 All right, well good morning you guys. Thanks for, thanks for patience, I appreciate it. So today we're gonna talk about retinal detachments and predisposing lesions, maybe. Okay. All right, does that look okay? All right, so we'll talk about retinal breaks and the things that predispose to retinal detachments. We'll also talk about prophylactic treatment of retinal breaks and lattice degeneration of things like that, as well as the differential diagnosis, and then we'll throw in optic pit maculopathy at the end. So retinal breaks, as you probably have been exposed to to some degree or another, are composed of a variety of types. So they're flapper horseshoe tears, they're giant retinal tears, or percolated holes, dialysis, and atrophic holes. And each of these carry with them certain propensity to cause retinal detachments. Some are more threatening and worrisome than others. Others are relatively benign and you can kinda watch them. But the main concern is that liquefied vitreous will pass through these tears or breaks in the retina and get underneath the retina, causing the retina to separate away from the underlying retinal pigmented epithelium. So flap tears, also known as a horseshoe tear. And this is where a strip of retina is pulled anteriorly. And so one thing to keep in mind with horseshoe tears is that the horse is always walking towards the optic nerve. And that's kind of how you can orient flap tears or horseshoe tears is that the horse is always walking towards the optic nerve. Usually these are symptomatic and they're associated with photopsis or floaters. The thing that's really alarming is when somebody has a giant retinal tear because these are hard to fix. You try to get the retina back up against the wall of the eye, but it has a tendency to slip down towards the optic nerve. So those can be a challenge. This is an example of an operculated hole. You can see how the operculum has pulled completely away from the retina. These are actually less threatening lesions because as they've pulled away and pulled this plug out of the retina, it's alleviated the traction on the retina so you don't worry quite as much about the vitreous pulling on the retina and causing a separation away from the wall of the eye. Rental dialysis occur when the retina essentially unzips from its origin in the far periphery. These are usually circumferential linear breaks. They're often associated with blunt trauma. I've seen these associated with soccer ball injuries and tennis ball injuries and all sorts of things. Sometimes people don't know when or how they were injured and they just show up with a dialysis sometimes it's been there for a long time. In fact, I just repaired one of these on a 30 year old female who could never really recall having had any blunt trauma but she had a large dialysis in her right eye that went from about six o'clock up to about nine o'clock. So it was essentially a giant retinal tear and I ended up putting a buckle on her to repair that sort of tear in the accompanying detachment. So atrophic holes are usually the least threatening of these tears or breaks in the retina. So this is what atrophic holes look like. This is just another shot of a couple of atrophic holes. They're usually not associated with an increased risk of retinal detachment. Once in a while they will progress so I think it's important to watch them but they're not always associated with an imminent risk of retinal detachment and often these are asymptomatic. So somebody comes in for a routine exam they're seen by their eye doctor out in the community and they come in and the eye doctor in the community says oh they've got a hole in the retina you look at it, it's a small atrophic hole and that does not necessarily need to be prophylactically treated with laser or cryo. So traumatic breaks can occur as a result of direct retinal perforation, contusion or vitreous traction. So especially with blunt trauma where an eye takes, if the eye gets hit with a ball or something like that and rapidly compresses and then decompresses that puts pressure on the vitreous base and that can result in a tear in the peripheral retina. Horseshoe tears and opriculated holes interesting are usually not caused by trauma. So contusion injuries often are seen in the inferior temporal or superior nasal quadrants as a result of the coup and contra coup forces. They're often large ragged, jagged breaks and are sometimes accompanied by commotional retina that you see in the posterior pole. Dialyses once again are found way out in the periphery so you'll see it essentially a peripheral and zipping and they can be relatively small, one aura bay up to very large tears in the peripheral retina and then sometimes you'll see traumatic macular holes as a result of trauma to the eye. And a young man who came to see me a few years ago he's about 15 years old. He's having a fight with his brother. His brother hit him in the eye with a curtain rod and it caused a traumatic macular hole which we were able to successfully repair. His vision ended up being 2050 but those are pretty typical cases where somebody takes a direct blow to the eye and then develops a traumatic macular hole. Younger eyes are a little bit more prone to trauma and getting breaks in the retina and part of the reason for this is that the jelly, the vitreous jelly is relatively formed and solid and adherent to the retina. So anything that pulls the retina away or pulls the jelly away from the wall of the eye can forcibly tear the retina in those cases of blunt trauma in younger folks. And somebody who's older has more liquefied vitreous. The vitreous isn't quite as tightly adherent and so as a result, usually the retina doesn't tear quite as readily or often they've already got a posterior vitreous separation so they're not gonna get a large posterior break as a result of blunt trauma. So with retinal detachments, often the diagnosis of retinal detachment is delayed. So only 12% in young eyes are identified immediately most are identified within 24 months but you see a lot of people who come in with asymptomatic retinal detachment. So I have a small peripheral retinal detachment that maybe started years ago and they were never aware of it and especially if they've got a relatively young eye then the eye will naturally lay down pigmented demarcation lines to surround and isolate the retinal detachment and keep it from progressing. Sometimes they'll get macrosis in these little sub-retinal deposits as well in cases of chronic retinal detachment. So posterior vitreous separation or detachment is often an instigating factor in retinal detachment. We often in our practice call it a vitreous separation because people often confuse the word detachment with retinal detachment and so you can say however you'd like but essentially it's a separation of the vitreous jelly from the back of the eye. Now that stops at the vitreous base so the vitreous base goes two millimeters anterior to the auricirata and four millimeters posterior to the auricirata and so as a result of that the vitreous is very tightly adherent in those areas and so consequently any forced attraction on the vitreous in those areas will tear either the parcellina or tear the peripheral retina because it's so tightly adherent. In fact, one of the things I think one of the real arts of doing vitrectomy surgery is learning to shave the vitreous base safely so that you don't go too deep and cut into the retina but you shave enough so that you don't provide a scaffolding for proliferative vitro retinopathy. So the vitreous is also firmly adherent at the margin of the optic disc in the macula along major vessels at margins of lens degeneration also choreo-rental scars. Most retinal tears of course result from traction of the vitreous which can happen spontaneously or as a result of a traumatic posterior vitreous separation and of course the evolution of the retinal tears of the vitreous jelly is pulled away from the retina which then creates a break in the retina and then fluid liquefied vitreous gets underneath that break and blisters the retina away from the wall of the eye. So posterior vitreous separation can often slowly progress over the course of years. We often think of it as a sudden event because your patients will often come in and say, oh, I was sitting there watching the ball game the other night and all of a sudden I noticed a bunch of new floaters and flashes of light in my peripheral vision. So we kind of think of that as a relatively abrupt event but often it's an evolution for a long time where it started years before and it usually starts with a liquefification of the vitreous over the macula and then the macula kind of starts to pull away or the vitreous jelly pulls away from the macula and eventually separates along the vessels and then usually it's last to pop off at the optic nerve but when it pops off at the optic nerve it often brings with it the telltale sign of the weissring and that's what you can often see as you look into the eye as you see the little tiny glial weissring that is floating in the posterior vitreous usually near the optic nerve. And so this is what a weissring looks like and you've probably seen this in clinic. The other thing that you can do if you can't see a distinct weissring or sometimes weissrings will condense and they just look like a little clump of debris in the back of the eye. So the other thing you can do is you can take your slip beam in the anterior vitreous and kind of direct it diagonally into the anterior vitreous and then you can see the posterior hyaloid face and that's also an indication of posterior vitreous separation. The other way to determine whether or not there's a posterior vitreous separation is with echography. So you can do an ultrasound of the eye and see whether or not the vitreous is separated away posteriorly. So of course, as we discussed the vitreous jelly remains attached to the vitreous base and this can result in traction and so forth. There are many conditions associated with vitreous separation such as a fakia inflammatory disease trauma, vitreous hemorrhage and myopia and all of these conditions can predispose people to a greater risk of posterior vitreous separation. It also increases the prevalence increases with axial length and age. So in autopsy studies they find that most people over the age of 70 have a vitreous separation and kind of the rule of thumb that we often use is 50% at 50 years old, 60% at 60 years old, 70% at 70 years old and 80% at 80 years old. And that just simply indicates that as we age we're more and more likely to develop a vitreous separation. And then of course, lens status affects the prevalence of posterior vitreous separation as well. So if you have a nice fake emulsification with an intact posterior capsule, the risk of getting a vitreous separation is only about 40% but if you have to do an intra cap the risk of posterior vitreous separation increases dramatically. It's almost twice as much. So the typical symptoms are flashes of photopsies. Sometimes patients will also kind of say that they see a gauzy type cobweb over their central vision which can be very annoying to them. Typically the symptoms will settle down and kind of subside over the course of a few months. They'll get better and better with time. But often they always have some little persistent floaters and then you can go in and if they're still symptomatic you can do Yang vitreolysis or sometimes a vitrectomy and that's a little bit controversial but I think in some ways the jury's still out on vitrectomy for vitreous floaters but it's something that I do all the time often. Those are my happiest patients and fortunately the risk is very, very low. Your main risks of course being the chance of getting a retinal tear detachment or endothelitis or sometimes hemorrhage in the eye but the chance of any of those things happening is very, very tiny and like I say in the cases that I've done of floaters for or if a trectomy for floaters patients are often very, very happy with the outcome. So vitreous hemorrhage is a very ominous sign in the case of a posterior vitreous separation. The reason it's ominous is it just is associated with a much higher risk of developing a retinal tear or detachment. So in general there's about a 15% risk of having a tear in the setting of a symptomatic posterior vitreous separation. If somebody has blood in the eye then there's a 70% risk of there being a tear. If they don't have any vitreous hemorrhage then there's only about a 10% risk and then of course the other sign to look for is tobacco dust in the anterior vitreous. They've got tobacco dust, well if they've got a tear in the retina they're about seven times more likely to have tobacco dust in the anterior vitreous. So the gold standard I think is scleral depression with the indirect ophthalmoscope. In Europe apparently they use the three mirror lens a little bit more and feel like that's an effective way to do it. But the thing about doing indirect ophthalmoscopy with scleral depression is that you can actually, the dynamic aspect of that exam is really important because you can get your depressor back there and roll it back and forth over the suspected area of pathology and if there is a flap tear you can see the flap lift up. And so I personally think that scleral depression is the gold standard for examining the peripheral retina. And you can do the wide angle photographs, you can do three mirror examination but none of those I think really replicates the dynamic exam that you can get with indirect ophthalmoscopy with scleral depression. If somebody does have a vitreous separation you should reexamine them generally and this says two to four weeks but I think two to six weeks is acceptable. And I usually just tell them that there's some risk of developing a tear in the interim. So we're kind of looking for a couple of reasons. Number one, we wanna make sure we didn't miss anything on the first go around. But number two, we wanna make sure that you haven't developed a tear in the interim. And if you have developed a new tear or something like that then we can address so we can treat it with laser or take it to the operating room. There are risk factors of course as we already discussed, aphakia myopia family history of retinal detachment or signs of stickler syndrome such as radio lattice degeneration. And I always just caution patients and telling them that if they do notice any new symptoms, a lot of new floaters, photopsias or any enlarging peripheral visual field defects that they need to come back in right away. So the options for following a patient with vitreous hemorrhage in these settings is you can follow them closely. You can do a calligraphy or you can do kind of an exploratory vitrectomy. Usually if you follow them closely the blood will kind of start to settle down and then you can see peripheral retinal pathology. But let's say somebody comes in with a dense vitreous hemorrhage. You can't see the periphery very well and you're not quite sure what's going on. I always do an ultrasound in those cases just to make sure that the peripheral retina is okay. And then we'll often let the blood settle down over the course of a few days and then have them come back and see if we can see the peripheral retina a little bit better so that we can find maybe a small tear that didn't show up on a calligraphy. Because sometimes the small little flap tears admittedly are a little hard to find and identify on a calligraphy. And it's not that you should skip that step but I think the combination of following them closely in a calligraphy is the right way to do it. And then sometimes you get to the point where you've done a calligraphy, you've followed them closely, they still have vitreous hemorrhage, you're not sure what's caused it. And then going to the operating room for exploratory vitrectomy to find out whether they've got a branch retinal vein occlusion or maybe like a peripheral curatal neovascular membrane that's caused breakthrough bleeding into the vitreous cavity or something like that has been the source of the vitreous hemorrhage and sometimes you just don't know until you get in there. So these are the lesions that predispose eyes to retinal detachment. So I think this is an important thing to kind of make note of. So Lattice degeneration does. Vitreal retinal tufts, cystic and zonular tufts will predispose an eye to retinal detachment, meridional folds and closed aura bays and peripheral retinal excavations. So Lattice degeneration is fairly common. It's present in about 7% of the population. But it's found in a significant number of eyes with retinal detachment and it predisposes people to developing retinal breaks and detachment. It's bilateral in about a third to a half of cases and it's more common in myopic eyes. Often in patients with Lattice degeneration you'll see one of two types of breaks. You'll see either atrophic holes within the Lattice degeneration or you'll see attraction tear at the margin of Lattice degeneration. If you see somebody with atrophic holes within Lattice degeneration, they're asymptomatic and don't have any sub-retinal fluid. Those cases do not necessarily need to be laser demarcated. But if they're symptomatic and they've got attraction tear at the margin of Lattice degeneration I would demarcate 100% of those. Those are high risk lesions and have a great tendency to progress towards retinal detachment. The risk of progression of course is more or greater in younger patients with myopia. And then often the challenge is is that they're sometimes asymptomatic especially if they have atrophic holes and you may have seen retinal detachments like this but sometimes you'll see these young patients who come in, they're 27 years old, they had no idea they ever had anything wrong with their eyes. And you'll look in there and they'll have a retinal detachment that's come right up to fixation. It's right at the phobia and they'll have just started to notice it within the last few days. But clearly they'll have had multiple demarcated pigment lines that it's broken through. They'll have some atrophic holes in the periphery and they don't have a vitreous separation in many cases in that setting. And so it's kind of like the stealth RD that starts to form and it comes in from the peripheral vision and they just don't notice until it's really close to the center point. And so those are ones that you kind of have to watch for. Those are actually patients that are often very nicely treated with the scleral buckle. The reason for that is that if they've got Lattice degeneration and you're going with the vitrectomy and do a vitrectomy, the vitrectomy itself creates some tension or traction on the peripheral retina including the areas of Lattice degeneration which can lead to more breaks. If you do a scleral buckle then you're not messing with the Lattice degeneration, the periphery. You don't have to induce a PVD. You can just put on a buckle and do cryo and often younger patients respond really well to that. In fact, there are a number of good papers showing that younger patients with an intact posterior hyeloid without a posterior vitreous separation and small atrophic holes do better with the scleral buckle. So for those of you who are interested in retina don't just throw the buckle aside. A lot of people are kind of saying that at this point and there are some programs that don't even teach training doctors how to do a buckle, but I still think that it's an important tool in our armamentarium, especially in cases like that. So there are three types of tufts. There are non-cystic tufts, cystic tufts, and zonular traction rental tufts. So the cystic and zonular traction tufts can predispose to rental breaks and rental detachment, but usually the non-cystic tufts don't. And so when you look in there and you see a little non-cystic tuft, it just looks like a little tiny nubbin in the peripheral retina. It's often close to the oorocerata. A cystic tuft is usually a little bit more elevated. It's a little bit more pronounced and often has some pigment surrounding it. So this is an example of some little cystic tufts. And once again, these are very benign and don't progress to rental detachment. This is, or I'm sorry, those are just the previous ones are rental tufts. This is a cystic tuft that's a little bit more elevated. It's hard to see, I think, the cyst within it, but the way I would distinguish those two is that the cystic tuft is just a little bit more elevated and often has pigment associated with it. And these are associated with rental breaks. Sometimes, first I saw one of these a few months ago and the patient came in a month or two later and had a rental detachment that had resulted from a tear right in that area where the cystic tuft was. So usually we don't treat them prophylactically, but they are something to watch. This is a zonular traction tuft where you've got a little zonule that's come back here and is pulling on the peripheral retina. And once again, that does predispose to rental detachment and tears. Meridional folds can also do this in closed aura bays and peripheral retinal excavations. Some people think this is probably a mild form of lattice degeneration. So sometimes you'll look in there and you'll see this funny stuff in the peripheral retina. It doesn't have the classic lattice appearance, but it probably is consistent with a peripheral retinal excavation. And this does also predispose people to developing a retinal detachment, but it doesn't have the classic kind of hallmark features of lattice degeneration with the white lattice-y-like vessels as well as the pigmentary changes that you can see with lattice degeneration. So this is an enclosed aura bay and I don't have examples of the other, sorry. So these are the things that do not predispose patients to retinal detachment. So cobblestone degeneration is a very common finding where you'll see little atrophic spots in the peripheral retina. And they become more and more prevalent as patients age. So it just looks like little cobblestones, little atrophic spots throughout the peripheral retina, more focused in the inferior peripheral retina, but these lesions do not predispose patients to retinal detachment. They look kind of scary and look kind of weird, but actually they often represent the greater adhesion between the retina and the underlying tissue. So often if there is a retinal detachment, it will stop at the area of paving stone or cobblestone degeneration. And then peripheral systroid degeneration is kind of like schesis. It's like a mild form of schesis and that doesn't predispose patients to retinal detachment either per se. So we already talked about cobblestone degeneration, but it's quite prevalent. It happens in about a quarter of people over the age of 20 and increases with age. So this is an example of cobblestone degeneration. You can see the little atrophic spots in the peripheral retina. And once again, these are never the site of a primary retinal break. Retinal hyperplasia can occur when there's traction on the peripheral retina. And so if you've got a cystic tuft where there's a little bit of traction, then you can get RPE hyperplasia in this. Once again, it's seen in tufts and lattice degeneration. I can also be seen in areas of previous inflammation and trauma. Sometimes you'll see spontaneously regressed retinal detachment. So somebody had a couple of atrophic holes, they get a small retinal detachment. Every once in a while, as a result of a young formed vitreous and intact posterior hyeloid, they'll get an internal tamponade that will kind of self-treat that retinal detachment. So you'll see an area of pigmentary hyperplasia that kind of looks like it could be in the configuration of a retinal detachment, but it's just simply the result of having had the retinal detachment spontaneously resolve. Hypertrophy occurs more with aging and is often seen in a net-like or particular pattern in the peripheral retina. And the histologic features in this case are similar to chirpy. Peripheral cystoid degeneration, like I say, this is kind of like a mild form of schesis and you see these little cyst-like lesions in the peripheral retina. And it can develop or turn into kind of full-blown retina schesis, which becomes a little bit more obvious. So with regard to prophylactic treatment of retinal breaks, a lot of breaks don't cause retinal detachment. So the things that would make you want to treat a break is if it's threatening, like if it's a horseshoe tear, especially in the superior periphery, you worry about fluid getting underneath that tear and causing the retina to detach. The other thing that you'd worry about is seeing sub-retinal fluid. Anytime you see sub-retinal fluid around a blur break, you worry that it can progress or will progress to retinal detachment. Retinal detachment itself is fairly rare. It's only about one out of 10,000 or one out of 15,000 people per year. And so less than 1% of people will ever have a retinal detachment in their lifetime. And of course the goal of prophylactic treatment is to create a choreo-retinal adhesion around the tear. You can't fix the tear directly, but you can wall it off and isolate it. So things to kind of watch for, like we talked about, symptomatic retinal breaks. If they're asymptomatic, you probably don't need to treat them. Sometimes we talk about the prophylactic treatment of lattice degeneration. Afakia and pseudofakia increase the risk of developing a retinal detachment. If somebody's had a retinal detachment in one eye already, then that makes you a little bit more prone to prophylactically treating somebody who's got peripheral retinal breaks or pathology. And then if they've got a sub-clinical retinal detachment, that's also a good thing to treat as well. So with symptomatic retinal breaks, like we talked about, in a symptomatic posterior vitreous separation, about 15% of eyes will have retinal break. If somebody's got an operculated hole, they're less likely to detach because there's no residual traction. If they're atrophic holes and they're asymptomatic, it's usually not a big deal. Even if they've got an acute PVD, I usually don't treat those unless I see sub-retinal fluid associated with the atrophic holes. So this is just, and these are slides that you can look at or review later if you want. I'll try to leave a copy with somebody. But anyway, with horseshoe tears, you almost always want to treat those with a dialysis, you always want to treat it. On a percolated hole, if they're symptomatic, I treat those. And atrophical, I don't treat it unless they have sub-retinal fluid. And then lattice degeneration that does not have any associated tears, usually we don't prophylactically treat that. Unless they've got a retinal detachment or have had a retinal detachment in the other eye, then I'll be a little bit more likely to treat them with laser demarcation. So with asymptomatic flap tears, often these do not cause a retinal detachment, but if they're symptomatic at all, I always treat them. And I guess the way I look at it is I'd rather treat them and err on the side of treatment because really the treatment's pretty benign. You know, the treatment usually doesn't cause any symptoms. The worst that can happen is they'll have a little peripheral field defect, but usually it's so far peripherally located that they never notice a peripheral field defect. Like we discussed, if they're asymptomatic, usually we don't treat those. So with lattice degeneration, once again, it's a little bit debatable whether or not it requires prophylactic treatment. Have you seen those of you who've rotated through the retina surface here? Do you usually see the retina attendings prophylactically treat lattice degeneration? Do they usually do it in the fellow eye that's had a retinal detachment? They do. I almost always do that. And the reason being is that, especially if the patient's been macula off and their vision ends up being like 20, 70 or 20, 80 in the eye that had the mac off detachment and now they've got their other eye that's got lattice degeneration. I think that it's a good idea to go ahead and put some laser treatment around the areas of lattice degeneration. And I think there are two reasons for that. One reason is that, number one, it might prevent them from developing breaks or tears in the peripheral retina in the event of a posterior vitreous separation. But the second reason is, is that even if it doesn't completely prevent that, it will often prevent or limit the extent of a retinal detachment if they were to get one and at least slow it down so that it doesn't just march through the macula and cause another mac off detachment. So Afakic and Sotofakic eyes, of course, have a higher risk of developing tears and detachment. A subclinical retinal detachment is one in the peripheral retina that has fluid that extends at least one disdiometer from the break, but not more than two disdiometers posterior to the equator. I just retook the boards for my, you know, 10 year anniversary or whatever, where I had to recertify. This was a question on the boards. So anyway, so just kind of keep that in mind. What actually constitutes a subclinical retinal detachment? A number of these will progress. So I always laser demarcate these. I don't think there's any reason not to. If it looks like it's fairly aggressive and it's, you know, they're really symptomatic and it's moving quickly, then I think that laser treatment, they probably in many cases need more than laser treatment because often if you've set up a laser barrier, it will break through the laser barrier. So if somebody's had symptoms for just the last couple of days, they've got a retinal detachment superiorly and it's extending, you know, let's say two disdiometers posterior to the equator, I think in general those either need a pneumatic retinopaxia or a vitrectomy or a buckle. They need something that's often a little bit more definitive than laser treatment. But if they've got an inferior retinal detachment, those usually progress much more slowly. So let's say they've had symptoms for a month or two, you look in there, it's an inferior retinal detachment. I think that those can be safely laser demarcated because they don't usually progress quite as quickly. So with retinal detachment, three types, regmetogenous, which means there's a break in the retina. Tractional or exudative. And the differential diagnosis in these cases is schesis tumors and curable detachment or elevation. So this is one that I often see referrals from doctors in the community about is whether or not it's a retinal detachment or whether or not it's schesis. And we'll go over the distinction here in just a minute. But there are the kind of quintessential link-off rules that help you to locate a break. Have you guys heard of the link-off rules for locating a retinal break in the setting of retinal detachment? So these are the link-off rules. So you look at the higher side of the retinal detachment. So if this side's lower and this side's higher, then there's a very high chance that it will be located within one and a half clock hours of the top part of the retinal detachment. If it's fairly equal and kind of coming down on either side like this, there's a very high chance it will be within the top one and a half to two clock hours. If it's an inferior detachment and once again one side's a little higher than the other, then it's almost always gonna be on the higher side. And really the intuitive approach to the link-off rules is whatever side is higher is where the retinal detachment's gonna be. And then sometimes we'll get an inferior bolus detachment. If that's the case, you have to look for guttering around the peripheral retina. I actually did see a case like this where a young man came in with an inferior bolus retinal detachment in the inferior periphery. In fact, I just did a buckle on him last week. And the only break I could find was a little tiny break right up at 12 o'clock. And he had once again kind of this guttering appearance around the retinal periphery. So proliferative retinal vitriol retinopathy is kind of the bane of retinal surgeons. It occurs in about one out of 20 cases of retinal detachment, so about 5%. And this is just where they get massive fibrous proliferation on the surface of the retina. And it kind of scrunches the retina causing starfalls and causing the retina to become stiff. And it's hard then in those cases to iron out the retina. But this is something that we try to do everything that we can to prevent in the operating room. And I think that's one of the reasons, one of the arguments for doing a very thorough vitrectomy with squirrel depression and carefully shaving the vitreous base and just doing everything that you can to prevent this. If you leave a lot of vitreous in a vitrectomy then it does in theory provide some scaffolding for the glial cells, scar tissue forming cells to crawl across and then potentially create proliferative vitro retinopathy. But it is the most common cause of retinal detachment or a pair of failure. So this is one grading system, kind of the most commonly used grading system for proliferative vitro retinopathy. So grade A is just haze and pigment clumps in the vitreous. B is where they start to get some wrinkling of the inner retinal surface but they don't yet have fixed folds. Cp stands for posterior, so that means posterior to the equator. And that means that they've got fixed folds posterior to the equator. And CA, A referring to anterior, means that they've often got anterior loop traction. Once again, if you leave a lot of vitreous in the peripheral retina, then what can happen is they can get anterior loop traction where the vitreous contracts in the periphery and kind of pulls the peripheral retina up towards the ciliary body. And those are really hard to treat because then you have to get in there and essentially dissect out the peripheral retina where that anterior loop traction is or sometimes end up doing a retinectomy. But those are not optimal cases. So this is a case of proliferative vitro retinopathy. So what grade would you say that this patient has a proliferative vitro retinopathy? So one through 12 is the clock hours. And I'm sorry, I didn't mention that. So if they've got a total of like three clock hours of proliferative vitro retinopathy or star folds, that would be like CP3, referring to the three clock hours of star folds. So this patient has a fixed fold here, fixed fold here, fixed fold here. And it looks to me like it's pretty much all posterior. It's hard to photograph anterior loop traction. But if you just had to take a stab at it, what would you say this grade of proliferative vitro retinopathy is? What's that? Yeah, yeah, I think that's a very good thought. So it kind of goes from about maybe four o'clock over here to about nine, nine, 30. So yeah, CP5 or six, somewhere in that ballpark. I think you're exactly right. So how about this one? What would you call this one? Yeah, yeah, I think that's an excellent thought. It doesn't look like it goes too far anterior. And you know, once again, it's really hard to photograph anterior PVR just because it's so far out there. I mean, I guess you could do it with maybe some of the wide angle ones, but they're just starting a lot of good photographs of anterior PVR. But this one looks like it's posterior to the equator. So one way that you can orient yourself when you're looking at a fundus is you can find the vortex veins. And the vortex veins in each of the four quadrants will usually indicate where the equator is. And then that kind of helps you to know whether it's posterior to the equator, anterior to the equator. This one looks to me like it's probably about, the focus of the starfold is maybe about seven to eight millimeters temporal to the fovea, which is probably still in the posterior range. So I'd probably say that this is CP PVR. And then how many clock hours do you think that is? Yeah, yeah, I think that's as good a guess as any. So it's probably like CP for PVR. What you find sometimes is, you know, you take a photograph of PVR. And what you'll find when you get into the operating room is that there are a lot of fixed membranes and folds right around here. But then these little tentacles coming out are just kind of the photographic artifact from that retina kind of being drawn in. So you don't necessarily always find membranes here on these little extensions, but usually you find a bulk of the membranes right here. So anyway, with the management of retinal detachment, of course, is that you find all the breaks, you treat them, it's very important to do a good preoperative and postoperative exam. So you know what you're getting into. Because your technique, your approach is going to change once you get into the operating room or once you know what's going on. And so you kind of need to come up with an operative plan. Are you going to do a scleral buckler? Are you going to do a vitrectomy? Are you going to do combined scleral buckler with vitrectomy? Are you going to need forceps so that you can peel membranes off the surface of the retina? Are you going to need gas or oil? You know, what are you going to need? What instruments are you going to need in the operating room? And it's just kind of, you know, it's like that with any case you do. If you go into a complex cataract with a small pupil, you might need a malugan ring or you might need ICG or something to stay in the anterior capsule. I mean, it's just kind of that whole approach. So you kind of just have to get in the mode of looking at the pathology preoperatively and trying to figure out and anticipate what you'll need intraoperatively. This is an example of a scleral buckle and it being sutured to the wall of the eye. This is what a buckle looks like inside. You see that little ridge. And this is how a buckle works. You do cry over the area of pathology and then sew the buckle to the out of the eye. So it's kind of an outside in approach. Now, you can also do a pneumatic rent apexi which ports the break internally. The best candidates for this, for a pneumatic rent apexi are eyes that are fake-ic usually and have breaks in the superior two thirds of the retina. Although I have to say, if they're below the horizontal meridian, I'm often pretty reluctant to do a pneumatic rent apexi. I think those have a pretty high failure rate. So I'm a little bit reluctant. I think with modern vitrectomy, I think that maybe it's harder to justify doing a pneumatic rent apexi in some of these cases that are a little more questionable. This is an example of pneumatic rent apexi. Some people do cryo treatment at the same time they do the pneumatic rent apexi. I think that's pretty common. What I usually do is I put in the bubble and then let the retina flatten and then bring them back a day or two later and then do laser treatment. So you can go either way. The argument for doing it the first way, doing the cryo at the same time that you do the bubble, gas bubble injection is that sometimes the view is a little bit tough and it's hard to do laser treatment. But since we don't have cryo in our office over the past 10 years, I've just gotten used to doing it with the laser. So overall, the chance of successfully repairing a retinal detachment is at least 80 to 90%. And if somebody's got a giant retinal tear, PVR, UVitis, or curable detachment or something like that, then the chance of successfully repairing the detachment is less. The difference between MAC on detachments and MAC off detachments is a big one because if they've got a MAC on detachment, they've got almost a 90% chance of keeping vision that's 20, 50 or better. If they've got a MAC off detachment, they've only got about a 30% chance of getting vision that's 20, 50 or better. So as a result, that's a really important distinction to make and it's important to take patients to the operating room in a timely fashion to try to keep them from developing a MAC off detachment if they're starting to get an attachment. So traction RDS are often, they often have kind of the scaffold appearance. So I just learned this last night. So scaffold means boat-like or boat-shaped. But what that means is that the detachment kind of looks concave. So you look in there, it's usually got a concave, whereas exudative detachments and regmetogenous detachments will often be more convex. It'll be more bolus. So scaffold or a tractional detachment is often kind of the scaffold appearance that looks concave. So if you take the traction off a tractional retinal detachment, often it will settle down on its own, provided that there's no regmetogenous detachment or provided that you don't create a tear in the retina while you're trying to peel the membranes off the retina. Of course that's a no-no. With exudative detachments, you'll sometimes see shifting fluids. So you put the patient upright and the detachment looks one way and then you lay them on their left side and the detachment will go to whatever is the lowest point in their eye. Often these retinal detachments are quite smooth and they almost never have fixed folds. So they don't get PVR like regmetogenous detachments do. So this is just a busy slide showing the difference. So in terms of differential diagnosis for retinal detachments, this is something that I don't think we ought to spend too much time on. It's in your book, it's in the Academy book, but it goes through this whole thing about cystoid degeneration, typical cystoid degeneration versus reticular cystoid degeneration versus typical retina schesis versus reticular retina schesis. And frankly, I think clinically it's very hard to tell the difference, and it essentially just has to do with where the retina is split. So with typical cystoid degeneration and typical retina schesis, it's the outer plexiform layer. With reticular, it's the nerve fiber layer. But clinically, can you tell the difference? I think in most cases not. And I've tried over the years to kind of see when I look at patients with retina schesis, whether or not it's typical or cystoid. Boy, after 10 years, I still don't think I can tell the difference. So I think that academically it's probably important to understand that they make distinctions, but I think that in many senses this is kind of a histopathologic thing rather than a real practical, real world clinical thing. So the most important thing I can tell you is that it's important to learn how to distinguish retinal detachments from retina schesis. And this is the type of question I get all the time from referring doctors. Is this schesis or is this a retinal detachment? And so here are some features that you can use to distinguish the two. In a retinal detachment, the surface often looks corrugated. It looks kind of wrinkly. In retina schesis, it's usually very smooth and domed. In a retinal detachment, hemorrhage or pigment are often present. In retina schesis, pigment and hemorrhage are almost never there. In a retinal detachment, they have a relative scatoma, meaning that the peripheral vision affected by the retinal detachment will look kind of gray and hazy. But it won't be completely missing. If they have retina schesis, that area will be completely dark. Usually they won't even miss it. They won't even know. But one thing that you can do is you can take your scleral depressor and you've got your indirect on and then you can move your scleral depressor into and out of the light. And with a retinal detachment, you can go to normal retina and then you can go to the area of detached retina. And they'll say, yeah, it looks a little bit hazier in the area of detachment, but they can still see the shadow of your depressor. If they've got retina schesis, then as you move from normal retina to the area of schesis, they in theory will not be able to see the shadow of your depressor at all, because it's an absolute scatoma. The other thing too is that if you shoot that area of schesis or detachment with a laser, if they've got a retinal detachment, then usually the laser won't take up at all because it will hit the RPE, but it won't create any burn in the retina because the retina's detached or separated away from the RPE. If they've got retina schesis, then usually when you shoot it with a laser, you'll see uptake of the laser. Sometimes you have to make sure you turn up the power enough, but usually you'll see uptake in the setting of retina schesis. And then shifting fluid, usually with regmetogenous detachments, the fluid doesn't really shift with retina schesis, but sometimes it will kind of shift or move. It kind of undulates a little bit. With retina schesis, it never shifts. So here's some examples. So is this a detachment or is this schesis? Detachment? Is this a detachment or schesis? Good. Is this a detachment or schesis? Detachment. You know that because there's a pigmented demarcation line along the back of the detachment. Is this a detachment or schesis? Yeah. Once again, very regular, smooth, dome-shaped, not corrugated, and no pigment. Is that a detachment or schesis? Detachment. Is that a detachment or schesis? That's schesis. That's right. So often with schesis, if you can get your OCT out, kind of in the periphery where the area of schesis is, you'll see the photoreceptor cell layer still there, but you'll see that clearly there's this portion of the detachment that's, or excuse me, this portion of the schesis that's elevated. And once again, if that's splitting through the outer plexiform layer, it should be splitting through this layer right here. And so anything that's outer plexiform layer and beyond will stay adherent to the wall of the eye. Anything that's inner or more interiorly located to the outer plexiform layer, you'll see it detached. So you can actually do this, yes? Yeah. What's that? A serious detachment versus a serious detachment. Well, sometimes serious detachments are kind of smooth and regular too, right? So that can be kind of a tough distinction to make. But usually with a serious detachment, the retina doesn't look quite as thin and atrophic as it does with schesis. So with schesis, usually the retina looks very thin. I mean, it's paper thin, so much so that as you're kind of looking through it, you can just see the vessels. Sometimes that's all you can see and it's hard to see the substance of the retina. Whereas with a serious detachment, usually you can see the substance of the retina a little bit, just a little bit more opaque. One of the challenges though is if somebody's got a chronic retinal detachment, often the retina really thins in those cases that it can look a lot like a schesis detachment. In fact, I saw one of these just a few months ago where as an older gentleman, I think 85 or so, came in, the referring ophthalmologist said, I'm not sure if this is schesis or a detachment. And I looked at him and he had some pigment along the posterior margin of the elevated area which made me think maybe it was a detachment. I was also able to do an OCT which showed that it was a detachment and not a schesis. And then the third thing is I found a break that told me that it was a retinal detachment rather than a schesis. But that detachment had probably been there for many months, if not years, probably years. So the retina had become very thin and atropic. One thing that you can see just going back here a little bit is sometimes you'll see these outer retinal breaks in the setting of retina schesis. So there are breaks on the outer wall of the schesis cavity. And these can sometimes turn into a retinal detachment. So you'll have a retinal detachment underneath this schesis. And occasionally when you see that you have to treat it like a retinal detachment. If it's far enough peripherally then you can just laser demarcate around that area and it's not a big deal. But every once in a while it requires doing a retract me. Alrighty, I think that we are close to done. Optic pit maculopathy. How many of you have seen and have seen a case of this optic pit maculopathy? So what you'll see is you'll see this little tiny hole or excavated area at the temporal margin of the optic nerve. And then often the OCT looks like this. And so I did one of these maybe all, I think it was late last year, it was in December of last year. So it was about nine months ago. I took it to the OR. I did have a tractomy. I peeled the ILM and put an SF6 gas bubble in his eye. And he came back like a month later and he had a full thickness macular hole. This is the worst, because it looked just like this. Where he had like a little tiny roof over the cyst and he had an opening there. But the weirdest thing was is that that macular hole spontaneously resolved over the next couple of months. I've never seen anything quite like it. But the nice thing is that he's doing great. He started out being 2400. And I think he's now down to 2050 or 2016. These usually have a poor prognosis if you don't do anything at all. So the things that you can do is you can put laser treatment right along here to try to keep the fluid from seeping out and getting underneath the macular. You can also put a gas bubble in there and try to push the fluid out. Or you can do the tractomy. And those are the three options for this. I've never put just a gas bubble alone, but I have done laser treatment and I've done the tractomy for these. And in my experience, the thing that works best is the tractomy. So I think that for me going forward, whenever I see somebody with optic pit maculopathy, they're always going to the operating room and getting the tractomy. Peeling the ILM is probably a little bit more controversial. I'm not sure whether or not it's helpful or useful. But I think doing the tractomy with laser treatment right along the edge of the optic nerve is often definitive and takes care of the problem. Whereas I've often been underwhelmed with the response of laser treatment at the margin of the optic disc. Furthermore, as I've reviewed the literature on that, it just doesn't seem like it's kind of a success rate. I mean, it's probably somewhere like a third of patients end up having the fluid kind of go away. So not a robust response. But anyway, I think that that is about the end. Do you have any questions about anything that we're talking about today? Okay. Okay.