 to be able to survive called until you've become a little bit more familiar with glaucoma so We're gonna try a little something where you guys I want like the junior reaching to the senior residence and then the senior residence can kind of cracked or like, you know Adjust things based on their knowledge, but we're gonna try it. It's a little bit of experiment Let's see how it goes. So introduction to glaucoma Just review the, you know, the five battle signs of the eye that you're gonna want to make sure you're checking on every patient every time on call All of these will relate to glaucoma Acuity fields people are exam motility. Maybe not so much in that intracular pressure So intracular pressure is obviously the most important thing that you're checking in when you're worried about glaucoma especially acutely for your call issues A lot of people will often ask Your pick, you know, your patients will ask well, how well I know if the pressure is high And the answer is, you know, almost always they won't know and then people want to know Well, why when the pressure goes up ankle closure do they have pain? But then the pressure can be 50 and patients have no idea and the analogy I always use to describe it is the frog and the boiling water which you guys probably all heard of which is You can put a frog in water and then you slowly turn up the heat and the frog doesn't notice and then it boils to death because it's like Oh, you know doesn't really notice that the water is getting warmer and warmer and warmer as it does so very very slowly But if you drop a frog in boiling water It hops out because it's the change from normal to markedly abnormal the eyes the same way So when the pressure goes up very rapidly over a short period of time from a low number to a high number Even if it's like 6 to 30, but it goes up really quickly that patient might be super symptomatic Versus if it goes up really slowly and it's maybe 60 But it's been you know, it went up slowly and it's been 60 for weeks. You might have no symptoms at all And then the reason why pressure is important one because it usually gives you an idea of what's going on and to It's the only means we have for treating glaucoma even though there's a lot more going on in glaucoma Then we fully understand all we have is pressure. And so that's why we always care so much about what's what is the pressure? What is the pressure and then always important to know you don't have to have high pressure To have glaucoma and I saw a patient today Not today, but this week who her normal tension glaucoma was missed multiple times by us and she now just has a central island in one eye Because her pressures have always been normal. She complained about progressively worsening vision her worsening RAPD was missed And then we did fields and she's got jazz and like no vision left So just keep that in the back of your mind when people complain about Very visual complaints. Make sure you're carefully checking for an RAPD and then think you know, could this be glaucoma normal pressure glaucoma Visual fields, you know in an acute setting in the emergency room, they're a little bit harder to do but They'll give you an idea whether or not they're Intact or severely restricted. So it's still a good idea in your acute patients your call patients to be doing visual fields Confrontational visual fields in clinic You know, we'll go over visual fields in a lot more detail in the separate lecture But almost always glaucoma starts with kind of those peripheral defects the classic nasal step and then it progresses to the Arquea defects Normal tension you can get the paracentral scatoma and then then you'll get the Superior and the inferior I do it and that will leave you with your central island and then you'll have blackout vision Well, that's essentially the wide range of glaucoma visual fields My favorite little meme, I'll give you guys a chance to read that and then You know, obviously you're checking visual acuity on all these patients visual acuity and glaucoma is deceptive, right? You all well anyone who's been at the VA has had this patient where you look at their field and it's just Black and then you look at their vision and their 2020 And you think how on earth is this possible and it's because that one You know tiny little intact portion of their nerve fiber layer is in their central macula is still sending signals And they can still see but literally everything else is gone And this works against us because patients don't notice their vision loss until the very very end Because your brain is essentially filling in Those gaps so your brain again patients ask how come I didn't notice that I was losing vision until it was really really late Your brain is acting Essentially like Photoshop. It's why none of us notice our blind spots even you know when I close other I close you still don't notice Your blind spot until something is moving and then you can actively see where it disappears into your blind spot But otherwise your brain is taking Context clues from what it thinks should be there and putting it there and it does that in glaucoma too So oftentimes patients see the Humphrey visual field print out with the blackout areas and think that's what they should be seeing But it's not they just kind of see what their brain is filling in And so that's why nobody notices their vision loss until it gets really bad or they'll tell you you know things just keep coming Like on the side I won't notice them and then all of a sudden there's a car there all of a sudden People are sneaking up on me on the side. They're not gonna tell you. Oh, I have a visual field defect They're gonna tell you people are sneaking up or having trouble You know, I can't read because their visual field down there is gone But they're not gonna say what a blackout vision in an arc you would defect down here And then people are exam is really like I said really important in glaucoma That patient that lost 90% of her vision if we would have just caught she's been seen here at Moran for the last three years for the last two years they've been complaining of vision loss in her left eye and No one caught this RAPD. It's like at the four plus RAPD now. And so it was it's clearly been there for a while So make sure in the clinic, you know, oftentimes the techs are checking pupils for you I love our techs, but they will miss an RAPD even a glaring RAPD half the time So make sure especially when you're When you're worried about glaucoma or you're worried about the optic nerve Double-check pupils look for an RAPD yourself. Don't rely on somebody else to do it Or you can screen for people are things by asking them, you know Just one I seem brighter than the other two colors seem different one eye versus the other So even if you walk in and they're dilated you can still like red desat them if you think oh gosh Maybe maybe I can't trust this pupil area exam. They're already dilated Well, I can still do a red desat or ask them brightness testing So don't forget to think about that, you know, the people are exam and then glaucoma, you know Oftentimes in glaucoma if it's even a little bit asymmetric, you'll still get an APD. It might be subtle But like a a decent-sized nasal step is enough to produce in one eye and not the other is enough to produce an APD Just keep that in mind. All right glaucoma you guys know It's not a problem with the faucet. It's almost always a problem with the drain That's just the basic anatomy and then the other major part of the exam It's not a vital sign of the eye, but that you should be doing on any patient Basically, I say any new patient that you see you should get a gonio one because Tell you what's going on with that patient and two because the only way you're ever gonna get good at doing gonio is if you Do gonio? So the more you do it the better it's gonna get certainly any new glaucoma patient to any clinic needs a gonio Dr. Roscoe will tell you at the VA if you're thinking about dilating a 90 year old guy who still got his lens in you Don't do that. Tell you go and yell him and make sure that his angles are open post trauma patients looking for angle recession or PAS Diabetic patients uveatic patients looking for PAS. So there really are a lot of patients where Even if you're not thinking glaucoma the angle can tell you a lot about what's going on And then the mnemonic for those of you who are first starting out looking at the angle and thinking what the heck am I looking at? It's I can't see this Stuff which is iris, ciliary body, scleral spur, Trabecular mesh work, and then Schwabbi's line. Grading the angle, you're trying to assess a number of different things When you're first starting out, you're basically just wanting to say what am I looking at? What are these structures? Is it open or closed? As you get a little bit better at doing it You're trying to say okay, where what are these structures exactly that I'm looking at? Where is the iris inserting? Anterior to Schwabbi's line is grade a between Schwabbi's line and skull, scleral spur visible is C And then if you can see the ciliary body, D or E And then the angle of insertion So what angle is it open? You know is it 30 degrees usually pretty narrow 45 degrees pretty open, so you're just kind of Getting as much information as possible and really that you know, this is just a guess you're looking at it and saying I don't know it looks narrow 35 degrees 30 degrees sounds good And then the iris configuration Most patients if they're normal will have just a flat iris The boat anteriorly is frequently what you'll see when you're worried about narrow angle or pupillary block Plateau iris is pretty uncommon and hard to see but that's where you get that hump of tissue Right at the angle. It's almost like the classic board finding is the double hump sign But you get this extra kind of mound of iris tissue right near the angle and then the concave That does anyone know what kind of glaucoma you frequently see a concave iris configuration But classically you're young myopic males Yeah So the classic glaucoma that you'll see the concave is your pigment area glaucoma You've got the young myopic patients the eyes stretched really long The iris actually bows a little bit Posteriorly and it's that posterior bowing that allows it to rub on the lens and that's how you get the pigment dispersion So if you're ever on a test and somebody says something about the gonio is Bowed posteriorly they're almost always trying to tell you this patient has pigment dispersion and then just some conio examples The only way you'll get good at figuring out what you're looking at is by one doing it and also looking at examples So the one at the top is just kind of a nice normal open angle You can see Celery body You can see a pretty densely pigmented Travecular mesh work and maybe like a faint sample E.C. line on that one who can tell me what a sample E.C. line is I know you guys all can Exactly so there's technically they think microscopically there's a little Transition area where the endothelium is ending which is what Schwalbe's line represents and then the The angle structures are starting and so it's a natural place where pigment can kind of Accumulate on this tiny little shelf and so if you would see anybody with a densely pigmented Line right at Schwalbe's line then you want to think pigment dispersion or pseudo exfoliation Post trauma is another one or uve addicts can get it People can get it post cataract surgery So sometimes you'll see some pigment especially inferiorly if you're going to owing someone after cataract surgery anything where there's been a little bit of Inflammation in the eye can allow pigment to build up on On Schwalbe's line When is it why is it important to know if you're looking at a sample E.C. line or the Travecular mesh work? SLT them exactly you don't want to SLT their endothelium that would be sub ideal and also oftentimes in like say this patient here when you get Really good at going owing You'll discover the corneal light wedge reflex Which basically tells you in a normal core in normal cornea you have the Anterior wedge of are the anterior kind of strip of your slit beam which is on that Epithelium and then your internal wedge of slit beam which is on the endothelium well when your endothelium ends These two strips join together. So that's happening at Schwalbe's line But if you have a pigmented Schwalbe's line it can look like Travecular mesh work and so it can mean the difference between an angle like Telling if an angle is open or closed. So if you see this pigment you might think oh, well, there's a Travecular mesh work I can see the TM obviously the angles open But if you do your corneal light wedge reflex you realize oh nope That's just a densely pigmented Schwalbe's line in this angle is actually closed a great resource It's like an atlas of every different Goni-O exam finding you would ever want to see in their videos So you can watch him literally sit there and just go near the angle and zoom in and show you exactly what You should be seeing when you're doing Goni-O correctly And it is it's pretty helpful. So if you have some free time instead of aging all your colleagues Go ask if yous at work Watch amazing Goni-O videos and then the final part of you know a Vinnie I exam Especially when you're thinking about glaucoma is evaluating the optic nerve and you know assessing the cupcake disc ratio And this is just you know, obviously a really elementary review, but you're assessing the health healthy room of tissue relative to the the cupping centrally and kind of It's a gestalt like how much you know what percentage of this optic nerve is taken up by cupping versus how much healthy room There is things you'll want to take into account when you're looking at a nerve like this and saying well Is this a normal nerve that just kind of has a physiologic larger cup? You're looking at the rim tissue as you get better at looking at glaucoma. You can also look at kind of the NFL Nerve fiber layer as it's emanating off of the nerve and you can start to see little focal wedges or defects that could indicate glaucoma versus just physiologic and then obviously this is where Rnfl OCT is handy where you get an Rnfl OCT on this patient and it's all green in 120 Well, this is physiologic versus, you know, if this is all They have superior thinning and pure thinning then this is glaucoma. So it's not always easy to tell And then nerve that looks like this if this is true glaucoma or not So all right getting into cases case number one 76 year old female Red painful eye past 24 hours. What do you want to know? What else do you want to ask? No previous ocular surgery never had anything like this before What's she doing when it happened? She was laying down getting massage at the patient who owned a massage studio and said Oh, I can't get massages anymore because anytime I lay down to get a massage I get a horrible horrible headache that just lasts like all night. So the provocative testing in glaucoma does sometimes work So never anything like this before no past ocular history. She wears glasses She had a mom with clinical history and remark on this lady in the ER She's kind of got a this weren't a glaucoma lecture. What else would you be thinking? Right, this is good. She had just had surgery and ophthalmitis inflammation scleritis uveitis and then obviously glaucoma. So here's her exam findings here She's hyperopin findings here into your chamber. She's a little bit too hazy and won't let you go near her Right away. So you're just looking by penline which you can do in the ER if you have to And then you know hard to get a view beyond her cornea because it's so hazy But there's like a you know, maybe a cataract there and you're you think you finally tuck her in to letting you do a gonio and She's hey, you can't see any trickular mesh work. It's all just You know, there's nothing to see in there With a bowed angle and then you gonio her other eye and it's really narrow so talk about Who's at risk for angle closure and what the pathophysiology is I think to understand with a cute angle closure crisis so They want Factors Oh So in a short eye, there's less space overall, so it's more likely to happen, and it's more likely to be bolder, more likely to wear them. So there are factors like that that are related, and that makes your family structure. Yeah, in this case, you know, it's kind of like current, so I can imagine like it's pulled into the corner. It's not like all the way open, that's why it's like most of the time it's dark, and then when they come into light, it's like it's coming in this mid-spot, and that's where it gets blocked. I understand, because that's like when it's super outside, it's like not close to the people. Sometimes when it's kind of there, it's like that perfect little spot where that big angle, don't break it. And that's why it's like always on financial, like personal lenses, because those are fat, whereas like IOLs are super thin, so I know I'm never happy. I'm sure it can happen. My first officially angle closure in a guy who had, he actually was pseudophagic. Okay, how are you guys doing? We're good, good? One more minute. Okay. I'll just answer emails. That's like a topical type of thing. Hi, I have pressure in here. It's like she has a cuticle closure. Her ankle is close to the hand. Are there any other things that's like you would think about? Do you know what we're talking about? Well, I think we're right there, but you can put that all the time. Oh, that's hilarious. Okay, the old asker would then push a sign or you'd block it. Yeah. Dispatch, but classic. You have a type of retro cataract. Yeah. So that's what happens when it occurs. Exactly. Yeah. So that's like you, all the lens 14s walk up with your regular lens. Does that happen in really dense coverage? I don't know if she's quite there yet, but. Oh, I will get there shortly. Okay. We'll give you guys 30 seconds to wrap up your discussions. And you can stay in your groups because we'll probably do a little more discussing. Okay. So who wants to talk about women presenting signs and symptoms for acute ankle closure? Just list them off. One of the groups. Med painful eye. Med painful eye. Puking into a bag. Yeah. They're miserable. These patients are miserable. So again, patients will ask, well, how will I know if I go into ankle closure? You won't know. They come to the emergency room. They are very unhappy. What else when you're looking at the eye? Easy cornea. Med dilated pupil. Easy cornea if it's acute, but I've seen plenty of patients where they've, especially your demented patients that can't tell you, you know, they, someone will just notice their eyes red and they've been in ankle closure a while. But yeah, those are the big ones. Good job. What about risk factors? Increasing age. Increasing age. Female. Female. Asian or like Pacific Islander descent. Perfect. Genetically like family history. Yes. Use of like anticholinergics or like topomax or something. Excellent. Good job. Then the difference anatomically between what the ankle configuration is and specifically what pupillary block is. Just a second. So we talked about signs and symptoms, shallow anterior chamber, risk factors, crowded anterior chamber. So you're short axioling and hyperopia. Also smaller cornea, age. And a lot of that just has to do with changes in the cataract. So even if they don't have fagomorphic glaucoma, just age related changes to the lens tend to shift everything forward. And so that's why it's rare to see acute pupillary block angle closure in young patients unless something else weird is going on. And then one of the things they think can also predict angle closure is the ability of the iris to retain water. And so some people will measure like your, how boggier or mushy your iris is with anterior segment OCT. That's kind of a newer field. But there's a lot of research into that. So that might start to be questions like on, on OCAPs. And then genetics, Asians and Inuits and first degree relatives. So the path of physiology of an acute primary angle closure is pupillary block. Meaning something is obstructing the flow of fluid at the pupil. The pupil is, when that happens fluid can't get out from behind your iris. And that's what causes everything to push forward. So it's, it's an anatomical setup that puts you at risk. But the actual instigating thing is something happening at the pupillary margin lens interface that stops the flow of fluid around the lens. And that pushes everything forward and only once everything is pushed forward does the angle completely close off. Does that make sense? So that's when you get your classic really narrow in the periphery but relatively deep or formed centrally that kind of Bombay appearance because you're having the accumulation of fluid behind the iris. And that is why a PI is helpful in pupillary block glaucoma because you're relieving that pressure that's pushing everything forward. Drilling that hole doesn't change anything about their angle. Their angle is still narrow. It's just you relieved the acute pushing forward from the fluid. So just to reiterate that normal angle, angle's nice and oh dilated position for some reason. That's where things tend to have a hard time. There's a lot more touch between the iris and the lens when the pupil's mid dilated. And so that's why things like closing your eye or laying prone, those things that put you in mid dilated or certain types of medications anticholinergics that kind of mid dilate the pupil are the biggest risk factors for sending someone into acute angle closure. Did you drop those? I did not. I think Griffin drew them. And then this is classically what you will see. So you can tell, right, there's something pushing that iris forward from behind. And this is the patient in that classic iris Bombay pupillary block appearing angle closure. Again, pupillary block, iris Bombay. This one has a more advanced cataract. So what's the treatment? Emergently, you're going to give them diamox. And then you're going to call the fellow or your chief depending on how comfortable the chief is. And you're going to have him do a PI. And the reason why the PI works is because... Laser iridotomy is a type of laser... That's the only reason why it works. You're not changing anything anatomically or structurally about the angle. You're just preventing that pressure build up behind the iris. And then on crisis, like you've truly gone into it, oftentimes we're going more towards early cataract surgery in these people, but not always. You can see why. Can someone explain actually why cataract surgery? What it's hard to have or almost impossible to have pupillary block angle closure in someone who is pseudophagic? So it's harder for them. Like it wouldn't be as common for the iris to touch. Exactly. Exactly. You're exactly right. So you can just see the difference on this anterior segment OCT between pre-cataract surgery, the angle is open, but it's narrow. And you can just see that lens is taking up space versus post-cataract surgery. There's a whole lot more room in the eye. And there's not a lot of opposition between the iris and the IOL. The only time I've ever seen a cute pupillary block in a patient without a lens was a patient who was a-fagic and she grew a membrane entirely over her pupil. And then you just yag the membrane and give her back her pupil and the problem is solved. But it's practically impossible. If someone's pseudophagic and you think they have angle closure, it's probably almost definitely not. It took me I think as a resident full on halfway into my second year to really understand who needs an LPI. So case number two, we kind of talked about this. Everything's the same except for, oh, what's that right in the middle of her eye? I don't know. Coroptometrist told her she had a cataract a while ago, but cataract surgery scared her. And pressure's high. She can't see anything out of that eye. And she's got a white lens. So what is the difference between someone who gets pupillary block angle closure and someone who goes into fake amorphic angle closure? Discuss. You have a minute. So she's the first person to do that. So I guess the first question is... Yeah, but that's just, but that's like fake amorphic, like the only cause of the cataract pupillary block angle closure. That's the question. Yeah, that's the question. Yeah, so you got the part where you're archaic. That's going to be so free. So... So I get examples of the cataract who goes into... from this both category. Cataract surgery? Yeah. So the surgeon cataract surgery, that's like, yeah. So that's what happened. So this was like the gift that Dr. Zabriski gave me when I was just finishing fellowship. She's like, congratulations, you're towards the end of your fellowship. This, it will be your first case. I'll be down the hall if you need me, but we'll add this on in room four. So this gets a lot of things. First of all, the difference between primary pupillary block angle closure and fake amorphic angle closure is the mechanism, right? It's purely since pushing everything forward. They do not have to be predisposed to angle closure to go into fake amorphic angle closure. They can have the widest open angle in the other eye with the bad cataract simply because that lens is taking up so much space it's just completely pushed everything forward and closed things up. So it's a different mechanism and it's not a primary pupillary block. There may be a slight component of pupillary block that develops and so oftentimes people will try an LPI in these patients and see whatever pupillary block component there is, but it is not curative. You'll find the pressure will still be high on these people and this is, as Brad was saying, kind of the only scenario where cataract surgery is an emergency. The cure, the only way we're going to get pressure down in this patient is by taking their cataract out. We can temporize them with diamox, try and bring the pressure down. We can, you know, do an AC tap if there's room, but you've got to get the pressure down and then you have to get the cataract out. So yeah, this was a lovely lady who presented, of course, on Friday afternoon at like 3.45, spoke no English. She came to us already while I tried to put a PI on her and her pressure's still 6 in her. She got IV diamox over the weekend and then it was super fun. You'll often find when you're doing cataract surgery on these patients there's a component of zonular loss too that's allowed everything to shift forward, right? So the zonules get loose when the cataract is that big. They get stretched and then everything just pushes forward. How do you do cataracts? You're cheaper like that. Right? So there's a lot, you can give them like pre-operative diamox or pre-operative manital to try and shrink the vitreous. There's a thing called a honan balloon which you will read about. I've never seen it used, but the idea is it essentially pushes it down to give you more of an anterior chamber. Or you can call your friends in retina and have them come in and do a little preparatory vitrectomy to give yourself some more room. Or you can do it yourself mid-case if you feel like Dr. Chia has done it, had to do it a couple of times where there's just no room to work and so you go in, you do a little vitrectomy, things have more room to fall back and then you have a chamber again. But yeah, it's not fun. It requires a lot of viscoelastic and yeah, you lose a year of your life when you do it. So essentially the biggest difference is the mechanism. A PI is not going to be curative in these people whereas in primary angle closure it can be and then the cataract. And so again, I think a lot of you have seen this, but my cat went into fagomorphic angle closure glaucoma while I was at Ascarus. So I came home and his cornea looked like this and then he had to get a nucleated. And now he's a one-eyed cat, but he's very happy. It's not a pain anymore. Oh yeah, he was really uncomfortable. And he had underlying ubiida so that probably was a component of it, but I could tell a cataract was developing quite a while. Well, the angle, in acute fagomorphic, the angle would still be closed just because the lens has pushed everything as part of it. But if you're looking, oftentimes, if you're trying to tell the difference between, is this primary angle closure, is there a fagomorphic component? You can look at the other eye. And if the other eye is open, then whatever's going on in that eye is probably just a fagomorphic. Oftentimes, really the biggest differentiation is important for testing purposes because I'll ask you, is this fagomorphic or is this primary angle closure? In the real world, it's usually a little bit of both, which is why in the real world, most of these patients end up getting PIs anyways because there's probably some component of pupillary blood going on in addition to the fagomorphic component. Okay, so, in your group's 26-year-old female with bilateral eye pain, redness, blurry vision, what do you want to know for her given that this is a glaucoma lecture? She's 26. It's bilateral. So anytime you see a question like this set up on a, you know, they're trying to get you to think about atopamax history. Yeah, they're trying to get you to think about atopamax. So, oh, any recent history of migraines, any medication changes? What are you on? Oh, epilepsy. Oh, what medication have you just started? And then the key for atopamax induced angle closure is it's bilateral. So if both eyes are in acute angle closure and they're young, it's medication induced until proven otherwise. And on a test, it's almost always atopamax. Do you give these people a PI? An LPI? Why wouldn't it help? There's no pupillary block. There's no pupillary block. That's right. So tell me what the proposed mechanism is for why atopamax can cause acute angle closure. Anterior rotation of the cellular body. Exactly. Good job. So anterior rotation of the cellular body, you can get cellular body effusions, rotates everything forward, pushes everything forward. Bilateral angle closure is almost impossible for people to present bilateral acute angle closure. It does happen, but almost always if they're presenting bilaterally, it's atopamax. And then the treatment is to stop the drugs and lower the IOP in the interim. It will resolve once you stop the atopamax. It will go away. Those effusions will resolve. The cellular body will rotate back to where it should be. And you just have to keep the pressure stable while you do it. There's no role for an LPI in these patients. So just a few other types. Angle closure glaucoma that you'll frequently see on call. Neovascular glaucoma. I mean, in testing situations, it's usually fairly obvious they're trying to point you towards angle closure. You'll see fluoride, iris, neovascularization. They'll have a history of poorly controlled diabetes or a CRVO, BRVO. Anything that causes ischemic changes in the eye can give you neovascular glaucoma. In reality, it's often really difficult to see these vessels, especially if the cornea is hazy or the iris is dark. So you have to really, really have a high threshold of suspicion in these patients to look for vessels. Do these patients need a PI? Why not? Right. So the mechanism in this is not, again, it's not a pupillary block glaucoma. You have vessels growing into the angle that are causing anatomic closure of the angle, but there is nothing pushing from behind that is causing the angle to close. So again, this is something that I would see as a fellow, the residents would call me and say, oh, hey, I think this patient needs a PI and it ends up being neovascular glaucoma. These patients, nothing. You can PI them and then they'll just bleed everywhere. Not ideal. So these patients almost always end up needing glaucoma surgery, usually a tube depending on their vision and their visual prognosis. And then malignant glaucoma. So malignant glaucoma is pretty uncommon, but I saw it maybe three times as a fellow, almost always at night when everyone else is, I think, the worst cases with Tina, everyone was gone to AAL, patient with a pressure of 70. And the key hallmark in malignant glaucoma is a uniformly flat chamber. So if you see that Bombay appearance, it's not malignant glaucoma, but if everything is just diffusely pushed forward and, oh, I don't know, they had glaucoma surgery or cataract surgery earlier that day or the day before, it's malignant glaucoma. The key that you'll see on a test is they'll say, oh, this patient, super narrow, angle closure, you do a PI and nothing changes. There's no, you know, there's no improvement in their symptoms. There's no improvement in pressure. The angle is still completely closed off. So no improvement after PI is the hallmark with malignant glaucoma. Here's an example of what it looks like. You can tell everything, you can see how it's different than that Bombay appearance. Everything is pushed forward. And then again, an anterior segment, OCT, showing just diffuse anterior pushing of the vitreous. Who can explain the mechanism or the proposed mechanism from malignant glaucoma? What do they think is happening? Why are things getting pushed forward? It's the... It's like the vitreous is basically, like, isn't it like a known kind of... That's true. It's like, as I was saying, I was like, wait, no, I feel like every explanation I've read is like... The classic explanation is you have, instead of the aqueous getting secreted into the posterior chamber, posterior chamber being in between the iris and the lens, it's actually getting secreted into the vitreous. And it goes posterior to the vitreous, builds up behind the posterior hyaloid, pushes the vitreous forward. So it's actually anterior pressure from the vitreous being displaced anteriorly. It's the classic teaching. Whether or not that is actually true remains to be seen. But that is why one of the treatments is to yag the hyaloid, because you're trying to disrupt the vitreous enough to allow that fluid from behind to come forward. So treatment for malignant glaucoma. Acutely, you're trying to lower the pressure as best you can with drops. They almost always need IV dimox. They'll end up getting an LPI just because you kind of have to do it to prove to yourself that it's malignant glaucoma. So you do your PI and nothing happens. You start them on atropine. 50% of the time over time, atropine will allow this to resolve. But it usually takes a long time for the atropine to kick in. So in the meantime, you can try to yag the anterior hyaloid face to try and disrupt that face so the fluid can come forward and relieve that pressure. I've never seen it work. I've tried to yag the crap out of this leaf, just nothing. And then I called Zabrisky and he said, oh yeah, I've never seen it work. But the one time someone's told me that it worked is when you actually yag through the PI. So I tried that and I just yag the crap out of her vitreous through the PI and still nothing happened. And she eventually went on to have surgery. So 50% of the time in theory atropine these can resolve with atropine. I think in reality most of these patients don't want to just get a vitrectomy. The zonulohyaloidoid urodectomy meaning you're actually taking part of the zonules as well. Almost always it's postoperative. There are case reports of spontaneous malignant glaucoma and those are kind of controversial. So almost always it's a postoperative patient. Frequently it's post glaucoma surgery but it can be or complex anterior segment. The one that I saw on call was a secondary IOL and then that patient went into malignant glaucoma afterwards. This weekend we had a patient who came in super high pressure and the blood was basically against the colonia and turned out they had hemorrhagic carotidals on B-scan. Does that count as malignant glaucoma? No. You bring up a good point which is make sure you're looking in the back of the eye. So you can do all that stuff and have the exact same exam findings with hemorrhagic carotidals being the mechanism that's pushing everything forward as well. So you still are obligated to do your full eye exam or a B-scan. But yes, hemorrhagic carotidals can present very similarly to malignant glaucoma. I think they did everything. They did like an LPI. And then they were like, oh, this might be something else. So in an ideal world, look before get a B-scan before. Because yes, you're exactly right. Hemorrhagic carotidals will look just like that. Is it something that changes the flow of the aqueous behind everything? No one knows. That's the theory is that you somehow disrupted the normal flow of aqueous. And so surgery is obviously the primary mechanism. I guess you can make the argument to do it as well. I haven't seen it. So that's kind of a cute issues with angle closure on call. You'll get less commonly on call. You'll get these problems which are the open angle problems. So our 57-year-old African-American male with vision changes in the right eye, he's probably not going to present to the emergency room, but he might. In fact, my very first patient on call, my two-year, was exactly this case. It wasn't Barack Obama, though. Barack Obama have glaucoma? No. Things you want to know, vision changes, maybe they're going to have specific angle closure. Those complaints are specific. Open angle glaucoma or something, people will always tell you the few ocular diagnoses they've heard of. He has a high stress job. And then this, really kind of a normal, benign, appearing exam until you check pressure and it's elevated in the right eye. And his optic nerve looks like this. So cases where these kind of patients will present, this is where one gonio is going to help you. You're going to gonio him. His angle is super deep. You know he's not an angle closure, but the pressure is high. He's got cupping. You're thinking, why is this guy presenting this is clearly open angle glaucoma. What often happens in these patients when they present acutely is the acute recognition of a chronic problem. They for some reason close their other eye and they realize, oh man. Wait a second, I can't see out of this eye nearly as well as I can out of the other. And then they come to the emergency room. So that is what happened with my lady who had a central island and then unfortunately for her she'd been following with an optometrist for like 20 years and had missed her glaucoma for more than 10 years and years. She ended up needing a trap. So Barack Obama says, good job you diagnosed me. Strong work everyone. Oh a beer. The PA students. These patients, you know, what are you going to do? Your options are you can decrease aqueous production or you can improve aqueous outflow. We'll go over drops again in a separate lecture but you guys know the main categories. You have your beta blockers, you have your UVO scleral, and then the newest one is the rock or roe kinase inhibitors which is repressa and rock-latan. And basically we just throw anybody that we're desperate on. We were like, well we can try repressa. That's approved in America. Yeah. At the VA everyone gets it now. It's repressive. Last night I hit like Japan. So when you decided you were going to be a clover. It was part of it. That's when I decided I was going to do advocacy. Because this lady had been just grossly mismanaged for years and years and years by an optometrist. Who was like masquerading as a... who told her that he was an eye doctor and essentially just let her go blind. That's when I got involved with advocacy which you guys should all do. Everyone should go to mid-year form if you get the chance. It's the greatest conference, especially as a resident. Anyway, digression. The question always comes up. Normal tension glaucoma or is this poag? I just threw this in here more because you're going to be tested on this eventually. But the biggest difference is pressure. In normal tension glaucoma the pressure is normal. In poag the pressure is elevated. You can make the argument that the cupping characteristics are a little bit different. They tend to have more sloped cupping in normal tension or more focal notching in normal tension. They think disc hems are more common in normal tension. I think that that's probably just because their pressures are normal but they're still unhealthy. Most people have you're hanging out at these pressures that for most people are fine but for them are unhealthy. They're going to get disc hems where for the poag patients still get a disc hemorrhage if there are pressures at an unhealthy level but for them it might be 40 and we're usually pretty good at treating those. I think that might be why you see disc hemorrhages more frequently in normal tension. Not because it's inherent to the pathophysiology. The thing to really know with normal tension is the systemic associations. When you see normal tension glaucoma especially if they're getting worse and their pressures are 10 you're going to want to screen. Do you have history of migraine headaches? Do you have a history of Raynaud's phenomenon? Patients with that kind of vasospasm history are more at risk for normal tension and then hypotension especially nocturnal hypotension so these patients will get blood pressure monitoring and theemia can cause it as well. So these patients get systemic workups especially when you're first diagnosing normal tension glaucoma to make sure there's nothing else going on that's contributing to the nerve cupping and it's essentially an ischemic idea, right? They're not carrying enough oxygen in their blood because one of these conditions or vasospasm is reducing the flow of blood to the optic nerve and they get long-term chronic ischemic damage to the nerve from one of these mechanisms rather than it being pressure that's causing the ischemic damage. Does that make sense? But we're treating the sleep apnea for the sake of sleep apnea. We're treating their...no, it can stop like if you have a normal tension patient that's progressing and they have untreated sleep apnea treating their sleep apnea will stop their progression or at least slow it frequently because you're increasing their oxygen carrying capacity at night you know they're often probably profoundly hypoxic at night your optic nerve is a watershed area just like your brain like those watershed areas in the brain so if you're not carrying enough oxygen by the time the blood gets to the internal parts of your optic nerve then it doesn't have enough oxygen to really saturate the tissues the way that it normally would so yes, if you're improving your oxygenation with the CPAP machine at night you're going to improve your glaucoma. So just a few other types of opening glaucoma because we're here in Salt Lake City like giving them oxygen also help them like giving them like natural oxygen yeah, I mean and some people with CPAPs I think do get some supplemental oxygen as well you're doing the positive pressure ventilation so they're oxygenating better on their own because they're keeping their LVLI open more but you're also providing some supplemental oxygen a lot of the time too same reason why like profound anemia would cause the same problem because their oxygen carrying capacity is significantly reduced so just a few other types to review your open-angle glaucomas Scandinavian patient in Utah and you see this on the lens what is it? Pseudoacetylation and then you go near them because you go near everybody and you see a sample E.C. line and a fairly pigmented trabecular mesh work and you send them to the cardiologist the GI specialist if it's around skin don't do any of that probably so the thing to know with Pseudo-X is that it's a systemic disease they just end up getting most of their effects in the eye I don't send them to cardiology as most common in people of Scandinavian descent and for some reason people who decided to settle in Salt Lake City as well and then you get the fibrillary material on the lens capsule in the iris, trabecular mesh work it often presents with markedly elevated IOP and they may have been people who have been stable for years like oh yeah they have Pseudo-X but no signs of glaucoma will follow them some people will make the mistake of following them once a year but that pressure can go up really quickly, very very fast over just a very short amount of time to really high numbers and then come to you a year later and their pressure is 60 and they're blind so Pseudo-X needs to be followed Pseudo-X without glaucoma needs to be followed at least twice a year that you're seeing them never let them go longer than that because they can just deteriorate really really rapidly and then cataract surgery you worry about when you do cataract surgery on these people you worry about their zonules and then you also worry they can go into angle closure not necessarily during cataract surgery but if those zonules are loose everything can get pushed forward really easily so these patients can go into acute angle closure and then treatment drops SLTs usually pretty effective on them angle based surgeries usually pretty effective because the problem is right there in the trabecular mesh work but often times it's pretty effective anyways and then last one I think you're young myopic male we kind of already talked about this oh my eye I get this brow egg every time I go running and then my vision is a little bit blurry and they have what is this what's the official word for what this is showing for cumberspindle and they have IRSTIDs that would be a shy stripe but it's pigment from that chafing of the iris on the lens capsule so if you dilate them and you see this kind of band of pigment again that's all findings consistent with pigment dispersion and it's usually young patients usually highly myopic they usually have that bowed iris cumberspindle sample ac line mid peripheral iris TIDs vision loss can be profound again I've had a couple patients who've been followed for years and everyone missed the fact that they had pigment dispersion syndrome and then when they finally go into acute glaucoma from it no one knows to be following them at more regular intervals and their pressures are 60 for a year and they go blind so again if you have a patient with pigment dispersion they need to be followed more regularly pigment dispersion without glaucoma needs to be followed just like a pseudo-x patient congenital glaucoma kind of a lecture for another day the classic triad who wants to tell me epipharah linking glauphorospasm and photophobia so any baby where they present like that always think glaucoma any baby that has corneal clouding think glaucoma a new baby with tearing think glaucoma butthelmos is classic but it's not part of the classic triad so they don't necessarily have to have butthelmos oftentimes these patients will get treated with nasal acrimal duct obstruction and people will miss that they have glaucoma so a baby with tearing it's not an NLDO until you've ruled out glaucoma so just make sure you're checking the pressure and doing glaucoma workup and then babies can't get alpha agonists because it will depress their CNS and they'll stop breathing and then they'll die and you don't want to kill babies and treatment is surgical so drops are a temporary measure but the treatment is to treat the ankle treating your glaucoma post-ops for MIGS troubleshooting their post-ops are kind of just your typical cataract patient troubleshooting when you're on call they might have a little bit more blurry vision because when you're working in the angle it's more vascular so they might have more cell they're at bigger risk for a high FEMA especially after a GAT they're almost always going to have a high FEMA so if you get a call from a patient who's had an angle based surgery cataract surgery MIGS procedure you just want to make sure that the high FEMA isn't an eight ball high FEMA it's okay for them to have a high FEMA you just treat it like you would treat any type of high FEMA with a Trab and a Tube the things you worry about are a lot more complicated coital effusion, supercoital hemorrhage over filtration, licking blood, under filtration and then the classic thing you'll get asked this on every OCAPS I got asked this twice on oral boards they showed me a picture of it anterior chamber and they said this patient had a blood clot surgery what is going on and you have to ask well is their pressure higher low what does their blood look like so just know this flow sheet it's a classic setup for a test question so leaking blood you would expect the IOP to be low you would expect the chamber to be narrow and you would expect the blood to be flat it all just kind of follows with common sense over filtration IOP would also be low but the blood would be elevated and it would flow it out through your blood will it make glaucoma if the pressure is high and the chamber is flat and then coital hemorrhage you can really have this is kind of what we're talking about coital hemorrhage can present anyway it can present with low IOP because the low IOP is what puts them at risk for the hemorrhage if that hemorrhage has been there for a while it can push everything forward and cause the pressure to be acutely high usually the chamber will be shallow because everything is being pushed forward by these giant coital hemorrhages behind you can often see them when you look at the eye they're kind of hanging out they're saying hi to you from behind the pupil then you feel terrible and then the blood is variable but the way you'll know it's a coital hemorrhage is because they'll tell you I sneezed and then all of a sudden my eye started to hurt like crazy or I bent over to pick up my newspaper and then all of a sudden I had severe pain and couldn't see anymore that's it, questions would you like to state that to check the pressure or to feel their eye that they can tell at the time? I mean if it's like a cooperative then like a two year old you have to do an EUA you're not going to get an accurate pressure because then they're screaming at you and they're bell solving and their pressure is going to be high when they're screaming at you and you're trying to eye care them or tone a pen them and the eye care is telling you you know you're too far away you're too close, you're too far you're going to get a pressure with a tone a pen and then from about age one to age if you were really suspicious you know say they were epithomic and had the classic triad then you would just schedule them for an EUA what other questions? is this what people had in mind by an introduction to glaucoma lecture? yeah that's great it was like they said to read chapter one but chapter one is not actually an introduction to glaucoma those chapters are always wrong these problems the moran, ophthalmology, learning i love that acronym experience