 Well, we were just chit-chatting about fellowships, so I'm sorry we're a little slow in getting started. So you said fellowships in retina? In retina. Okay, anybody? I'm happy to contribute if you want. Yeah. Well, what do you think? What's your current take on the fellowship situation in retina? Most of them don't give you enough time to really sort of absorb a lot of the medical as well as the circle side. I think. Yeah. And it takes a long time to learn, so there were a bunch of us that would basically take on junior partners who had finished their fellowship, and we usually said it takes five years after they've finished their fellowship to sort of get them in the mode of handling patients, handling, referring physicians, handling arts. Right. I mean, we can talk about various fellowships around the country if you wish. Let's do the lecture. That's what we're here for, and then maybe if we have some time later on. Sure, sure. I'm sorry, gang. I apologize. So today we're talking about lasers and ultralightism. I'm an O4s. You're a pardon? I'm an O4s. Old fart of red. Now go ahead. Thanks. So we're talking about posterior segment lasers, so we'll be talking about photo coagulation, trans-pupillary thermal therapy, and photodynamic therapy. And so coagulative necrosis occurs at 149 degrees Fahrenheit. The area and volume or diameter and depth of laser treatment is directly related to the power and duration of the laser, and much more so than the theoretical differences between wavelengths of the laser. So we'll talk about indications for treatment and delivery systems. We'll discuss wavelength and color, power and duration, anesthesia, lens selection, and then pitfalls and complications. So some of the indications for photo coagulation would be pen-rental coagulation for neovascularization, focal laser treatment for macular edema, closure of microannurisms and telangiectasia, like in Coat's disease, creation of coriorental adhesion. So this is, of course, used in treating retinal breaks and retinal detachment, focal ablation of extrafovial cortoneovascular membranes. Now, when Dr. Sinclair was training, this was a very common thing. In today's world, some of these lasers you probably don't see or use very much at all and probably won't get a lot of experience with in residency, I would guess. The other thing, too, is since some of the studies like protocol S of the DRCR network came out, I think that PRP is still used but not used as much as it used to be. One of the things as I was reviewing these slides from this talk is I thought it would be really interesting to pull up all the Medicare data and kind of see what the laser codes have done over the past 10 to 15 years. And I would guess that you would see a dramatic drop-off in laser codes. For instance, focal laser treatment for diabetic macular edema, have you guys had a chance to do that or had much experience with that in residency? We have people that we do have AS to see if they might be like a good kid. More from like MAC, MA is like they'll do focal for it. Yeah, I don't think so. So did you do any micro post laser here at all for macular edema? Steve, did you do micro pulse in your practice? I've done a huge and published a lot of micro pulse. I just want to know whether anybody's done it here. You know, we don't have micro pulse in our office and part of it is just everything's been so taken over by anti-vegeta therapy and then... The pharma world is just dominating our workplace. You're right. But in addition to that, if they fail anti-vegeta therapy as the first line, then we usually go to Ozured X or some sort of steroid or alluvian. But anyway, so it is. It's really changed over time. Yeah. Other things that... So you can use focal laser treatment to treat central serous choreorectinopathy. And then you can also use photo coagulation of some intraocular tumors. So things like curvil homangiomas and sometimes it's used even to treat curvil melanomas, small curvil melanomas. There are different delivery systems that can be used for laser. Of course, there's slit lamp delivery system. There's micro-pulse laser. So Steve, I'm really curious to hear about your experience with micro-pulse laser. Frankly, I haven't used it and I'm not very familiar with it. It was something that came into vogue after I finished my fellowship. And we don't have micro-pulse laser. I've seen the presentations and papers, but I don't have any practical experience with it. So what's your experience with micro-pulse laser? Practical experience is that for mild, macular demo, when the vision is good and the fovea is involved, do you want to do any kind of laser treatment or do you want to give anti-veg injections when the vision is relatively good but the fovea is involved? So we found that Jeff Luttrell and I published that this micro-pulse laser works very well at resolving the edema and actually improving the vision. But you've got to measure the vision in real-world context. You can't use visual acuity because visual acuity, come on, gang, we've used it for 170 years and it does not measure vision. It has never been validated. It's the longest thing in use in medicine, but it's never been validated. But we all use it. But when you use different, let's call it vision testing, that measures real-world vision under real-world context, it shows significant improvement. And in AMD, we're seeing dramatic reduction in the development of chordal neobascularization and a really significant reduction in the progression of geographic atrophy. So we're sort of beginning to think about it and 810 now is used much more than 532, the yellow wavelength of erodex. The 810 is now sort of becoming preferred for the micro-pulse treatment. I don't know how often you have it up here. You use it for more photo-coagulative kind of processes. So I've been interested in hearing sort of that. But for macular treatments, when we're starting much earlier in the disease process, I think the micro-pulse is going to have a real mixed relationship with the antigen. So do you use it in macular degeneration to coagulate drusen and things like that? Yes. So, you know, there was the capitrile that was done during my residency years. Did you do that? Yes. But it didn't work, right? The takeaway is that it didn't work, right? The rates of croital neovascular, even though you got rid of the drusen, it created enough injury, and this is what we're worried about with the nanopulse laser injury kind of trials, too, is that although you can reduce drusen, what are you doing to that pigment epithelium that is injurious? So you're still going to get the croital neovascularization as a secondary quality, because now they're showing that croital neovascularization is the worst drusen, yeah. But the worst things are the pseudo drusen, the calcified drusen, and other things, and pigment epithelial hyperpigmentation, and other changes that are going on that we're sort of not realizing yet that are really predicting the progression of the macular degeneration. I think you're going to see a lot of this in the next five years, and I think pharma is going to try to get into it, but I think in the meantime, if I predict, I think micro-pulse laser will come to the fore. Interesting. Still need to be done, gang. Well, I mean, with all the I'm happy to... With all the complement factor factors that are coming out and being tested for dry AMD, it'll be interesting to see what the yin and yang of laser versus complement factor inhibitors will be. Right. So laser energy is absorbed by melanin, and that's what creates the photocoagulation. So the laser goes into the eye. It hits the RPE where the melanin is, and that creates the coagulate of necrosis. So macular is anthophil. So the pigment that's in the central macula absorbs blue light relatively well, but not yellow or red. But you're saying that the red is actually kind of the laser of choice now for... It's now becoming, again, in the photocoagulation world, we try to reduce the injury as much as we could, because what Greg... Well, what a bunch of us showed is that so you photocoagulate the microaneurysm or the telangentasia or you're treating the edema as we used to do in the ETDR study, but 90% of your laser energy is absorbed by the RPE. And that laser scar expands 300-plus percent over time. The problem here is it extends over 25 years. So most of the studies that were done with two-year follow-ups or barely three-year follow-ups when you're using visual acuity as your outcomes, they didn't show the bad effect of the photocoagulation. I'm sorry. I'm annotating on top of it. Please go on. No, that's fine. Those are wonderful insights. Thank you. The other thing is back in the day when I was an intern here from 2001 to 2002 and then at Iowa from 2002 to 2005, AntivegF came out right at the end of my residency in the beginning of my fellowship. So you probably know Jim Folk from the Capitrinal, so Jim was one of my mentors at the University of Iowa. But anyway, back in the days before AntivegF therapy, we'd see a bad diabetic or bad central renal vein inclusion and we'd always use red laser treatment. And the reason we'd use red is because it's not as well-absorbed by hemoglobin, whereas blue, green, and yellow are much more absorbed by hemoglobin. So we would just be desperately trying to get as much laser treatment into the renal periphery as we could, but we'd always use red, and that's because it wasn't absorbed by the hemoglobin. So this just talks about the different wavelengths, different colors that are used. So green and yellow in photo-coagulation. We would use focal laser treatment using yellow laser primarily when I was in my residency in fellowship. Blue laser treatment is not something that I think has been done for a long time. By the time I came around, it was all green and yellow mostly, and then red to penetrate through vitreous hemorrhage. And then infrared, 810, as of course is used in micro-pulse laser treatment. So these are some of the sample settings. You guys have done pan-retinal photo-coagulation for diabetic retinopathy. Have most of you done PRP? Do you guys still get a chance to do PRP? At the VA, you do quite a bit. How do you decide how much laser to put in and how many sessions to do it over? How do you decide? I mean, yeah, go ahead. I think for us, we're learning, and so the first time that you sit down and you use a contact lens or you know that everything's inverse. So a lot of it for us at the VA is based on how well and how quickly we can do it and how much the patient can tolerate. Because I think we do have a lot of patients who need very dense PRP, but you just kind of do what you can and then if it's not enough, then you just bring them back. Yeah. So do you always use a slit lamp with a contact lens like a super quad or a roto-spheric or a rodent stock? If you guys use the rodent stock, sometimes if they have a really heavy brow or a prominent brow, sometimes the rodent stock's nice, it's got almost like a little more of a shaft on it so that you can get around the brow. What kind of anesthesia do you use for pan-renovatory regulation? Topical. Do you ever do a subconj or block them? The retrovolver? So, you know, when I was in my residency in fellowship, we'd often block them. That was kind of the routine. We usually do a retrovolver block for pan-renovatory regulation. I'm not using the indirect to do PRP. I don't know why, maybe it's just the fact that I'm not as much in one area and I kind of scatter it around a little bit more. I'm moving around a little bit more, but sometimes I think the indirect is almost a little bit better tolerated when I do it that way. In some ways it's a little faster, too. But, Teresa, I think to your point, I think it's good to get as much in as they can tolerate in a session and then bring them back if you need to. Also, the billing for PRP changed here where it used to be a 90-day global period and now it's a 10-day global period. So, we get paid a lot less now for PRP. But, you know, if you do PRP, it used to be that when I was in my residency in fellowship a lot, the attendings at Iowa felt strongly about not just blasting them with PRP and doing like 1,500 spots in one session. So, we'd often do like 4 or 500 spots and break it up into, you know, two or three sessions. Steve, what's your MO for laser treatment? Yeah, the downside of PRP. I mean, it's amazing to me that even though the diabetes goes on forever, it really stops the, let's call it progressive retinopathy of the capillary occlusion. Now, you can sometimes get a little bit more capillary occlusion toward the fovea from the temporal side, but always the question has been how much PRP do I put in? Do I fill the ischemic areas that I may see on wide-angle and geography? Do any of you do this? Or do you just put it in everywhere? Because the secondary downside is the constricted visual field. Because remember, if these spots, if you're putting them one burn, you put them up one burn with the part or one burn with the part, they expand to coalesce to form a solid peripheral visual field defect. That's 15, 20 degrees. If you're taking it tight into the disc, that's the temporal side on that eye, that's 15, 20 degrees outside of your visual field. I'm sorry, go ahead. I'm just sort of saying these are some of the downsides. Their downside is if you're trying to put in a lot of PRP with the indirect, remember you can aggravate the macular edema by just burning the hell out of them. So the whole question I think that's now coming down is how much PRP do I put in? How hot burns do I put in? How close do I bring it back? Do I just treat the ischemic areas? Is the relatively ischemic area at the border of what I can see as capillary non-profusion contributing? Right. Those are just all comments that we don't know. Well, the other thing too is nictolopia. So night vision problems. So constricted visual field and night vision difficulty. And those are tough things with PRP. So how do you decide in whom you do PRP versus in whom you do antipage of therapy? Any thoughts on that? My ability of the patient to come back? Yeah. Yeah, that's for me. And that's a very subjective assessment, isn't it? I mean, but if you have somebody and you're worried particularly about payment issues or their ability to get rides or take off work to come in, you know, and you've got to get something in there that's going to keep them progressing to a tractional retinal detachment or massive vitreous hemorrhage or something like that. So it's really variable. I've got a young lady who's probably in her early 30s. She's been type one diabetic now for 20 years. Super reliable. She comes in to see me every couple of months. We're down to every couple of months now. And I give her an Avastin shot in both eyes every couple of months for her proliferative diabetic retinopathy. But she doesn't want the constricted visual field. She doesn't want nictolopia. She's super reliable. She's got great insurance. She's got it together. And so she prefers antipage of therapy. And a patient like that, I think it's a great treatment and also kind of kills two birds with one stone and that you can also treat any diabetic macular edema that's kind of cropping up or it helps to keep the macular edema at bay. But how long do you keep it up? What are we using for endpoints with antipage in PDR? In her, it's indefinite. And I think that she... And we've had that very frank discussion about this numerous times that this might go on for the rest of her life and she's like, okay, bring it. I'm fine with this. But it's nice to have some PRP in because I think it decreases the VEGF drive. And so it kind of keeps things under control in general, anyway. Yeah, but just to amplify what he said is we don't have a long-term follow-up to know what happens with the ischemic retinate in the aftermath of when you stop antivegf once you've involuted the neal. Right. But later on, gang, what's going to happen here and how often do I follow this patient? What do I do in order to try to define my long-term thing? Because I think the patients like you have are rare. Yeah. In other words, to keep coming back and keep doing it. And then it's not until, oh, shit, I got my vitreous hemorrhage. Well, you know, and the other problem too is if they get hospitalized or if they're, you know, if they're really... Which diabetics often are. They're really sick people in general. And so they get hospitalized and go to a skilled nursing facility for a while. They fall off the map, and then they're proliferated. He goes crazy. So anyway, these are just some sample settings. MPS-style laser. Again, you probably won't see this in your residency or fellowship. I think it's pretty rare anymore. But we used to do the MPS-style laser occasionally when it was an extra foveal-protele neovascular membrane. We do that in my residency and early in my fellowship. But then antivegf therapy came along and it just entirely changed everything. Anesthesia, we've touched on this a little bit. There's topical subconjunctival, retrobolbar. For retinal tears and sometimes localized retinal detachment, I really like subconjunctival because you're not blocking the entire eye. You don't have to patch them afterwards. And yet it seems like, especially if you let them sit there for 15 to 20 minutes, it provides adequate anesthesia to be able to do your retinal tear, retinal detachment, demarcation. In terms of lens selection, there are a couple of different lenses that you can use. You can use the negative-power planokon cave lenses or the high-plus power lenses. And these each result in different magnification, laser spot magnification. So if you use the focal laser lenses, like the Goldman III mirror, the Yanozzi lens, it doesn't magnify the lens spot very much. You get a lens spot that's fairly true to what you have on your laser setting. Whereas for panoramic population, if you're looking for a wider angle lens, a super-quad or a quadrospheric lens, you'll get increased spot magnification. But the other thing, too, to Dr. Sinclair's point, that you get laser creep is what we always would call it. You get expansion of the laser spot size. So I think that when you're doing panorental photocrygulation, I mean, I look at my patients who had panorental photocrygulation in the 70s or 80s, and their peripheral retinas are just hammered. I mean, they've got basically confluent laser. And I'm a little more ginger with their laser. I want to treat it enough that I control the neovascular process. But I don't just... I don't carpetbomb them. I try to be a little bit more discreet in the way I treat it. Nevertheless, you've got to treat enough to keep the neovascular process that are controlled. Any questions? Steve, any comments? No, very good. Yeah, I think this whole aspect of how much peripheral laser treatment we've got to do to try to control the process and get the good results we've all experienced, but not create the nyctalopia that, you know, they... And even under misopic conditions, you're that romantic restaurant. And these people, even though they don't have gross macadamia, do have significant difficulties. So I think all the PRP, we're going to reevaluate in terms of making much, much lighter burns. And even some people are trying... Micropose laser for PRP, but they're sort of on the cutting edge and we don't know yet. But we're just going to lighter treatment and maybe just treating the ischemic areas that we see rather than bringing it tight into the disc and one to two disc timers from the vascular arcades, which we used to do just as a gross treatment. So all of these things, I think, are... PRP is still part of our regimen, but we're working on trying to change that treatment aspect. Great insights. These are some of the potential complications. The worst ones I've seen are accidental foveal burns or laser treatment, really heavy focal laser treatment, adjacent to or through the fovea. And I've seen some patients who have come in with just really, really bad maculates as a result of this. The other things are things like we talked about. So, you know, things like peripheral visual field constriction, nyctalopia. And then if you create a break in Brooks Membrane and the RPE, then they can get critical neovascularization. So that's why when you do focal laser treatment, you start out really light. You start out with a setting typically of like 80 milliwatts and then gradually go up until you're getting the treatment, the desired treatment effect. Now, as I understand, a micro pulse does not have those same types of complications, typically that focal laser treatment traditionally has. Exactly. The whole idea with the micro pulse now, and there's been a huge amount of basic research to sort of show, within this realm of for 8, 10 nanometers or for 532, this amount of laser milliwatts, but the key there is 5% duty cycle. And 5% duty cycle, you're getting no retinal injury that we can proceed by anything, even two or three years afterward. But the whole question is, all right gang, if this is a healing laser that I'm applying, how often do I have to apply it? And I'm a surgeon. I like to see when I'm treating, I want to see the burns. But the thing here is we don't want to see this with the micro pulse. We just want to induce some sort of healing like the anti-veget. So again, this is undergoing, I think, a huge evaluation at this point in time. What are the best modes of treatment for central serous or soft cruising or soft cruising? But that's another time, another thing. Well, that's one of those things. The micro pulse is coming, I think coming to the fore, but it still is, we're trying to figure out how to put it into our range. Next topic, transpupillary thermotherapy. This is, in my mind, really fallen out of favor. I don't know anybody who does this anymore. It used to be used for curvil melanoma and sometimes curvil neovascularization. It's a thermal laser treatment. And sometimes they would use a sandwich technique where they would treat the tumor with transpupillary thermotherapy and then they'd also plaque it. Part of the concern about this is that if you just do transpupillary thermotherapy for small melanoma, then it would create kind of a fibrotic cap on the top of the melanoma and sometimes then it would grow posteriorly and extend through the sclera. So that was one of the concerns about transpupillary thermotherapy. I only know one doctor. So I treat tumors and I only know of one doctor who's doing TTT at this point in time. But again, this is almost becoming a relic but still something that we need to talk about or mention. Yeah, I think the shields, if I could just comment, the gerian carol shields are still doing a little bit but it's falling way down. You're right. Because underneath this curvil melanoma you can't figure out with ultrasound or whatever how deep it's gone into the coroid end or sclera. That's the problem. Well, that's the challenge. And the problem is if you create a fibrotic cap and then you get posterior extension of the tumor, that's just, that's a very bad situation. I mean, then you're looking at almost an exaneration type of situation. So the next topic is photodynamic therapy. So we used to use this a lot for curvil neovascularization. I actually still use it for central serous coriorentinopathy. I actually think, especially if you've got fovia involving CSCR, I think it's actually a really good treatment for that with multiple small points of sort of indiscrete leakage around the fovia when you're worried about doing focal laser treatment. So with central serous coriorentinopathy if you've got like one specific discrete smoke stack area of leakage on your fluorescent angiogram and it's a disc diameter away from the fovia, you know, I don't really worry about treating that with focal laser treatment. I feel very comfortable treating that with focal laser treatment. But if they've got a couple of little smudgy leaky areas right around the fovia, I do worry about treating that with focal laser just because my concern is about causing paracentral scatomas. So I've actually had quite a bit of success treating these with photodynamic therapy. So photodynamic therapy is, it's a red spectrum laser, so it's I think 689 nanometers on the wavelength. It's 689 nanometers. And so usually when we do it in conjunction with vertiporphin, we inject the vertiporphin, we wait 15 minutes and then we treat with photodynamic therapy for two seconds. It's also, it works really well for curative hemangiomas. So curative hemangiomas often just melt away once you treat them with photodynamic therapy. And in fact, I've treated, I have treated a diffused curative hemangioma associated with Sturge Weber syndrome with photodynamic therapy and had success doing that as well. So photodynamic therapy still has its role in the world. If you talk to the vertiporphin people, they will advocate for treating it, treating macular degeneration. Sometimes it's actually useful in some types, some subtypes of macular degeneration, like sometimes polypoidal or rap lesions can be really responsive to photodynamic therapy. And so, but you know, usually I treat those. I think that more and more anti-veget therapy has become the first line treatment. Most of those things get treatment with anti-veget therapy. And then depending on the response, you can do an ICG angiogram and see if there are any feeder vessels that would potentially respond to photodynamic therapy. The other thing that's cool that will be coming online for photodynamic therapy is treatment of small curative melanomas with a light-activated molecule that we inject into the eye. It gloms onto the curative melanoma cells and then we treat it with a PDT wavelength laser, 689 nanometer laser. And that activates those light-activated, it's actually a bunch of light-activated molecules attached to a viral capsid, it attaches itself to the melanoma cells. And then you hit it with this and it creates a bunch of free radicals that then destroy the tumor cells. So we're involved in the clinical trial for that in our practice. And it's actually a really cool promising technology. It's in phase one, phase two studies right now. But that looks like it may have a lot of potential to treat small curative melanomas in terms of treating larger curative melanomas. So right now the threshold on that study is curative melanomas that are less than three millimeters in thickness. If it's over three millimeters in thickness, they're not eligible for the study. But then the question someday will become can we treat medium-sized curative melanomas with the thickness of four or five, six millimeters and will they respond to this sort of treatment? So anyway, that's something that's on the brink and really exciting. Photodynamic therapy. Do you guys see much photodynamic therapy here? We do. We just do. Ernestine does it a lot. I'm trying to think of what this patient had. No, it wasn't that. I think it must have just been CSCR that we did it the other day with. Yeah. I've only seen Ernestine do it though. I haven't seen anything else. Just to throw out some. I'm a little bit concerned about PDT treatment because remember what you're doing is this is a dye that is carried for the porphyrin in predominately the albumin of your blood in the serum. And that dye, you're hoping, is going to be absorbed by this, let's call it problematic endothelial cells of the choreocapularis and pigment of the ileum that are causing the leakage. But the difficulty there is you're having a significant leakage that's coming through into the sub-retinal space that you're activating now with your dye, laser. And that does create photoreceptor burns, well not burns, let's call it injury, that we have not really assessed very well by, again, by our usual visual acuity, high contrast photo, photopic kind of vision. But when you test these people, so I've talked with the vertebrate porphyrin people and said, come on, what is this half, half laser kind of, why haven't we done a controlled trial so we can look at the dose response curve for either, for the laser because you're giving a standard dose for the treatment. But I still haven't received much, much response yet. So I think we've got... A lot of people have gone to reduce fluence, PDT, or they don't do the full fluence, so they reduced the power by half. Yeah, but this is just a guess, gang. No, it is. We need to do some sort of better analysis of that laser intensive. Right. And the, and the thing for, you know, for doing central serious types of leakage. Right. Because you're right, there are those that don't respond to the standard focal laser photo violation or micro pulse that we need to do it and we just, I've got to figure out, you know, I think, how can we do it better? That's all I'm saying. I'm sorry, I don't... Oh, those are... My, my, my, my enthusiasm. So that gets ahead of me. So I was at a DRCR network meeting, an investigators meeting when we were working on protocol T. And then after, you know, protocol T and protocol S came out, I think it was, Neil Bressler said, well, is it time to just throw away our lasers altogether? So anyway, I don't think it is. But it's interesting because this whole section is something that's, that's not used as much, but I think that during residency and fellowship potentially, I think get as much experience as you can with it. Because one thing that I've noticed is that my general ophthalmology colleagues often feel really uncomfortable with focal laser treatment because they just have hardly done it. They're worried about causing foveal burns and things like that. So anyway, while you're in the training setting, get as, you know, if there's an opportunity to do a focal laser treatment. And especially if you've got somebody with diabetic macular edema and you've got a tight little cluster of micro aneurysms and the supertemporal macular or something like that. And it's not fovea-involved diabetic macular edema but still clinically significant diabetic macular edema. Those are ideal patients to do focal laser treatment on. So, you know, get as much experience as you can doing laser treatment on those folks. Like do it lying. Yeah, there you go. So these are just some of the milestones in vitro rental surgery, which is our next topic. And so, you know, it was really taboo for a long time to touch the vitreous. I mean, the thought process was that if you touch the vitreous, the patient would go blind. And why would those patients go blind? Well, often it was because they developed these massive rental tears or massive tractional rental detachments and then they'd go blind. So anyway, nobody really knew how to safely remove the vitreous from inside of the eye. So, 1850, Helmholtz invents the ophthalmoscope. 1919, Jules Gonen introduces this technique that he called ignapuncture. In 1949, Custodus develops scleral buckling. And in 1955, Zugio Dodo introduced Open Sky Vatractomy. And then in 1959, Heruda published on a closed system Vatractomy System. But the person that we're going to talk about a little bit more is Bob Machamer. So Bob Machamer is one of my heroes. So he's got a really interesting story. He grew up in Germany and to put himself through medical school, he worked in a steel mill and the milling process and how to make, you know, really precise fine instruments. So in the late 60s, he got this NATO scholarship to go to Miami to the Baskin-Palmer Eye Institute. And there he started working with closed vitrectomy surge, closed vitrectomy systems to remove the vitreous. And as a result of that, he developed the first vitrector and the vitrectomy cutter. And he did this kind of on his own, on his own time with his own instruments. I mean, reportedly in his garage, who knows where he actually developed it, but he developed the first vitrector. And so he always kind of thought that in order to make progress, we have to do things that are unconventional, that everybody else thinks is a little bit crazy. But as a result of his work, he became the father of modern vitrectomy surgery, so to speak. So in 1971, he developed this visc cutter, which was a 17 gauge vitrectomy cutter. Steve, what year did you do your fellowship? In 78. 78. So I mean, for Steve, this was kind of brand new technology when he was doing his residency in fellowship. I know for my partners, Greg Brinton and Mano Swartz, I mean, this was brand new stuff. I think Mano was in his fellowship from, in, I don't know, 77 or so. And anyway, brand new stuff, really exciting stuff, but it was a one-port parse plaintiff attract me. And here's a picture of that. And so they would go in through the parse plaintiff, but this thing was huge, a 17 gauge cutter that they would put into the eye. And you compare that to today's 25 and 27 gauge cutters. I mean, the thing just looks massive inside of the eye. Yeah, we would just stick it inside the eye and we'd just say, for a while, and they'd say, do you think it's enough, Steve? After 15 minutes, maybe, maybe, and then pull it out. Here's a video of the visc cutter in 1972. So you've got this thing as big as your finger. Yeah, right. Well, the thing is, I mean, you look how far back they are posteriorly, do you think, are they not getting into the auriciratum, potentially causing peripheral retinal breaks? But this is the cut rate. So what do our current cutters go? About 10,000 cuts per minute. This thing did, what, like 15 cuts per minute? I was gonna say 15 to 20, yeah. Yeah. Anyway. Yeah, and we didn't have any good lighting, so you couldn't see the damn stuff that you were cutting. Well, I think the first 10 patients that Bob Maughlin did this on ended up being like NLP blind eyes. But then, eventually, they refined the techniques and they got better and better. But, you know, these are likely eyes that were heading for the bucket anyway, so to speak, and that, you know, these were eyes with dense vitreous hemorrhage or bad membrane or something like that, eyes that probably weren't going to see anyway. But I just, you know, the amount of gumption and courage that it took to do this on the first series of patients is pretty impressive to me. So these are some of the milestones. They eventually got it down to where it was a three-port parched plane of attractomy, 20 gauge. And that remained the standard for several decades. And in fact, in my training, we did 20 gauge of attractomy mostly. So in my fellowship from 2005 to 2007, 25 gauge and 27 gauge, or excuse me, 23 and 25 gauge were just coming on board. But still, the majority of the surgery that I did in my fellowship during the mid-2000s was done with 20 gauge of attractomy surgery. So, you know, we were taking down conge and sewing in the infusion line and doing all that stuff, which in today's world we hardly ever do. In fact, I can't even remember the last 20 gauge of attractomy that I did. I used to do them a lot for trauma cases because I thought they were really useful in trauma cases. In the current world, in our surgery centers, we don't even find 20 gauge of attractomy stuff. I don't even know that our current surgical centers stock 20 gauge of attractomy packs. So that's how far we've come and how much it's diverged from, you know, 20 gauge of attractomy surgery. But anyway, things have just gotten better and better over the past several decades to the point now where we do almost all of our cases 25 and 23 gauge. So Steve, you do attractomy surgery still? Yeah. So, Dave, they've suggested that when I come out here, I, please, not because they have an adequate number of, but yes, I sort of started attractomies. I work with Don May because the whole bad thing back then is you had one instrument that you were sticking inside the eye, trying to do suction and infusion. We didn't have any lighting except through the microscope. And Don was the first one to suggest three ports of fusion, suction, and illumination. And everybody was saying, why do I have to make three, you know, holes in the eye when I've been used to doing one? But that really inaugurated the ability to do the separate instruments that we wanted to to get the right lighting inside the eye that we could illuminate it. That's what really, I think, promoted the whole systems and the faster cutting rates, as you've mentioned. Really enabled us to control the suction, the traction. We came to Larry Uduzzi, Larry Uduzzi's office in a course, and I think it was Dr. Mockerman who basically stuck a needle inside the eye with a curved tip and stuck it under a membrane and ripped it off. And we all went, whoa! But he was able to show at that time that at least we could delaminate the membrane from the surface of the retina. That was the first demonstration. It was amazing. Definitely. What we're really going for now is to be able to control what we do in a microscopic way. Will we be able to get robotic hands that will do it better than our own hands? Not yet. We really haven't got eight degrees of freedom of motion and endoscopic surgery is great except that we don't have the depth perception with the endoscopic surgery that we've had with the biome that was inaugurated by Eckhart and the guys I'm sorry. Oh, that's great. That's awesome. But he's lived it. I started vitrectomy. So it's sort of fun to see. It's fun to hear that perspective. Just a little bit of trivia. Does anybody know where endophoto-coagulation was developed? Endolazer? Yeah. So my partner, Mano Schwartz, developed endolazer photo-coagulation here at the University of Utah. It's a 20-gauge vitrectomy system. So when I was in my fellowship and we did a lot of 20-gauge vitrectomy surgery, that's a one-millimeter incision. If we're doing 25-gauge vitrectomy surgery, that's a half-millimeter incision. So the nice thing about these smaller incision sizes is you get much less post-operative hypotony. And so you don't have to worry about that quite as much. And occasionally we've seen bad or ugly complications as a result of post-operative hypotony and bleeding related to post-operative hypotony, so there's a lot of proidoles and things like that. So these are some of the advantages and disadvantages. Of course, some of the advantages include that it creates a shorter operative time because you're not taking down conscious time, but we'd always take down conscious time with flaps temporarily and nasally to put in our ports. We don't do that anymore. The patients are way more comfortable. In fact, I came out of my fellowship. I did a 25- or 23-gauge vitrectomy surgery. This is in my first few months of being out here in Utah. And I did it for a patient who lived in Layton. I don't know if you guys know Trevon Wall and he's an ophthalmologist up in Layton. And I did this vitrectomy surgery and Trevon saw him like a day or two later after I'd done the surgery. And he called me and he was kind of a little agitated. He said, I thought you said you did a vitrectomy surgery on this patient. I said, well, yeah, I did do a vitrectomy surgery. Well, that's impossible. How can his eye look so quiet and look so good after vitrectomy surgery? And he just didn't realize that, you know, using 25-gauge vitrectomy surgery that there was very little redness to the eye. Fortunately, there was no subcontractable hemorrhage in this patient. And the patient's eye really looked pretty quiet and pristine. And he just couldn't believe that the patient had had a vitrectomy with a membrane peel just days before. So anyway, it does result in increased patient comfort as well as faster visual recovery. And again, you know, these are some of the things that came up. And I think that they're not as much of a problem now, as I said, there were some initial concerns about the increased risk of endothelitis or potentially epithelial downgrowth into the incisions into the wounds because we weren't taking them conch. And then there were initially concerns about the increased risk of retinal tears. Actually, as it's turned out, there are probably fewer retinal tears with small-gauge vitrectomy. So these are some of the indications for vitrectomy with regard to macular disease. So we do a lot of it, be rental membrane peels. We take care of vitro macular traction. And then of course, repair macular holes. Submacular hemorrhages are sometimes evacuated using vitrectomy surgery. And again, there was a submacular surgery trial where they removed sub-phovial coronal neovascular membranes. I don't see this done by anybody anymore. But again, when I was starting my training, the submacular surgery trial by Matt Thomas in St. Louis was a big thing. When I finished my fellowship, again, this had really fallen out of favor, but anti-veget therapy had come along and as a result, the outcomes were so much better. This is an epiretal membrane. On average, they get about two lines of vision improvement or halfway back to 2020. This is an example of vitro macular traction. Often these patients will have metamorphopsia and blurred vision. And they often will improve a lot once you go and appeal that epiretal membrane and relax that traction when their visual acuity improves thereafter. These are the stages of macular hole. I'm sure you've seen these or reviewed these in the past. And this is what it looks like on OCT. I don't really believe that's a stage for macular hole. This comes from Heidelberg. They say that's a stage for macular hole. What's the definition of a stage for macular hole? PVD. I don't think that patient has a complete PVD. I would, but that if you looked at the optic nerve that you would still see vitreous tethered at the optic nerve. So I don't think that's truly a stage for full thickness macular hole. Or at least I wouldn't call it a stage for full thickness macular hole. Did you use detraya at all around here? I have used detraya. I don't think it works great. It's got a 26% success rate. It sometimes causes disc chromatopsia where their color vision gets thrown off and sometimes even serous macular detachments. I think detraya is a very mediocre to poor product. I would second that across the country. I think that pretty much it's what people have said. I didn't know if you had used it at all around here. The other thing, the pricing of the medication was pretty expensive. I think it was $4,000 per dose is what the way they priced it. We've got a private surgical center down the road here where we can do a vitrectomy for $4,000. With my vitrectomy is I'm going to have a 98, 99% success rate with very low rate of complications. And if I use vitreah I'm worried about disc chromatopsia and serous macular detachments and things like that. Again, in the cataract world here do you use any intravitrile, in other words infusion antibiotics during your cataract surgery? You don't. Intravitrile? Well, I'm sorry, in your infusion fluid do you use any antibiotics? Like intracameral? Yeah, for cataracts. Yes. What do you want injection right now? I'm going to be in the case. There's this whole you know the rate with the tractomy of endothelitis is somewhere around 1 in 2,000 to 1 in 5,000. And I think the secondary effects of these antibiotics can create all kinds of problems. And I'm sorry, I've been very critical of the cataract world in trying to prevent endothelitis. Again, with a very, very low consequence, but I think and unrealized problems of these intravitrile antibiotics. I'll just let you know. Yeah, but you know at the same time we are covering endothelitis today, but one of the things you look at the data that's come out of Europe and their rates of endothelitis are so much lower than what we've experienced in the United States with their intracameral use of antibiotics. I don't know. And for an anterior segment surgeon what are the most catastrophic complications they can have? Yeah, but when you talk about between 1 in 2,000 and 1 in 5,000 it's... But it's higher for cataract surgery. Vitrectomy surgery has a lower incidence of infection. Again, this is fairly obsolete, but occasionally they used to do persplitivitrectomy for curvilneobascularization. So you can also use persplitivitrectomy of course for complications of diabetic retinopathy including coverage, diabetic tractional detachment and diabetic macular edema. I don't see this being done as much anymore with the advent of anti-veget therapy since Rise and Ride came out looking at loose sentence for diabetic macular edema in 2012. I think that the number of people doing diabetic vitrectomy with membrane peel for diabetic macular edema has really gone down. So that's not completely fallen by the wayside, but anyway this is an example of a vitrectomy surgery and we're getting a little short on time. This is a 23 gauge system that I'm using. This is a gentleman with diabetic retinopathy and vitreous hemorrhage. So I usually use a 0.34 step to stabilize the globe. Here's the 23 gauge trochard that I'm serving. With 23 gauge wound construction it's a lot more important to be careful about your wound construction and there's a lot of debate about the optimal wound construction. I go in at an angle of 30 to 45 degrees when I go into the sclera and then I usually orient more perpendicular to the globe as I go in. Of course, then hooking up the infusion line putting in the other ports here so I go in superior nasal and superior temporal and so I'm sitting at the head of the bed so this is upside down. But this guy had he had vitreous hemorrhage and he healed the epiretal membrane and had some diabetic macular edema so we went in and cleaned him out and healed the epiretal membrane. This is the lens we use so this is called a clarivit lens it's a contact lens. We've got a great assistant who's been with our practice since 1985 she's really capable so we have the luxury of being able to use these handheld lenses because she's so good at it in places where that's not a possibility so compare this with the visc cutter that you saw in Bob Mockimer's surgery from 1972 it's just a far cry this video is actually several years old so at this point in time it was 5000 cuts per minute but I'm removing the vitreous hemorrhage here you can see the wisps of vitreous hemorrhage coming into the port on the cutter and then you can see the pooling of the hemorrhage here over the posterior pull so you see that this gentleman has had auto-coagulation in the past so here I'm just removing I'm aspirating some of the vitreous hemorrhage off of the posterior pull so that I can better visualize the macula and see what's happening in the posterior pull I'm injecting some ICG into the eye to stain the epiretal membrane and so by doing this I can then see the epiretal membrane and better and more completely remove it as well as the internal limiting membrane so one of the thoughts with diabetic macular edema is that it's beneficial to remove the internal limiting membrane and that helps to alleviate the diabetic macular edema again he had a little bit of pooling of hemorrhage over the posterior pull over the macula you can see the exudates here in his macula there's his optic nerve but I'm using the aspiration or I'm using the silicon tip extrusion cannula to just puff some of the vitreous hemorrhage off the surface of the macula and that's in an effort to clear so that I can better visualize the membrane and then here I am with the ILM forcep and just grasping the epiretal membrane and the internal limiting membrane so there are different ways of starting on a membrane peel some people use like a barbed 25 gauge needle some people will just do a pinch and pull type of start to the epiretal membrane peel I usually just do a pinch and pull just very gingerly grabbing the epiretal membrane and internal limiting membrane and then starting to peel you can see the internal limiting membrane and epiretal membrane right there this is, I believe that's his phobia right there, but anyway it's got a lot of exudates just adjacent to phobias so we're trying to help him out by doing the to clear the vitreous hemorrhage as well as peeling the membrane from the macula so as to help with any diabetic macular edema which he clearly had and then sometimes people put just a little bit of air in the eye and it seems that by putting a little air bubble in the eye at the end of the surgery it helps the sclerotomies to close especially if you've done an angled entry it kind of pushes the flaps together and helps to create a position between the flaps of that angled entry and just helps the sclerotomies to close a little bit more easily with 23 gauge vitrectomy sometimes you'll see a little bit more hypotony than you do with 25 gauge vitrectomy so in that situation again sometimes having a little air bubble in the eye at the end of the surgery is beneficial for the end of the surgery so that's vitrectomy surgery for a diabetic in a nutshell vitrectomy can also be used for complications of anterior segment surgery and this is certainly something that as a retina surgeon we get a lot of calls on our colleagues will call and say I've had this problem in the operating room can you clean out the nuclear fragments and things like that or put a lens in the thing I find myself doing more and more is putting in secondary IOLs these days so I'll put in an aqueous and suture it to the sclera sometimes we do an anterior chamber lens but this is post-operative endothemitis we've talked a little bit about this time frame is important less than six weeks is acute over six weeks is chronic the reason that's important to keep in mind is to just kind of keep in mind what sort of bacteria potentially takes treason that could potentially be causing the endothemitis but anyway that's essentially the end of the lecture we could go through the endothemitis for track to be studied but this is all changing very rapidly and the thing that's cool about life in the retina world is just to see the developments and see how many things are changing and evolving and the reality is that what we're doing currently for macular degeneration is going to change dramatically in the next five to ten years so things like long term anti-veg F agents and intravitral injections and all these things are just going to change so markedly in the next five to ten years it's really a cool time to be in our profession any parting thoughts or comments Steve any thoughts or comments