 So, a couple of things, I think always, they always seem to come up on clinical examination. So, about the optic nerve head, if you use a 60 degree lens, that gives you, you know, like about a one-to-one. With a 60 degree lens, the height of the slit equals the disc diameters and millimeters right directly from the scale, right? So, you've got a 60 degree lens and you're looking at the optic nerve and you dial down the slit to match up with the optic nerve. It's a one-to-one relationship. Okay? With a 78-degree lens, it's a 1.1. And with a 90-degree lens, it's what we usually use, it's 1.3. And those numbers just seem to come up a lot. So, you know, Super 626 is the one I'm asking about now, I think. Is that right? Yeah. Okay. So, that's like the closest to 60 diodes to that. So, that equals to 1. Yes. You just say 1. Yeah. Yeah, 60-degree lens. That's an old lens. But that's Super 66. Okay. So, that's a good point. So, maybe that's the reference now. It's the Super 66 is the one that works. But the 90-degree is 1.3. Okay? So, it's 1.3 times what you read. And the normal sized optic disc is approximately 1.5 to 2.2 millimeters. So, the other thing that they say is that, like here, you're looking with a direct ophthalmoscope, the small aperture is about 1.5 millimeters. So, the small aperture on the direct is about the size of a smallish, kind of the small end of the optic nerve. So, most optic nerves are just a little bit bigger than the small aperture on the direct ophthalmoscope. That's another thing that comes up sometimes. And, let's see. What comes up is, as far as the vertical cup to disc ratio, the normal, quote-unquote normal is considered somewhere between about 0.1 and 0.4. But as many, as 5% of individuals without glaucoma will have a disc size greater than 0.6 or a cup to disc ratio greater than 0.6. And another question that I see a lot is that a cup to disc asymmetry greater than 0.2 is found in less than 1%, you know, 1% or less of individuals. So, that's really a breakpoint when you're looking at cup to disc ratio about asymmetry. More than 0.2 is pretty unusual. I think those are some things that seem to come up. I know that the size of the optic nerve relative to the 90 diopter lens is a specific question on my MOC. Okay, let's see. I mean, if you guys have any questions, of course, ask me a bit. So, in terms of the number of axons, in a child, it's like 3.3 or 2.2 million. And it's pretty much like 1.1 million. 1.2 million is the number that I have. You know, about 1.2 million axons. And then diameter, I guess it's a moving world. So, diameter, kind of like the worst thing is like 1.5. And then the posterior, it increases. It's just going to, like, with the sheath. Yeah. I actually don't know that. It's not my area. But, yeah. Yeah, those kind of things always, they always just kind of keep coming up with those kind of size questions and stuff like that. What was the thing with the direct, if you're looking with the smallest aperture, that size? That's about the size of kind of the small end of the normal optic nerve range. So, you know, optic nerves are, you know, about 1.5, and that's what the size of the small aperture of the direct up-downs. So, the idea being is if you look at the, look at that, and your optic nerve is smaller than that, that would definitely be a small optic nerve, because that aperture size is kind of the smallest end of the normal range. So, I think another thing that, again, we're just all over the tests that I took were questions about the major clinical trials of glaucoma. So, I thought we'd go over that just a little bit. So, this is a table, I don't know if I, if I show that little graph right there, do you recognize that graph? Yeah. So, that's a very famous graph from the ocular eye prevention treatment study, okay? And what that shows is that the way that you're able to stratify risk based on corneal fitness, right? And, you know, I did it once, but if you, if you take these numbers here, because on this side is pressure. So, if you take this table and you collapse it, all right, and you collapse it so that you no longer have the stratification that you get from corneal fitness, and all you get is the stratification based on intraocular pressure, right? So, if you collapse that onto one side, the only variable you have is intraocular pressure. And it's really pretty amazing because if you collapse it down and do the numbers, and you look at individuals with a mean pressure greater than 25.75, which is basically 26 or above, right? And you look at the risk based only on intraocular pressure, the risk of developing glaucoma over that five years is something like, as I remember doing them, is it something like 21 or 22%. But the thing is is that you would have no idea that some in that group actually have a risk of near 40%, whereas others have a risk of less than, you know, 6%. And so that's, does that make sense? So that's the power of what that added stratification of corneal fitness brings is it separates that group, you know, any of those groups based on if the only variable you have is pressure. The idea being is that it just shows the power of the predictive value of central corneal fitness. In fact, as you remember on that table, they don't have it in here, but on that multivariate analysis of the ocular hypertensive treatment study, central corneal fitness came out number one. It's amazing, you know, even more than pressure. So that just says that, I mean, central corneal fitness is just a number that when you're treating glaucoma patients, you just have to have it. It's absolutely as important as measuring pressure. You only need to measure it once, really. But just having the front of you, all the time we built our EMR, you know, we built it so that the central corneal fitness would just come forward all the time. So it's always right there on that report that you can have because it comes up every time you make decisions. So the idea of this table is just to show the power of the predictive value of central corneal fitness. Now, if you were to say, so obviously, you know, people with thick corneas, do you over or underestimate their pressure? Overestimate, right? Thick corneas. And what would you say, and this is a little bit arbitrary, but, and I think if they ever asked you a question on this, they would make it obvious, but where did you think that a thick cornea kind of starts? What number do you have in your mind? Is it all the k? That's kind of a thick cornea. What's that? 560? Yeah, something like that. Again, it's kind of arbitrary. But hopefully if they ask you a question, they would say they would show it like a 620 or something. Over 600 is definitely there. But yeah, I kind of think of the, in my mind, kind of the normalish range is, you know, 520, 530 to 560, 570, you know, kind of in there. Less than 520, I definitely think of that as then, less than 500 definitely then. And the same going up, you know, 580 and above is definitely, definitely greater than 600 is definitely big. Okay. So you over or underestimate the minimum thickness? Yeah. So for men and women, how much does that differ? Men and women? Yeah. Not that much, really. I mean, that probably does. But in the clinic, it really is not very similar. Okay. So then going on here to some of these clinical trials, and you know, they've been coming up for years. So the SIDGET study or the collaborative initial Welcome to Treatment study, there's about four big ones here that you really, you definitely ought to know. And they are the four, I think there's four listed here. So the SIDGETs is one of them. And what did that study look at? What they're actually lowering IOP? What's that? What they're actually lowering IOP? Yeah. So it's basically the SIDGETs is surgery versus medicine. And it is the U.S. equivalent of the early Morfield study, Morfield in England, published a study when I was a resident, so that would have been about 93 or something like that, that indicated that surgery first seemed to be very effective in halting visual field progression. So they really started advocating surgery first. And so in response to that, and it was a very good study, but in response to that, the National Institute launched a study here in the United States that kind of met the modern day criteria of a kind of a practice of the flying study. One of the most important variables of which is that it's multi-centered. The Morfield study, great study, but it came out of one institution that you know that the major, major studies now that really define the way we practice multi-centered. So they started recruiting, I think, at about 93, which is about the time that the Morfield study came out, and they recruited 607 patients all with open-angle glaucoma, but they did allow secondary open-agles and humanitarian exfoliation disease. Multi-center randomized all the buzzwords you need. And basically the bottom line of this study is that they found and they were randomized, you know, right off the bat, right? They were first diagnosed right off the bat, surgery or medicine. And if you look at the results, although the IOP was lower than the surgery group, initial medical and initial certain therapy resulted in a similar visual field outcome after nine years. Okay, so that's pretty impressive. Early visual acuity loss was greater than the surgery group, no surprise there, but the differences between groups converged over time. Okay? The quality of life impact reported by the two treatment groups was also very similar. The overall rate of progression of open-angle glaucoma in the cities was lower than in many clinical trials, and that's an important thing about this trial and another question that comes up. So they were randomized to surgery or medicine right off the bat, and they did about as well, and the visual field, excuse me, the visual loss was worse in surgery early, but they kind of converged over time, and the quality of life was rated about the same between the patients, which is interesting. One very important part about this study is that the rate of progression in this trial was lower in both groups than in most trials, and the reason for that is probably that in both arms of this study there was very aggressive pressure. I think the surgery group was like 48% lowering from baseline, but the medicine group was 35%. I mean, it was really excellent pressure lowering, and the reason was on the medicine side is that there was a very set protocol, but they allowed the use of prostaglandins, so there's the biggest difference. Many of the other studies didn't have use, either they weren't available or they didn't allow them, but they allowed the use of prostaglandins and they allowed multi-drug therapy. So that's really interesting study and basically it kind of didn't change then what is typically done in glaucoma and that is restarting medicines. Now the only thing about that is that some of the very latest and more recent publications by the Sages study seem to say that people with very advanced disease early on that got surgery early on and probably didn't do any better. So there's an argument there. So, what does that mean to me? Well, sometimes when you have a patient that comes in and it feels already wiped out or it's super severe and maybe you might be seeing it for the first time or they just recently got diagnosed so it kind of fits the Sages profile. One of the things I do on them is I just kind of max out their drugs right off the bat. They come in at a pressure of 35 their field looks terrible and rather than just start them on a prostaglandin and bring it back and then start them on this and bring it back, I'll just start them on at least two agents to start with like a prostaglandin and dorsal mix and wall or something like that. And just get an idea are we going to get there with medicine or not and try to make that just and move to surgery. So, doesn't this say that it seems like we just have someone who's new and we start someone who's showing a mild visual field defect and they just started at a pressure of 21 and it seems like we're starting people on one drop and not decreasing them by 36%. I mean, that's really what we should be doing. Well, yeah, I mean I would say that when you start treating on anybody there's always exceptions. You know, you have these people that come in and they have glaucoma their pressure is 12. But if you've got a classic glaucoma patient new or just starting treatment or maybe just brand new you're deciding to start treatment. Yeah, they've got a pressure of 22. I would say at a minimum when you start a drop you're looking for a 20% drop at a minute. And if you don't get that I would stop that drug and try something different. But I agree with you. I mean, you'd like to see around, you know, a minimum 20% but you'd like to see about a 30% drop of pressure for someone with genuinely you know, looks and smells like glaucoma visual field defect, you know and you're starting them on treatment. Yeah, you'd like to see about a 30% drop and it's not unreasonable especially if the visual field defect is, you know, moderate or so. You've got a teeny little nasal step out there or maybe you'd accept a 20% drop but if their visual field is significant I'd say you're looking for a 30% drop to kind of start out. So that's the city side. Very important study. You know, it's 20 plus years old now but still very, very important. And the other thing about that is that, you know, they lowered the pressure and the patients did it really quite well and they got the pressure down a lot. Okay, so then the ocular hypertension treatment study super important, that table that I was just showing you is from that. So this is another, all of these studies I saw almost every one of them recruited in the early 90s. The advance one is a little bit earlier than that but so ocular hypertension by definition they didn't have glaucoma right they just have high pressure recruited a whole bunch of patients and they were randomized comparing observation with medical therapy. So they either randomized to either observation or treatment of medicine. And they got about in their study they got about a 22.5 decrease in pressure. Now there's also in all of these studies it's interesting whether you're not using placebo or whatever in the control group there's always some lowering and in this group also in the control group there was about a 4% lowering a pressure right kind of a regression and here's where this number comes in and those that were treated there was about a 50% reduction in the risk of developing glaucoma that's the number to have in your mind there was about a 50% reduction in progression to glaucoma at 5 year follow up. So the untreated group was about 9.5% conversion to glaucoma and in the control group in the treated group it was 4.4 so there's your about a 50% difference. So that's a there's just an important number to know and that's again established some of the treatment parameters for treating antibiotic retention. The risk of glaucoma glaucoma was increased with these are the factors that are important to remember age, vertical and horizontal accompanist ratio the pad of standard deviation on visual field and the IOPF baseline and then central corneal thickness kind of came into the equation so just as a historical note when this study was first organized and randomized central corneal thickness was not included in the screen and some of the study participants some of the physicians just argued we've got to do this and thankfully they did and then they actually went back and measured central corneal thickness on these patients and it turned out that that was the most powerful predictor it was. So that's where this kind of idea of this really powerful risk stratification for glaucoma for ocular hypertension came about which is the older the patient the greater the accompanist ratio initially the worse the visual field in terms of the pad of standard deviation like there's a little bit suspicious there and then there's there IOPF baseline and there's central corneal thickness you can weigh those factors out so I kind of think of it if you look at this table right here I think of the people that's my up and left people that are up and left have higher pressures thinner corneas and increased baseline accompanist ratio so you've got a patient with a pressure of 26 corneal thickness of 480 and accompanist ratio of 0.5 the first time you see them even though their visual field is normal their risk of developing glaucoma in the next 5 years is 47% so that's I kind of think of them in that category thin cornea, higher pressure higher accompanist ratio and then down in this corner you've got the lower pressure still after the hypertension so their pressure is not 26, 22 their central corneal thickness is 600 and their accompanist ratio when you first see them is 0.2 their risk of developing glaucoma in the next 5 years is probably less than 2% so those are kind of the categories, so I don't actually calculate out the risk although you can, I mean you can plug in the numbers and actually generate a number but I kind of think of them in those groups and everybody else falls somewhere but those are really the critical things out of the octalagra tendetry study and this is really an important study that we refer to all the time so just a couple of things that have come the original paper with that data, with the risk association and the 50% decrease of post 2002 subsequent papers in 2007 the same predictors of the development of POEG were identified independently in both the oats observation group and the same study done in Europe so those two were found to be equal including baseline age IOP, central corneal fitness and cup to this ratio and then the visual field the thing about the visual field for me I'll be honest with you the visual field for me you know it doesn't factor into my kind of just thinking and the clinic that much because if you start to get a visual field that looks a little funny you're kind of almost talking about glaucoma so I'm talking about the hyper tens if their visual field is stone cold normal and their OCT might be stone cold those are the ones I'm talking about but their pressure is 26 how do you stratify their risk? well that's when you really go with age the older they are, the more likely they are their central corneal fitness is huge in that setting and then what their baseline cup to this ratio is those are the main things for me and of course the pressure and then here's another very important thing so in 2010 they published and they said the subjects in the original observation group received medical treatment for a median of 5.5 years after their period of observation subjects in the original treatment group continued to receive medical therapy so basically you had this ocular hypertension group that got therapy right off the bat then you have the second group that were followed in the observation arm for 7.5 years and then some of them started treatment based on their own choice or they met certain criteria that their risk was higher now that they had the information that they knew their risk was higher so some of them were elected to be treated so you've got these two groups that have been treated for 13.5 years straight they worked for 7.5 and then treated for 5 5.5 the proportion of subjects who developed POEG was .22 in the original observation group and .16 in the original medication group the primary person of the follow-up study was to determine whether delaying treatment resulted in a persistently increased risk of conversion to glaucoma although the two groups diverged with respect to the development of the original study period there was no further divergence in the capillary curves after both groups received out of glaucoma treatment the bottom line being it did not hurt these people to observe them it didn't mean that then once they started on treatment that their risk was still 50% higher right? it didn't show that at all so it justified the idea that these very low risk patients observing them is perfectly acceptable and did they stratify the thin CCTs again or? I'm not sure exactly I think they just kept the same I think they just kept the same risk profile going forward and when they treated those I think they were treating more of a higher risk group but it didn't affect the final outcome in terms of how many of them converted during that five and a half years where the previous observation group is now treating okay trial number three which is also very important is the early manifest glaucoma treatment trial this is the one that is to compare immediate IOP lowering with observation so the difference about this study is that these folks had glaucoma they weren't glaucoma suspects but they had glaucoma they had all the diagnostic criteria of glaucoma and they were stratified to either be observed or be treated and I think I've mentioned before when I give this lecture this is the one that was done in Sweden it was a national institute study, US funded study done in Sweden because you'd never get that through an IRB to observe people with glaucoma in a trial there's too much data to say that but they needed to answer the same question and so it's newly diagnosed patients who were 50 to 80 years of age had early glaucoma were identified there was exclusion criteria it was multi-center and they were randomized to either no treatment or treatment this is a different treatment protocol to receive batoptic and laser trapeculoplasty that's how they were treated now the one thing about this trial different than SIGIS is that the treated group here only got about a 20% pressure lower so in this group at 6 years 62% of the untreated patients showed progression whereas 45% still a really big number of the treated group progressed so the treatment did reduce the progression by 25% but it's argued in this study the reason why so many of the treated progressed is that the pressure lowering was modest at best there's only about 20% but it again showed it just helped to establish that even in a glaucoma patient treatment does make a difference okay I've said this to you before even when I was a resident that had not been clearly established there were still papers being published I started my residency in 1991 there were still patients papers being published in the late 80s early 90s arguing that treatment glaucoma did not have that lower pressure and that's why several of these states so early medicals glaucoma treatment trial treatment helps even if they've already gotten glaucoma and then the last one that's listed here is the advanced glaucoma intervention study and this is a study that had kind of a weird start because I was wondering what worked best to do laser trap and then more laser or laser trap trap now that seems like an odd question to ask but this was the earliest of these this actually started recruitment way back in 88 and so we were just trying to find out how to treat these advanced patients with this disease and you know this is the really this study has produced a whole bunch of papers it lists gosh 14 of them here but the one that is the most important is ages 7 so if you're going to learn one of those, learn ages 7 and ages 7 is the one that showed and I've talked about it here the pressure the patients do better these are eyes with average IOP of 14 or less during the first 18 months or eyes of pressure of greater or 18 at all visits those that had pressure of 14 or less at all their visits did better it's a simple conclusion that seems pretty logical but it never really did show the pressure lower at every visit versus those whose pressure was higher at every visit those with the lower pressure did better and the average pressure amongst that group was 12 so that's kind of where the idea came about getting the pressure down around 12 and these advanced patients seems to be there's another one that you might hear about is that in 2009 ages reported that IOP fluctuation was an independent predictor of progression meaning that if the pressure was kind of variable at inter visits that that seemed to result in more progression that's actually been a little bit reputed by some other painters so that's not a super hard fast finding but it certainly wasn't important any questions about those studies that they are all the time they're very important the other thing that I would encourage you to go over on your own and I'll guarantee there's a lot of it going to be on your and that is the table of glaucoma medications and you know basically it just breaks it down into the various pharmacologic types of glaucoma there are basic mechanisms of action the usual kind of percent decrease that one can expect and major side effects okay and if I could just point out I know you know all the basic things but I could just point out a couple that maybe you're not aware of or maybe not thinking about that are very very real and in analogs one of the things that they list under systemic side effect is flu-like symptoms or joint and muscle pain or headache I've heard all three of those many many many times they feel like they've got the flu or maybe a little more common is that they feel like they have a cold I've been stuffy I've been stuffy all the time and they won't necessarily associate it with the initiation of the eye drop but joint muscle pain I've seen that be just shockingly profound you know and headache so those are all very real of course you know all the ocular side effects you know the lash growth etc etc those systemic side effects of prostate planets are very very real and I'll guarantee it you'll hear about it the Bay of Walkers you know and they're all real you know I've heard them all one thing about the the Bay of Walkers is that the topical tolerance of the Bay of Walkers is really outstanding I mean Timmelwald almost never causes an allergy irritation is minimal so that side of things is great but the side effect profile on the systemic side is significant and the absolute at least in my mind the absolute contraindication of Bay of Walkers is asthma or reactive airway disease you can put somebody in the unit with the drug Timmelwald if they are found asthmatic or something like that so that is absolutely real and then the other one that we can't underestimate with the topical Bay of Walkers is the depression low mood very very real I always watch for and the other one is sexual dysfunction so I always watch for a patient of mine who I know is on a Bay of Walker if suddenly they appear on a new antidepressant or an ED drug I think those are two things to watch for and if I see that many of my patients and they're on a Bay of Walkers I should talk to them about let's try coming off this and see if it makes a difference or if they are on those drugs to start with I definitely think twice about adding a Bay of Walkers to that because so apriclonidine and bromonidine is what we use for alvegan now again the overwhelming thing is the topical of those drugs especially the bromonidine there is absolutely in my mind absolutely no doubt about it the difference between the generic bromonidine and the brand name alveganp in terms of allergy I wish we could get the alveganp but it's incredibly expensive for so many but there's just such a difference bromonidine 0.2% is so much more allergenic than the alveganp is alveganp the normal alvegan that's the brand name it's almost always I don't even think they have the right for alveganp which has a different preservative that's the pure right plus the concentration is half it's 0.1% but the other thing to absolutely remember about the alphabetic magnets is the fatigue and dry mousin those are huge in terms of systemic side effects and both of those can be profound the fatigue can be profound of course you know it's contraindicated in infants right we published that paper first here the first I think index case was one of my patients here a little baby that didn't know had been a one after the NPA just got super lethargic and so we collected a few cases one of them was from Hyderabad actually put a baby in the evening with respiratory suppression incredibly less common if not unheard of with apricline or alveganp because it just doesn't cross the blood brain barrier there's a real difference I know up in the neuro clinic they won't even test a border cocaine for kids for testing for like a border so that's probably not necessary probably not, yeah there's a very different penetration of the blood brain barrier but the apricline seems to do fine and then the fatigue so it's contraindicated in kids but you'll hear it in adults you have to be aware of that when they talk about fatigue I put an older lady on Bremonidine to start with and I got a call about a week later or something from the family and they said you know Grandma we so tired since starting these drops I said well it can happen she said well you know ever since she started these drops she hasn't gotten out of bed and we're just opening her eyes to fit her drops let's stop that but that's how profound it can be but some lady in the bed for a week it's real okay a couple other things you know about dimox I really think of dimox as a temporary drug nowadays to get into surgery however you know I've got a big practice with lots of glaucoma patients and I've got a number of them that are on chronic dimox because they're either a super high surgical risk and they do okay on it so yeah okay they would absolutely prefer to just keep taking that and maybe risk their one eye to have surgery or something like that and again you know remember when I started in glaucoma everybody's on dimox we didn't have anything else you know they're on timelol, pylokarpine and dimox how's that for a reaction I mean we have the most unhappy patients in the world but that's what we have so that's what we use I have a long history of people being on chronic dimox so I'm not afraid of it but obviously it's got a long list of side effects and mostly we think of it as a temporizing drug to get the pressure down immediately and get it in surgery but I have a number of patients who are on a long term how hesitant I feel like a lot of times we see all these really bad diabetics and they have bad renal function and they need to be on dimox how much of a contraindication is that I'm not afraid about it and someone like that I truly think of it as a temporizing drug but someone with good renal function and otherwise relatively healthy it is something to keep in mind as a potential chronic therapy and again 25 years ago it was the therapy everybody was talking about we have a bunch of people in the VA last year putting them on chronic dimox but I think that's partly because the system there is that we're changing, we're not checking creatinine levels and potassium levels so it's a viable option to consider sometimes the one thing I think of also about the topical carbotic inhibitors dorsolomide dorsolomide as you know is the generic dorsolomides azopt azopt is more comfortable there's no doubt about it but I really think about those as darn near the safest topical drugs from a systemic standpoint maybe even safer than the prostaglandin not only because of the bad but those are really I think systemically very very safe treat babies that's usually the first drug I pull off if I want to try a topical agent or a pregnant woman for example so that's I think that's the thing to know about polycarpene and we sell music that it's on here I guarantee you got to know about those things that's where they test you from I think I've said before when I took my my bores which back when I took it was exactly the same as the OCAPS and it was just the same test there were like three questions on a drug garanite garanite was like some old oral carbotic inhibitors not even on the chart anymore I don't think I remember looking it up and the only place it was was on this stupid chart in the book just know these even some of these kind of orphan drugs like phosphine iodide understand a little bit about that and manitol I have never given manitol it's always on try the phosphine iodide the thing to remember about that it's it can be a very very useful and helpful drug in kind of complicated aphaking glaucoma so it is a drug that in a child with aphaking glaucoma can be like a home run drug so it is I mean I have several patients on phosphine iodide and it was not available for a long time but it is now in the pharmacy so the last thing I wanted to mention and we'll go a little bit early is about about endothelitis following filtering blood surgery you know we hate it but it is real but I think the thing to note the incidence of post-operative endothelitis with glaucoma surgery with or without any fibrosis drugs has been reported to range from about 1.3 to as high as about 8% so that's kind of how I think about it 8% is too high these days but to say 1 to 3% is probably fairly legit I think ours is lower than that here we have the day to improve that but it's a real risk most commonly it's caused by those high thin blebs certainly the presence of a leak increases the risk to eradicate so every time I see one of my patients back that has a bleb looking for a leak as part of it I don't pain the floor seeing every time in the strictest sense you should but I just put in a drop of fluoresce right off I just used their eyelid to kind of paint the bleb you know how you do that right you kind of move it up and down over the bleb and it kind of paints the bleb with the fluoresce that you put in and that does a good job of detecting the leak but I look every time every time I have a patient that has a bleb I check for a leak just kind of kind of do it because that is a very different perspective and what's the most common organism to cause a late bleb associated endothelitis I was thinking it was a strep species I mean some of them are the strep the strep for it that's what I think is the most common cause acute post cataract endothelitis it's usually a staff species of some sort right the layout set of bleb associated is usually a strep species most common age flu is actually fairly common what's the difference between a blevidus and a strep or a bleb associated endothelitis what do you look for vitreous involvement that's the number one if you've got vitreous involvement by definition you've got an endothelitis so you've got to get on that if it's just cell in the anterior segment you're walking a little bit of a fine line there but I think you can treat them as a bad blevidus and very carefully and if it seems to be strictly limited to the conjugal the anterior segment is totally quiet of course the vitreous is quiet then that's kind of a pure blevidus you can treat that top the one thing though is that if you do have what you think is a blevidus you have to treat them pretty strongly with antibiotics you can go right to fortify but you can also go to just frequent you know kind of broad spectrum topical and when I think of broad spectrum topical I might put them on a like a ophoxicin or bigamox type drug and then maybe polyture and use them together in a bad blevidus but if it looks really bad especially if you've got any kind of anterior second inflammation putting them on fortified antibiotics is not a bad idea and sometimes I just use like bigamox or something frequently in a fortified bank and I usually do that we fortunately don't see it that often and you know a lot of the I truly believe that that this modification of the modern trapezolectomy where we broadly apply the mitomycin has absolutely made a difference in terms of the frequency of the infection because it just changes the morphology very much that is really an important change just since I've been on these so and does the tubes don't have the same rate of ophthalmitis? it's significantly less but it's not zero but almost always when you have an endothelmitis associated with a tube there's an erosion I would say I have not seen one an erosion present so that's the other thing anytime you've got a tube patient you've got to look for an erosion every time and if you see an erosion you've got to fix it I don't think you can just watch it so if I see an erosion I start it on antibody topically just prophylactically and then get them scheduled to patch it up with a blem leak I've known people and I've followed I have sometimes followed a little blem leak on antibiotic hoping that it'll seal up put them on an aqueous suppressant put them on an antibiotic see if we can get it to seal up I'll watch it interestingly I'll watch that one more than I'll watch a tube erosion a little bit the tube erosion has just seen destined to get infected because you've got hardware in there so it's just asking to get infected so I usually patch those really quickly and then I've watched a little bit and I know some I can say some have watched a leak for a long time alright so those are the things that I wanted to talk about with Trevor based on my recent history