Dr. Gerson: So, Optos, Daytona and OCT, the dream team for retinal imaging. So, if I asked you--if you think of "dream team," who do you think--what do you think of when you think of "dream team"? Any thoughts, anyone? What's that?

Unidentified Woman: Two great products?

Dr. Gerson: Two great products put together. She's in marketing. She's a marketing spy from another company.

No, I think the first--you know, two things. Number one, I'll show you something that my mom always told me. If you want to get people's attention and keep it, you have to grab it right away, so I'm going to do that right now. But, it also kind of gives you some insight into how I think of things a little bit--.

Unidentified Man: --All right, let's get down to business, shall we?

Unidentified Man: [Unintelligible--.]

Dr. Gerson: --So, that's a dream team, right?

Unidentified Man: Let's see, which is better? One? Or two? One? Or two?

Unidentified Man: They look exactly the same.

Unidentified Man: Just pick one. Or two.

Unidentified Man: I don't know, two.

Unidentified Man: Okay. One? Or two? One? Or two?

Unidentified Man: [Unintelligible.]

Dr. Gerson: I think probably more appropriate that most people, when they think of a dream team, they think of the olympic basketball dream team.

So--but, just like in the olympic basketball dream team, a dream team is something that people have to come together or things need to come together to get to--get a job done, and oftentimes, from different perspectives. So, things that do things--people or things that do things a little differently to get to the same answer.

So, in the dream team from basketball, it was, you know, Magic Johnson making all the great passes to Michael Jordan to make his slam dunks, and Larry Bird shooting from the outside. So, they all did things a little bit differently in order to win their games.

So, it's kind of like sweet and salty. So, you've got Goober for your peanut butter and jelly. And then, just--which is really better? One? Or two? One and two are kind of a team to put together so we can figure out what people need for glasses or in politics, although I think this is probably the least likely, of all of these, to have any realistic sense to it.

But, putting it into our perspective, into what we look for for a dream team, for what we have in our offices for what we're doing, I think the correlation between the periphery and the posterior pole, both in imaging and in October, is really the dream team.

So, we can have two things to put together to say, "What's going on in the periphery? What's going on in the center?" But--what's going on in the center, both from a color perspective, what we can see, but also from an autofluorescence perspective of, "What can we not see? And what does OCT tell us?"

So, really, we're saying, "What's going on beneath the surface? What's going on beyond, below, beneath what we can actually see?" So, really putting together the dream team of what you can see clinically, along with what instruments can tell you or what's going on that you really cannot see, clinically.

So, I'm going to go--kind of jump around a little bit between OCT, autofluorescence and then just wide field imaging. And then, I think I'll be able to show you how all three really fit together to really make it crucial to have this combination to really see everything you need to in your practice, when you're looking at the retina.

So, obviously, we hope that all of our patients are going to be normal, but some of them aren't. And when they're not, we need to be able to look at them with whatever means we have to figure out that they're not normal and what's going on? This is just an example--just a movie going through the different slices of the Optos OCT and just showing how much data there is to interpret.

This is a running loop, and this is actually a loop of the macula in my eye. And so, it's just showing you all the different scans that this particular scan protocol took. But, something I think that's really important to realize is great technology is crucial, it's really important. But, just as, or more important, in the technology is a smart doctor to go along with it.

Because you can have the greatest technology, but if you don't know how to use it and integrate it into what you're doing, then the technology isn't really helping you that much. You have to be able to take the technology, take the information it's given to you, and figure out, "Well, how's that help me to diagnose and treat my patient so that they do better?"

So, I'm going to start off with what is fundus autofluorescence? You may have heard of this. This is something that's becoming a lot more common in optometry journals. There's a lot of it in ophthalmology journals. It's really kind of cutting edge stuff.

So, when we talk about retina or--we probably think of it more in glaucoma. We think of structure and function. What's happening to the structure? How is that affecting your patient's ability to function? And so, we need to look at that when we look at the retina or we look at the macula, and we need to assess someone's structure and their function.

And so, fundus autofluorescence--so, we think of OCT as a structural test. It tells you whether things are anatomically sound or not, but it doesn't really tell you anything about how well a person's really seeing or what's really going on at that moment in time.

Fundus autofluorescence, though--it gives structure, but I think it also gives function because you can really--and I'll show you that, in some of the cases I'll present. It really gives you a good idea of how well that person's eye is actually functioning. How well they're going to see, based on the image.

And so, on the left here is an image of a fundus autofluorescence of somebody that has RP, and then the OCT is that same patient. If you look centrally, the OCT is very normal, right in the center and underneath the fovea. This is someone with pretty good vision. So, if all you did was check this person's vision, it would be good.

But, what you can tell by this darkened area here - and I'll go through what this means in a little bit - but, that's abnormal. It's not autofluorescing as much as it's supposed to. So, that's telling you function's probably fairly poor. And in your RP patients that have 20/20 vision, most of them, their visual function is very poor. So, this is just kind of leading up to that.

So, what is fundus autofluorescence? It's really a new--it's not all that new, but really it's new to be commercially available. So, it's a new form of imaging, taking advantage of optics and wavelengths and capturing--to capture and assess retinal disease.

And what it's really looking at--and it's looking at the RPE and the RPE's metabolic activity. So, kind of a one-liner would be this--it's assessing the metabolic activity and health of the retinal pigment epithelial. And that's what it's doing.

You're--and there's a lot more of it being talked about in different clinical trials, in literature as end points for clinical trials, and really something that I think that we're going to find to be really quite useful in managing patients with macular disease or even peripheral retinal disease, helping to tell us what's really going on, and where is it happening?

So, what it does, it captures a response using different filters from molecules in the retinal pigment epithelium. What it's looking at, in particular, is something called lipofusion or lipofuscin, which is something you probably hear of when talking about macular degeneration or other age-related processes.

So, in these age-related processes, there's more lipofuscin, and that's what's going to shine or become bright or hyperautofluorescence.

Now, there's--I've recently found out there's more than two devices available, but the main two are Spectralis, by Heidelberg, and now the Daytona by Optos. And so, it's really nice and--that I think the unique thing about the Daytona is not only does it give you the autofluorescence of the posterior pole, because we all think, "Well if someone has a disease that's going to be relevant, it's going to be in the macula."

But, the truth of the matter is, a lot of times, macular disease may be starting in the peripheral retina. And so, maybe we'll be able to detect and diagnose and then potentially treat macular disease when there's a healthy macula, from what we find in the peripheral retina.

So, I think that that's something that's really important for us to realize, that wide field imaging isn't just a color imaging modality now. Now we can do it in fundus autofluorescence and really get a deeper view of what's going on.

So, again, mentioning as structure or function. And really, it's a measure of the functional ability of the RPE. So, it's kind of both: structure and function, and it really goes along really nicely. It complements OCT because we're not giving you the same information. You put them together, and you have a lot more than you do with either one on its own.

It's invaluable in AMD, in particular, because what's where we have a buildup of this lipofuscin. And it's something that's real interesting in different macular dystrophies, something that we probably see more than we realize because we're not able to--haven't been, at least, able to test with fundus autofluorescence.

So, kind of like with a fluorescent angiogram. With the fluorescent angiogram, you look for things that are either too bright or too dark. And that's the exact same thing with fundus autofluorescence. Instead of using dye, it's autofluorescence through filters.

And so, you're looking for either areas that I have hypo-fundus autofluorescence or hyper. So hypo, not enough, so it's dark. Hyper are areas where there's more than there's supposed to be, so they light up.

So, kind of similar principles, from that perspective, when you're looking at fluorescent angiograms. And so, probably the biggest things that cause the hyperautofluorescence is accumulation of the lipofuscin within the RPE. So, then, the opposite: it's darker if there's not enough.

I think the easiest way to explain this--I--you know, I gave the one-liner earlier, "What is fundus autofluorescence? It's a measure of RPE metabolic activity." And so, if something is bright, it's dying. If something is dark, it's dead. And that's kind of the easy way to look at it. And when we look at some of the images, it kind of helps you understand it that way, because I think we need to make things practical and easy to understand.

So, if something's dark, the damage is done. If it's bright, that's an area that's active. It's dying. So, if someone's dead, there's not much you can do about it. If someone's dying, well oftentimes there's things you can do to prevent that from happening.

And that's the same thing we'll learn in eyes is that, if an area is already dead, metabolically, well, there's not so much to be done. But, if we know that it's metabolically active, it's in bad shape, well can we revive it? And I think the answer we're going to find is yes we can. And that's where we're going to need to be focusing our activities on what we're doing.

Here's an example showing wide field and then zooming in, actually, on a different patient of optic nerve head drusen, something that sometimes is kind of difficult to discern from optic nerve head edema. But, then, when you have fundus autofluorescence, it makes it really easy. You can actually delineate each of the drusens very, very easily. Makes it really easy to see.

Other clinical applications. Kind of like OCT, it's a non-invasive, quantitative, objective way to diagnose problems. And I think that's something that's always important to look at, that it's objective and quantifiable so that--the way I explain to patients is a test is subjective either with A, or we can screw it up. When it's objective, you can't mess it up. It's going to do the right thing every time. It's going to do a good job every time. You can't mess it up.

So, it's objective, and you can measure. It's quantifiable. You can measure what's going on. It's a great way for monitoring disease progression. Not only has it progressed, but if there's bright areas, is it progressing? Is it--is this something that this patient had go on in the past? Or is it going on now? And I'll show you some really good examples of where that's really practical.

Here's just some examples. This is an example of a drug-induced maculopathy. Something that's been in the news over the last 12 to 18 months in eye care is Plaquenil and that there's new Plaquenil screening guidelines. And if you're going to be seeing patients that have Plaquenil and screening for toxicity, doing a visual field and taking color photos doesn't do it. That's no longer accepted as the gold standard for monitoring these patients.

What you have to be doing is multifocal ERG, which I have--I haven't met someone yet that's not in a university that has one of those; spectral domain OCT or fundus autofluorescence.

So, autofluorescence in--spectral domain OCT: those are the two choices.

If you're not doing one of those two, then someone might question whether you should really be following someone that takes Plaquenil, because you're not going to find the toxicity early. You'll find it late in the game.

This is someone that had a drug toxicity that's not early. It's kind of late in the game. It's still bright, so maybe something can be done. It's not dead yet. So, when you see something that's bright, you can say that there's hope.

Now, this is someone where you see a lot of dark in the macula, a lot of hypoautofluorescence. So, this is someone that you wouldn't expect to be seeing really well. And in fact, she doesn't. She's 2100. This is someone with Stargardt disease.

And you can, I think, really tell a couple things. Number one, you can really understand why central vision's so bad. But, number two, you can really see the extent that this disease goes to in the peripheral retina, that it's not just affecting the macula. You can see all the little flecks pretty easily. And spots that are bright are areas where there may be some activity--over activity, where there's more damage to be done.

We're really showing you the extent of something that's Stargardt--you really probably think of it as a macular dystrophy, but it really affects much more of the retina than just the macula.

So, what about this patient? Would fundus autofluorescence have a role here? Would it be helpful? Now, it's be really easy to say, "Well, gosh, this is someone that clearly has geographic atrophy, and so that's measuring, with the Optos, the traditional P200, showing the geographic atrophy, and this is used in the Optos OCT showing that thinned and atrophic macula. And that's why you see the choroid so well, because there's not much retinal tissue to absorb any of the waves going through it. All is going to image the choroid.

So, you might ask, "Would fundus autofluorescence be helpful here? If this is someone that's already 2100, let's say, and their vision's already poor, does it really matter if you get more information? If you know more information?"

I would tell you, "Yeah, it is, because this person doesn't have good central vision, but they have good peripheral vision." Well, what does that mean? Where does the center stop? And where does the periphery start?

Well, wherever that line is, you hope that that line is stable. And you hope that that line of where the central vision is, and is not good, isn't expanding out. Well, that's something that, unfortunately, I don't have fundus autofluorescence on this particular patient, but that's something that, in clinical trials, is being looked at. It's being looked at.

Well, if we look at geographic atrophy and we think we have a treatment for it, can we tell if that's treatment's working? And as accurate or more accurate than any other measure is area of fundus hyperautofluorescence. So, dark area here. So, that's how they're measuring it. And they're also saying, "Well but if you see a bright area, like you do there, or you do there, that's where it's likely to be expanding." So, that's where this person's likely to lose more vision.

So, hopefully, if someone has an area in the center, an area in the macula that's already dead, hopefully there's not more surrounding that's dying. Hopefully, their disease is actually stable.

Now, let's talk about AMD from a little different perspective, about peripheral changes in AMD, because when you think about AMD, if you're going to look for it, I'm sure you, like me--the first thing you do is you look with the lens or with an image that you take, and you look in the fovea. You look in the macula. And that's where you look for AMD.

Now, it's true, that's where you look to see what's happening with the vision with AMD. But, that's not necessarily the only place to look to see if something has AMD or other changes. So, these are images--these are slides originally created by Jerry Sherman, but these are images that were taken as part of the Rakovic eye study, which was a huge study that was done with lots of people imaged.

And the really interesting thing here is you see not only does this person have geographic atrophy. They also have some peripheral drusen just--not really all the peripheral, but they also have lots of peripheral retinal changes.

And so, how do you know which came first? The chicken or the egg? Did they have the peripheral changes first? Or the central changes? You don't really know, but if you think about how many older people you see that have peripheral retinal changes, is that maybe telling you who's going to ultimately develop macular degeneration? And if you knew that, would it cause you to act differently? I think it probably would, for most of us.

And you can really see--I think it makes it a little bit easier to see these changes and the extent of them in the periphery when you have the fundus autofluorescence. So, I think it really helps.

This is just a zoomed-in picture of the fovea, of the macula and optic nerve, showing really great detail. It's pretty awesome what great detail you can get from a wide field image. Or it's not just wide field imaging. It gives great images of the macula.

Now, here you see it in green separation, and then here you see it in the fundus autofluorescence. And so, you see that there's just an area of the macula that's gone.

Now, the good news is, at least over here, there doesn't appear to be any intense bright hot spots. So, maybe it's not growing, but it also shows you that there's some dead areas over on the other side of the optic nerve. So, affecting a person's peripheral vision. It's not just about their central vision, but other parts of their vision are important as well.

Now, the other thing that's interesting is that lots of drusen here, and you think it's pretty widespread. You would expect that whole area to look the same. But, when you look at the autofluorescence, what's really going on beneath, it's not. So, it gives you a different picture than what you can see, clinically. So, I think it holds a lot of value.

Now, going back to the patient I showed you a little bit ago, geographic atrophy of your vision is 10 over 120, so 20 over 240. And you can see the color, and you can see the SLO image is taken with the OCT on the Optos OCT.

Here's a little bit closer up of that, and you can see that you don't really have very good delineation of the macular structures in the fovea, and that's why this person has poor vision.

Here's the other eye. Basically the same as the fellow eye. And what could fundus autofluorescence tell us? Well, it would tell us if one eye was truly--was better than the other, it'd probably tell us which eye was better. If I would tell you, you know, one eye sees better than the other, you'd be able tell more so by fundus autofluorescence than you would by color.

You'd also be able to tell--like I've already mentioned a couple times, is this something that's gone? Or is it gone and growing? And you'd want to know that. You'd want to know that for your patient on what's going to be happening to their vision.

Now, we're going to jump off of fundus autofluorescence and go to wide field imaging. And I'm going to start out with this one and talk a little bit about diabetes. And if you look at these images and you see just--there's two small peripheral retinal hemorrhages. What does that mean to you?

And I'll tell you, to me, that means that person has diabetes and high blood pressure until I can prove otherwise, because both of those are pretty easy to prove otherwise. Pretty simple finger stick and, you know, cuff around a person's arm. It's really easy to be able to tell. But, you only know to do those tests if you can find something that tells you that you need to do those tests. And so, peripheral imaging oftentimes does that.

And here's a fantastic example. It's real hard to see here, when you have it all wide, and you see the whole picture, so I'm showing you the forest first. I'll show you the trees here in a second. But, this is a 44 year-old healthy patient that used to have pre-diabetes but cured it with lifestyle, and his doctor's happy and not worried. Everything is good. Nothing to worry about.

There's the red-free image, and you can see what got me a little bit excited. And then, there's just a zoom-in of it, so you can see what that one little peripheral hemorrhage looks like. And a lot of people tell me I'm crazy. "You see one peripheral hemorrhage and you get worked up about that?" Yeah, I do, because if that was me, I'd want to know why it's there. I wouldn't want to just assume, "Oh, maybe I"--you know, "I fell down or I--playing basketball, someone hit me in the head, addition that's what caused it." I'd want to assume there's something wrong until I can prove otherwise. Well, that's what happened in this case. When you see an ambulance, that's never a good sign.

His in-office random blood glucose was 463. Now, for those of you that don't know, that's a little bit high. His in-office A1C was over 13. So, he's averaging over 300 for his blood glucose. So, it's not just he had a, you know, couple donuts before he came in. His blood sugar's always out of control.

[Unintelligible] be able go to the primary care physician either today or tomorrow because he's busy. He can't make it. So, he went two days later, and he was put on a combination medicine for his diabetes.

And the only way that we knew, because the doctor was happy, he was happy, was because we found one peripheral hemorrhage. That's it. And that's what it took to get this guy back on track, finding that one peripheral hemorrhage. And I think that's a pretty powerful case.

And I always try to follow-up on these patients and find out what's going on. And he's doing okay now. He's not happy that he's on medication, but at least he realizes why, and he understands that, "Wow, it's a good thing that I had that image done. I wouldn't have known how sick I really was." I mean, that's someone that probably should've gone to the hospital. The reason he wouldn't go to the hospital that day is because he said, "Oh, I'm busy. I got to go to work, and I can't take a day off today."

So, these are just some more images of diabetic retinopathy, again showing that you can have something from he images of peripheral retina and not sacrifice the posterior pole. Because if you do, then it kind of defeats the purpose. If all you see is the peripheral retina. But, you don't. You see the posterior pole, and you see in red-free. You see just tiny little changes become very, very easy to see. So, that's why I really like something like this, because not only does it make it easy for me to see, but it makes it really easy for me to share it with my patients and show them.

You know, if I'm showing another doctor something pretty subtle. You get it. It's easy. But, to have something actually jump out enough to show to a patient is a different story, and I think that's something that we're really able to do.

And again, this is a patient that, when you look at the forest, everything looks pretty normal. But, when you start really looking a little bit more closely in amongst the trees, you see something there that doesn't look quite right. And let me show you the red-free. And so, you see a hemorrhage.

So, to me, that looked kind of like a flame hemorrhage, and so I assumed that was probably blood pressure. So, what's next? I checked her blood pressure. So, it hemorrhages in my office. It's diabetes and blood pressure until I can prove otherwise.

So, I checked her blood pressure, and I couldn't prove otherwise. She has high blood pressure. And so, her blood pressure was 150 over 94. So, it's not incredibly high, but that's high enough that she needs to go to the doctor and get medicated.

Now, does she have a primary care physician? Not really, but she said she was going to go take care of it. A month later, she comes back, she's lost a few pounds because the doctor that she went to go see was the one at the weight loss clinic she was going to. So, somewhere you go to lose weight, and there's a doctor on staff to make it, I guess, legal to do the things that they do.

So, it's someone that--she went there and said, "You know, my eye doctor said that there was something wrong with my eye, and that I had high blood pressure. Can you check it?"

So, they checked it. They put her on medication for her blood pressure, and that's the prescriber - the person at the weight loss clinic. And so, a month later, when she came back, you can see that hemorrhage is gone. So, it'd be easy to assume, "Well, the hemorrhage is gone, she's on high blood pressure medication, she's lost a few pounds. She's in good shape. I don't really need to worry."

Well, I asked her, "Did they check your blood glucose?" She said, "No, they just--all they did was check my blood pressure. Said you were right, and gave me a prescription for medicine." I looked at my chart, and shame on me, I didn't check it either.

So, I checked it that day, and her--she hadn't had breakfast that day. Her fasting blood glucose was 134. Diabetes is anything over 125, when you get it to say--to do that more than one time. So, just one fasting blood glucose is not definitive of diabetes, but it shows that someone should've checked it along the way, whether it was me or the weight loss doctor or somebody else.

So, we found that not only does she have high blood pressure, but she also has diabetes. And so, again, interesting to find something that really changes the way that someone lives and their outcomes, because now they know what they have, and they can do much better because of it.

So, diabetes is a big deal. And that--the numbers today--for 2010, the numbers are higher than these. But, in 2000, there's about--people born in 2000, about one in three would ultimately develop diabetes. Higher for African-Americans and Hispanics. Now it's higher than that. It's between 35 and 40 percent. So, it's pretty shocking.

If you're sitting at a table of three, that's saying at least one of you, if you were to be born today, would develop diabetes. If you're sitting at a table of two, probably one of you, if you were born today, would develop diabetes.

What's interesting is that in about 20 percent of people that are diagnosed with Type 2 diabetes, there is already non-proliferative diabetic retinopathy. And I think that's a really key take-home point, because that's saying, you know, "What comes first"? Well, that's not saying the diabetic retinopathy comes before the diabetes. The diabetes is already there. It just hasn't been diagnosed. Nobody's looked in the peripheral retina. So, it gives all of us a great opportunity.

You know, if you think about it, I'm about a 40 year-old guy. And if--and most people I'm assuming, in my shoes, if they're like me, 40 year-old guys don't go to the doctor. And the only way I'm going to go to a doctor for a lot of my patients, is, "I can't read anymore. I can't see up close. There's something wrong."

So, I go in, I get my eyes checked, and if I'm doing a full exam of my patient, I'm checking their peripheral retina, I may be finding the hemorrhages that--because I'm the first interaction they've had, as a medical professional, for maybe a couple years. And maybe that's why we're going to be diagnosing diabetes, because 20 percent of the time it's there before they know they have the diabetes.

So, I think that's something really powerful that we can really take home and realize that, for how many people there are that have diabetes now, that's not a number that's going down. That's a number that's--has been going up, continues and will continue to go up unless something fairly dramatic is done to change the way that--really, that we live in this country.

Now, with diabetes, we used to think of it as Type 1 and Type 2. But--or we should think of it, rather, as Type 1 and Type 2 and not just insulin dependent and noninsulin dependent because, oftentimes, people with Type 2 diabetes develop a dependence on insulin. A lot of people will.

So, you can't just assume that if someone takes insulin, that they have Type 1 diabetes. Either way, it's important to be looking at the eyes and really looking for changes and looking for even peripheral changes. Diabetic retinopathy is not just in the posterior pole. It's anywhere in the retina.

So, what we want to do is we want to find it. If they have retinopathy, we want to find it. We want to stage it. We want to kind of grade it so that we know, "What's the level of severity? How often do I want to see this person back because of the likelihood that it may get worse?"

So, obviously, the more severe it is, the more often we're going to see them back, but hope they don't develop proliferative diabetic retinopathy, because these are people that, if something's not done, then they're not going to do well. They need to be diagnosed, they need to be referred for treatment and receive that treatment in order not to lose vision, in order not to go blind.

And then, the other thing we look for is macular edema, and I'll show you some more OCTs of macular edema. But, I don't think you necessarily need to have an OCT to diagnose macular edema. We can see that clinically. But, I think you really do need to have an OCT to follow these people over time.

Because how do you know if it's getting incrementally better or worse? You don't. You can't tell, looking in clinically. I think you really have to have an OCT if you really want to follow people with diabetes, and any macular changes, over any period of time.

Now, this guy came into my office and said, "My vision's been changing. I was recently released from the hospital. The reason I was in the hospital is because I was having some blood glucose issues. I couldn't keep them under control, and it's been like that for a long time. Even in the hospital, they had a really tough time getting things under control. And now, I'm on three oral medications. No previous history of any eye problems." And this is what he looks like.

And you can pretty easily see that there's some changes just outside the macula. So, if we had the macula here, and there's changes just outside of it, this is someone that might be, and was, 20/20. So, they have really good vision. But, their eyes don't look really good.

And is this someone you really want to give glasses to? Probably not. If they just got out of the hospital because of their crazy blood glucose, then you might want to have them come back and recheck and make sure you don't have to remake their glasses.

But, we can see, funduscopically, when we look at an image, that there's change, and we can see that in OCT. Even though he's 20/20, you can see there's definitely some changes within the retinal layers there. There's some exudates.

So, even though they're not, maybe, showing up great on a color, if we look right, smack dab, in the middle, you can kind of see in there. You can really see it there. So, combining the two things - a wide field imager that has macular or posterior pole detail, along with an OCT - tells you what's going on.

And you can't just say, "Well, his vision's 20/20." Because if all he did was say his vision was 20/20 and look, with your 78, optic nerve to macula and back, it's all good. You don't notice that there's something pretty severe going on here, and that he's actually pretty lucky and not too far from having really lousy vision. So, it's important to put everything together.

Again, normal vision, but we have exudates here. You can even see some of the fine changes in the retina on the OCT, right? The fovea is very normal. But, just outside, there's some subtle abnormalities.

So, really good vision doesn't mean a really good eye or really good health within that eye. I think that's something really crucial for us to really start paying attention to and really realize that. And I think we'll see some more with some fundus autofluorescence when I show you some of those.

So, with this patient, are glasses a priority? Well, probably not. He actually had several more hospitalizations over the next two months, because I knew that because I said, "We're going to have you come back in three or four weeks, and we're going to redo your refraction."

And he couldn't make the appointment. He rescheduled, couldn't make the next appointment because he had been hospitalized because of his blood glucose. Obviously out of control. So, we don't want to give someone like that a prescription.

Now, once he gained some sense of control, he was actually sent to a retina specialist because even though he had really good vision, and right, smack dab in the center it looked really good, just outside that fovea, like I showed you, there was edema.

And a lot of times a retina specialist will treat that. They're not waiting for patients to lose vision. They'll treat them sometimes, when they still have good vision, to prevent the loss of vision. And so, that's what we're really trying to do. We're really trying to make sure people don't lose any vision.

Four months later, and he still wasn't ready for new glasses because he was still fluctuating. Blood glucose wasn't doing good. And this is something that, you know, you'd love to give them a new pair of glasses so they could see better, but they'd need a new pair every day for how much their blood glucose is going up and down, up and down. And if all you did was look at the optic nerve, and just to the very center of the macula, you wouldn't have seen anything going on in their eyes. So, the history and the imaging, in this case, made a real difference.

Now, again, pairing structure and function--and this is looking at autofluorescence, OCT, and this is looking at microperimetry. So, that's what this SLOM--I just--I don't know if I made that up or if someone else has already made that up, but it's Scanning Laser Ophthalmoscope Microperimetry.

So, it's like visual feel but on a micro level--microscopic level testing for visual functions. So, that's really kind of the ultimate in structure and function. And that's something that the Optos OCT [unintelligible] can do. It can do microperimetry.

And so, we're looking at, "Well, what's going on in the fovea? And then, how does that correlate to where someone can see things? Can you really pinpoint the exact spot where people are seeing and not seeing?" Yeah, now probably we can. We can see what changes lead to visual changes, and what changes are just things that maybe you and I get excited about but ultimately doesn't do something to a person's vision. So, really giving us much more detail where it's really important and practical.

So, this is a lady who was recently diagnosed with diabetes. She comes in saying that she was diagnosed with diabetes two weeks earlier. And we check her vision, she's 20/60, and get a little bit more of the story.

"How'd you find out about your diabetes?" "Well, my foot was hurting, so I went to the hospital, and they had to amputate a toe. And they checked my blood sugar and told me I had diabetes. So, I've had diabetes for two weeks."

And I said, "Well, I think you've probably had it a little bit longer than two weeks, and I'm glad your"--you know, "your vision isn't terrible, but it's really not all that good. It's 20/60. She said, "I know. I know it's not very good, but the endocrinologist said to wait to come to you until things were under control, because you wouldn't want to give me glasses until things were fairly well controlled, because my vision was just going to fluctuate. But, it's already been two whole weeks, and it's still not good, so that's why I'm here, because I've only had diabetes for two weeks."

I said, "Well"--and she kept saying that. I said, "Well, when was the last time you went to a doctor?" She said, "That's the thing. I went 20 years ago, and everything was fine." I said, "Really?" I said, "And when was the last time you had any blood work done?" She said, "Yeah, I had an A1C done 20 years ago, when my youngest child was born, and that was normal. So, I don't really understand how I have diabetes now." She just didn't get how not going to the doctor didn't protect her from developing diabetes.

By the way, she's a nurse, which is really kind of the scary part of the story. So, don't assume just because someone's a fellow healthcare professional that they understand what's going on.

So, I saw--her brother is a patient. I asked him, "Where does she work?" So, I'm thinking, "That's not where I want to go." And she works at a retirement home, so I don't need to go there for a while.

So, 20/60, new diagnosis of diabetes, and you can just see, lots of hemorrhages, exudates, cotton wool spots. I mean, we're just seeing the whole gamut of what happens to the retina. All the bad stuff that happens has already happened to her.

Now, interestingly, sent her off to the retina specialist, because I know she was already receiving systemic care, and I knew, for her eyes, the only way she was going to get better was if her macular edema was addressed.

So, I sent her to a retina specialist, and here's the pre and post-Avastin injections. So, this is 20/60 to 20/25, 10 days after Avastin. Over here is 20/60 to 20/25 two days after Avastin. Pretty remarkable how quickly Avastin works.

I think it's also pretty remarkable how bad this macula still looks, but it's seeing 20/25. This one's seeing the same as that one. Now, you know, I think I'm pretty good with a 70 diopter lens or a 90 diopter lens, but I can promise I wouldn't be able to tell the difference between this and this. I think I'd be able to tell the difference between those two, but these two, there's no way I'd be able to tell any difference.

But, her vision went from 20/60 to 20/25. So, what would look the same, clinically, would have a dramatic difference in what the vision is. And without OCT, you can't tell what that is. So, this is a pretty good case of really helping me understand that.

Now, she started doing well. Her vision improved. And unfortunately, then, she developed this large hemorrhage. She dropped back to 20/60. Sent her back to the ophthalmologist.

And I actually see her ophthalmologist--I see him pretty regularly outside of work, and I saw him this last Tuesday morning. And he said, "You know, I just want to"--he had sent me a letter two weeks ago saying that Tracy's [sp] doing great. She's coming back for a refraction. She's finally stable to get glasses."

And then, I saw him on Tuesday morning. He said, "Yeah, I just saw Tracy yesterday. She re-bled again." And so, she's on two years now. She's had at least 10 vitrectomies, and she's now getting monthly Avastin injections. He started astretchin [sp]. It was at six to eight weeks, and then she re-bled. So, now, she's back to once a month Avastin injections.

So, kind of a sad case, but you saw what she looked like at initial diagnosis. And by no means was that her diagnosis. But, the reason that's important, I think, and where this really comes full circle, is the people before that, that had one hemorrhage, that you have to assume they have diabetes, that's probably how she started. She probably started with very subtle changes.

And if she would have had her eyes checked, and someone's seen that, then she would've been diagnosed earlier and, ideally, her diabetes would've never gotten so out of control that she's had all these problems. So, that's where that single hemorrhage becomes so important to prevent.

Both of those people were at diagnosis, but one we diagnosed from one hemorrhage, the other one diagnosed two weeks before images were taken because she had a toe amputated and is now almost blind in one eye. So, catching things early is pretty key.

So, what does Tracy need? Another vitrectomy to salvage her vision? Well, she does, but more importantly, she needs systemic health. And that's something that, you know, when we can intervene early, we can help people get that. At this point, yeah she still needs that, but it's pretty late in the game. She's pretty sick. And if her eyes are that sick, you can bet the rest of her body is probably equally as sick and not doing very well.

So, the main treatment for people now that have macular edema, it's--most of your patients are probably having an injection of Lucentis along with some form of laser, because that's what this study was published about, oh, actually almost two years ago now. It was what it says, that people that do the best are people that get a combination of Lucentis plus laser.

Now, you're seeing--on the bottom here, you saw a little video of someone actually getting a Lucentis injection. Interestingly, I had a patient in yesterday with myopic degeneration who's been getting Lucentis injections. She's had six.

And I asked her, "What's the worst part?" She said, "The anticipation." And I always tell people that, but it kind of confirmed it for me to talk to this patient about it. She's a young woman. She's about 45, which I used to think was old, but now I think is really young. So, this really young 45 year-old was telling me the worst part's the anticipation.

"The actual injection is a breeze, but to actually have to sit there and think about it or know that I have an appointment tomorrow or next week, that's the worst part. The actual injection, not a problem at all. I don't mind that at all. If I need to get injections to keep my vision, I don't care. That's no big deal. Just don't tell me about it."

So, all this talk about vision and diabetic retinopathy--you know, if I asked you who--let me ask you, who's seen a patient with diabetes in the last week? Probably all of us, unless you've been, you know, on vacation here in New York. If you haven't been on vacation all week, you've seen a patient with diabetes.

And then, if I asked, "How many people have seen a patient with diabetic retinopathy," you'd probably think, "Well, I don't know if I've seen that." Let me put that into perspective. This is from a publication in August of 2010 that laid out some numbers of a study of a thousand people.

And basically, if you really crunch the numbers of--if you look at how many people in the U.S. have diabetes, what percentage of people with diabetes have retinopathy, you'd find that about 4 percent of Americans - not people with diabetes - about 4 percent of Americans have diabetic retinopathy.

So, how many people do you see in the average day, when you're at--in clinic? Ten? Fifteen? If you see 15, that means you're seeing someone with diabetic retinopathy every other day, whether you realize it or not.

Remember that person with the one hemorrhage? Diabetic retinopathy, whether you really realize it or not. So, just using all these different ways to put this into perspective what a big deal it is to find things early.

Here's an example of diabetic macular edema on Optos OCT. You see the PIL is still intact? This person has good vision, but that doesn't mean that there's not problems. You see these cystic spaces here, just right next to the fovea. It's 20/20, but it's--this person's not in very good shape. It's not going to take much for them to be 20/60, 20/80.

But, you need to find someone at this stage in the game, not once they get to 20/80. They can go have treatment now and always remain good vision instead of wait 'til it drops and send them and hope that they can regain the vision that they've lost.

Now, I want to show some other non-diabetic pathologies. I want to show, in particular, some autofluorescence. This is someone that came in that had central serous. And he's a known case. He knows that he had had it in the past.

So, what do we see here? Well, we see, you know, a lot of typical things, the typical gray background. The optic nerve will look darker, the blood vessels are kind of blacked out. But, then, when we look in the macula, we see that there's a little more darkness than normal, and these bright spots. So, that's telling us that there probably some activity here. His central--he came in because he noticed a change in his vision, so his central serous is acting up.

Now, when we think of central serous, we probably think of just one little spot, right? That smoke stack that--where the smoke plumes out of? Well, the fact of the matter is, it's not just one spot in central serous. And this is a great example of showing how that's not the case. You can see that the--it actually affects--pretty much the whole macula is affected by the central serous.

Now, these are some follow-up visits. This is a follow-up visit a month later. And I apologize, the image is a little dark, but you see those bright spots are no longer there. Not active. And then, a month later, looks like that. And so, really pretty quieted down. So, you can see the central serous resolving itself over time.

Now, here's what he looked like on follow-up with fundus picture, and you can see that, yeah, there is some RPE change. And you look at OCT, there is some subtle change there. But, he's back to 20/20 and happy.

And so, using all three of those, using the OCT, using what it looks like, centrally, in color, but also using what it looks like, centrally, with the autofluorescence, really tells you, is it active or not? Had he had it before or not?

Because here's--I think the next one's going to be a great case of someone that--it's current active with their central serous, where they have both RPE and neurosensory fluid, 20/20 vision, by the way, because the fovea is in tact.

But, you can see this is someone that--it's nothing just any one spot. And this is a very--common what you see in people that have had central serous, because you see this tracking, where they had fluid here. Then, it kind of tracks downward.

Now, it tracked downward outside the fovea, so that didn't affect the vision, but that doesn't mean it didn't happen before. So, this is someone that's--has chronic recurrent central serous that, at this point, just isn't affecting the fovea. It's awfully close.

And a little different than the patient with diabetes, central serous is something that generally doesn't get treated, because it usually goes away on its own. But, it's so important to know what's going on and know how close it is and tell them what to monitor, what to look for, and when you're going to see your patient back, because of the information that you have.

Now, this happens to be another guy that I saw just this week. And he came in--he's--I think he's 38. He came in, and he says, "Yeah, you know, I had something going on in my eye about 10 years ago, and they brought in all the residents, and everyone wanted to look at my eye." And he said, "And they told me I had the eyes of a 50 year-old black woman."

I was like, "Okay, that's kind of interesting. Let me take a look." And I said, "Do you remember what they called it." And he said it was--he kind of knew. He said, "They said it was like a multi-inflammation choroid." He couldn't quite put together--multifocal choroiditis was what he had been diagnosed with.

And he's 20/25, but you can see that the macula's not quite right. There's some very subtle change. This is the SLO image, where I had--I should've maybe turned it more to where you can see the SLO changes. But, you can even see the subtle changes in the macula. And if I blow those up, you can see it a little better.

So, even if he's 20/25, that's pretty good quantity of vision, but his actual quality of vision probably isn't quite that good. And his other eye looked the exact same.

Interestingly, he had no spots in the peripheral retina at all. Now, unfortunately, I couldn't image him on the autofluorescence, but I think that would've been really interesting, because there's probably lots of change that was just below the surface that I couldn't see that would've told me, "Yeah, that's probably what it was, because I can see all those--the multi-focality of it. I can see it in all the different spots." Because as he presents today, it doesn't look multifocal. It's just only a couple spots in the macula, and that's it. There was nothing else, at least today.

Now, if somebody's wondering, "What are your RP patients--what do they really look like? Because when you see them, sometimes they--it can look pretty subtle, and they may have good vision, they may have really bad vision?"

And I've seen that - that there can be dramatic differences in what people with RP look like, funduscopically but also with autofluorescence. And this is a guy that actually has pretty poor peripheral vision, and you can see why. You see lots of dead tissue surrounding it.

And in the macula, you see how it's a little bit brighter right there? That's a fairly typical ring to see around the macula, and you wonder if that means that, in this person, that the macula is starting to get affected? If his central vision's going to start to get affected? That's likely the case.

Now, let's go back to this case. I actually already told you what this was, but I want to show you the same patient from a couple different perspectives. So, this is a woman that--her name is Debbie [sp]. It's 2100 and has Stargardt.

And there's about the same area, a little bit less of the area, but fundus autofluorescence. To really show you the extent--you can't really appreciate too well what's really going on there. And it doesn't matter if you're looking at this image or if you're looking in the eye, that's what it looks like. You can't really see the extent of it. You just see the macula.

And then, you look at this, and you say, "You know what? It really extends out. All these little flecks." I think what--what's, I think, interesting is to say, "Well, gosh, that area there, that's pretty bright. That's active. That's an area where it's getting worse."

And whereas I would love to tell Debbie, you know, "Look, the central vision's already gone, and this is as bad as it's going to get, I can tell your central vision's already gone. Centrally, it's as bad as it's going to get, but that central area of 'bad' looks like it's probably going to grow a little bit." And it's going to grow into her blind spot, which is going to make it seem even bigger.

So, using this, it really kind of helps me to explain to her what's going on, because you look at this, you have no sense of activity. You have no idea. Is that something that's staying the same? Getting worse? Getting--it's not going to get better. You can make that assumption. But, you don't know if there's likelihood of it getting worse.

Now, here's actually what her OCT looks like. And you can see there an extremely thin macula. Well, we know that because there's all that atrophy there. And that's why you can really see the choroid. When there's no macular or when there's no retinal tissue for the OCT to go through, then it's imaging really well into the choroid. So, you can see the choroidal vessels, which I thought was kind of cool. But, very, very thin, pretty bad-looking macula. She's 2100. She has been for about the last 15 years.

I just want to show you some more examples of pathologies, again using the Optos OCT. These are two different patients with drusen. And to really see, you know, where the drusen are, where they're affecting and what--people will call this a drusenoid PED or pigment epithelium detachment. Pretty easy to see there when you have the OCT.

Here's just another person with really extensive drusen and changes underneath the macula. So, using OCT to really show that to you and see what's really going on.

How about macular holes? Well, we know what--really what causes a macular hole is the vitreous pulling, pulling, pulling until it just tugs off a little chunk. Kind of like an operculated tear anywhere else.

So, really, what this is is that's a flat tear in the macula. But, then, later, it might look like that, where that flat is completely torn off. So, now, you have your floating operculum. Now, that may or may not make any difference in the outcome or the vision, but it allows you to really see what's going on.

Macular holes were something that OCT really taught me a lot on how they happen. They don't just happen. They're not atrophic. Something's pulling, pulling, pulling 'til what's there gives way and can't hold anymore.

Now, this is actually a patient that I saw yesterday in the office. A 35 year-old Caucasian female. She got hit in the eye the night before with a volleyball. She noticed that her vision was kind of funny. No flashes, no floaters, but there's a part of her vision that's missing since she got hit with the volleyball. Should she come in? And my staff says, "Yeah, maybe you ought to come in. We should check you out."

No pain. Anterior segment's normal, no high finga [sp]. They did a--my staff did a visual field on her, looks like that. So, if you see that, what are you expecting to see, knowing that she got hit in the head with a volleyball?

What you're hoping you're not going to see is that she has a retinal detachment, but that's kind of what you're expecting to see, from what you've been told. That's what she looks like. We show a little bit more closely, and that's actually an area of commotio retinae. And so, it's--what--if it's in the macula, it's called berlin's edema, but basically what it is, it's from blunt trauma, and it's swelling to the retina, and kind of whitens or creates opacification to the retina, but you're still able to see the blood vessels.

And so, it's not detached, she didn't have a retinal tear, but she has this area. And the protocol for it is to follow up weekly until it goes away. So, luckily, for her, she has just this. She has--basically, it's like having a bruise in the retina and not a retinal detachment.

It made me better to be able to image this and, you know, look in and see it clinically, but also image, because if something does happen, I can at least say, "Well, when she first came to me, this is what was going on. She certainly didn't have a retinal detachment, regardless of what may happen later down the road."

So, as--I think, from a medical/legal standpoint, this is a really good one to be able to have to really say, "Yeah, I dotted my I's, crossed my T's. This is what was going on then, regardless of what happens to her tomorrow."

So, I thought that was kind of an interesting case. Too bad this isn't two or three weeks from now, because I'll have another image of her next week and the week after, and we'll be able to watch this over time as it's getting better.

So, hopefully what I've been able to share with you is that, you know, having great technology in your office--it's fun. Yeah, it's important, but we all--you know, everyone always tells you how important it is. "You got to have this. You got to have that." But, what I'm going to tell you is it's fun. It's fun to be able to provide the best care for your patients, to know that you have the best in technology, the best there is to offer to your patients.

It's fun to be able to do that and know that you're practicing to the very highest level, the very highest standards of care that anybody--anyone can have, and that, really, your patients deserve it, and that it's important to have access to these things, because your patients deserve the best care that they can possibly have.

And I think now we can really provide it, and we can really--you know, we can see things that, when you're combining OCT with wide field imaging, with autofluorescence, you're seeing things that you just cannot see clinically. And I think that's what's really important. You're seeing things that otherwise wouldn't be there, as far as you're concerned.

So, hopefully this has kind of sparked some interest, and--to either ask questions now or go to the booth and see what these things can do.

You may be surprised. You know, if you go to the booth, have your own eye imaged. You may be surprised, because you may have had color images taken--you're kind of rolling your eyes like, "I don't want to see it," but, you know, you may have had images taken of your eyes before, and everything looks normal. But, how do you know that it's really normal unless you can really see what's going on?

So, have yourself imaged and prove to yourself that your eyes are normal or maybe that they're not.