 Okay, so secondary open-angle glaucoma, and I'm going to start with a little bit again just to review. You guys have been hearing this nonstop, but multi-factorial progressive optic neuropathy with characteristic loss of retinal ganglion cells and atrophy of the optic nerve. And then we usually think about IOP dependent and non-IOP dependent, and IOP is just a risk factor. So characteristic patterns of optic nerve damage, and we went through this last week, and visual field loss. Who couldn't remind everybody what type of visual field loss you get? Arq. What else did I hear? Paracentral scatoma. Paracentral scatoma. That's a classic. Nasal step. What's the top three causes of nasal step? Glaucoma. Glaucoma, glaucoma. Very good. Paracentral island also, you know, keep that in mind when you see these patients. And you can even get, you know, a lot of times too, you can get almost a, basically a hemifield defect as well, but superior arc and inferior arc are also pretty classic. What other things would you want to look at? So they've got identifiable contributing findings of secondary open-angle glaucoma. What does secondary mean? What's the difference between primary and secondary? Nico, you'd like her about to talk. Yep, secondary. You know, there's like a mechanism that's causing optic nerve damage in high IOV. In primary, it's a wide definition of idiopathic, where we can't find anything. We can't find any underlying cause. So, dysfindings, anomalous vessels, remember, keep in mind, you know, the disc can look asymmetric because there's anomalous vessel pattern. During embryogenesis, the way these central artery and central at the vein end up basically being formed and then diverging. And that can give you very different looking optic nerves. Does a small cup to disc rule out glaucoma? So can you have glaucoma with 0.1 and 0.3 in the other eye? Absolutely. And can you not have glaucoma with 0.7 and 0.8? So you have to look at the rib. You have to look at the whole, it's the totality. And obviously with secondary, it's really that history and it's going to be that clinical exam and angle findings are really important. So dischanges, we talked about this the other day, and again, cupping or what we refer to as cupping, deep, large suspicious cups. You can have normal cups, you can have not a deep cup, and it's really the progressive loss or change to the neurofiber layer. So it's the rim. Notching, nasalization of vessels, but none of these are all really pathodemonic. I think the way we're starting to think now, it's adrense hemorrhage or neurofiber layer or diskeying hemorrhage that really becomes more pathodemonic. What do you think about if you see a hemorrhage? What's the first thing you should think about? Really simple. No pressure. No pressure? What about the pressure's fine? Basically, Pat, what? Still uncontrolled. You see a hemorrhage, their glaucoma's still uncontrolled. So what's happening? What's changing? And we've changed from, when we see a hemorrhage, we've changed our work up a little bit away from just IOP to what else is going on? Do they have sleep apnea? What's their blood pressure? What other contributing factors? And it's always good to ask, are you on an anticoagulant? What else could give you a hemorrhage in the retina? Diabetes, what else? Hypertension? Vain inclusion. Vain inclusion? You know, an impending vain inclusion. You may be able to see a few other hemorrhages along the way and then say, OK, this is a vascular vent. Mastrofe? Also, somebody is coughing, sneezing, you know, and if they're on an anticoagulant, they can get hemorrhages anyway. So it's just another thing to keep in mind. But generally, a neurofiber layer hemorrhage on the disk is uncontrolled glaucoma, even if their pressure is 16. And what else do I have here? Just some progression of optic nerve damage over time. How long do you think this would take to occur? So the first thing you should ask me is, well, Dr. Roscoe, is it a pressure of 20? Or is it a pressure of 40? So let's say it's a pressure of 20. Think about the studies we talked about last week. They started to see neurofiber layer changes and visual field changes and optic nerve changes over. How long? Board question, 1 to 5, 5 to 10? What do you think? How many think this would progress at a pressure of, say, 20 over five years? How about over 10 years? Generally longer. It's a slowly progressive optic neuropathy. But if that pressure was 40, then maybe it could be over, I would hesitate to say maybe a year, two years, three years. But it's going to be much more rapid. And then again, up in that first photo, in photo A. So that optic nerve on the right-hand side could very well be glaucoma. You may look at it and say, oh, that looks normal. But that could be a glaucoma's optic nerve. Morning, Lee. So again, visual field changes. We talked about all the different things you could see. So you've got your paracentral scatoma. You've got your nasal step. You've got your hemorrhage, central island. The other thing too, and I think I talked about this the last time, if you see a hemorrhage, definitely do a central 10. Because you may miss a neurofiber layer hemorrhage. So the large studies that were recently completed, the adage study, showed that if you had a disc hemorrhage and did a 24-2, that visual field was normal. But if you did a central 10, you actually did see some early damage. And you did see damage within the central 10 degrees, which I also thought was really interesting. So secondary causes. Well, let's go through some of the secondary causes. So Nico said we have to have, it's a reason to have the glaucoma. It's a reason to explain why you have elevated IOP, or optic nerve damage. So something I love, exfoliation or pseudo exfoliation. Pigmentary dispersion. Lens-induced glaucoma. We'll go through some of these. I personally still get them confused. Every time, I just got to go back and memorize them. But they like them on the boards, because it does kind of confuse you. Basically, when I look at these fecalitic lens particles and fecal antigenetic, I mean, the key thing to me is got to get rid of the inciting factor, whatever that is, whether it's the cataract, whether it's the remaining lens particles. And there's a lot of times an inflammatory component. Tumors. Always think about tumors. If you see, OK, we'll get to that. I'm going to give you guys some ideas. Inflammation, trabeculitis, fuchs, posnarslasmin. I've actually seen one case of that. That's really cool. Posnarslasmin, we really don't understand it. It's really interesting. Elevated episcleral venous pressure. Think about that as well. Look for dilated torturous episcleral vessels and trauma. Hyfema, angle recession, steroids. Always ask about steroids. Always ask about trauma. Were you ever on steroid drop? Did you ever have inflammation in your eye years ago? Did you ever have surgery years ago when you were on a topical steroid? And then trauma, angle recession. Always goneo. How do you make the diagnosis? What's the one thing you need to do to make a diagnosis of primary open angle glaucoma? Confirm the angles open. Absolutely. Goneoscopy. So secondary. Also, sneak thick facade can be insidious. When would it not be insidious? When would it not be slowly? When would a patient notice that pressure is going up? Symptoms. OK, what would give you? So I guess the question is, when would you have symptoms of high pressure? And when wouldn't you have symptoms of high pressure? Yep, exactly. That's exactly it, when the onset is more acute. So if you have somebody that comes in, so could a patient have a pressure of 40 and not even feel it? Yep, no corneal edema, right? So it's been a slow creeping. And that's exactly what we were just talking about, Beck. You know, the case of somebody who's had a PI years ago. In fact, explain, I think that's a great case. This patient comes in, had a PI in the past. Yeah, she had PIs in both of them. Well, she did have symptoms, though. She had symptoms, yeah. She had redness and pain. How high was her pressure? It was 35. It wasn't terrible. The year told me 80, but I don't know what they were mentioning. But yeah, she had PIs in both eyes, but she still had an ever-natural lens. And it was, you know, enough to cause a problem. And she just had the lens out like a year ago. But now this time, she actually won't. Did you have corneal edema? No, actually, the corneal was pretty clear, yeah. And 35, generally, if she's got good endothelial cells, they don't get a corneal edema. Pressures in the 50s and 60s, yes, absolutely. But I think the key thing there is when you have a pain in PI, you want to go to your own. You want to make sure that that angle doesn't have angle closure. I shouldn't say angle closure, but chronic angle closure or creeping PAS, perfylentyrsineakii. And if she did have that, then she may have not been symptomatic with a pressure of 35. The other thing, too, was she did, I don't know how she thought of it, but she had a bag of drops at home. She told me she gave herself a pink drop that was chloride, but that was all that I knew about. It was one of those bullets that we carry around like to clean out the PI after we do injections and things like that. Oh, really? She's sort of chloride. Yeah. But then she picked up this other drop, which was COSOFT. OK. It's so good. She gave herself a drop of COSOFT. Interesting. I'm a little better. That's pretty interesting. Good for her. So slowly or rapidly progressive, we talked a little about that can be painless. Again, if it's a slowly increasing IOP. And secondary open angle. So by definition, it is open angle. So secondary open angle, and you've got a dugonianoscopy, and you have to confirm that. We talked about can be asymmetric, but also can be bilateral, depending upon the etiology. And I guess what are some of the things to consider if it's asymmetric? Sort of went through that list of secondaries. Will it be asymmetric? What? Psyduck's filiation. Psyduck's filiation? Is it truly asymmetric though? Or I should say, is it truly unilateral? That's the question. So on the boards, they will ask you, what is the most common, I remember this from God, my board's 20 something years ago, what's the most common cause of asymmetric? Secondary open angle glaucoma, and it is pseudo exfoliation. But I don't know if they said secondary if they just said open angle. They may have just said open angle. But it's, in a sense, bilateral, but it does present asymmetric. What else would be asymmetric? Trauma. So always think about trauma. Fuchs, ice, those would all be asymmetric. And ask about the history, so family history, medical history, trauma, surgery, and medication history. And those are some of the things we talked about last time. So back to our list, exfoliation, pigmentary, lens-induced, tumors, interocular tumors. Again, always go near, look at the iris. Think about, so how would tumors actually give you secondary glaucoma? I'm sorry, what, Lee? The lens diaphragm effect would kind of... Okay, so if it's pushing forward, right? So would that be secondary open angle? Or would you see distortion of the iris and almost perhaps some angle closure? Right? So that's a little bit of a mix, but no, absolutely. Look at that iris. Look at that iris contour. So something behind the iris, ciliary body, cis, ciliary body, tumors, masses, absolutely. What else? Distortion or anatomical changes? No, but good thought. Could be causing bleeding or increased oxygen demand, which is the abascurization. You can have the abascurization, yeah? Absolutely, yes. Tumor cells are being involved. And tumor cells, yeah? Think about tumor cells too. So if you see more pigment in an angle, okay, so here's a good question. You see more pigment in an angle. What should we be thinking about? Pigment dispersion is one. Pseudoxfoliation? And tumor. Yeah, very good, huh? And trauma, trauma can do it also. So four things. So different reasons for having pigment released from the eye. But look at that angle. So if you see asymmetric pigment, definitely start to think about, well, what's giving you that pigment? So fuchs, what about fuchs? Fuchs is a cool one. The boards like fuchs, they like fuchs. I don't know if I've ever seen a fuchs. I've questioned fuchs. What would you see in fuchs? It's usually unilateral. What's a telltale sign? Heterochromia. Heterochromia, which eye is abnormal? Not gonna tell ya. Let's keep going. Oh, so totality of the workup. So we're gonna do anything different. You're gonna do anything different for your secondary open angle glaucoma than you would for your primary. Okay, right? So if you see something abnormal, the iris, you're gonna send them to Harry and have a mask and look at his, and look at the angle. Trying to think what else you would do differently. So let's go back to all our causes. Let's go through each one. Exfoliation, what would you do differently? Anything different? So what we're learning, we know it's genetic, right? So you wanna know more about a family history? Maybe you're gonna ask them. We now know that there's other elastoid type abnormalities. Actually, the work that's coming from here. So you may ask them. I always ask my patients about other things. COPD, asthma, AFib, pelvic organ prolapse, hernias, vasculopathy, things like that. Pigmentary dispersion. Yes, Lee, go ahead. For exfoliation, they're saying that the thyroid. So you would always, and all these patients do an OCT. We don't yet know if the lamina crevose is actually different in exfoliative patients. We also don't have any clues to why one eye gets the exfoliation and the other one doesn't. Because if you do conge biopsies, you will actually find, well actually, if you do biopsies anywhere in the body in these patients, you will find exfoliative material. So lungs, meninges, heart, uterus, gallbladder, vasculature, conging type of skin. So this elastoid material is all over their body. Just doesn't necessarily cause any problems unless there's some sort of stressor, is what we think. We think the stressor actually may be ultraviolet light, but that's a whole other discussion. So you would do an OCT in your head? You would always do that, yes. So in any patient with glaucoma, you're gonna look at their optic nerve, right? You're gonna do an OCT. What about pigmentary dispersion? What would you do differently? Okay, so always look at translumination defects. And we'll show some pictures of those. Always transluminate. If I can't tell you anything. Goniogonio, goniogonio. My second thing is transluminate. Transluminate. Look at their iris before you dilate them. Otherwise you will miss things. What's, so good translumination defects. What else would you do with this patient? What are you gonna look for in the anterior segment? Pigment. When would you see the pigment? When the iris has friction, so when the iris is moving, so after you dilate them. When else may you see pigment in these patients? What do you wanna ask them about? Huh? I love these exercise. These are the coolest patients. These are so cool. I remember I had a girl, she was 16 years old. She came in to see me, she was a gymnast. Her anterior segment was full of cells. Every time she went on the trampoline. Runners, basketball players, soccer players. If you are, it's not, I shouldn't say lucky enough, but because it's unfortunate for them. But they can disperse pigment. Do you think they always have elevated IOPs when they disperse pigment early on? No, no. So you can see an anterior segment full of cells and they may not have an elevated IOP. But over time, if that pigment keeps getting released, that pigment's gonna clog their trabecular mesh work and their pressure may go up. So you're gonna hear stories of, oh yes, after I run, my vision gets blurry and I get a bit of a headache. So then what you wanna do with that patient, and I just had a patient the other day do this. He's in the 60s, actually 50s. He looks like a, he looks, he's classic for a pigment dispersion, but I couldn't get him to actively disperse. You want to try to get these people to actively disperse when you wanna check their pressure. And your management is going to depend on what their pressure does when they actively disperse. So if they throw off pigment and their pressure stays in their teens, you may not do anything. They throw off pigment and their pressure's going up into the 30s, you know you need to do something. And there's a whole big discrepancy with, you know, whether or not to do a peripheral iridonomy. And I think a lot of us would still do a peripheral iridonomy if they're actively dispersing and their pigment's going up. Now you would say to me, well, why are you gonna do a PI if their open angle and their pigment dispersion? So why would you do a PI? Yep, so Bob Rich, probably back in the 70s and 80s, has shown, and actually there's some pretty cool ultrasounds now. When you do a PI in these patients, the thought is that there's a buildup of anterior segment pressure pushing the iris back, and then there's friction of the iris on the zonules because you get translumination defects in mid periphery. So if you do a PI, you're actually going to relieve that pressure differential between the anterior segment and the posterior segment. Or anterior chamber and posterior, yeah, posterior segment. And allow that iris to come forward. Does that make sense? So it's not bowing back. The other thing that's interesting about these patients, they tend to be males and they tend to be myopes. So always like, oh, and what else do, are they more predisposed to? What do pigment dispersion, what are they more likely to have if they're myopic too? Lattice. Lattice and retinal detachments actually. Retinal detachments is the key kind of keyword. And what's interesting too is it's disproportional to their myopia. So in and of their myopia, so their myopia increases them through retinal detachments, right? But if they've got pigment dispersion, it puts them at a higher risk. So we think that there may be something that's genetic that's different about their eye. So these patients also, you want to warn them about retinal detachments. Lens-induced glaucoma we'll get to, intraocular tumors we talked about, fuchs, positive schlassmen. That's a really cool one too. How do these patients present? What? Redness. Redness? Actually pretty quiet. They're always pretty quiet. But eye pain, what else? Just a genilateral. Genilateral? Men or women? Tends to be a little bit more on younger women. I always think of my pigment dispersion as my middle-aged man or younger man, although my 16-year-old gymnast didn't fit that bill. And positive schlassmen I think of more women. And maybe it's just because I saw a girl. But, and they tend to be generally younger. And they'll come in and they're actually, their eyes not too red. They're pretty quiet. But they have a little bit of discomfort, a little bit of blurring and really high pressure. Fairly high pressure. 30s and the 40s. How do you want to treat them? Steroids. It's an inflammatory cause. You're going to see these fine sort of stellate KPs, but they're not even classic KPs. But, and if you go any of them, sometimes you say that you can see, you know, some inflammatory cells in the trapeculum ashwork. But they're actually really, really pretty quiet highs. They're really interesting. And then surgical trauma. We'll talk about an angle recession. Go through this. So again, a little bit about exfoliation. It's the most common identifiable cause of glaucoma worldwide, cunning for majority of open angle glaucoma in some countries. Progression is anywhere from 15 to 40% of cases. And it's estimated that 80 million people worldwide. So where, oh, this is actually cool. Where was Lindbergh? Anybody know who, I'll talk about him in September, actually, when I present about exfoliation. John Lindbergh. There's actually a John Lindbergh society. And it's been resurrected by Bob Rich. And it's pretty cool. So he first discovered it in 1917. And he discovered it in Helsinki, Finland. And he was an ophthalmology resident who found the material, went to present and do his dissertation at that time. That's how they got their degree to practice. And he presented it as a resident to some of his professors. And they also sort of perpued him. And one of them actually took his idea and took his discovery and then went on to talk about it. And basically say that he was the one who discovered it. So came back, then it turns out, so then John actually got the recognition for the discovery. And it was in 1917, so it's been 100 years. And the other thing that was really neat, it was in Helsinki, Finland. And I recently met his grandson. And I thought that was really cool. Distinct disease, very specific mechanisms of development. But we don't know what's the contributing factor. And we know that there's a genetic predisposition. The majority of people say, oh, what gene is it? What's the gene? LOXO1, LOXO1. And what does LOXO1 do? I don't expect you guys to know this details, but. So it converts tropolus into elastin. And these patients have, they have a genetic abnormality within the LOXO1 promoter. It's actually for the messenger RNA. And it's a suppressor gene. And we're not quite sure what's going on with LOXO1. So these patients have LOXO1, but it may be dysfunctional. And in the material itself is LOXO1. So it seems like something is wrong or dysfunctional with the LOXO1 enzyme. And it collects. And you get these microfebrile or deposits that are almost kind of gluey that can't dissolve. And we also think what happens is, if you think about AGV trauma, anything that damages tissue, if the tissue's damage, if the elastin's damage, it wants to repair itself. And we think that's what's happening is because there's damage, the LOXO1 gets activated, but then there's something dysfunctional about the LOXO1. So the elastin tissue is not repaired properly. That's sort of the hypothesis. And it holds with UV. UV damage is elastic tissue. Genetic predisposition, as we talked about, most patients actually have a lot of it, something like in Iceland, it's like 98% of the population actually has the genetic abnormality or the risk allele. But yet they don't go on to present with exfoliation. Largely overlooked, especially in the US. What's the, you have any idea what the percentage is, actually, in the US? Kind of rough estimate. It's age-related also. So if you're older, greater percentage of the patients will have it. In Utah, it's about 3%, 3% to 6%. So over 60 is about 3, over 80 is about 6. And that's consistent with the United States. Other parts of the world, it can be as high as 30 or 40%. And then Bob Rich always talks about it being potentially reversible or curable if we can figure out what causes it. Increase in prevalence with age. We used to talk about it being Eastern European, Scandinavian. Do you think that's true? No. So it was first discovered there. But it's actually prevalent in Turkey. Huge population, probably about 30% of the Turks will have exfoliation. Guatemalans, Mayans, we have a big population actually down there that was discovered. Actually, Alan Crandall was the one that picked up the exfoliation in his patient population. So we're actively looking at them. Africans, Indians, Japanese, large patient population in Japan probably runs about 20% to 25% in Japan. I think the key thing here is you need to look at these patients before you dilate them. You need to look at translimination defects. And then you absolutely, absolutely have to look at them after you dilate them. Because exfoliation can be very easily missed. Why is it important to know that this is their cause of their secondary opening glaucoma? What's different about exfoliation patients? Whatly? Zonulatahisins, OK. If you're doing cataract surgery, you may want to do cataract surgery early in them. What about their glaucoma? Going back to that optic nerve that's going to take 10 years to progress, are these patients going to follow that rule? No. These patients can go blind rapidly. It's really scary. It's really scary how quickly these patients can lose vision. And sometimes it could be really young. And then on the other hand, you could have an exfoliation patient that never develops glaucoma. And they do perfectly fine. And we still don't understand why. And what's the difference with that? What's unique? Why some patients and others and not others? And one of the things we think about, too, is just because you have the material doesn't mean you're going to get glaucoma. And maybe the patient with exfoliation who's developing glaucoma would have gotten glaucoma anyway. So maybe they have a genetic predisposition just to open angle glaucoma. And now on top of it, you put this material and they've almost gotten a double whammy. Sort of the way we're thinking about this. Here's some of the prevalences. Greece, Turkey, Navajos, US, average is 3%. As we said, Chinese, Spain, Japan. That actually is a little bit higher now. It's closer to 20. But yeah, sort of all over the place. I don't know about the Eskimos. I don't think anybody's gone back and studied them again. A lot of patients with open angle glaucoma will have exfoliation. That's another thing to realize. You guys are coming out of a phenomenal training department. So you have a patient with open angle. Always go back and think, did somebody miss something? Never take someone's diagnosis for 100%. Go back and question that. And obviously in Iceland, the majority of patients with open angle have exfoliation. It's a really high number, 74%. Glaucoma, much more rapid progression. And we don't know. You brought up something, too, Lee. That's a good point. Is it the laminocrobosa? And that's why. Is there something genetically abnormal about the elastin in the collagen and extracellular matrix within the laminocrobosa that makes them more susceptible to IOP fluctuations if they have exfoliation? Because again, this is a genetic abnormality throughout their whole body. Or is it just the extreme fluctuations? These people fluctuate all over the place. They don't follow the book. Their pressures are all over the place. Tons of fluctuation, rapid progression, and just worse overall disease, greater medical failure. One thing that's interesting. So I thought this was really cool when I heard this. And I work really closely with Bob Rich. And I go to, there's think tanks every year that we have just on exfoliation. We get all the people from all around the world. Japan, Turkey, Iceland, Finland, the people that originally discovered this when we sit around and we talk about exfoliation. And Bob Rich always tells about a case where he had a patient who developed exfoliation but had a sector erudectomy very early on. And that area where that patient had a sector erudectomy never developed exfoliation on zonules. I thought that was really cool. So there's some sort of dynamic interaction between the iris, zonules, the lens. And also, if you take the cataract out sooner or earlier, I should say, you may slow down the production of the material. So there's this push now to take the cataract out earlier. Even if they don't necessarily need it, you may have better outcomes because those zonules are not as traumatized and as abnormal. But maybe it's affecting the material and the material production itself. So somehow the zonules are not as disrupted. But you may have less material and less block hormone progression. It would be a cool study to do. Yes? Do you know why it's peripapillary? So they always talk about peripupillary. You can see peripheral as well. But classically, they talk about it being peripapillary. And it has to do with peripapillary rough. And it may be. So the other thing with exfoliation is there's more ischemia occurring to the eye. And we're not quite sure if it's because the blood vessels are not, they're stiffer because the material in the smooth muscle of the vascular wall or they're actually occluding the microvascular. The other thing that's really cool about these patients. So Lou Pasquale at Harvard did a study. He published this if you guys are interested. But he looked at capillaries in the nail beds of patients with exfoliation. And their nail bed capillaries in their nail beds are much more tortuous. So there's something abnormal about their vascular system because of the elastin. And these patients with exfoliation, back to your question, have more iris ischemia. So also keep that in mind. And that's perhaps why we see it's basically an end vessel right at the iris pupillary rough. But we may be having pupillary defects because of ischemia as well. And you get ischemia in these eyes. Which also may be the reason why they've got worse glaucoma. So it's sort of a chicken and egg what's coming first. There was a little bit of a tangent. Material, what do you call these? What do you call this? What do you call this ring sign? What? A bullseye? A bullseye, or they call it three ring. I don't know if you hear one, two, three. But it's a three ring sign. And you can get translimination defects definitely in the heart periphery as well as a pupillary rough. Always look at the pupillary rough. Always look really carefully. Sometimes the material can be very difficult to see, very difficult to diagnose. You can see capsular contraction as well. That's another thing to think about. You see a patient who comes in. They have a history of open-angle glaucoma, come from an outside dock. They have a cataract extraction. And you see thymosis. And you see contraction of the capsule. What should you think about? Exfoliation. That patient may have exfoliation, and it was never diagnosed. They're also more likely to go on to have lens dislocations. And I think the interesting thing is we've been trying to figure out if doing cataract surgery earlier prevents the later lens complications from lens dislocation. And nobody's been able to actually quantify that. It's sort of a, again, a thought. Iris pigment in the angle. We talked about unilateral heavier pigments. What do you call this? What does this patient have? Policies line. What gives you a sample leases line? What? Exfoliation? What else? Pigment dispersion. So it just means, why do you get sample leases line? What is that? Where is it? Tell me where it is. Where is sample leases line? Antirdeshwabi's line. Yep, right there. Antirdeshwabi's line. And where do you tend to see it? Inferior angle or superior angle? Yeah, inferior angle. Why? Gravity, conduction flow. What about over time? Let's say this patient's pigment dispersion. So here's a good question for you guys. Exfoliation and pigment dispersion. What's going to continue to have more pigment over time? And which one's going to continue to get less pigment over time? OK, pigment. Why? Is it the iris or is it more the lens iris dive from the cataract? Well, that too. Yeah. So I always think of the cataract coming forward. And the iris basically gets pushed forward and you don't have that friction. So over time, a patient with a heavily pigmented angle due to pigment dispersion is going to get less pigment. So over time, where is that pigment going to be? So here's another interesting question. Where are you going to see more pigment in a pigment dispersion patient who's, say, 75 years old? Inferior angle or superior angle? You may see it in the superior angle because the inferior angle may clear. So because of convection and because of aqueous fluidics, the thought is that the inferior angle is going to clear faster over time. You also should think about pigment dispersion in patients who may have very little pigment in their angle. And again, just because of that reason, that angle has been cleared. But the damage, and they also may have normal IOPs. So don't be fooled if your pressure is normal and you've got damage, but you've got translimination defects. And you still may see some asymmetry between the eyes in terms of pigment. Ghost cell glaucoma as well is another one. And or trauma, hyphema, clearing blood. But you're not going to see a sample these days. You're going to actually see blood then in Schlem's canal. What else do you think about if you see blood in Schlem's canal? Another cause for secondary open angle glaucoma? Episclerol venous pressure. Yes. Think about elevated episclerol venous pressure. Can you have blood in Schlem's canal and have a pressure of 12 and not have anything wrong with you? Can you have blood in Schlem's canal? So does everybody with a little bit of blood in Schlem's canal need to be worked up for glaucoma? I had a patient at the VA like this a few months ago. No. Sometimes you can see it can't be normal. Just reflux. I mean, it's a dynamic vascular system. You can see some blood in Schlem's canal. It doesn't mean anything. Yes, Lee? Along the same lines. That's a good question. What do you guys think? If you see blood vessels in the angle, are they always pathologic? Why Niko? The Pyros vessel? Yeah. That are more tortuous and more on the anterior surface. So correct. So yes. And it's the pattern of the vessels. Again, it's not too dissimilar to the retina. If you see collateral, you guys are going to see collateral vessels. And you're going to see shunt vessels. And these are not the fine sort of spidery vessels that are consistent with ischemia and neovascularization. So when you see neovascularization, it's going to look very different. And you also want to look at the configuration of the angle. And then you take the whole patient into the picture. What gives you neovascular? I mean, this isn't in this talk. But what gives you abnormal blood vessels in the angle? What gives you neovascularization of the iris? Ischemia is the number one thing. So you worry about carotids, ocular ischemic syndrome. What else? Diabetic retinopathy. Tumors. Tumors can absolutely give you iris. Neovascularization. Uveitis, also, and sort of congestion, chronic inflammation. And then, obviously, all the normal ischemic CRVOs and CRAOs, et cetera. Pigment dispersion, your younger male myopes, wide IOP fluctuations, up to 40 to 50 with symptoms. So again, and you want to get them in an active state of dispersion. So that'll be the difference between pigment dispersion syndrome and pigment dispersion glaucoma. Do they have elevated IOPs, and are they having optic nerve damage? Burnt-out pigmentary. Again, you look, and you see these trans-elimination defects. And maybe they've got a faint sample E.C.'s line. They've got normal pressures, but they've got optic nerve damage. And is it symmetric or asymmetric? What do you guys think? Could be asymmetric. Actually, could be either. Really depends upon their myopia, too. But you may see it tends to be this, I would think of more as being a little bit more symmetric. Because generally, they're going to be about the same. If they're minus 4 and 1, they'll be a minus 3 and 1⁄2 or 3.50. But it can actually present either way. Reverse pupillary with block, we talked about. Treatment. What's the zent male line on the capsule in the back? So you'll actually see pigment also on the anterior hyaloid face. And you can see it where the anterior hyaloid face actually comes up to the lens posterior. So if you can, if you can, oh, and this actually was really annoyed. I have to take my boards again. And I was at a board course. And they showed a really wide dilated eye. And they showed the zonules. And they had some pigments. They had some schmutz, couldn't even tell it was pigment, schmutz on the zonules. And on the anterior hyaloid face as it comes up to the lens. And my mind always thinks exfoliation. So they were like, what's giving you these changes or this debris on the zonules? And I said exfoliation. And I was wrong. And it was pigment dispersion. So they were talking about the zent male. So if they happen to show you they like pigment on the back anterior surface and on the zonules. And pseudo exfoliation, they like, people are rough. But this actually could be either. This is sort of classic for pigment dispersion. But I've seen patients like that with exfoliation as well. Oh, we didn't talk about this. What did they get on their cornea? Croukenberg, Croukenberg's Bendels. Oh, yeah, and here. What's this? There it is. Yeah, it's an IR line. Heavily pigmented angle. And this is the reverse. Oh, we were just talking. I forgot I had this in my slide. The ultrasound after a PI. It's really cool. I mean, that iris comes up. It's really neat. I always thought this was a really, I like pigment areas really cool. It would be neat to look at the genetics. Fakolitic, fakolitic glaucoma. So fakolitic glaucoma, large cataract macrophages. And again, I wish there was an easy way to sort of remember this stuff. It's just memorization. But macrophages, plugging the trabecular mesh, wear a hyper-mature cataract, what do you need to do? Take it out. Take the cataract out. Lens particle glaucoma. So different from fakolitic. Fakolitic, the cataracts there. What's lens particle? Part of it's left over, so there's some cortical material. So lens particle glaucoma, too. Do you have to have this right after the cataract surgery? You can, but you don't have to. What about 10 years later, you do a yag cap and you disturb the cortex that's there, l-schnick pearls, and you break up this material. Did you then get lens particle glaucoma? Sure. Yeah. It's sort of a reaction. The material clogs the trabecular mesh work. What do you want to do for this one, too? Steroids, aqueous depressants, clean up the material. So I have a question. It really depends upon the presentation and it depends upon how much of this inflammation. Because don't forget, you can have a really hot red eye because of the elevated IOP as well, and not so much from the inflammation. So again, it depends upon the presentation. I don't think I can give you a Pozner-Schlossmann. Hit them hard with steroids. Don't be scared of the pressure. These patients, it's tough to say. You can also have goniome, do gonioscopy. You may also have a component of angle closure, too. If this is a complicated cataract and they've got a lot of cortex material, a lot of manipulation, maybe the capsular bag is not intact. The rye may be hot and red because of. But it's usually, it's not so much inflammation as a pressure spike because of this material that's there. It's not like the FACO antigenetic, which we're going to talk about as well. That's really an anaphylactic inflammatory process. So FACO-lytic glaucoma, hypermature cataract, lens particle, white fluffy cortex in the anterior chamber, generally capsules not intact. Again, it's just, you know, it's more complicated. I always think of these as the more complicated cataracts. Treat the inflammation, treat the IOP, and you may need to go in and take out the material. And that really gets to your point, Lee, is, is this going to resolve over time? If it's a little piece of material and eye's not so inflamed or pressure's not so high, you may not have to be as, it may not be as critical to get into that eye and take the material out. But if it's a really hot red eye with a lot of inflammation, even all the steroids in the world is not going to help you get all that material resorbed in an appropriate time span. But keep that in mind, actually. Even like I thought that was a really, I forget who presented that case. It was really interesting to think about a YAG capsule years out, you know, 10, 15 years out. And the patients got, you know, inflammation in a high IOP because the material got disrupted. And then phacoanalytic, anaphylactic. So, again, that's really more, that's really more inflammatory as well. And that's when the lens protein. So I think of that always as the bag that's not intact and that lens material's leaking out. And then there's an inflammatory reaction. So there you've got to take the lens out, actually, as well. Ocular inflammation, glaucoma, steroid responders, gonioscopy. Oh, so why no myotics? Why don't you want to put these patients? Actually, myotics work really well in pigment dairy dispersion also. But young myopes, you really don't want to use pylote. We don't use pylote as often anymore. We used to use pylote on these patients. But increased risk of retinal detachments and also the headaches and the symptoms. Why no prostaglandins? Why don't you? I mean, we do, but traditionally speaking, you always want to think that your prostaglandins can be aggravating inflammation. Leaky, it breaks down the blood aqueous barrier. Prostaglandins break down blood aqueous barrier. And they give you CME as well. That's very, very well documented. The other thing they can actually do is reactivate herpes. So they're pretty benign, but there are cases where they actually can throw you a curveball. So what is this? Poshers-Lassman up front. Fuchs heterochromia. Oh, Fuchs heterochromia erudiciculatus. Also on gonioscopy, what do they have? They may give you pictures, photos like this. Yes, yes, very, very fine. So that gets back to your question. That's another case where you can have very, very fine. And they're not crossing the trabecular mesh work. They're sort of this low line. And they just look, their angles just look a little bit different. Recurrent bats of elevated IOP, mild iridus, trabeculitis. We talked about this. What is this? That's classic actually. That's the Poshers-Lassman. They get these fine, fine, fine. They're not even really stellar. It's really not KP's. They're just this very stellar, yeah, sort of little inflammatory. Do you keep these patients on long-term anti-inflammatories? No, no, not at all. You just treat them when they come in and they get to know their disease. And it actually, they outgrow it. So it's generally younger patients, middle age. Middle age women, again, is what I think about. And possible causes. Do we know what causes it? Yeah, I think there may be a viral etiology underlying it. You gotta see them. Yeah, you absolutely have to see them. But if you, you may have one or two cells in the anterior segment, it's really not an iridus. So it's gonna be different than an iridus. In your differential, always consider herpes. But again, it's this sort of fine. What would you see if you had a herpes? Do you get this sort of fine? Generally, herpes is much more of an iridus. Any sort of infectious etiology is gonna have larger KP's. This is very, very fine. And a very quiet anterior segment. And they're not really red. They're blurry, a little blurry, their pressure's high. But it's really the trabeculitis. But you gotta see them, yeah. And you know, and some of these patients too, if they really know their disease, you can always, you never wanna give anybody a standing prescription for steroids. But the ones that really know their disease will also know to start it and then come in and be seen. Oh, and then aqueous suppressants because you are dealing with elevated IOP. Trauma, high incidence of rebleed, larger hyphemes, greater likelihood of elevated IOP that's pretty intuitive, compromised angle. Sickle cell, you know, the big thing here is, you know, carbonic anhydrase inhibitors. Think about sickle cell, higher risk of rebleeding. When do they tend to rebleed? How many days? Three to seven. Three to seven, generally within the first week. So you wanna immobilize them. Gonioscopy, you know, it's, you wanna know if there's an angle recession component, you're not gonna be able to see it, especially if they've got an active hyphema, but at some point you wanna get that patient in and you wanna do a gonioscopy and you wanna see where that angle's torn. Angle recession is going to, down the road, five, 10, 15 years. You know, it's really hard to speculate but that patient needs to know if they've got angle recession there at a higher risk of glaucoma over time and they need to be followed, basically for the rest of their lives, which is a hard thing to tell a young kid who's got an high hyphema. You know, keep going. You know, when you're 50, 60 years old, don't forget about the fact that you had trauma to your eye and keep getting examined. Hemaletic, ghost cell glaucoma, these patients will have, ghost cell glaucoma's pretty cool. It's this khaki looking, red blood cells with no more, you know. And you know what's actually cool too? You can see ghost cell glaucoma. What do you wanna look for in ghost cell glaucoma? What's another telltale sign when you think about ghost cell? What? Yep, look at the anterior vitreous because you may still see some ghost cells there or even some, you know, RBCs but if they had a vitreous hemorrhage, think about ghost cell glaucoma. Angle recession glaucoma, tear in the ciliary body, longitudinal ciliary muscle fibers, unilateral secondary open angle, talk about when does it occur, other eye developing POEG. And they can always have mixed mechanism too, you know. They can have angle recession and they can have POEG. Risk factors for progression, pretty obvious. Elevated IOPs, diurnal fluctuation. Which study? Which study talked about diurnal fluctuation? That was last week's lecture. It was here. Chris, Mike, Nico, Becca, you guys here last week, I think so. Ages study. What are the two things the ages study taught us? Two things. I don't remember, two things for ages. What? Yes and no, but that wasn't what that taught us. 18, yes, 18. 18, patients had less progression if they were under 18 and diurnal fluctuation is bad. So patients went on with more progression if they had diurnal fluctuation. And if they had IOPs that were over 18. So now when you look at studies, it actually reports that as a separate outcome. Percentage of patients that had IOPs of 18 or less at all time points. And that was because the ages study. Think about nighttime IOP, sleeping position. We talked about all these. These are sort of the way we think about glaucoma now. Blood pressure, hypoprofusion, ischemia. Recommendations and treatments we went through. And then prognosis. Prognosis really is the cause of the glaucoma. Any questions?