Objectives of this presentation are:

  • To Understand the epidemiology of diabetes and diabetic retinopathy
  • To Understand the fundamental pathophysiology of diabetic retina disease
  • Learn the Features and Classification of diabetic retinopathy and diabetic macula edema
  • To be able to apply the Evidence based clinical trials to the management of diabetic retinal disease

Lecture location: on-board the Orbis Flying Eye Hospital in Binh Dinh, Vietnam.

Lecturer: Dr. Wai-Ching Lam, University of Hong Kong and University of Toronto

Transcript

(To translate please select your language to the right of this page)

DR LAM: Okay. I thought yesterday, when we were doing the OCT — this is the last slide about the bull’s eye or chloroquine maculopathy. So they described this as the flying saucers — changes. So I’m gonna show you… So that is what it looks… They call the changes. And that’s what they mean. The flying saucers. So you can see the shapes of the flying saucers. The reason is because there’s thinning of the outer segment, around the macula. Not at the macula. So you can see that the eye doctors are very imaginative. I wouldn’t think of this as a flying saucer, but someone else has. So I just wanted to kind of bring that up from yesterday, because I don’t think I was able to show what the flying saucers looked like with my hand. Okay. All right. So… Some epidemiology. This is from the WHO. And I think most of us are aware of the prevalence of diabetes. And it has been estimated the global prevalence of diabetic retinopathy has risen from 4% in 1980 to now almost double, in 2014. And the increase is kind of worse in the middle and lower income countries. Countries like Vietnam is — I’m sure you’re aware of the increases yourself. And we understand that diabetes affects not only the eye, but the other parts of the organs, like the heart, the kidney, and the extremities. And what is worse — that the estimations in 2012 — there was 1.5 million deaths attributed to diabetes. This, as we all know — diabetes affects the younger age populations, different than the age-related macular degeneration that affects people who are older. And it is common to have eye problems among the diabetic patients, up to about 35%. A third of the patients will have eye problems. And the longer you have diabetes, the more likely you’re gonna have eye-related problems. And what’s important is that those conditions, such as macular edema, that affect the visual acuity, increases as somebody who has diabetes for longer. So we’re gonna talk a little bit about the pathophysiology of the diabetes. First, you know, we know that the sugar goes up, and so that is the glycosylated end product, from the diabetes, for high sugars. And there’s also the presence of the oxidative stress to the… With free radical formation, because of the ischemic changes that happen with diabetes. That will cause the loss of pericytes, which is the earliest changes in the anatomical structures of diabetic retinopathy. But interestingly, we sometimes forget there’s also an inflammatory component that is responsible for causing the increased leakage of fluid. Because there’s damage to the tight junction between the endothelial cells. So the buildup of the basement membrane, causing the vascular changes, and the leakage of the fluid — all of that attributed to what we describe as diabetic retinopathy. When the damage starts to become severe, the circulation becomes a problem, and you get ischemia. From the ischemia, you can get the complication related to bleeding, tractions, and retinal detachments. We know that the high sugar, the hyperglycemia, is the major cause for the diabetic retinopathy. And we also have to realize the inflammatory components of the diabetes is something that sometimes people have forgotten. So I’m gonna just cover some of the features of diabetic retinopathy. Which you probably are very familiar with. The first feature is — probably most of you are aware — is the microaneurysms. And this is caused by loss of the pericytes. So that’s Cybersight, just covering the small microaneurysm from the picture of it. So they appear as little red dots. Sometimes hard to distinguish that from retinal hemorrhages. And very commonly, they are seen in the center part of the eye. What we call — near the macular regions. To distinguish it from dot hemorrhages, the best way to do that is fluorescein angiogram. So in the fluorescein angiogram, the microaneurysms will look like a dot hyperfluorescence, because the dye collects there. And if it’s just a hemorrhage, it will be a blot hypofluorescence. It will be dark. Another feature is the intraretinal hemorrhages. So remember, diabetes is a retinovascular disease. And so it is within the retina — those blood vessels have problems. And that’s where the hemorrhage is. It’s very different than the macular degeneration, where the hemorrhage is in the subretinal area, that goes into the retina. So we can see the hemorrhages there. We can see also the hemorrhages… They’re usually deep in the retinal layer. And yesterday, we saw the OCT appearances of the cotton wool spot. It is essentially an ischemic damage to the nerve in the nerve fiber layer of the retina. And then you have this — what we call IRMA, or intraretinal microvascular abnormalities. So basically they are dilated blood vessel channels between the artery and the vein, from a response to ischemia. Sometimes it’s hard to distinguish this from neovascularizations. The way to identify them is to do fluorescein angiogram. A retinal neovascularization will leak. An IRMA does not leak. So the presence of IRMA means that ischemia — there’s another feature here. You can see that the narrowing of the vein — we call it venous beading. So that is also a sign of ischemia. So another feature is this venous loop. And what I mentioned before, venous beading. So when you see that, it means there is severe ischemia. So here is the venous beading. Sorry, venous loop. Sorry. And you can see there is ischemic non-perfused blood vessels. And right next to this venous beading, you can see there’s early retinal neovascularizations. And you might even have some intraretinal — or IRMA. Microvascular abnormalities. So in terms of the classifications of the diabetes, we classify it when it is mild, when we only see just microaneurysms. We classify as moderate non-proliferative diabetic retinopathy, or moderate-severe non-proliferative diabetic retinopathy, when there are retinal hemorrhages and exudate in addition to the microaneurysms. And we call it severe if there is this 4:2:1 rule. What does it mean by 4:2:1? If you have intraretinal hemorrhages in four quadrants, all four quadrants, and you have venous beading or venous loops in two or more quadrants, and the one is the presence of IRMA in one or more quadrants. But you don’t have any signs of proliferative diabetic retinopathy, such as retinal neovascularizations that hemorrhaged. When you have that, that means this is a severe non-proliferative diabetic retinopathy. And… Yeah, yeah. And so if you have those features, if you have two out of three of these features, the risks of proliferation is very high. So I’m gonna show you some features of a severe non-proliferative diabetic retinopathy, where this square identifies areas of IRMA in two quadrants, and you have a cotton wool spot, suggesting ischemia. Another picture, showing area of cotton wool spot and venous beading. So if you have the… If you have severe or very severe non-proliferative diabetic retinopathy, the chance of developing proliferative diabetic retinopathy is from 14% in one year or half of them, if you have very severe. And then in three years, a third of the severe ones become proliferative. And more than half will become proliferative, if you have very severe ones. So this is… If you have all three of those high risk features, or if you have two of those high risk features — if you have all three, the patient can get proliferative diabetic retinopathy in half of them. Half of them will progress to have that. Which is a significant concern. Therefore, it’s important to identify those features, so that you can see those patients on the regular basis, or even start treatment, if they are not gonna come back on time. Because if you don’t treat them, half of them will have severe visual loss within five years, when the proliferative diabetic retinopathy is not treated. So these are some of the features of proliferative diabetic retinopathy. It’s important to recognize the high risk characteristics. If the patient has these high risk characteristics, they are more likely to develop vitreous hemorrhage and cause loss of vision. So basically, if you have retinal neovascularizations, that is high risk, but it will be higher if the retinal neovascularizations are large. And how large you need? Well, if it’s not on the optic disc, then if it’s more than half a disc diameter, it’s considered large. And if it’s on the optic disc, either a quarter to a third of the disc diameter is considered large. So that means, when you look at the patients, you look at — if there is any retinal neovascularizations, if it’s on the disc, and if it’s large. And also if there’s any bleeding. So if you have all of those, then this patient is going to have a high risk of severe visual losses, because of bleeding and complications related to it. Proliferative diabetic retinopathy. On the other hand, if you only have retinal neovascularization that is small, and is not involving the disc, and there’s no hemorrhage, so there is one out of the three features, then you don’t need to treat right away. You can watch this. Because sometimes those neovascularizations can go away by itself, if their diabetes gets better. So don’t forget that the patients have diabetes. So it’s important to review their diabetes status, their blood pressure status, and their cholesterol status, and make sure that they are well looked after also. We talked about the severe non-proliferative and very severe non-proliferative diabetic retinopathy. So I’m sure you’re all very familiar with the screening kind of protocol. So for any type II diabetics, they should get screened as soon as they make the diagnosis. The reason for that is — most often is that they already have some retinopathy in their eye, because they don’t usually go to get the eye… They don’t get to find out that they have diabetes until late. So for the type I diabetics, if they were found to have diabetes before puberty, then they don’t need to be screened until they reach puberty. And that’s because they are not likely to get any severe retinopathy before reaching puberty. So, on the other hand, if they have the diagnosis after they reached past puberty, then they should screen five years after the diagnosis of the diabetes. So, again, the idea is that it takes time for them to develop retinopathy that will require treatment. And once you find out that they have retinopathy, then you’ll have to classify them, whether they are mild or moderate-to-severe. If they are mild, then they can be seen once a year, because it will take time for that to become a problem. But if they are moderate or severe, then they need to be seen either three months, if they’re severe, or six months, if there are moderate changes. Then, if they don’t have any retinopathy of diabetes, then for the type I, then they need only to be seen once a year. And for the type II, it can be a little less frequent. One or two years. Okay. So now we have diabetic retinopathy. Then we decided the patient needed treatment. The most common treatment is laser. So, in fact, the protocol — the study of using laser treatment for diabetic retinopathy is back in 1971. So it’s a long time ago. So they were able to show, by doing laser, the panretinal laser photocoagulations, they were able to reduce the risk of severe visual losses by as much as 60%. So the laser has been the standard of treatment for the proliferative diabetic retinopathy with high risk characteristics. But the problem with laser is that it is destructive. Meaning that it takes away a lot of the good retina, creating scar tissues. And patients lose their peripheral vision. And they also have a problem at nighttime, seeing in the dark. Because of the destructions of the peripheral retina. And if there is macular edema, the laser, the PRP laser, the panretinal laser, can make the macular edema worse, because there’s more inflammations after the laser. So up to 20% of those patients who get laser treatment still experience severe visual losses, despite the lasers. So people wanted to know if we can do better using, for instance, anti-VEGF, when we already use it for the treatment of diabetic macular edema. When do we use laser for treating patients with diabetic macular edema? So those patients who have clinically significant macular edema, or CSME, is the one that will benefit from macular laser photocoagulations. So we’re gonna spend a little time looking at the classifications. But this is very different than the fluorescein angiogram pictures of, like, focal laser, diffuse laser, or macular ischemic. The assessment of CSME is by clinical examination, and not by fluorescein angiogram. So the first one is when you have an area of retinal thickening, in this — in the kind of bluish-grey area. That is, within 500 microns of the center of the fovea. So if you have that, that is CSME. What that means is that this area of retinal swelling is going to move to the center and cause a problem to the vision. So this picture is here. This is the center of the fovea. So this area of retinal swelling is within 500 microns from the center of the fovea. So this patient has CSME. And will benefit from laser. So another definition is that when there is hard exudate, just like the yellow stuff, within 500 microns from the center of the fovea, with an area of retinal edema next to it, that is also CSME. So here’s the center of the fovea. So this is the area of the yellow exudate, within 500 microns from the center. With this area of edema. So what that means is that this edema is causing the fluid to track towards the center, and you already have some exudate present to show that it’s doing that. So again, so this patient will benefit from laser treatment to those leaking microaneurysms, and they will help to prevent decreased vision, because of the macular changes. And the last one is that if you have a very large area of retinal swelling, that is, within one disc diameter from the center of the fovea, that itself is about one disc diameter in size or bigger, then this area of edema is also considered CSME. So you can see this is the optic nerve. So this area of retinal edema is slightly bigger than the optic nerve, and it is within 1 disc area from the center of the edema. So you can see this edema is going to, again, threaten the center of the fovea, and cause damage to the vision. So laser to those leaking microaneurysms will help to reduce the edema and prevent the loss of vision. So, as I said before, those classifications that I told you are based on clinical examinations. It has nothing to do with the changes you see on the fluorescein angiogram or OCT. Because they don’t do those tests. They just do the examinations. So with the fluorescein angiogram and OCT, now we have somewhat of a newer classification. We classify them either as local, diffuse, or ischemic, or a mix. So this is diffuse, and that one was focal. So this is ischemic, because the FAZ, the foveal avascular zone, is bigger and irregular. And they can also have macular edema. Okay. So… This is the study that was done — the ETDRS, early treatment diabetic retinopathy study that was done in the 1980s, and they showed that by doing macular laser, you can reduce moderate visual losses by up to 50% in patients with CSME. So, for a long time, laser is the standard of treatment for diabetic macular edema. So we wanted to find out how the anti-VEGF compared to laser treatment. But before we do that, let’s talk about the types of treatment that we do. How do we do the laser? Most people now, they do focal laser, instead of the grid laser. Basically focal laser — it’s that you use a small spot size. Short durations. With a lower energy. Targeting those microaneurysms that are leaking. And the purpose is to close those microaneurysms. It will turn the microaneurysm into either white or black. Do you know why it will turn either white or black? So in a microaneurysm that has a lot of blood in it, it will turn black. In a microaneurysm that doesn’t have a lot of blood in it, it will turn white. Because the blood within the microaneurysm will create much more energy uptake, and the blood will coagulate and turn black. And when you do it, of course you try to avoid the foveal avascular zone, and not to damage any of the fovea or the macula itself. So the treatment is — those patients who have CSME, then you will start the laser treatment. Now, there are quite a lot of studies looking at comparing the use of anti-VEGF, compared to laser or compared between the types of anti-VEGF, as well as comparing to steroid. Yeah. I’m not gonna go through all of them, because that would take me probably all day and tomorrow to do that. So I’m going to just highlight some of those ones that you should know about. So the first one that I wanted to talk about is the DRCR.NET Protocol I. So I think you all know that DRCR.NET is a group of doctors in different centers in the US — now has expanded outside the US — who are interested to do studies, clinical studies, to find out answers about management of diabetic patients. So this Protocol I wanted to find out, number one, is that — if laser is as good as using anti-VEGF — the anti-VEGF is ranibizumab. And if the laser should be done right away, or you can wait. Remember I mentioned about steroid, because there is a component of inflammation for the diabetic retinopathy. So they also wanted to find out — is steroid also helpful or not helpful? So the study found out that those… So this line here… Yeah. The blue line is ranibizumab, Lucentis, with deferred laser. Meaning that they wait. They don’t give the laser right away. They give the injections, and then wait. If the swelling doesn’t go away after three months — then they would do the laser. You can see that their vision is better than those who had laser at the same time as they’re getting their ranibizumab or Lucentis. And the combination of laser and Lucentis is much better than those who only get laser alone, which is the purple line. And what’s interesting is that, for the triamcinolone, the steroid injections, the patient gets better initially, and then after the first three… Six months, then they become worse again. And the reason for this deterioration after the 24 weeks or 6 months is that the patients developed cataract and started to make the vision not as good. So that is confirmed when they looked at those patients who already have cataract surgery. And you can see the yellow line, which is the steroid patients — that drop that you saw before didn’t happen. They will continue to get better. Get very close to those who are getting the Lucentis injections. So in fact, Lucentis, steroid, are much better than laser alone, when you treat the patient with center-involved diabetic macular edema. And you can see here, when you compare those who have laser right away, or those who have laser later on — their vision improvements are not that much different. In fact, the one that waits for the laser treatment has better vision than those who have laser right away. And that’s — the reason is, when you do laser, you’ve actually damaged some of the tissue or retina around the center part of your vision. So as good as it is, it also can cause some decrease in the vision. So it’s probably better to wait to do the laser, and not do the laser right away. So only those patients who didn’t get better right away with the injection — that you should use laser to help. So that it’s the deferred laser group. On the other hand, if the patients already have cataract surgery, then cortisone injections, steroid injections, are doing very good. As good as the Lucentis. And they have found that more than half of those patients who didn’t have laser right away never have laser for the five years that they watch the patients. But they need more injections. And they, on average, need four more injections. What’s interesting is that about a third of the patients still have some edema at the end of the five years. So that means they will need some additional treatment besides the laser and the anti-VEGF that we have. So then the question asks: Well, can we use more anti-VEGF? Higher dose? Double the dose of Lucentis? Does it make it better? So the Protocol 3 is done with not only half — four times the dose of ranibizumab. From 0.5 milligrams to 2 milligrams of ranibizumab or Lucentis. And they treated the patients and followed the patients for two years, and they found out that there is actually no difference between the 2-milligram group and the 5-milligram group for the vision. The improvement of the vision. There’s not much difference between the low dose and the high dose of Lucentis. In fact, if you wait ’til 24 months, the low dose group have better vision than the high dose group. Surprise. So it’s not logical that more is better. But at least not for anti-VEGF, for treatments of center-involved diabetic macular edema. So the higher dose really doesn’t help. But actually may even make it worse. And the explanation is that when you use 0.5 milligrams, you’re already getting the maximum from blocking all the anti-VEGF. So giving more than the maximum is not gonna help. Then the other question is: If one anti-VEGF is better than the other anti-VEGF, and if injection is as good as laser, so… To answer the first questions, to see — there are now three anti-VEGF that we have. Right? We have the Avastin. We have the Lucentis. And we have the Eylea. So people want to know, and that question has been asked for many times already: Is one better than the other one? And this is Protocol T. When they actually looked at the dosage. So it looked at the use of Eylea, Avastin, and Lucentis for treatments of diabetic macular edema. But they use 0.3 milligrams, because that’s the US-approved use dose for diabetic macular edema. For the rest of the world, it’s 0.5 milligrams. They looked at 660 patients in three equal numbers of groups. So about 200 in each group. And they followed the patients during the first year, every four weeks, and then in the second year, 4 to 16 weeks, a month to four months. So the patient gets one of the three anti-VEGF. If after six months the edema is still there, they can have macular laser. So here is the result. It’s interesting. The Avastin has to use the rescue laser the most. It means that the patients who get Avastin will have more edema after six months. So that therefore they need laser done. So it happened in the first year and it happened over the two-year period. And ranibizumab, interestingly, has also a higher than aflibercept, in terms of the use of rescue laser. And it is statistically significant in these comparisons. So when they look at — in the first year, at 52 weeks, they see that in aflibercept, the vision improvement is about 13 letters. And for Lucentis, it’s 11 letters, and in bevacizumab or Avastin, it’s a 10-letter improvement from baseline. So the difference is not too much between them. But if you look at those patients who have good vision to begin with, there is actually no difference between the three anti-VEGF. They all get about 8 letters of gain, overall. They get an 8-letter improvement. But when they look at those patients who have not good vision to begin with — like 20/50 vision or less, then they found that the aflibercept, the Eylea, has the most improvement in the vision. 19-letter gains, compared to Lucentis, which was 14 letters. There’s one line of difference between them. And then one and a half line improvement compared to Avastin. So from this, people thought Eylea is a better medicine to use for diabetic macular edema. At least during the first year, compared to Avastin or Lucentis. So then the second question is: Is this going to last? What happened in the second year? Is it going to see the same benefit that will stay over the two years? So this is the two-year result. Again, if you look at the overall number, overall patients, there’s not much difference between the Eylea and Lucentis. And both of them are better than the Avastin by about 2 letters. Again, they want to find out if there is a difference between the baseline vision. So those with good vision at the baseline, at the beginning — again, there’s no difference between the three groups. They all did well. They all did about the same. In fact, Lucentis this time seems to do a little better than Eylea. But it’s not statistically significant. And if you look at those patients who have bad vision, 20/50 or worse to begin with, that were getting better in the first year, it has shown that Eylea is better than Lucentis — that difference becomes much narrower. So at two years, Eylea no longer appears to be better than Lucentis, in terms of treating diabetic macular edema. The difference is only 2 letters. But it is better than Avastin. It is about 5 letters, which is one line, of vision improvement. I know here you use Avastin a lot. So this gives you an idea, if the patient is given either one of the three anti-VEGF, and how they do. So it appeared that when you use Eylea, there is an initial improvement during the first year that is better than Lucentis. But after two years, they are the same. So overall, both Eylea and Lucentis are better than Avastin. Avastin is still better than laser. And this is just to show that the central subfoveal thickness has been significantly reduced by getting rid of the edema with the anti-VEGF. And all three are very good in reducing the macular edema. So I’m gonna move on to talk about steroid. What about steroid? And we know that from the Protocol I, the one that we talked about, steroid worked as good as the Lucentis, especially in the pseudophakic patients. And it’s important to know that when you test the patient for those inflammatory markers, they are increased in diabetics. And the more severe the diabetic, the more those markers, those cytokines, have increased. This showed that the more severe the retinopathy, the more the inflammatory marker or the cytokines. So we know that the anti-VEGF is very good to lower the VEGF level. But it is not of any effect on the inflammation. On the other hand, steroid can be effective on both the VEGF suppression and the inflammation suppression. So particularly in the case of pseudophakic patients, then if they’re not getting better with the anti-VEGF, steroid will be an option to consider. Because when using anti-VEGF, up to 40% of the patients did not get that much better with the anti-VEGF, and up to 20% of them did not get better at all to the anti-VEGFs. So perhaps in this 25% of non-responders, steroid is an option. So I know that when I was working with our hands-on trainees, they don’t consider steroids a treatment option, because they worry about all the complications related to the steroids. The cataract and glaucoma are the two most common complications. Like I mentioned before, if the patients already had cataract surgery, then it’s not a problem. And you can test the patient to see if they are still a responder. Only about 30% of the patients who get steroid get pressure increases. So the other 60% don’t get pressure increases. So, you know, next time you can look at the — considering steroid as an option, especially in those patients that you’re not getting better, after 6 or 8 Avastin injections, they’re not improving. So another property of the anti-VEGF is that it can improve the severity of the diabetic retinopathy. Here is an example of a two-step improvement of diabetic retinopathy severity score, from a level 6 to a level 4. The reason I want to show you this picture is that I’m going to show you the study that’s shown — using anti-VEGF, you’re gonna get two-step improvement of the diabetic retinopathy from just the anti-VEGF interventions. So this is using Eylea. And two doses. The green and blue one is 2 milligrams every 4 weeks. And the yellow one is 2 milligrams every 8 weeks. You can see that both treatment regimes have more improvement of the severity of the diabetic retinopathy. In the VIVID trial, almost half the patients who received every 8 weeks injections has two-step improvement of the severity of their diabetic retinopathy severity scale. So the decision is to do a Protocol S, to look at if laser, PRP laser — not macular edema anymore — we’re looking at treating patients with proliferative diabetic retinopathy, with much more severe forms of diabetic retinopathy, to see if laser versus laser plus Lucentis — to see which one is better. They want to find out if anti-VEGF is as good as laser, and they also want to look at the safety of laser, compared to that of injections, for proliferative diabetic retinopathy. And the secondary question is: Are there other benefits of Lucentis, in terms of their vision, their peripheral vision, the macular edema, and if they need vitrectomy? So this is to look at those patients, when they start with diabetic macular edema to begin with, compared to those who did not have diabetic macular edema. And you know those patients who had diabetic macular edema at the beginning — they’re going to get Lucentis injections. So no surprise is that those with diabetic macular edema has more Lucentis injection, compared to those who did not have diabetic macular edema to begin with. And if you look at the visual field between the Lucentis and the laser group, and there are more changes, more mean deviations from the laser group, compared to the injection group, from the Lucentis group, and that’s expected, because laser causes loss of peripheral vision, when the injection doesn’t — so that’s the Humphrey visual field. Then, when you look at the percentage of the eye developing centrally involved macular edema, over the two-year period, more patients, about 30% of the patients, with laser developed macular edema, compared to only about 9%, 10% of the patients who got Lucentis injections. So those with laser has more macular edema than those who’s getting Lucentis injections. And if you look at the regressions of the neovascularization, meaning how well they do with the PDR, proliferative diabetic retinopathy, there’s no difference between those who are getting injections of Lucentis and those getting laser treatment. So even we think laser is stronger, to get rid of the laser — the truth is it’s probably not the case. And injections do as good as the laser, in terms of getting rid of the retinal neovascularizations. And if you look at the diabetic retinopathy improvement, there’s two steps improvements of the diabetic retinal scale. Almost half of those patients who get Lucentis has improvement of their retinopathy. Not their vision. Improvement of their retinopathy. And if you compare the complications, they are the PRP group has as many, if not the same types of complication, compared to the injection group. And the number of vitrectomy that’s needed is actually more in the PRP group than the Lucentis group. So the conclusions for the Protocol S is that the Lucentis has better vision… In fact, it’s no worse than that of PRP, in terms of the… The vision is actually better at the end of two years, for the Lucentis group. And the Lucentis has less visual field losses. They don’t need as much vitrectomy. They tend to have less diabetic macular edema. And if they’re getting Lucentis, they don’t usually end up needing laser treatment for PRP. And there’s no complications noted. So from the Protocol S, they say if the patient comes in with diabetic macular edema, and you’re already going to give anti-VEGF, then don’t do the PRP right away. Even though there are proliferative diabetic retinopathy changes. If the patient can come back — of course, if the patient is not gonna come back on a regular visit, then you might have to do the PRP. Because that might be a problem, to monitor the patients. Well, what is interesting is that if you don’t have diabetic macular edema, Lucentis still is better than laser in preserving the central and the peripheral vision. But this is much more expensive, to treat patients with the Lucentis injections, for the proliferative diabetic retinopathy. So I think at the end it’s probably shown that the Lucentis is as good as laser in managing patients with proliferative diabetic retinopathy. And if the patient can afford it, it may be better to use anti-VEGF than to use laser for the treatment of the proliferative diabetic retinopathy. So this is a two-year study. So we don’t know whether it’s going to be the same for the five years. So we are not saying PRP is not good. It actually can be done very quickly, after three visits, because, remember, we talked about the number of lasers that you need to do. You only need about 4,000 burns. Each visit can be 1,000 burns. And you can finish the treatment in three visits. And it’s much less expensive than the Lucentis. And you don’t have the complications of infections or having to have a needle in the eye. But just remember: About half the patients with proliferative diabetic retinopathy also has diabetic macular edema, which will require anti-VEGF injections, either Lucentis or Avastin. So when you used the anti-VEGF, either Avastin or Lucentis, the diabetic retinopathy can become less severe. And they might not need as often laser treatment or surgery or vitrectomy. So something to think about. So now about vitrectomy — we know we do vitrectomy for vitreous hemorrhage or tractional diabetic retinal detachment. The other indications are ghost cell glaucoma, and if the patient has vitreous hemorrhage that lasts more than three months, then the vitrectomy is necessary, so that you cannot only get rid of the blood — you also can treat the underlying retinopathy. That’s the end of the presentation about the management of diabetic retinopathy. So we talked about laser treatment for the macular edema, we talked about laser treatment for the proliferative diabetic retinopathy. For the laser treatment for the diabetic macular edema, you should wait. You don’t do it right away. Give time to allow the anti-VEGF to settle down the macular edema. If, after three injections of Avastin, the macular edema is still there, then you should then add laser treatment. And if you find after 6 or 8 injections of Avastin the macular edema is still there, you may consider using steroid, especially if the patient already had cataract surgery. If the patient has diabetic macular edema and proliferative diabetic retinopathy, then you should start with anti-VEGF. There’s no rush to do PRP laser. And if the patient can’t afford the injections, PRP laser is still a good way to manage proliferative diabetic retinopathy. And when you have vitreous hemorrhage, then you should consider vitrectomy, when the vitreous hemorrhage is not going away. How can we test to see if the patient steroid responder or not? What is the protocol? Very good question. There are different ways that you can try. And some people have given patients topical steroid drops, like Pred Forte, four times a day, ask them to do it for a week, and you can then check the pressure. If they have increased pressure. If they have increased pressure, it means the patient is a steroid responder. Then using the steroid as a treatment for injection is probably not a good idea. Okay? For intravitreal injections of steroid, if there are the cheap, inexpensive ones — triamcinolone acetonide — and people use either 1 milligrams in 1 CC, or 0.5 milligram in 5 CCs. 0.5 CCs, I mean. 1 milligram or 0.5 milligram. If you give 1 milligram, it lasts a little longer. It lasts about 6 to 8 weeks. If you give 0.5 milligrams, it lasts usually about 6 weeks only. And there’s also the option to use a long-acting dexamethasone implant. The commercial name is called Ozurdex, and they last between 3 to 4 months. And dexamethasone tends to have less risk of increasing intraocular pressure, compared to triamcinolone. The reason why we don’t inject dexamethasone as a solution is because it clears from the eye very quickly. It only lasts less than a week. That’s why, if one uses dexamethasone, you have to use that implant in order to have this long-acting property.

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June 2, 2017

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