 All right, so we're going back to Barcelona, and this is the apartment building that that Gaudí Had designed it's really cool It's now people are still living in there But you could do tours of his old apartment on on top and all but absolutely wild It's on one of the main streets of Barcelona And just the design is is 60s drug trip even though he built it in like 1880 And this is the top and here's where it gets really wild. He's got this undulating top on here with kind of African modern art on there so very very wild and so you go through there's there's flower pots on here and There's this undulating design and they walked of course they put fences around it so that people wouldn't wouldn't fall off But that wasn't part of the original design. This is what it looks like So you've got this kind of African looking modernist Art sticking up and I'm not quite sure the symbolism of why there's four of these guys here and one of them here But each one is different each one of the masks has a different appearance to it and This is all you come out from the top apartments and if you look right here The coverings over the windows on the top almost look like a battleship And so this was the very top here and you can walk through here, and they've got a little bit about his history That was there, but just interesting each one of these masks is unique and Almost looks like imperial troopers, you know from From Star Wars, so we have to keep slipping Star Wars in here today. That's going to be our theme And then one other look and again, you can see there's just some of them here And then there's these abstract designs on the corner. Nothing is even It all undulates through and as I said this looks like the side of a battleship, you know And they've opened up the gun ports But this is really the attic of the apartment building and then this is the entrance way going up with these Rod-iron things on the balcony. So there's very very wild architecture. Okay, so today We're going to talk about glaucoma. We can't talk about glaucoma without understanding what the anatomy of the Trabecular mesh work is and so there's a couple different ways we can describe the trabecular mesh work The first is if you're looking at the mesh work in a goniomere and so Adam Let's start with that. So we're going to look say we're looking at this trabecular mesh work in a goniomere What's the most anterior part that you see? All right, what is Schwabby's line? What should be right there? Okay, so our decimates membrane on the inner surface of the cornea terminates it often leaves a little bulb and That Schwabby's line and when you look through with your goniomere, you'll see a little white line Now I really encourage you guys when you're seeing new glaucoma patients to goniomere them because You know on the on the pictures here those lines are this wide You know when you look at in the book But when you look in there you look with the mirror and the patient's squeezing and there's a bubble under your You know under your ear thing that you're holding there and you see others a couple lines of guys that open Is it closed? You know the only way you're going to be able to tell what an angle looks like is you got to do hundreds of them So, you know in glaucoma people come in start doing them often All right, so we start with Schwabby's line. We come down from that Adam. What's the next layer you see? Okay, and how do we divide the trabecular mesh work and which is which which is more anterior? All right, so the non-pigmented is this more anterior area you see and then the area you see down here is more the pigmented area And then as you come you see a little kind of a white line right here at the posterior surface. What is that? Okay, the scleral spur and then lastly you can see part of the Ciliary body or even iris and so when you look at the scleral spur What the scleral spur is if you think about it the trabecular mesh work is shaped like a triangle and it sits You know with this little spur this little lip of sclera sticks out So if you make your thumb and fingers like this the mesh work fits in there like a triangle apex here and base here The scleral spur goes all the way around 360 degrees and will help to kind of support that and keep that Trabecular mesh work there now Russ. There's another You know way we describe the trabecular mesh work And we kind of divide it into zones if you will and what what kind of descriptions do we use there? All right, that's the inside most part Okay, and what's the third? UVL exactly so if you kind of divide it this way You know there's there's corneal sclera. There's UVL and then the most importantly or at least to me is Judge the cantaliculum. What does just the cantalicular mean? So that's this area right here right next to Schlem's canal. I hear Schlem's canal right here. What is Schlem's canal? Exactly so you think about it think of it as a flattened like a bicycle tire in or two It's not a round structure. It's kind of a flat oval structure, but again it goes 360 All the way around and that's Schlem's canal when you look at close-up the reason why the Judge the cantalicular trabecular mesh was important is this is where a lot of the resistance To outflow from the eye occurs and so people think this is where the money is in open-angle glaucomus When you look at the mesh work, it's got bars of these little collagen with some elastin fibers around them And these bars have endothelial cells around them also and Then so aqueous fluid will passively diffuse through here, but when you get to the judge the cantalicular area It's not just open. It doesn't just passively diffuse. There is some active transport that goes on there now This is not tight junctions like a blood vessel, but there is some junction Junctionality here and some resistance to flow So when we when we think of the aqueous, you know you want to Track let's let's call it track a milliliter of aqueous Ashley so we're going to track the aqueous. Where is it produced in the celery body? Okay, and then where does it proceed from there? All right, so here comes it comes through the director mesh work Just the cantalicular tissue Schlem's canal. Where does the aqueous going it leaves Schlem's canal? It's an easy one to remember because they're called aqueous veins And so it actually percolates from Schlem's canal You know this little Venus system that goes around and it's called aqueous Veins and sometimes people call these collector channels and the reason that this is important is We've got some new little micro incisional devices now They're going into the director of measure to treat glaucoma people are saying how many of these should you put in? We're just figuring out where they work best and it turns out where these aqueous veins gather They call these collector channels it turns out that if you put one of these devices Into Schlem's canal near one of these channels, then it works better and so that the person who's really responsible for You know showing us that these exist is actually I'm Rob Stegman from South Africa If you ever want to look up the most awesome videos I've ever seen in ophthalmology look up Rob Stegman and he's got these videos where he will unroof Schlem's canal and Then he'll put dye into them or he'll squirt something clearing to them And you will actually see on the surface of the Episcopal era the aqueous veins And you see them blanching out and then going back down hip with some dye in there And it'll show where these collector channels are beautiful beautiful videos So if you get a chance take a look at those and here's a close-up. Here's that juxtapenolicular tissue here Schlem's canal And it's kind of this collapsed inner tube look to it does have some endothelial cells around them And the reason that that's important is now we're starting to look into surgery where we don't Try to treat glaucoma by opening up the whole Trobicular mesh work and then letting aqueous flow from the anterior chamber under the conch We're now doing some procedures where you actually unroof Schlem's canal and then put a little suture in it or blow it up with Visco elastic or something so that you have a more controlled way of getting the aqueous to come out Now this is showing you one of those aqueous veins and collectors so here is the mesh work here Schlem's canal Here's this aqueous vein and then it goes out onto the epi-squaral Surface underneath the conch and they'll be right here And so I tell you guys this every year when you're in the VA and you're looking at these people with the slit lamp Look just beyond just behind the limb us and see if you can find aqueous veins And if you if you really look hard for them You can see them in most people and what you'll see is you'll see some veins But you'll see some box carring of the RBC's in there and that'll be because there's little clear aqueous flowing through in there too So you have to look deep in the epi-squaral through the conch and top with your slit lamp, but try it and see if you can't see those Okay, so the most common type of glaucoma is open-angle glaucoma and Brian Can we tell that a patient has open-angle glaucoma by doing a light microscopy of the mesh work? And why is that? Well, we don't know what causes it, but the interesting thing is on light microscopy There's no difference between a glaucoma this angle and an angle of someone who doesn't have open-angle glaucoma of the same age So when you look at irregular mesh works in younger people, they're a little more cellular They've got more endothelial cells are not quite as compact as we get older the trabecular bars compact There's less cells around them, but to be honest you take a 70 year old with open-angle glaucoma 70 year old without open-angle glaucoma They all look the same on light microscopy now in EM you can pick up some differences So it's hard to diagnose open-angle glaucoma on light microscopy So when we think of glaucoma, we think of it We divided into a few different areas and the simplest way I like to think of it is, you know You've either got open-angle glaucoma You've got angle recession glaucoma or you've got narrow-angle glaucoma So when we're looking at open-angle glaucoma, glaucoma where the angles are open you can have Primary open-angle glaucoma or you can have secondary open-angle glaucomas and so Niko This is a secondary open-angle glaucoma. Why would I be showing you this picture if we're talking about glaucoma? Can you see the angle from this picture? What do you see in this picture though? That's interesting Exactly, and what's the pattern of the transillumination defects and it's radial And so when you look you see that this patient has these radial Transillumination defects so you shine the light straight through the pupil that light bounces off the retina comes back and you see these Oranges transillumination defects here What is that indicative of? Pigment dispersion exactly and why is it in this pattern? Well people argued about this for years why? Pigment dispersion glaucoma occurs. It was interesting There's a guy at Dartmouth who finally just took some you know donated eyes with Pigment dispersion glaucoma and looked at the path and said okay What is it that causes this and what they did is when you flip this over and you're now looking at the posterior aspect This is a posterior iris surface. These are the where the zonules insert it turns out the zonular bundles that hold the lens in place Are running along here and for some reason you get posterior bowing of the iris in these pigment dispersion cases And it scrapes against those zonular bundles so this you can see lines up if you can imagine the lens would be sitting here and these Bundles of zonules run this way and then insert here in the ciliary body and as those scrape on the iris You get dispersion of pigment so this is a secondary open-angle glaucoma pigment dispersion syndrome and Pigment dispersion glaucoma here. We see here's an iris Cornia trabecular mesh work look at all the pigment in the mesh work Now where else beside the mesh work does the pigment in pigment dispersion syndrome settle and we're still at Niko chance to save yourself He's looking quickly in his book On what surprisingly not really Where else do you see in a slit lamp do they settle the cornea? That's right. Just do you have it's all in perspective Just remember we tell all our cardiology colleagues the purpose of the heart is to pump blood to the eye So keep that in mind. So right here what you get is you get Pigment dispersion on the endothelial surface of the cornea and it sits in a particular pattern It sits in a broad triangle in the lower third central part of the cornea and when you get that Pigment dispersion settling there That I think is just due to where aqueous You know currents flow on where they go, but in any event you get pigment sitting there on that lower third central cornea shape like a triangle It's called what anybody who's triangle arts art Arlts Triangle and so you see that in pigment dispersion syndrome and it's called a another word we use for it is a Krukenberg spindle and so you see these and that's a real tip off for pigment dispersion glaucoma Okay Eileen another cause of secondary opening of glaucoma would be I mean this is not just pigment dispersion Well, it's kind of recess, but it's recessed because something is pushing the iris away because it's growing up into the angle here Exactly and arising from where? From the ciliary body so you can get secondary open angle glaucoma from an infiltrated process And that is a tumor most commonly a malignant melanoma the ciliary body which will then grow Up into the angle here and can give you a secondary open angle glaucoma And here you can see just another view of it. This is cornea iris root And right in here into the mesh root now there's a tumor coming from the ciliary body growing right up into the angle So secondary open angle glaucoma due to an infiltrated process All right, we got an easy one here. I guess chris you're next Pseudo x and how does pseudo x cause glaucoma? Exactly that material Which is you know here deposited on the surface of the Crystalline lands you can see where the pupil is scraped as it People moves in and out that material will actually get deposited in the trabecular mesh work, but interestingly enough It's even more than that Exfoliation is really an interesting Entity not only do you get the exfoliative material clogging up the mesh work? If you will it's kind of like leaves clogging the storm storm drain on the street You get that but you even get exfoliative material actually inside the cells Just to canniliculately and and even affecting the little vessels coming out And so it's more than just clogging it up But if you want to think about it, it's actually the most you know The biggest part of it is actually just that exfoliative material clogging up the drain if you will And so again, you get a secondary open angle glaucoma And you can see all this exfoliative material sitting here on the surface of the lens And this just shows you it in retro illumination And so this is very common here in utah. So you'll see this a lot You've really got to watch these people carefully because they can get into trouble in a hurry So people with with significant exfoliation You know they can look really good and in a short period of time the pressure can shoot way up and then go down the tubes in a hurry And so you really want to keep a close eye on these guys with exfoliation and remember we saw this when we talked about the lens You've got the so-called iron filing Pattern of this protonaceous material sitting on the lens capsule But in addition Here is the trabecular mesh work and here's all that stuff Sitting on the inside surface of the cornea and clogging up the mesh work And so you can get a significant fairly severe secondary open angle glaucoma With exfoliation now when you're treating both exfoliative glaucoma and you're treating pigment dispersion glaucoma These respond pretty well to argon lasers Because argon laser works by being absorbed by pigment and making heat And so because there's pigment and pigment dispersion, but also in exfoliation You can get a pretty good bang for your bucks and do argon laser now We're now using the slt select laser, which also works pretty well in these secondary open angle glaucoma is due to both pigment and exfoliative syndrome All right Renee What are we seeing here? What if they've had no cataract surgery? Okay So that's a good differential because we're talking about glaucoma obviously and so you want to think about What are you know lenticular causes of glaucoma? And that's another broad category of glaucoma and so If you've got a glaucoma where the patient has a You know just a big nuclear cataract and they're a little hyperopic and the angle's getting narrow or narrow Or what kind of glaucoma do we call that? Fakal morphic glaucoma, so it's the size and shape of the lens that's narrowing the angle and causing you glaucoma What was the first entity you said? uh-huh Fakal lidic glaucoma and what is fakal lidic glaucoma? So here you see here's the Iris cornea mesh work. Look at these macrophages and again if you want to sound intelligent You say british costus will tell you that so see macrophages, you know If you talk british you sound very intelligent So it was you know 0.2 centimeters long and it had macrophages in it. So you sound very intelligent when you do that So you can see these Stuffed macrophages. They're just huge. They're you know when you look at a patient with fakal lidic glaucoma If the cornea is not too edematous from the pressure you can see these Gigantic macrophages floating around they're just stuffed with pigment But not only do the macrophages clog up the mesh work, but just the pigment does too And so the treatment for this is what? Yeah, cataract surgery not only remove the lens But also you want to flush out the anterior chamber real good and people you stuck about You know irrigating the anterior chamber. Well, you know when you do faco you've got a lot of ia going in there anyway, so I mean, you know, we flush out the ovd pretty good anyways I'm not sure what what they mean by flushing it out But you know if you do have a case of fakal lidic glaucoma when you get the lens out of there As you're moving the ovd, you know, just got to swing around the anterior chamber and let that fluid You know flush out all these macrophages and this protein and then Doing the cataract surgery is curative. But again, this is a secondary open-angle glaucoma because the angle is still open in this case And this is actually an anterior chamber aspirate And so before we had oc t's and other ways of looking in there people were concerned about what this was And so you'd actually aspirate it you would send it for culture But then you could also just squirt it out and and look and these are macrophages just stuff With protein again All right, so we talked about Open-angle glaucoma and this is a really crude schematic, but it's a good way to think about it now You can go to closed-angle glaucoma or you can go to angle recession Well, there's been a trauma and the angle's been torn loose All right, so nick what do you think about this patient? What would you be concerned about here? You've got a unilateral injected eye with a mid dilated pupil What if I tell you that that pupil doesn't move very well and this one's normal over here One more hint. Here's the slit lamp. What is this slit lamp show? Something we see on the little patients all the time at four to six months There's something on the That's actually on the surface. Look at the slit beam What is that showing the irises Yeah, look at the his look at the look at the picture of the the slit beam hitting the cornea And then look at it hitting the iris and you could actually literally see that bowing forward And in fact in the periphery It's almost touching and so that's called iris Bombay and so when you get a relative pupillary block Then you get aqueous building up behind the iris you'll get forward bowing of the iris And eventually you'll get angle closure glaucoma Now this doesn't usually happen in people with normal You know appearing angles usually these are people with narrowed angles either they're narrowed From how the patient's built Or they're narrowed secondary to the lens swelling as time goes on even eventually you can get the faco Morphic glaucoma they talk about the lens coming forward But it's interesting depending on what part of the world you're in now if you're in in singapore In your patients are ethnic chinese More than half of your glaucoma patients will be angle closure or chronic, you know narrow angle glaucoma More than half same thing in hong kong So very very common in people of chinese ancestry And where you see them reported is singapore and hong kong and so very common in utah We don't see this that often i mean occasionally we'll see narrow angle glaucoma or texas glaucoma But because it's it's uncommon you want to keep your radar up higher because you don't want to miss one of these And so you see that forward bowing So what happens is is you get some kind of a relative pupillary block there where the aqueous can't Go through and the setting where you can trigger one of these where you got to be really careful Is if you have someone with a narrow angle an angle at risk and you dilate them They don't go into an attack of glaucoma right away, but when they go home You know two hours later that dilation is wearing off once it hits that mid position The opposition of the iris to the lens is the greatest right there in that mid dilated That's where they'll get the attack So you want to check the angle first before you dilate somebody and the techs here are really good And they'll grab me two three times a week and say can you look at these angles before we dilate? Because you want to make sure that you're not going to have an angle at risk And this is one that we didn't catch early enough jack. What am I showing here? Here's a slur body Here's the angle back here What's happening here? Clustats okay And what do we call it where there's this almost like a connective tissue sticking the iris to the peripheral cornea Uh-huh This is a chronic, you know angle closure or chronic narrow angle, but what do we call it actually when you get This you know peripheral iris stuck to the area of the peripheral cornea blocking off the mesh work It's a three-letter abbreviation Give some sounds like This is called we abbreviate this p.a.s peripheral anterior synica And so when you get the iris and the periphery stuck up to the cornea eventually that can permanently block it off So that's why you don't want to miss Like a chronic angle closure And so the problem is is these acute attacks you can tell those easily but someone who slowly but surely Narrows their angle and then eventually closes it off This is kind of the slow creeping chronic angle closure These are the ones that are tough to diagnose and then you know patient will come in and their pressure will be creeping up slowly But surely you see them the angles closed pressures 40. They're not having pain and they're you know, they're cupped out So you want to catch them before they get to this point and here you can see Another one and so you can have secondary angle closure glaucoma due to peripheral anterior synica Adam, what's another reason you can have secondary angle closure glaucoma? This is subtle, but it shows it right here Very subtle see those little vessels there So you can get exactly you can get secondary angle closure from neovascularization So anything that can cause ischemia in the eye, you know central vein occlusion Just ischemic eye in general diabetes. You can get neovascularization of the iris And those little neovascular vessels eventually Will grow through there and you will actually get the iris and the periphery sticking to the cornea So neovascular glaucoma can give you a secondary angle closure What happens is is as these little tiny blood vessels here's the tiny blood vessels very fine tiny blood vessels The little endothelial cells can have some contractile properties with them too So as these abnormal blood vessels grow they can contract and they can shrink the tissue and eventually Narrow the angle and then once it sticks then it'll stay stuck So that's secondary open secondary narrow angle glaucoma due to neovascularization All right, Russell there's another reason for Angle closure and you know iris bombay and all and What would this be showing? Okay, so you can see right here. This is it looks like kind of like a dinosaur Going up there But but if you look you'll see where the iris pigment up through them was actually Stuck to the anterior lens capsule. This is not an artifact and then when we looked at the path The pigment stayed stuck on there. So you get what's called a posterior synechia Which is sticking down of the pupillary margin To the lens posterior and that can give you An occluded angle and then secondary angle closure from that And so sometimes you can get A membrane that grows completely across the angle blocking it off and someone who's got say chronic uveitis chronic inflammatory disease You can get an angle where it's occluded. It's got a membrane completely around it or you can get 360 degree synechia posteriorly and they call this succlusion with an s so secluded Pupil and so those will again keep the aqueous behind the iris instead of in front of it And you get a secondary angle closure glaucoma. How do you treat this? At least acutely Yeah, so you can do a laser peripheral aridectomy If you guys haven't done one of these before They're really cool You put your little you know mirror on for doing the laser pi and you crank the yag laser up to five So you really crank it heavy and you put a double burst in it And you aim for a thin part of the iris there and then you just hit the button and it goes it goes And you can instantly see aqueous gushing through there and then you'll see the iris go backwards It's pretty cool when you do it And so you have to be careful when you're doing it. You don't go wow You know with the patient, but it's rare to get instant gratitude when you do something But this is instantaneous. So it's pretty cool when you do do it All right, ashley What's different about this angle? It's recessed. So here's the mesh work up here. Here's an aqueous vein here and look here's the iris root Right here. So when you think about a recessed angle, what's the most common etiology for this? Blunt trauma. So usually it's blunt trauma. So someone to get hit. This is one that you'll often see Secondary to the two dudes And for those of you who don't know, you know all ocular trauma in In uh young males is caused by two dudes never one two Uh, just sitting there mind of my own business, you know on these two dudes jump me, you know It's it's the same story two dudes and so the two dudes jumped in me as trauma to his eye And you get this recessed Angle this is usually associated with what other finding when you see them acutely In the eye Hythema and so when someone has an acute hythema from a blunt trauma You don't want to be putting a gonio mirror on there and match it on the eye where that's you know got fresh blood in there So you wait about a month let the hythema go away if all is okay, then you bring them back and you do the gonio Now bonus question for you ashley How soon after a blunt injury with angle recession does glaucoma occur? Nico 10 years very good 10 years seven to 10 years And so the reason that that's important is easier young dudes, you know there The last guy had with the traumatic hythema and a recessed angle He wanted to know hey man, when can I lift again doc, you know, and it's like, you know You got blood in your eye. You really don't want to be like, you know pumping your bicep curls, you know right now And so of course his blood trauma was he got hit with a paint, you know He's doing one of these paint gun battles And of course he took off his glass. No, he didn't take him off I said, well, you weren't safe to go. Well, they didn't make us You know, and it's like so He's the other guy. So we had a long conversation with him about birth control, you know Don't pass on this stupid gene, you know to another generation but But you really have to put the fear of god in these guys and what I mean by that is You have to let them know that they're at risk for developing glaucoma 10 years from now So when you're a 19 year old dude, you don't really think about that But again, I've had in my career several times where someone has come back in With blurred vision and this is back when we had paper charts You pull out the old paper chart sure enough 10 years before they had blunt trauma recessed angle The pressure slowly builds up. They don't notice it Then they end up coming in with a blurred vision. The reason it's blurred is their pressure is 45 now Their cup is 0.99 and they have a little temporal island of vision. Everything else is wiped out And it's slowly gone on so they didn't notice it So you got to put the fear of god in these guys and say, you know what? You could go blind from this for the next 10 years So you have to come in once a year and sometimes the blind word helps I don't usually say blind to people. I say loss of vision I say blurred vision you never say blind But in a dude with an angle recession, you say blind You say come back every year or you could go blind Happens immediately it's a blunt trauma where that Eye gets deformed a little bit and the aqueous pushes everything back and the tear actually occurs Not so much even at the iris root. It actually tears into the face of the cylinder body So you can get an aero dialysis where the iris root will tear loose But oftentimes what will happen is is the face of the where the iris root meets the cylinder body will tear So you can see the iris root is still attached and that tear goes into the face of the cylinder body Where here's a normal angle down here in comparison So secondary angle recession 10 years out the glaucoma occurs and then eventually I think what happens is is that traumatized Mesh work eventually just scars over and I'm not sure the exact etiology and why it takes 10 years Okay So this is just to kind of show you this is the same eye with the front and back picture at once Here we have Look at the angle recess there Not only that they had a traumatic cataract. So there's a little summer in June here and of course here's the Total 0.99 cupped optic nerve with chronic angle recession All right, so we're going to talk a little bit now about what glaucoma does to the optic nerve and so Chris, what do you think the cup to disk ratio is right here? It's way out here at least 0.8 sometimes hard to see right there. So at least 0.8 And so you'd really worry about that and the nice thing now is is in the olden days when I was a resident We would just have to draw them and take a guess or maybe take some stereo pictures of them Now you've got you know, you've got oct's you can you know mark out what the cup is You can look at the nerve fiber layer you've got all kinds of ways of looking at what glaucoma does But remember in the in the end stage glaucoma is a disease where the pressure is too high For the optic nerve to tolerate And it's not a disease where the pressure is too high. It's too high to tolerate So there are people who get glaucoma with even a low pressure There are people who don't get glaucoma with a high pressure And so you want to be really careful with your terminology But the bottom line is you lose The nerve fibers as they're coming in here and people will argue back and forth And maybe they'll talk about this when you guys do glaucoma Is this a disease where they get mechanical disruption of Good humors into the nerve fibers that goes in the laminar crebrosa. Is it ischemia? Is it a combination of both? We don't know but what happens is is you get The nerve will cup out and you'll get posterior bowing and you'll get damage to those nerve fibers As they're coming through the optic nerve and through the laminar crebrosa and again, here's a big At least 0.8 cup although this one's got a better rim But look how deep that is And the problem is is you want to stop the disease before you get to this So this is more than a 0.9 cupping this is I even call this more than one because you can even get excavation underneath the edge So when you look at one of these you can actually see right here Sometimes you can actually see a blood vessel will go in and it'll actually dip around to where you don't see it And so when you get severe cupping You have what's called a beanpot and I've you ever seen like the boston beanpots Where it's it's wider in the middle and narrower at the top And so this is severe cupping interestingly this patient had trauma There's a scar through the cornea and adherent lucoma to the Ruptured lens with a summering drink, but again totally cupped out disc And here's what I was talking about see how that vessel goes around the edge and then disappears behind there And so you can actually see vessels disappearing around the edge So the idea is is you want to get it before it gets to this point Here's posterior bowing of the laminar crebrosa Where it's crunched back here. So this is the end stage. You don't want to let it get to this point And here you can see secondary atrophy Look at the widening of the subarachnoid space of the nerve there and again, look at that overhanging And it comes in this looks like one of those things that tabin climbs, you know Where you it hangs out more than you and you grab it with your hand and dangle and then scurry over the top of it So Who could do that? I lean too Okay, so I lean think of that you're scaling that it's a big cotton with little cotton canyon Where the big cliffs are and there you are climbing that little lip right there Here's a close-up now if you look look at the nerve fiber layer there. It's completely gone I mean the nerve fiber layer is gone. We want to prevent it from getting to this point So that's end stage glaucomodous optic atrophy no matter what the etiology Okay, well, I don't know Nick. This one's an obscure one. This is an optic nerve scenic cross section I'll give you a hint patient had a sudden rise of pressure This is an obscure one cost us The key thing I want to point out is a focal area of power So this isn't like a ms nerve or something a little focal anterior just behind the laminocrobrosa Area of of this pale staining to this nerve So there's a focal infarction there and this has a weird name to it Anybody know it? Oh, I skipped you. Oh my god. I skipped her name. Okay, so you get to go back What is this sorry? Schnabel's optic atrophy. So it's interesting Schnabel. I don't know who he was. It's not like fuchs. He's obviously a german But if you have an acute pressure rise like an acute Angle closure glaucoma pressure shoots up to 50 you can get these focal areas of Pale ischemia some people even theorize that you're actually pushing Vitreous into the area you're pushing fluid into there and so you get this focal Area of optic nerve damage in ischemia. It's schnaubles cavernous optic atrophy And i'm glad you said something because otherwise it would have skipped you and here's a nice stain for Alcien blue. What is Alcien blue stain? Ucopolysaccharide exactly and so that's why people think that maybe the high pressure is actually pushing Vitreous into the nerve there and so Ucopolysaccharide is one of the components of vitreous along with a lot of water and so this is a special stain For mucopolysaccharides here stuffed into the optic nerve and schnaubles cavernous optic atrophy Another thing you can get let's see. I guess we can add them First of all, what part of the eye are we looking at here and what are we seeing? Okay anterior lens capsule and what's going on when we go to the higher power Yeah Focal anterior evacuated spaces the little lens epithelial cells have been disturbed again. This is someone who had an acute pressurize What do we call these guys? Exactly. So those are the two cool words in barcoma schnaubles atrophy and glaucoms lecken, you know, so that sounds real good Sounds like you know the german Internist, you know telling the young guy when he comes in you have glaucomflecken. Oh my god. Does pedicillin treat it, you know So here we have glaucomflecken. And so these are a focal ischemia Of the anterior lens epithelial cells and when you see them You'll see that little whitish gray spots that form under the anterior capsule and then eventually they fade with time So that's a sign of an acute pressurize for whatever reason Now eventually the glaucoma, we showed you what it does to the optic nerve. So russel What's the what's the most part part of the retina that's affected by glaucoma? the ganglion cell layer And the nerve fiber layer will eventually thin out now Look at this picture here because next week you guys get a week off I don't know why they do that, but you'll just be sick of path. So you get a week off But February 2nd, we're going to do retina And we're going to spend the first 10 minutes talking about what ogre's onions and retinas have in common Layers so know those layers of the retina for the second So glaucoma affects just the inner layer the ganglion cell layer and the nerve fiber layer And here you can see Here's a normal macula on top. There's the multiple ganglion cell layers And here's the glaucoma this macula at the bottom where it's very scant So end stage glaucoma affecting the retina eventually affecting the fibers Now there is an odd type of glaucoma that I don't know a whole lot about. I don't think any of us do And this is congenital glaucoma And so congenital glaucoma in the olden days again when I was a resident You put agonio on these kids when they're sleeping the OR or kepi lens You look at the angle and you'd see this little velvety membrane Across the angle and they call that bark hands membrane And so people theorize that this membrane would grow across the angle congenital glaucoma So if you went in there with a knife and just slice that membrane open Then the angle would open and the glaucoma would be improved Well, it turns out it's a lot more Tricky than that and really there is kind of a Meldevillet angle in a lot of congenital glaucoma cases with This little membrane going across it so you can't just really cut it These kids are tough to treat because you know kids scar they're like rabbits They scar they heal real rapidly and so they don't really respond real well to surgery But this is a close-up again this bark hands membrane they call it And you just look that's just a Meldevillet mesh work It just doesn't develop properly And that's what you see very commonly in a congenital glaucoma All right, so we want to talk about Another entity of diseases that can cause glaucoma rusted. I asked you already You did Okay, actually This is a weird-looking Weird-looking eye. This is a 25 year old and their other eye is absolutely normal And this eye has been given a blurring and pain for a while. What the heck are we seeing here? No injury to the eye No pastocular history ice. What does ice stand for? Exactly actually our syndrome just ice iridocornial endothelial syndrome So it's a syndrome That has kind of three different ways it can present Depending on if you're a lump or a splitter And so the key is it's unilateral Usually it'll start showing up in your teens or 20s and so it'll progressively increase Now this is the most common Kind of subset of ice and what's going on right here This is called essential iris atrophy. That's the most common Kind of subset where you see it's called corectopia Or polychoria polychoria That's costus catellus polys many Pupils so many pupils and so you can see multiple areas where the iris is stretched It's atrophy that's abnormal. This is called essential iris atrophy All right, Miko. What's the second subset? Oh, he's looking frantically in there. Oh my god. What is it? Not quite That's the third one. So you get you get partial credit because that's the third one. What's the second one in the triad Chandlers and then how is chandlers a little different than essential iris atrophy? It's dispersed and you get corneal edema with it So for some reason, you know, everybody gets some kind of iris atrophy Everybody gets a little bit of pigment But in chandler syndrome for some reason you get more effect on the endothelium and you get more corneal edema And of course the third one you said was Iris neva syndrome and here you see a nice picture. These look kind of cool when you see them in clinic Here's a broad slip beam of the iris and you see a little velvety appearance to the surface of the iris And you see these little bumps Pigmented cells sticking up through it Now what eileen is the common etiology to all of these? What's the, you know, final common denominator of all of the ice syndromes? Exactly. So they So they they grow and what is it? What do endothelial cells lay down when they're growing? Yeah, and what's that based on membrane called of the endothelial cells? Does some is membrane exactly so you get what's called desmetization Of the anterior chambers so these abnormal cells grow Across the angle closing off the angle they grow on the surface of the iris And eventually of course as they're growing on the iris you can get the iris pulled in different directions that iris atrophy You can get little pigmented cells growing with this And in fact, this is a cool one. This is one that that we had this was actually on the cover Of the archives of ophthalmology about 15 years ago And we had this patient and and they did a big peripheral or a decommunic try to control the pressure This is a p as stain and this is the posterior. So this is the anterior surface of the iris There's a p as positive membrane There's decimates membrane all along the surface of the iris But note these little pigmented cells poking through And when we looked at it in close-up, here's decimates membrane And you have these little pigmented cells and so this is the the you know pigment component to it okay, so the three parts of the Ice syndrome, you know central ice atrophy chandlers and then the The you know iris neva syndrome and so you can see this is the iris neva's portion of that. They love this on boards It's on there every year. So something you got to know even though you rarely see these you got to know these And there's a close-up decimates membrane this little pigmented bump popping through it They have little pigmented nevi, but if you look at them There'll be this velvety surface of the iris from the decimates membrane going across there And then these little pigmented cells will be popping through Now there is a another category that you have to memorize that can cause secondary glaucomas And well, I guess you're you're next You are next So there's a whole category here, and I'll give you a hint george wearing who sadly passed away a few months ago Categorize these with the so-called step ladder classification. Does that ring a bell? Anybody there's another group of secondary glaucomas Okay Exactly so there is another entity that that will do these and and In the olden days again when they used to teach us that Mesoderm is what forms the anterior chamber angle They called this an anterior chamber cleavage syndrome Because what they thought was that this mesoderm would grow into the angle and then eventually cleave and form the angle Well, it's not mesoderm it's actually Neurocrest cells that do this but in any event as the Mesh work is being formed and the anterior chamber angle is being formed They sometimes will have some malformations. They call this anterior chamber cleavage syndrome But george wiring had a good step ladder classification. Again, it's multiple different entities under the same broad umbrella And so he would put from the simplest to the more complex and it's a good way in your brain of memorizing these knowing the step ladder so the first Thing that you see in this particular entity is right here and what are we seeing right here? Embryo toxin and so people thought that at one time this was due to some toxin forming or the baby was formed And so you will get a thickened shawabi's line that's more anterior So when you look at kids with this you look with the slit lamp you'll literally see A line that's kind of concentric with the limbus but further away And so you'll get a thickened anterior Displaced shawabi's line they call it posterior embryo toxin And here you can see kind of this thickened funny looking You know termination of decimates memory. So posterior embryo toxin And then eventually you can get posterior embryo toxin with some Bands of stuff coming up from the iris Adherent there that can close off the mesh work, but actually make the iris adherent. What is that next one? renae No Not yet. No, this is in the periphery still not in the center Aksenfeld reigers and so people used to separate these Aksenfeld reigers now people are just putting them together So Aksenfeld's originally you had Little, you know bands of stuff going to the posterior embryo toxin from the peripheral iris Reegers anomaly was the same thing with loss of Iris and so you'd get iris atrophy in those areas. So now they call it Aksenfeld reigers Then you go further down The stepladder and you go further down the stepladder. Then you can get a central area of opacified cornea Nick any stabs on what that would be? Peter's anomaly. Okay, so see at least you listen. That's a good sign so Peter's anomaly and what's interesting about Peter's anomaly is You get areas where you can get strands of stuff adherent to the iris I mean from the iris adherent to the cornea, but they're more central But what's weird about this is you will get an area in the central posterior cornea Where for some reason decimates and endothelium just don't form properly And so you'll get this area. They call this an internal ulcer Now you have to know all these damn german names of von hippel So von hippel described a bunch of stuff And you know and one of the things you described was this internal ulcer of Peter's anomaly and and again some of the ways I think about this is What's weird about Peter's is it looks like someone took a bite Out of the central posterior cornea. So you get corneal Edema in that area, but sometimes it's like the iris. I mean the lens went up and bit the cornea And so you'll get a central anterior subcapsular cataract Kind of underneath the areas where there's that defect in the cornea And so I like to remember it as you know, maybe the lens, you know Took a big bite out of the cornea and then pull it back down again So you get this central ulcer with corneal edema and you can also get some focal anterior subcapsular cataracts in these So again These anterior chamber cleavage syndrome just like the ice syndrome They love asking questions on these because it's obscure There's a lot that you have to learn and so that's the whole point of boards is separating wheat from chaff And so that's the way they delineate people is looking at things like the The anterior chamber cleavage syndromes. And so here's that cornea. Here's some edema and sure enough, here's that central Ulcer of unhipple in Peter's anomaly So George Waring wrote this in the 70s and it's a classic paper It's called the stepladder classification Even though they're arguing about what causes it and what it does it's still a good way to memorize this So keep that in mind And this is from God these apartment building roof and here again is the Sagrada Familia Church which they're working on Right there. So next time it's going to be retina And so, uh, please know the layers. That's important