Chapters Transcript AI in Ophthalmology Education Course: Current Concepts of Ophthalmology 2025 So I thought I'd start out before we talk about the mask graders, I would thought I'd start out with what. Age-related macular degeneration is and there is an updated AMD simplified severity scale that just came out and it's uh based on the AREDS study. So I thought we would just start with this because I thought it was a lot easier to go over the mass graders um in comparison to this. So the new, this is a new classification you sign one risk factor for each eye with large resin. Uh, as a reminder that's greater than 125 microns, assign one risk factor for each eye with pigmentary abnormalities. Assign one risk factor if neither eye has large drusen, but both eyes have medium drusen. As a reminder, less than 125 microns, greater than 63 microns. Um, Late macular degeneration is defined as neovascularization, neovascular AMD or any geographic atrophy, and previously this was non-central geographic atrophy. Um, previously non-central geographic atrophy was not defined as late AMD, so, um. That is one change, and the second change is that particular pseudore have been um entered into this new classification, which were not mentioned previously. So if we were gonna actually just go through this, let's talk about um. And I, where there's large drusen. Pigmentary abnormalities are absent and reticular pseudodruzin, also known as subretinal juzinoid deposits, are absent for similar features in both eyes. Um, so this patient would have two risk factors, 2 risk factors, no reticular pseudodruzin. The risk to progression in 5 years to late macular degeneration is 12%. Now let's just compare that with a patient who has the same risk factors but does have reticular pseudoin and you can see that increases almost by twice, um, a little bit more than twice, so 29%. That is important to note. Um, let's talk about large druzin. Um, one, a patient has a large drusin pigmentary abnormalities, but no reticular pseudodjuzin, similar features in both eyes. This patient has four risk factors. No if if they have no reticular pseudogies in their risk of progressing is 50%. If reticular pseudodjugen are present, that increases to 72%. So we can see the role of um reticular pseudodjugen now in this updated um severity scale, and we also have talked about the features of age-related macular degeneration. So why does this matter? Why does it matter that we're talking about masqueraders? Well, age-related macular degeneration is a leading cause of blindness globally. It's increasing prevalence affects daily uh daily activities and quality of life. Um, diagnosis from AMD of AMD from non-AMD mask graders really affects the indications of treatment and timing. It's crucial for timely and appropriate treatment and follow up. And misdiagnosis may lead to inappropriate treatments such as unnecessary anti-vagF therapy for wet or referral for the new treatment, newer treatments like such as complement inhibitors in dry macular degeneration. Um, proper diagnosis really can set up appropriate expectations and counseling. Genetic disorders require systemic, uh, monitoring and coordination. Inflammatory conditions may require adjunct therapy, identification of medication toxicity, um, is essential, and in some cases, um, there's a role for PDT. So AMD mass graders have a huge list associated with it, but the way I thought I'd break up this talk is to talk about the things that mimic, uh, dry macular degeneration and things that mimic wet macular degeneration. So drusen like, uh, deposits, yellowish flecks sometimes are confusing, villiform lesions, um, and fluid. So fluid can look a certain way when we are looking at imaging, so there are other causes of CMB, um, sometimes it's related to RPE dysfunction or clearing cavitations. Um, and then atrophy, atrophy can have a whole host of reasons. Multimodal imaging is essential for differentiating AMD from mimickers. Um, we understand fluorine, angiogram is and angiography and ICG um can tell us about vascular patterns, hyper permeability, and other lesions. OCT visualizes retinal um, and cordonal structures, and OCTA is particularly good at confirming uh the presence of macular neovascularization. Near infrared and autoluorescence are also used and will be shown throughout this presentation. So the objectives are really to talk about the masqueraders of dry AMD. Not all drusen are the same, not all yellow spots are drusen. Patients presenting with atrophy could be many different things. And masqueraders are what, not all hyperreflectivity is exudation from neovascularization. History, age of onset, past medical history, family and drug usage is critical to figure out, and genetics can sometimes sort all this out. So let's start out with not all Druden are the same. Many of you may remember this from our basic science book, um, but I think this is a really critical, um, reminder of the anatomy of where Druzen form. So deposits that accumulate within or above Brook's membrane, and they're, uh, comprised of various, um, vectors. Um, they can be described as hard or soft. They can coalesce into Druze RPE detachment. They can develop into acquired vitalliform lesions, and they're a common precursor of exit of AMD and GA. As a reminder, Bass of linear druin are our typical types of druzin. Particular suits and and we've already seen the importance of understanding what these look like, um, they extend above the RPE so they're in a different location. Um, they're really highlighted on your infrared and highlighted, but I've shown you, um, uh, some representative examples on this slide. Then there's cuticular dzin, different from the basal linear druzin that are the regular Druzin. These are basal laminar druzin, and they're on the spectrum of AMD, but there's an earlier age of onset and there's a stronger familial component. Um, there may be associated with mutations and complement factor, and um they can develop into viteliform deposits, geographic atrophy, and have CNV associated with it. This is a really typical um example of what they look like on OCT and they look like the seesaw pattern. On fluorineangiogram, they have that typical stars in the sky appearance, um, saw tooth pattern here, um, on the OCT and critical to for us to to figure out in these patients is, um, if it's found in an early age really to look at their renal function because um MGN2 is associated with these type of ruin, so to know. So, moving on, not all yellow spots are drusen. Here's a case of a 20 year old with 2020 vision. If you look at his uh maculars in both eyes, he has this yellow spots in his macula. When we look At this patient, this patient actually has a condition called benign yellow dot maculopathy and it's autosomal dominant inheritance, non-progressive, and it's diagnosed at an earlier age, um. If we look at the multimodal imaging, the funnest autofluorescence really shows the hyper autofluorescence of these patients, um, yellow spots which don't happen with regular druzin, and there are no elevations at the level of the RPE. So although clinically it looks like there's yellow dots there, um, and if this patient is older, you may be, um, uh, rightfully confused, um, these are signs that this is something different. North Carolina macular dystrophy, and this is taken from the stone stone rounds, and I just want to point out all of us think of uh North Carolina dystrophy as as big craters in the in the macula, but one of the, one of the um variants of this, um, does have these yellow spots again, um, they hyper rust and they um don't have elevations at the level of the RPE. Here's another patient who's a 30 year old presenting um for screening for new onset diabetes. She does have a family history. Her mom has macular degeneration, has been followed for years. So this patient um came in, had these like pigmented lesions in the macula. And I followed her over a course of some time and you can see on the OCT how those might be confused with um Jeruzin, but there are these elevations. Um, fundus autofluorescence showed hyper autofluorescence of those lesions that was pretty progressive in the circular type pattern. And this patient had maternally inherited diabetes and deafness. Her diabetes was actually um initially, uh, diagnosed as a different type of diabetes which is Modi that does not have any pattern, uh, type of changes associated with it, but the these patients have pigmentary or model changes in the macula and it is a very common um ocular feature. They have diabetes onset in their mid-adulthood between 30 and 50 years, and they also have the sensory uh neural hearing loss, um, and their diabetic retinopathy can be varying. Here's actually I obtained pictures of her mother's uh mother's uh fundus, and she also had this, and this was actually a disease that hadn't been even diagnosed in her mother, um, and when we. So her diagnosis was determined from her fundus exam. Here's a mother's um autofluorescence image, and again this is passed through maternal mitochondrial DNA. So in summary, not all yellow spots are drusen. Looking at the time course, their history is key, uh, multimodal imaging, this all impacts treatment and outcome. How about patients who are presenting with atrophy? Um, so This is an advanced form of non-exitative AMD. Key features presented um presents as well demarcated areas of atrophy, um, and they have this characteristic darkness associated with RPE loss, um, where, uh, there can also be hyperaulorescence in areas that are, um, dying. So here's a case of a 45 year old who presented with visual complaints. She had the typical RP excrescences and some dark areas and bright areas and funduzolorescence. She was followed over a period of time. Similar in both eyes and pigmentary changes in the macula. This patient had Pentocin polysulfate toxicity when she was first seen this was an unknown um cause of pattern dystrophy but uh unknown cause for macular dystrophy but the uh FDA approved this drug for bladder irritation, institial cystitis, and it was only um recent. that it was determined that this did have retinal toxicity and toxicity is dose dependent as high as 25% after a cumulative dose of 500 g um and really important for us to note that there's no druzin, um, there is RPE thickening and elevation that may progress to atrophy and here we see how the uh the spots melt away. Replaced by atrophy and this pigmentary changes can be seen um extending beyond the macula in wide field imaging. There's this other newer condition that's been described that actually shows a vertical elongation of pattern dystrophy, and I'm only presenting this here to show you that the the rate of progression of atrophy can be quite rapid in these patients and looking at the vertical atrophy is a sign that perhaps you're not dealing with regular age-related macular degeneration. So time course, pattern of atrophy, history again is key and don't forget about medications. All of this impacts the treatment and outcome. And finally, not all hyporeflectivity is exudation. Just because you're seeing hyporeflectivity on the OCT doesn't mean there is neovascularization. This case of a 68 year old man presenting uh with 2020 vision in both eyes has these pigmentary changes in the yellow kind of areas in the macula of both eyes. I mean we look at at it on fundus autofluorescence, we see hyper autofluorescence, um, in those areas and on OCT you see these areas, these bumps, um, where there's areas of hyporeflectivity in there, um, that could mean that there is fluid, um, that is related to neovascularization or or something else. This is pattern dystrophy. This is a disease that involves the RP in the outer retina. It presents at 40 to 50 years old and it's autosomal dominant. Um, it's commonly misdiagnosed as AMD with CMV, um, but these viteliform type lesions can actually go through a series of stages. They can have that very elevation where they're very solid, and then they can have a pseudohypoion where there's clearing where there can absolutely be confusion of if there's neovascularization there. These lesions then erupt into the villo eruptive phase and then they they collapse in the atrophic phase and that's really where patients um lose vision. Um, again, those patients can develop CNV but that's not always present. Here's a case of a 45 year old with blurred central vision, um, 3 years ago looked. Like this, and then that resolved without any intervention. Thick, uh, thick choroid, um, a little shaggy photo receptors. So this is central serous retinopathy. So retinal fluid is present here due to RPE dysfunction and of course we know it's association with steroid use or the that created by your body in response to stress. Again, characteristic in these patients is that the cords, shaggy photoreceptors and angiograph, uh, angiograms are very helpful in these patients where they show the leakage either in a smokestack or expansile dot appearance. With with chronicity, they can develop CNV, but this is, there's not an indication for anti-vaF when they present and without CNV. This patient over time did develop uh macular neovascularization and hemorrhage hemorrhaging, um, and did receive it at this point and have at this point. Here is a case of a 55 year old with central distortion and has these characteristic appearance of hyporeflectivity on the OCT uh in one eye just under the uh retina, but in the other it's in multi-layers. This patient had macular telangottasia. This is acquired a bilateral, um, and appears in middle aged patients, and all stages can mimic AMD. Crystals can look like druzin. Um, they have right angle venues, cavitations on OCT can mimic exudation, and OCT can be used um to find CMB. So in summary, pattern dystrophy clearing does not mean there's neovascularization. If there is neovascularization treatment usually is a finite number of injections. CSR remove the causative agents, spontaneous resolution. PDT can be helpful in this, and in chronic cases you can develop neovascularization, which does respond to anti-veg F, and MacTel, um, can develop neovascularization. So takeaways, um, I hope you learned um about the new grading classification system of AMD, um, recognizing that not all drusen are the same, not all yellow spots are druzin, not all hyporeflectivity means there's neovascularization, and patients presenting with atrophy consider genetic medications, inflammatory things, and look at the pattern of atrophy. Um, family and drug usage history is crucial and genetics can sometimes, uh, sort it all out. Um, I'd like to give acknowledgement to, um, my, my students, but also, uh, my colleague, uh, Janice Law, we had a, uh, we did a learning course at the academy together where, um, we, um, hope to do that again. Thank you. Published January 24, 2025 Created by Related Presenters Rukhsana Mirza, MD, MS
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