 And then the other key thing is that there's no associated vitritus with it. So that was what I was talking about, that clear view to the retina. There should not be vitritus with ocular histone. So this is a more typical picture, but you can see these scattered punched out spots and then the associated parapapillary changes here. So another interesting condition that can cause CNBMs is angioid streaks, and angioid streaks you get this thickened, calcified brooks membrane, and then you get breaks throughout that membrane. And they can, it emanates off of the optic nerve and it can really look like blood vessels. And this is a pretty glaring case of angioid streaks, but sometimes you can see it clinically and it's much more subtle and it really can look like blood vessels and can be hard to pick up. If you're diagnosing angioid streaks for the first time, it's important to do a systemic workup because they do have systemic comorbidities. It's typically the most common thing I've seen it with is pseudosanthemolasticum. The other retinal finding you can see on exam with pseudosanthemolasticum, does anybody know? Is that like the subcube day orange? Yeah, subcube day orange. So it's like this orange pill appearance and you typically would see it in the temporal macula for pseudosanthemolasticum. But you can also see it with peges, beta thalassemia, sickle cell, other stonelos, and so in this case right here, this is the coital navascular membrane that's coming off of this break and brooks membrane and you can see the edema through there. So I mentioned systemic workup. They do have increased risk of coronary artery disease, coronary artery sclerosis, and GI bleeding. It's also important to recommend safety glasses for these participants because there's patients because they can have a very high risk of a coronal rupture with even very minor traumas to the eye. I don't think I mentioned this for the histo, but really our standard treatment is anti-bed Jeff agents for CNBMs. In the past we've done focal laser and photodynamic therapy, but for histo and angioid streaks, we start with anti-bed Jeffs. Now, the other thing to keep in mind for patients with angioid streaks is they'll often just get these spontaneous hemorrhages that aren't associated with the CNBM. So to diagnose that and differentiate that, you would need to do a fluorescein angiogram to look for the coital navascular membrane. So another common cause, and this is pathologic myopia is a more common cause than angioid streaks for CNBMs, and we see this quite a bit actually. And it's pretty common in patients that have an axial length greater than 26.5 millimeters. The nice thing about myopic CNBMs is they respond pretty quickly to anti-bed Jeff agents, and they often don't need quite as many or as frequent injections. One thing that you'll see in patients that have had old laser for CNBMs is over time that laser can kind of creep and scar and encroach closer to the center of the macula. So this is a patient of mine that I've been treating for a coital navascular membrane from pathologic myopia. And he has this parapapillary atrophy with myopic appearing nerves and RPE changes. He's actually in his 80s, but there's really not any drusen present. But you can see this subretinal hemorrhage associated with this thinning and atrophic changes here. And I did three injections, and I've been following him for a year now, and he hasn't recurred. This is what his OCT presented like. So I think that's about it for CNBMs. I think the last thing to keep in mind would be idiopathic. I think a lot of the idiopathics have probably had some sort of inflammatory disease, maybe a subtle pick or multifocal. So moving on to vitriomacular traction syndrome. So this is an 88-year-old I saw last week, and she really had no complaints at all in her vision. But somebody did an OCT in their clinic, and then she ended up in my clinic. And this is what her OCT looked like. I think she was 2020, 2025. I think the nice thing about the OCT, as you can see, where the hyaloid is lifting off in this perifogial region. And then it's just really stuck right there in the center causing these cystic changes. But the outer retina looks unaffected. And so we're just watching her. And then later in the day, I saw this lady who does have visual complaints, and her vision was 2200. And she's had a loss of vision inside for a couple weeks. And on this OCT, you can see that there is a full thickness macular hole. And if you scroll on your OCT, you can see that the hyaloid is still attached, and there's still traction right here. And you can see also that the hyaloid is kind of lifting in that perifogial region, but still adherent just right over the central phobia. So for the vitreous, which is made of collagen and hyaluron, over time, it starts to liquefy and collapse. And typically, like I showed you on those OCTs, starts perifogially, and then it'll spread to involve the phobia and the optic nerve and then the peripheral retina. Persistent abnormal vitreous attachment can lead to retinal breaks, vitriomacular traction, macular hole formation, and then remnants of this vitreous are implicated in the role of epiretinal membrane formation as well. So for vitriomacular adhesion, they really have no visual symptoms. And it can be focal, where you just see like a tiny little elevation over the phobia, or you can have this more broad base of adhesion there. But the key is that there's no visual symptoms. And then for vitriomacular traction syndrome, that they have decrease in vision, and they have metamorphopsia. Half the time this could separate on their own, but if they have a decline in vision, then that's when intervention would be warranted, which would be most likely surgery. Macular holes are pretty rare, 3 per 100,000. But we see them pretty frequently. We see them enough. It feels like it's more than that. But they can be bilateral, but it's not often that they would occur at the same time. You can see them spread out over years or months. For some reason, there's a higher female to male ratio that's never really been defined. And then the cause is this abnormal vitriomacular traction with this firm adherence at that thin area of the ILM right over the phobia. So gas originally described the various stages of a macular hole. That top of CT is a little hard to see. But you can see the vitreous here, adherence, and this cystic changes in the retina. And then I don't know if this projects very well, but in this stage 1b hole, there's a outer retinal break and kind of a defect right there. So these are stage 1a and 1b. On your clinical examination, you'll see a little yellow spot or a yellow circle in the phobia. 50% of stage 1 holes resolve on their own, so we don't recommend intervention at that time. And then, but you would watch them closely to see if they progress into a stage 2 hole. So this is a stage 2 hole. And you can see, and I don't know, it projects better on my computer than up there. But you can still see that their vitreous is attached. But we basically unroofed the schesis cavity right here and now it's a full thickness macular hole. And typically, it's less than 400 microns, and you can see that kind of opening. But on my computer, you can see that the hyaloid is still attached there. And we would recommend surgery for a stage 2 hole. Only 2% of these would resolve on their own. So this is when you would intervene if they present. And then a stage 3 hole, if you can imagine this little bit of the retina is kind of lifted off. And there's often an operculum that's overlying the hole. And it's full thickness. So the vitreous is now lifted off the fovea, but it's still attached at the optic nerve. And then for a stage 4 hole, you have a complete full thickness macular hole. And it's defined by a y-spring. So the vitreous is separated off the optic nerve as well. So you have a complete PVD for a stage 4 hole. The idea behind surgery for macular hole repair is releasing the traction associated on the macula. There is some people that recommend peeling of ILM. Others don't peel ILM for repair of macular hole. And then the idea is that we place a gas bubble which dehydrates the edges of the hole and with face down positioning, you kind of occlude fluid from getting to the hole. And that allows glial cell proliferation to close the macular hole. We do have a pretty high success rate of surgery in terms of closing the macular hole. It does depend on the size of the hole as well as the chronicity of the hole. So if you have a hole that's been there for longer than six months, you're less likely to close it. And I think the thing to keep in mind with counseling of patients before they undergo surgery is that surgery does improve vision, closes the holes, but often the visual recovery, they don't often get to 20-20 after surgery. They're often left with some focal distortion or abnormalities with their vision. It doesn't return to perfect vision after surgery, but it's better than the natural of an unrepaired macular hole. The other thing that I just wanted to touch on briefly is medical treatment for vitriomacular traction syndromes. And so there is one medication that's FDA approved for release of vitriomacular traction. It's called Acroplasmin or Getria. I think it came out maybe six, seven years ago. And it does have pretty good success in releasing vitriomacular traction. It's a recombinant protease against fibronectin and laminin. I think that a lot of retina specialists have done away with using it because of these patients. There was a small number of patients who had permanent visual loss after this medication was injected, and then they had abnormal ERG findings. And it's not sure exactly what happened, but people think maybe there was some disruption in the inter-botoreceptor matrix that led to visual loss. So I haven't done an Acroplasmin injection probably in four or five years. I haven't heard of any of the other retina attendings doing any recently either because of this. But it was approved for vitriomacular traction syndromes, and then it also had a high success rate in closing macular holes with a really small focal adhesion. If you had a broad epiretinal membrane or broad traction syndrome, it didn't have as high of a success rate. So I don't know if you'll run across that, but your book does mention it. And then epiretinal membranes, this is a pretty common finding on clinical examination. And on autopsydyes, 20% of autopsydyes over 75 have an epiretinal membrane. It's felt to be a proliferation of glial, RPE, and hyalocytes at the vitro-retinal interface, and that leads to the epiretinal membrane. On clinical exam, you'll see this transparent kind of sheen with this proliferation on the inter-retinal surface. It can be bilateral. It's often asymmetric. Many patients have minimal visual complaints. It can progress and cause distortion to the macular contour, and if it is visually significant, then surgery would be recommended to remove the epiretinal membrane. And epiretinal membranes can proliferate and start to cause this kind of steepening of the foveal contour. And this is what causes a lamellar macular hole or a pseudo-hole. And so you can see that it's not a full thickness macular hole, and it's kind of a different pathogenesis. You don't see any vitriomacular attraction here, but that epiretinal membrane is kind of proliferating and you're losing your contour here. So on examination, though, it can be difficult to tell without an OCT. These can look like a full thickness macular hole. One way that you might see on exams is the Watski Allen sign. I don't know if anybody does that anymore with OCTs, but they used to quiz us on the Watski Allen sign. So what you do with the Watski Allen test is when you're looking with a slit lamp with your 90 or your 78, you just have a narrow slip beam that you're holding over the hole or the pseudo-hole, and you ask the patients if they see a break in the beam. And so if they don't see a break, then that would be a negative Watski Allen sign, and it would be a pseudo-hole. If they see a break, then that would be a full thickness macular hole. But now you just do OCTs, and you don't have to do that. I was trying to just pull patient. So this is just a post-operative appearance after an epiretinal membrane peel. This is within a month. And there's been some improvement in vision, but he's still 2040. So just to show you that surgery can help, but it's not always perfect. And sometimes the foveal contour never returns to what it looked like 20, 30 years ago. So moving on to toxic retinopathies, this is a 41-year-old. She came in for follow-up of her plaque-onell monitoring, and she's been on plaque-onell for about six or seven years, I think, and she's been noticing these swirling white lights in her vision. And this was her 10-2 that was done. This is a pretty typical finding on someone who has plaque-onell toxicity, this paracentral scatomas. And then the OCT that she had was very classic. And this is where you hear of the flying saucer sign. And so there's loss of the outer retina and the ellipsoid zone and the paraphobeal region, but it's preserved subphobally. And so if you can imagine that it's supposed to look like a flying saucer. See, I tried to Photoshop one in, but I'm not that good with computer stuff to be able to do that. So then I copied one. And I think it's somewhere later in the presentation. I really tried to do my own clip art, and I couldn't do it. You guys are lucky I could get images off of Axis. It took me a while to figure that out. So this was her fundus autofluorescence. And so you can see the abnormalities here and what's beginning to look like a bull's eye maculopathy. Multifocal ERG was significantly abnormal. So plaque-onella is felt to be toxic to the retina because it binds melanin in the RPE cells and damages the cells and then leads to this irreversible scatoma in bull's eye maculopathy. The retinal damage can continue after you stop the medication because the plaque-onella is just very slowly cleared from the retina. Note in the last few years, there's been this extra macular distribution of plaque-onella damage that's been described in patients of Asian descent. And so it's important in patients with that ancestry to maybe consider doing a 24-2 instead of just a 10-2. And I'll show you some pictures of this extra macular distribution. There's a pretty low risk of plaque-onella toxicity early on. But if you've been on the medication for 20 years, the risk goes up to actually 20%, which is pretty high. So the screening guidelines, which will go over from the Academy really jump in at five years. Patients that have a higher risk of plaque-onella toxicity are those that are on a higher dosage. So the ideal dosage would be the less than 5 milligrams per kilogram of real body weight. And then you also might see older recommendations where 6.5 milligrams per kilogram of ideal body weight. But the more recent recommendations are based off of the real body weight. Kidney disease can increase plaque-onella toxicity. If you're on tamoxifen at the same time, you actually have a five-fold increased risk. So that's something important to monitor. And then if you have coexisting macular disease, macular degeneration, patterned dystrophy, you have a higher risk of plaque-onella toxicity. Oh, this is where I couldn't do this myself. But this is supposed to be the flying saucer sign. OK. And then this is the ultra-white-filled de fluorescent imaging. This is a normal. This is a typical bullseye. This would be a mixed pattern with extra macular and macular damage. And then this would be this extra macular pattern that you would see in, perhaps, an Asian population. So the current screening guidelines, and this was just updated a couple of years ago from the Academy, but you want to do an initial full exam within a year of starting the medication. If you're a low risk, then you repeat the exam at five years. But a lot of people would start yearly exams at that point. But the Academy official recommendation is to start at five years. If they have a higher risk, then you would screen annually after you're first seeing them. And then the testing that you would want to do would be the Humphrey visual field at 10-2. Consider a 24-2 of Asian descent, a spectral domain OCT. And then additional testing to consider if you're really not sure, if they have a higher hit risk, would be autofluorescent imaging. Really pretty low yield monitoring for color photos. Let's consider the high risk. Is that the kidney disease? Kidney disease. If they have macular degeneration, if they have any macular disease, I follow them pretty closely. Yearly after? Yearly, yeah. Even not after five years. Yeah, sorry. Kidney disease. The high risk for the kidney disease, if they're on a higher dosage, the tamaxifen, and then the macular disease. So another medication that can be toxic to the retina by binding to the RPE cells than the melanin is benethyazine, so that's thyroidazine and chlorpromazine. Chlorpromazine doesn't really cause a retinopathy very often, but you can get eyelid pigmentary changes. And thyridazine can cause a very severe retinopathy that can come on within weeks of starting the medication with this numular atrophy of the RPE. And in the late stages, it can look a lot like coridorabia. There's no screening recommendations because it's so rare. But if they have any visual complaints, then they would need a full exam. And cessation of the medication. I've never seen a phenethyazine toxicity. I don't think it's that common. I don't have any patients that have it. So I pulled this from your BCS book, and you can see the widespread pigmentary changes that cause pretty severe vision loss. So the BCS kind of organizes toxicities based on where their location of damage happens. And so the classes that can cause toxicity to the RPE cells are plaque linol and the thyridazine. And then these other medications can also be toxic to RPE cells. Clofazine can cause a bullzymeculopathy depharoxine, which is an iron chelating agent, can cause macular dema and RPE changes. Dideoxynosine, which is used for HIV and can be mitochondrally toxic, can cause some mid-peripheral pigment changes. These MEK inhibitors are chemotherapy agents used in metastatic disease. And they can get central serous-like changes with these kind of multifocal pockets of subretinal fluid. Sodenafil can also cause subretinal fluid. It's felt because of vasodilation. It can cause extravasation of fluid under the macula. And then alkyl inhibitors, which are these inhaled chemicals that bring on euphoria. And they're called poppers. They can cause a little yellow spot in the central macula. There's also different medications that can cause more damage to blood vessels and cause problems with the retinal blood vessels. And so one that we see pretty common would be interferon. You can get an interferon retinopathy with these scattered cotton wool spots throughout the medication. They're sorry, it's throughout the retina and associated retinal hemorrhage. Those typically go away once you stop the medication. Different medications for migraine headaches can lead to retinal vein and artery occlusions. Oral contraceptives and then estrogen, like hormone replacement therapy, can cause retinal vein and artery occlusion. So that's something to keep in mind with a young woman that comes in with a vein occlusion. That's pretty common cause of that. Procanomide can cause this profound ischemia and dope damage to the second order vessels in the retina. And then these two are used intraocularly and cause retinal vascular problems. And they're not used as frequently anymore because of the vascular problems. But gentamicin can cause this profound visual loss and macular ischemia. And then more recently, there's been case reports in the literature of intracameral vancomycin causing a hemorrhagic occlusive retinal vasculitis. So intracameral vein was used as endoplamitis prophylaxis after cataract surgery and cause basically a severe retinal vasculitis. And it's felt to be a type three hypersensitivity reaction. And so most cataract surgeons have gone away from using intracameral vein because of these cases that were described a couple years ago. And then there's medications that can also cause macular edema. So if you have someone coming in with macular edema and you don't have a reason and you wanna look at their medications, the taxines and nicotinic acid, they do not have any angiographically gauge on your fluorescent angiogram. So it would be considered angiographically silent macular edema. But the glidazones, which are oral hypoglycemic, they can cause severe fluid retention and pulmonary edema and fluid and macula. And that would leak this kind of classic petalwood leakage on the angiogram and fingerlamide, which is a treatment for multiple sclerosis. And that, the macular edema comes on within a few months of starting the medication and then it resolves once you stop the medication. Another interesting toxicity to the retina would be the crystalline retinopathies. And typically you see this with tamoxifen. With tamoxifen, you can see these kind of scattered crystalline deposits in the macula. They can have pretty severe vision loss, which is irreversible. Canthazanthine can also cause crystalline retinopathy. The nice thing about canthazanthine is that it goes away once you stop the medication and they don't have vision loss. Does anybody know what canthazanthine is used for? Have you ever heard of it? So it's an oral tannin agent that was, I think pretty popular maybe in the 70s or 80s. But I don't see anybody really on it. That's all it was used for, I think, was tannin. Other things to keep in mind in your differential for crystalline retinopathy, ethylene glycol, methoxyfluorine, which is an inhaled anesthetic that's no longer used in the United States. Talc emboli, for talc emboli, the crystals deposit in the arterial. So you'll see them in the vessels. Instead of with tamoxifen, they're in the retina, but you'll see that they're clearly inside vessels for talc emboli. And then I thought this one was interesting. I've never heard of this, but this was in your book, colon nuts, which are ingested by the Igbo tribe of Nigeria. And they can get a crystalline retinopathy without any associated vision loss from these nuts. I've never heard of that. Methanol and quinine are toxic to ganglion cells that can cause very severe vision loss. And then there's some medications that can cause abnormalities with color vision. So the classic ones are soldinophil and todallophil, and they get this transient blue tinting of their vision and some temporary ERG changes. Digitalis causes the yellow tinting of the vision. Isoretinone can cause a drop in night vision with reversible ERG changes. And then a bigobatran can cause abnormalities with your visual field and then 30 Hertz flicker changes. And this is just kind of miscellaneous toxins to keep in mind. I think one I've always wanted to see but have never seen a silver toxicity where you get those black tears and the cord. Have you seen it? Well, I have, but it was a research study. And we were actually using silver electrodes on the outside surface of the eye. And you can get argerosis. So you can get that. We didn't really see it in the retina too much. Oh, you don't have. But they don't have some lamp exams because of it. Oh, interesting. Yeah. I guess when I was reading about it, just it sounds like people are starting to take silver as like a homeopathic kind of naturopathic medication in the last couple of years. And what are they taking it for? I don't know either. But they get these kind of ocular pigmentation. Their skin can get this kind of bluish color. And they get black tears and this really dark coroid with granule deposits in the coroid with silver. OK, so moving on to photic damage. So this is light damage to the retina. It can happen from mechanical damage. And this would be from like a YAG laser where you mechanically disrupt the tissues with these acoustic shock waves. Thermal photic damage is our hot laser photocoagulation where you get excessive absorption of light, increase in the temperature with coagulation and scarring. And then photochemical damage is solar retinopathy. So there's no increase in the temperature, but these biochemical reactions cause tissue damage in the outer segments of the photoreceptors. This is also microscope exposure. So if you're an operating room microscope or prolonged cataract surgery could cause potentially damage to the macula or retina surgery with a light pipe right of the macula. So this is kind of your classic solar retinopathy picture, which has been, everyone's been talking about the last couple of years since the eclipse. But you get this kind of yellowish spot bilateral with outer retinal damage. And the vision can recover somewhat over three to six months. And then photochemical retinopathy. So this could be welding exposure with stray light that can cause retinal damage, laser induced injury with these high powered kind of green and blue lasers that you can get from wherever. And then retinopathy from ophthalmic instruments. This case, I was just going to show you. These pictures aren't great, but this was a case I actually saw when I was a fellow. And one of the residents was doing, well, she thought she was doing a YAG laser for PCO, but she actually had it on the SLT setting. And so she was burning the retina. Because the SLT is like a 400 micron burn. And it just went right straight back and got the retina. Because they used to have the dual laser. Yeah, they got rid of that because of that. Because of this. Yeah, because of this. But this happened when I was a fellow. OK, I have some questions for you guys. So the four sons of Histo. Does anybody remember them? Ocular Histo. Punched out lesions. Yes, punched out lesions. Very popular. Yes, pigmentary changes. Novotratus. Novotratus. Last one. See you in the end. Not always, though, right? Not always. Not always, yeah. OK, so shoot, I wasn't supposed to tell you that. So I wanted you to tell me your differential for bulls and maculopathy. So these are the rare things that you guys tell me the more common things. Hydroxychloroquine. I told you, I'm really not good with computers. Hydroxychloroquine. What else? Lopathy. The first thing on your list. Stargarts, cone rot dystrophy, hydroxychloroquine, AMD, chronic CSR, and an old kind of chronic macular hole. And then all these rare things that hardly ever show. Except for on a test. OK, crystalline retinopathy. The tannin agent. The tannin agent. Tamoxifen. The colobines. The colobines. Nuts. Nuts. Talc. Talc. Ethylene glycol. Ethylene glycol. And there is one more. See, fluorine, yes. Oh, this is a multiple choice. OK, stage two macular hole. What is the defining character? What is one of the defining features of a stage two macular hole? CC. Yes. I didn't specifically cover this. So vertebrated porphyrin is PDT. And it is approved by the FDA for only one of these conditions. But we use it for all of them. So the only one. C. C, myopia, CMVM, PDT is FDA approved for that. I think the things we use it more commonly for are central cirrus and choroidal hemangioma. But they're off-label. CMVM from myopia is the only one that has the FDA indication on that list. OK. Is that what you're going to do? Yeah. Explain real quick how PDT works. Yeah, so basically you inject vertebrated porphyrin. And they infuse it through the bloodstream. And then it gets taken up by the choriocapillaris. And basically vertebrated porphyrin is like ICG, right? And then you have a laser beam. I can't remember. So we use the, I don't remember the properties, like the exact properties of the laser to do it. But it's like 25 joules per centimeter squared. And basically you identify the area that you want to treat on fluorescent angiogram or ICG. And then you basically hold the laser over that area. And then that activates the dye and then causes damage to those blood vessels that are causing the linkage and kind of coagulates them with a really light power. There is some risk of choroidal ischemia with the PDT as well. But we use the reduced fluence of the vertebrated porphyrin and the reduced fluence of the laser energy. So there's less damage with ischemia associated with it. But usually we don't do it that often anymore. I do it mostly for central cirrus. And it works really well for central cirrus, like we were talking about FAA just recently. And then we'll do it for some patients with AMD that are kind of fed up with injections. They're kind of end stage. They don't have this great visual prognosis, but they don't want to come in as frequently for AMD patients. If they have good visual potential, like they're 20, 30, I don't recommend PDT for them. I kind of wait till they're worse than 2050, 2060. So which drug causes macular edema without leakage? Angiogram. It's the nicotinic acid. So both phenylglomide and risiculatazone cause leakage on your angiogram. And then this was the last question I had. And I just kind of touched on briefly in the toxicity section. So a 19-year-old man, acute central scatoma with a yellow spot in his macula. What drug could have done it? Hey, that's the poppers? Yeah. So they can cause this kind of central yellow spot in their vision. I think that was it. Do you guys have any other questions?