Once it’s greater than 2.5, it doesn’t matter if it’s 3 or 5. The field should be consistent. And refraction. You want to make sure the patients have the correct refraction with the correct mirror add for the test. So when you have a bad test, always check to see if the correct refraction was used. So is the visual field abnormal? The more clustered points, the more adjacent points in the same hemifield, the more that is a measure of abnormality. You want to see that it’s in a nerve fiber layer distribution, that it’s an arcuate, that respects the horizontal. The deeper the defect, the more likely it is truly abnormal. And the more reproducible. So you need to be able to look and see that same defect. On one or more visual fields. So again, here’s an example of a patient that had a defect. It was clustered, and it was in one hemifield. You get the impression that it’s not emanating from the blind spot. Arcuate defects should emanate from the blind spot, not just be peripheral defects. And then it’s retested and it disappears. And the majority of abnormal — of first abnormal visual fields in the ocular hypertension treatment study reverted to normal on subsequent testing. So reproducible is important. And then: Is the defect from glaucoma? This is a patient that did have glaucoma. But then had an occipital stroke. So this defect… Sorry… So this defect is progression, but it’s not progression because of glaucoma. It is — the patient has a homonymous visual field defect from an occipital stroke. And then progression. We look for change over time. And you can just scan multiple visual fields, and look for it. The Humphrey visual field has a program called GPA. The glaucoma progression analysis. And here they take the patient’s own visual fields, and they make that a baseline, and then compare subsequent tests to the patient’s own baseline. And here we can see the patient was relatively stable at first, and then developed a superior arcuate nasal step defect, and then an inferior defect, so had progressive, ongoing loss. And that will show you — in points that change from the baseline, it’ll give you an open triangle the first time it sees that abnormality, a half filled triangle the second time it sees that abnormality, and a closed triangle the third time. And when you get three adjacent closed triangles, it will say definitive progression. But you can certainly start to see that this progression is of concern here. And then this plot on this graph — it plots the visual field, the VFI, the visual field index, which is a measure mostly of localized loss, and we can see that it’s — the defect is increasing. I think I’m gonna go past frequency doubling perimetry. Some people may have this. It’s a different way of measuring the visual field, rather than just with light. One of the nice things about it is that it can be done in ambient light, without a patch. And it is quite accurate and sensitive, and it corresponds usually with the defects we see on other types of perimetry. And this can be done — this is a quick screening, done in a minute, just to give you a sense that there’s a problem there. But a normal visual field does not mean that the patient doesn’t have glaucoma. In early glaucoma, you may not see a visual field defect. Particularly if you have generalized loss. So in glaucoma, you can have localized loss. Or you can have just a little bit of glaucoma damage everywhere. In generalized loss… (dog barking) Oh, sorry. I have a dog in the house, if you heard that. In generalized loss, you may not see a visual field defect early. But in localized loss, you will start to see it a little bit sooner. But there can be substantial structural damage that may exist before it’s detectable in visual field testing. So here it’s showing… Maybe there’s a little something brewing here, with early structural damage, and then when it really breaks through, and there’s localized loss, you’ll start to see the arcuate defects. So you can have loss of your nerve fiber layer. That’s progressing. And loss of your disc tissue that’s progressing. But the visual field may not find that at first. But then once it finds it, the rate of decline can be quite steep. So you want to try to find things before you get too far along on this curve. And this is an example of a patient that has glaucoma on this side. On the right side, things look pretty good. Normal sized nerve, good rim tissue, top and bottom. Maybe a little bit of peripapillary change. Sometimes it’s a little hard to distinguish some peripapillary change from a little bit of a crescent. On the other side, though, there’s some loss of the nerve fiber layer, there’s a disc hemorrhage, there is definitely peripapillary change, and we can see on this older OCT, the nerve fiber layer is normal on the right, but certainly some abnormality inferior on the left. But we look at the visual field, and the visual field on the right eye was normal. And on the left eye, maybe you’re starting to show just using statistical analysis — you can see it, but just looking at the field, you might not appreciate that there was anything wrong here. So again, you can get some loss in nerve fiber layer, and have either none or very subtle defects in the visual field. So structural damage can often be identified before functional damage. So that’s where it’s really important to do your clinical exam, really look at those optic nerves. If you have photos, use them, and if you have availability to use OCT, use your OCT, because OCT is going to give you a sense of if there’s damage earlier than visual fields. It provides qualitative and quantitative information about the optic nerve and the nerve fiber layer. It can help you assess glaucoma, and the structural-functional coordinates helps you with diagnosis, progression, identifying where the abnormality is, and it helps distinguish glaucoma suspects from glaucoma. There is excellent reproducibility, excellent correspondence with what you see on exam or in any kind of photography. And there is also a lot of statistical software that has now been developed, particularly on the Cirrus OCT, that really helps with progression over time. The thing that we look at first is usually the TSNIT scan. And that is just — you can see the ISNT in here. It’s temporal, inferior, superior, nasal, temporal. It’s the measurement of the nerve fiber layer in a ring around the optic nerve. You sort of snip that ring, you lay it out on a graph, and it gives you the height of the nerve fiber layer, around the optic nerve. And here we can see there’s a defect inferiorly in the right eye, and that’s showing up here. So it’s color coded. When they’re making all these assumptions about what’s normal and what’s suspicious and what’s abnormal, though, we’re comparing that patient to a normative database. And there are many limitations to the normative database. First of all, the number of people in the normative database for all the instruments is surprisingly low. It’s improving over time, but it is low. It does not include children under the age of 18. So there is no normative database for children. And it doesn’t include high refractive errors. So one of the groups of people that we would like to use this on the most are patients with high myopia in particular and patients with high hyperopia. It’s sometimes hard with high myopia to distinguish between what’s normal and what’s abnormal, and the OCT doesn’t always help us there, because there are different patterns of loss in high myopia. The humps of the superior and inferior nerve fibers are sometimes overlaid. And there aren’t a lot of ethnicities in the database. Most of the participants are White. So you have to be aware of what database is used and whether or not it’s generalizable to your population. Also a lot of them don’t have wide variability in the size of the optic discs, tilted, anomalous optic discs will also not be… Will not be easily measured and compared to their normative database. But one thing that you can always do is take a baseline for your patient, and use your patient’s baseline as that patient’s normative, or just their baseline. Because glaucoma is all about progression over time. So if you are not sure — if you get a suspicious-looking normative database, but the patient doesn’t have a lot of other risk factors, watch that patient, if you have ability, to follow a patient with OCT over time. Then you have time to make an assessment. As long as you have confidence that that patient will come back. You can use their baseline. Just look for change over time. And also always remember, with a normative database, you would expect one in 20 normal eyes to fall below the green zone. So in reliability, the different machines have different ways of looking at reliability. You certainly want to look at signal strength. This is on the Cirrus. On the Spectralis, there’s something here. The Q score. You want it to be, I believe, in the 20s. But you need to also look at the scan. So with the signal strength, you want to be 7 or above on the Cirrus. But you need to look at the quality of the scan. Look at the measurements, make sure there are no shifts where the patient moved their eye and looked away, and look at the quality of scan. Make sure it’s not hitting the top. Make sure it looks like a good quality scan, that there aren’t any unusual artifacts. You also want to make sure there are not any big black boxes here, which means they just didn’t measure in those areas. This is a nice normal scan. It’s a good quality. It has good double humps on both sides. This is the same. And then we can look at structure and function. And that’s one of the beauties of the OCT. It really can help us compare. Here we see the dotted line is the left eye. There’s a problem with the superior nerve fiber layer here. And you can compare that both to the normative database and to the patient’s other eye. And here we can see on the actual scan this red area is showing that that’s the area of abnormality. So again, this is the ring that this — the TSNIT scan covers. The ring around the optic nerve. But you can also look at the Q on the Cirrus. So this patient in the left eye has diminished superior nerve fiber layer, and we can see that as diminished inferior field of vision on that side. The Cirrus also has something called the ganglion cell complex, and other instruments have something similar, where it looks in the macula at the thickness of the ganglion cell layer. And we can sometimes find defects in the ganglion cell layer before we see that in the nerve fiber layer. Particularly in myopes, particularly in people with normal pressure glaucoma. And that corresponds to the earlier central visual field defects we see in these patients. Here we see in the right eye inferior nerve fiber layer loss here. We can see it in the TSNIT scan here, in the measurements down here, and we can see it in the macula of the patient. How it has an arcuate pattern, extending right to the macula. And this patient has a superior defect, with a little bit of central involvement early. We’re gonna just move through this for a moment. Here we have what looks like pretty normal nerve fiber layer on both sides, but it is a little bit asymmetric on the left. We can see it’s still coming up green on both sides. So if you do a quick glance at this, it may look perfectly normal, but we can see some asymmetry, with the left side having lower nerve fiber layer inferiorly, and maybe a little something brewing here. Certainly showing it to you in the cup a little bit also. And when you look at the ganglion cell complex, again, we can see some defect in that left eye, inferiorly. And that corresponded to a superior visual field defect that’s juxtafoveal. And again, we can see even in 10-2 visual field. And sometimes if you have very thin focal defects on the nerve fiber layer, it may not show up in that ring scan. Here you can see it a little bit, subtly, here. You can see it if you look at the scan itself. But if you just looked at the TSNIT curve and the little plots here, you may miss it. And this patient already did have a little superior visual field defect. So unfortunately OCT is not that helpful when the glaucoma becomes advanced. When glaucoma becomes advanced, it bottoms out, and we say it “hits the floor”. And then you won’t see progression. And that can happen between 40 and 50-ish microns. In both eyes. And then it’s not that helpful to follow the nerve fiber layer OCT. You sometimes can follow the macula OCT a little bit longer, but at this point, when it gets this advanced, it’s much more important to follow visual field, and in this case, I would follow a central 10 degrees, and maybe even a central 10 degrees with a size 5 stimulus. There are wonderful progression programs now. Just as we see with visual field, there are OCT progression programs, where you can look at scans over time, you can look at statistical analysis over time. Here is, again, visual fields over time. And then I’m just gonna go through here. With the OCT and the Cirrus, it has wonderful programs, where you can compare the scans from the two baseline tests to the current test, and we can see changes, and decreases. And we can see here it gives you a whole table. Where you can see when there’s statistical change over time for your average, inferior, and superior rims, and you can also scan up here, and these abnormalities that are being shown are changes from the patient’s baseline. Not versus their normative database. So OCT program — progression programs have greatly improved. Many other OCT instruments are also very helpful. The RTVue has very similar types of tracings. I don’t want to spend too much time on this. And they have also very good progression programs and ganglion cell measurements. So OCT is excellent at detecting early glaucoma. It may be difficult in the presence of medial opacities, such as cataract, corneal disease, or vitreous hemorrhage, but it is not very useful in advanced glaucoma. And you still need a good scan, just like you need a good reliable visual field. Any test that you do, the first thing you need to assess is: Is this a reliable test? Are my subsequent tests comparable to my initial test? At this juncture, let’s go through those questions again. And then we’ll open it up to discussion. Which of the following is associated with a decreased risk of glaucoma? Low blood pressure, Asian ancestry, thick cornea, or disc hemorrhage? That’s right. Thick cornea. Very good. So when you have a thick cornea, the intraocular pressure is falsely elevated. And so there’s a decreased risk. The other low blood pressure — disc hemorrhage are certainly associated with increased risk of glaucoma and Asian ancestry is associated with increased risk of angle closure glaucoma. When checking IOP with Goldmann applanation tonometry, the mires should be as thick as possible, directly align, inner edges align, or outer edges should align. We should have some music playing. Very good. You want to align those inner edges. And if you have staff that checks your pressures for you, please ask them this question. It’s always very surprising to me that even senior technicians that I’ve met for the first time, when I ask them this, many of them get this wrong. So please work with your staff to make sure that they’re aware of this as well. In gonioscopy, it’s important to perform gonioscopy in myopes, in hyperopes, in eyes with shallow chambers, in anyone diagnosed with glaucoma, in eyes with high intraocular pressure, or all of the above? Yay! 100%. Great. So yes, it’s definitely angle closure and narrow angles are more common in hyperopes, but it can develop even in myopes. You may not want to check every time you see a myope for sure, or even every time, but you want to have a gonioscopy on record, and if there’s anything suspicious, follow it over time. Glaucomatous visual field defects typically have the following characteristics: Respect the vertical meridian, cluster in arcuate pattern, spare the paracentral area, and are easily distinguished from defects that develop after a branch retinal vein occlusion. Very good. So glaucomatous defects cluster in arcuate patterns. They follow the nerve fiber layer pattern. Branch retinal vein occlusion can cause a defect that also looks arcuate. Any defect that respects the vertical meridian you need to be cautious about a central nervous system defect. Retrochiasmal defect. Glaucomatous defects don’t typically respect the vertical meridian. And features of glaucomatous optic nerves include notching, saucerization, disc hemorrhage, peripapillary atrophy, and generalized loss. Or all of the above. Great! Another 100%. Yes, these are all features of glaucomatous optic nerves. Notching, the rim can be saucerized, generalized thinning, peripapillary atrophy, or generalized loss. So I just want to mention that it is very important to look at your optic nerves, to really think through the whole patient. Think about their risk factors, think about their pressures, how that might contribute. Really look at the optic nerves, and if you can assess visual fields and OCTs, make sure that they’re consistent with glaucoma. And reproducible and reliable. Thank you so much. I think I will stop my share now. And Q and A. Okay. So there have been a few questions, and if anyone else has questions, please type away. So the first question is: Should I start antiglaucomatous therapy while doing other investigations? It matters… So a lot of this matters how likely you are to be able to follow the patient over time. So if you are able to follow the patient over time, and if things don’t look severe, you can watch for a little bit. Most cases of glaucoma are very slow, so you have a little bit of time. And so you want to balance the risk of starting someone on a treatment for life that they may not need versus waiting a little while. Certainly if a disc looks advancedly cupped, or if you’re very worried or if you’re not sure that patient can come back in a timely way, you can certainly start medication. Otherwise, it is nice to get a few pressure readings before you start treatment, if that is an option. So the next question is about a 2-year-old child that’s been diagnosed with glaucoma. That was on Combigan and dorzolamide, but the pressure is still high. The parents apparently can’t bring the patient to a higher center, so what other treatments are suggested? Again, I know in different countries, there’s different availability to medications, but a prostaglandin analog is fine for children, and if the angles are open, which you’re not gonna be able to assess clinically in the office with the child, but you can try prostaglandin analogs… You know, in children — I really need to know a lot more about this child before I can say definitively. Because if it’s congenital glaucoma, you may really just be moving on to a surgical procedure. And there’s no substitute for that. In a child with congenital glaucoma. The next is about diaton tonometer, and I’m really sorry. I don’t know what a diaton tonometer is. So I’m gonna have to pass on that, but we can look it up and maybe get back to you. The next is about measuring pressure in two meridians in high astigmatism. Are you calculating the arithmetic average? Yes. And at what level of astigmatism do you start doing that? Yes, you take the average of the horizontal and vertical meridians when you have a patient with astigmatism. And I usually do that when I see any mires that are not typical. So if they look a little steep, or a little bit splayed, I will measure in the two meridians and take the average. So I usually don’t look at the chart, at the refraction, and see what the astigmatism is. I look at what the accuracy of what the mires look like on the tonometer and take the mean. Does a large optic nerve represent a protection factor for glaucomatous development, and can a large disc size mean it will never develop glaucoma? No. Thank you for bringing this up. This is very important. A large optic nerve is not a protective factor. It just means that the patient at that period of time may not have glaucoma, or you need to take the size of the disc into account if there’s a large cup, but patients with large optic nerves can still go on to develop glaucoma. And it brings to mind one patient of mine who I followed for ten years with suspicious optic nerves, and then went on to develop progressive glaucoma damage. So I’m so glad you brought that point up. Patients with large optic nerves can still get glaucoma. What are the tests for prodromal stage and stage of constant stability? I think what I understand is being asked is: What are the best tests for early stage versus looking for progression over time? If you don’t have access to OCT and visual field, you can watch the optic nerves. It is harder to do, like, detailed drawings, but you can just watch the optic nerve, and that can give you a lot of information. And for those people that have OCT and visual fields, I certainly encourage you still to really look at the optic nerve. You can’t just rely on your tests. Everything has to coordinate. You’re testing with your clinical exam. But earlier in disease, OCT is more valuable than visual fields. In advanced disease, visual fields become more important, and OCT is not helpful. And in the middle stage, both OCT and visual field can be helpful. So a primary open-angle glaucoma suspect is somebody — so the question is what is a primary open-angle glaucoma suspect, and how do you follow such cases? A primary open-angle glaucoma suspect is anyone who has some of the risk factors or some of the indeterminate findings that we’ve discussed. So people with risk factors, be it high intraocular pressure, or narrow angles, or family history, or maybe a little bit of suspicious findings on visual fields, or inconclusive appearance to their optic nerves. You’re not sure. Is that a normal optic nerve or not? You can follow people. If you’re trying to figure out if they have glaucoma, then they don’t have advanced glaucoma. And then you have time. You have time to watch people over time. As long as you feel confident that patients will come back. And it’s very important not to say: You don’t have glaucoma. Let’s see you in a year. You have to say to them: I’m concerned that there may be a little bit earlier glaucoma, or that you’re borderline glaucoma, and it’s very important that we watch you over time. And then just look. Glaucoma is all about change over time. So if you have a suspicious-looking optic nerve, and you’re not sure, you have some time to watch it. As long as people can come back. So I mentioned… So someone refers to a no-cup disc. And that’s usually a very small optic nerve, where all the nerve fibers just squish through it. So it asks me: When you see this for the first time at a comprehensive evaluation with clear margins and normal color, do you do anything? What happens when in a previous eye fundus the patient you see had 0.1 or 0.2. So what I think you’re getting is that you’re concerned that the disc may be swollen. You’re seeing a patient that you thought had a 0.2 cup one time and then comes back with no cup. So you have to first determine if… Did you assess them the first time? Do you call everything the same? Because there is a lot of inconsistency between how one person describes a disc and another person. But if you’re worried that there may be disc swelling, certainly the things you mentioned about having a sharp rim, that the nerve fiber layer is not — the peripapillary nerve fiber layer is not swollen. And you can tell that there’s swelling of the peripapillary nerve fiber layer when it blurs the vessels crossing over the edge of the disc. So if you lose the contour of the vessels as they cross over the disc, that’s certainly of concern. So I showed visual fields, 30-2 and 24-2. Are you starting with a 30-2 and switching to a 24 at some point? In general, we just do 24-2. So it’s very rare to do 30-2. I may have had some 30-2 because that’s what was done in the ocular hypertension treatment study, but there’s great variability around the edge ring, so I would stick with 24-2 as your baseline standard test. What do you consider a relevant decrease in retinal nerve fiber layer thickness from one measurement to another? Are you waiting to get into the red? So a good point is that you can have diminished nerve fiber layer, and it can all stay in the green, compared to age-matched controls. So you want to look for progression against that patient. And we’d like to think that all these instruments are incredibly reproducible, but you have to look for consistent change over time, because we have seen even 5 micron or more changes in a patient from one test to another that reverses. But if you can see consistent ongoing loss over time, that’s what’s important. But we call that “green disease”, when people get worse, but are still within normal limits. It can be progression and change, but it’s still within normal limits compared to age-matched controls. But if you compare that patient to their own baseline, it will show progressive loss. How do you manage a glaucomatous defect observed for the first time on OCT with no visual field loss? So if you see a defect in your OCT, and the patient has no field loss, you have to take a look at that patient first of all and see if there’s any reason to see that OCT. To see that defect. One, you want to make sure that that OCT is reliable. So you want to look at the quality of the scan. You want to look at the actual scan and see if that defect, that abnormality, is in a nerve fiber layer pattern. But you can certainly get OCT defects with no visual field loss. But you just have to see if it correlates with the clinical exam. So I saw young children with a cup to disc of 0.8 and a pressure of 10 to 14. So they were concerned that they may be steroid responders who were not detected. When I see them… Vernal keratoconjunctivitis is already burned out and not needing treatment. How should I approach their care? I think the first thing I would do is go back and look at that child again and see if they have a large optic nerve. If you have a large optic nerve, you can have a cup to disc ratio of 0.8 and it can be normal. It matters how young the child is, and if you have availability to do a visual field. Some young children are much better at visual fields than my adults, because they’ve played on video games, and are just good observers. So you can always try a visual field. But a cup to disc ratio of 0.8 is not necessarily glaucomatous. It may not be burned out steroid responder. It may just be a large optic nerve. But you have to go back and assess the size of the optic nerve. I should have mentioned also that if you have OCT available, you can see the size of the optic nerve on the OCT. It will tell you the size of the nerve, and that gives you a great accurate reading of whether or not it’s a large or small optic nerve. So that would be my first piece of advice. Is to check the size of the optic nerve, to see if the cup to disc ratio of 0.8 is significant. How reliable is a visual field performed once the patient is dilated? The most important thing is to be sure to get the full near add. You can do it postdilation, and while a very large pupil can cause a little bit of distortion, the biggest issue is that you need to give a young person a full near add. And that’s why a lot of people, when they get dilated visual fields, they’re not reliable-looking. It’s because they were not given the full near add. So if you have to do it once they’re dilated, put the full near add in, but then ask the patient: Does the fixation light look clear? And if not, you can sort of switch in and out lenses. Do a quick little refraction in the perimeter, to make sure the fixation light looks clear. But you can’t just put it in and get the age-corrected near add if they’re dilated. They usually have to have a full near add, which is usually about +3. 25. (dog barking) Sorry. The mailman is here. Which evaluation method should I rely on most for diagnosing early glaucoma IOP and disc assessment? So I think what this person is asking is: Is there one thing that is most important? And unfortunately with glaucoma you kind of have to do the whole thing. You have to look at the whole patient. Really look at their risks. Certainly the disc is the heart of the issue. But again, it’s sometimes hard to evaluate what’s normal and what’s abnormal. So really look at the disc, but really try to get a picture about the whole patient. The next is about accuracy with the pneumotonometer. Pneumotonometers are great, really great. How important is fluctuating IOP reading, both diurnally and between eyes, more than 4 millimeters, when all investigations are normal? Very good point. Variability of intraocular pressure readings is an important risk factor for glaucoma also. And asymmetry. So if everything else is normal, I would just watch that person as a suspect. But you can certainly add that to your list of risk factors for glaucoma. If there’s greater variability and asymmetry. So the next is: Can you comment on how you incorporate 10-2 central visual field testing into your glaucoma workups? They’re asking is it for early or suspects, where the ganglion cell analysis shows defect, rather than relying on 10-2 only for advanced cases. That’s a very, very good point. If you see a ganglion cell defect, I would suggest doing a 10-2 visual field. Normally I do reserve it for the more advanced cases, or for the myopes that have earlier juxtafoveal loss. So you can have a visual field that has just an early central defect. And again, we see that mostly in myopes. And then I do a 10-2 visual field even if they don’t have advanced glaucoma. But your point is very good. If you see a patient that has an abnormality, an arcuate clear abnormality on the GCC, the ganglion cell analysis, on OCT, it would be very nice to get a 10-2 visual field for that. May I follow the patient only with OCT in beginning glaucoma? Yes. So early on, you can just use OCT. So when I have early patients, I do tend to lean more towards OCT. If available, I like to get people started on visual fields, just so that they get experienced with it. And it’s probably good to get a baseline visual field. But if they are very low risk suspects, you can certainly just do OCT. How to deal with large cups in children with normal pressure? Will 24-hour IOP check help catch the higher pressures? So again, this comes back to whether that large cup in the child is glaucomatous or a normal variant. And the first thing I would do is go back and assess the size of that optic nerve. And then if the optic nerve is large, look at the health of the rim all around. It can be thin. It can be a 0.8 cup with thin rim all around, but in a large optic nerve, that can be normal. So yeah, 24-hour pressure checks can help catch pressures, but if you’re sitting the patient up to measure the nighttime sleeping pressures, you’re going to lose the elevated pressure that happens when people lie down. But I think the biggest issue is, again, looking at the size of the nerve and trying to figure out if this is physiologic or not. OCT can then also be helpful. How often do you encounter regressed glaucoma, and how do you confirm diagnosis? The most common scenario we see for regressed glaucoma is pigmentary dispersion. So some people that have pigmentary dispersion, which is most common in 20 to 40-year-olds, will “burn out” and regress. One way we see that is normally in pigment dispersion there’s 360 degrees of darkly pigmented trabecular meshwork. That pigment over time tends to clear inferiorly, before superiorly. So if you see a dark band of pigment in the superior trabecular meshwork and nothing — light pigmentation inferiorly — that may be a case of burned out pigmentary glaucoma. Other than that, glaucoma doesn’t often regress. It often worsens over time. And the next is: What factors do you consider to set a target intraocular pressure for normal tension glaucoma treatment? If a patient has progressive normal tension glaucoma, we certainly want to have a good sense of what their baseline pressure is. And aim for a 20 to 30% decrease in pressure. That’s sometimes hard when you’re starting with normal pressure glaucoma, but first determine if the glaucoma is progressive, because the collaborative normal tension glaucoma treatment study showed that a very high percentage of patients with normal tension glaucoma did not progress over a 7-year period. But certainly the risk factors… We didn’t talk also about blood loss — can sometimes be a factor in normal tension glaucoma. Also see if there were any factors that may have been present that aren’t present now. Like an acute blood loss or a surgery, where they may have been ischemic, or any time they might have been hypoxic, that is not happening now, or prior low blood pressure that is now better. So look for factors that may not be currently present, and then you can also then be a little bit more lax on your target. Next: In children, age 6 months, with normal pressure and normal corneal diameter, but there was total cupping — so is this a case of glaucoma? These kinds of questions are very, very hard to answer. There certainly could be congenital anomalies, congenital optic nerve hypoplasia, and there can be things that happened in the past, so I think it’s a bit out of the scope of this talk. The role of total deviation and pattern deviation on visual field in deciding whether a patient has glaucoma or not. So I would love to cover this in a full glaucoma and visual field lecture. But total deviation tells you every point in the visual field that is deviated from age matched controls. Pattern deviation highlights, brings out, the localized defects, and gets rid of the generalized defects that can sometimes be from cataract or refractive error. Sometimes generalized loss can be from glaucoma, but most often it’s from media opacity or incorrect refractive error. So the pattern deviation on the visual fields is most important in determining whether or not a patient has glaucoma. What does an enlarged blind spot indicate on visual field test results? It can mean that, one, you have a very large optic disc, and you’re seeing an enlarged blind spot. It can mean that the patient has extensive peripapillary atrophy, because that will cause a blind spot around the optic nerve as well. But you want to make sure that the blind spot is not coming from papilledema and optic disc swelling. Yes, that person is asking: is that my dog barking? It is my dog barking, yes, and the mailman came during the lecture, so there was a lot of barking. Can you please recommend some books about OCT and glaucoma? Let me look that up, what’s the best reference at this point. And we can answer it through Cybersight. And the next is: Oh, are we allowed ethically to treat the patient who is a glaucoma suspect? Yes. So if you have a high risk suspect, then you can treat that patient, to decrease their risk of developing glaucoma. So it really — it matters how high risk the glaucoma suspect is. But yes, it is ethical not to wait. The ocular hypertension treatment study supported that. That if you have a high risk glaucoma suspect with ocular hypertension, that particular study looked at ocular hypertensives, that you could decrease the risk of developing glaucoma by treating them earlier. So yes, it is ethical in high risk suspects. What is the differential diagnosis you think about when you first notice a normal tension glaucoma suspect? That’s a whole lecture in and of itself. But we think about… In the differential diagnosis of normal tension glaucoma, we think about prior episodes of elevated pressure, did they have steroids in the past, did they have stroke episodes, did they have low blood pressure. But let’s maybe set up a time to have a normal tension glaucoma lecture. In patients who do not follow the ISNT rule with prominent notching but with normal pressure and normal OCT on visual fields, how do you manage? So if you have prominent notching, you have to be very concerned that there may be a problem. The only time you should see anything that looks like notching, but is not glaucomatous, is maybe a very tilted optic nerve. Some tilted optic nerves can look like there’s notching. Sometimes you can have congenital defects that are notching. But many patients that have normal pressure glaucoma have notching. But you should then see an abnormality on the OCT. So when in doubt, you can follow people for time. If the visual field is normal and the OCT is normal, you can watch that person and make sure that they stay stable. What type of field analysis is most appropriate in children? Most children can do a 24-2 SITA Fast. It takes maybe three minutes. And now there’s SITA Faster, which really — they’ve taken out some of the extra testing that was done for blind spot testing and false negatives. And it goes very, very quickly. And if you have a cooperative child, a lot of children can really do very good visual fields. But I would do a SITA Faster if you’re using a Humphrey visual field. And someone is asking for contact for exchange with some patients, and Lawrence, perhaps you can put that up through Cybersight. I can also post an email, if that’s appropriate, with Cybersight. So I’m gonna leave that up to Lawrence. And Orbis to decide. Well! That was a lot of… Ooh, more questions. And I think we’re gonna have to make these the last couple of questions. Do we treat normal tension glaucoma in children? So the question is… Whether this is truly normal tension glaucoma. Normal tension glaucoma is very, very unusual in children. So there are some congenital abnormalities of the optic nerve that can give focal loss. I remember having an 11-year-old that had a coloboma of the inferior optic nerve. And it looked just like — I kept thinking when I saw that child, if I saw that patient for the first time when they were 50 years old, I would think that they had normal tension glaucoma. But she had a coloboma. And that’s why it’s important to watch people over time. So it would be very unusual to have normal tension glaucoma in a child. So I would look for whether it’s a congenital abnormality or something else going on. What follow-up process do you follow to assess large cups suspicious with normal IOP? Again, my apologies for my dog barking. I watch the optic nerve. And also if you have OCT available, you can look for sequential OCTs. And also visual fields. So it’s pretty much the usual. So you’re gonna watch them as you would watch any other glaucoma suspect. Thank you so very much. I am active with Orbis, and if there are any issues, please do contact Orbis, and I would be happy to go over anything else. And it’s been a great pleasure and an honor to be able to spend this hour and a half this morning with you. Thank you again.
April 29, 2019