Diabetes & Endocrine ECHO: Update on Diabetic Retinopathy – 5/18/17

So let me introduce Dr. Arshad Khanani, who is a vitreoretinal specialist. He works here in Reno at Sierra Eye Associates, did his
training in Texas before coming to Reno and he’s been my go-to guy for patients
with diabetic retinopathy since as long as I can remember being here. So it
is my pleasure to introduce him to you, it’s been a couple of years I think sicne we did this right? So I’m gonna turn it over to him and then we will loop
back and finish up our cases. Great thank you so much, exciting to be here as usual.
I think it was two or three years ago we did this and a few things have
changed since that time, I mean the basic management have stayed the same but
there’s some new guidelines that came out this year by ADA to manage or to
screen (inaudible) retinopathy patients. One of my good friend Charlie
Wyckoff actually was one of the authors on that paper, he’s based out of Houston.
So we’ll review some basic things about diabetic retinopathy. Please feel free to
ask any questions, if you have no questions, dumb questions, if you have any questions related to my presentation or in general about eye exams or anything you
do, please do let me know. So just the anatomy, basically first we’re gonna talk
about anatomy, and then we’re gonna talk a little bit about guidelines and screening, and then we’ll talk about some pathology. And there’s going to be a lot of pictures you know, Evan is too smart to think about this t3 t4 I’m more like a visual guy (laughter), so that’s why I became an opthamologist because I like to see things. I don’t have the brain cells to process all those lab results you guys
are talking about. So, you know, you look at this picture, this is the right eye so
always when you have a photo you always worry whether it’s the right eye or the
left eye. So you know there’s an acronym MOOM, M-O-O-M, so Macula on the left side, Optic
nerve, Optic nerve, Macula. So you start, you know, either eye, if you start on the
macula you know the left side is the right eye, if it’s on the right side it’s
the left eye. So that’s how I remembered. So fovea is the central vision part of the
eye, optic nerve head, obviously you can see that and you know you check that
for abnormality and other things in your clinic. You know with the direct ophthalmoscope, I think the most important thing you can rule out is mainly
papilledema. You know and I was in training I did an internship in internal
medicine, and the attending always saw the papilledema, I never saw it, but we always pretended, like “oh yeah I agree”, and then you know it’s like, well ther’s no papilledema (laughter). So a lot of times it’s very hard to look through the direct scope, because the patients are not dilated yet. So one trick for medical students is obviously with some dilating drops.
Have some, you know, short acting phenylephrine tropicamide handy and just put a few drops in. And they really have no contraindication even the patients
with hypertension or pregnancy and you can really get a much better exam if
you dilate the eye. So if you look at the circulation here you have, can I point with this? Uh, you can. Okay perfect. So you can see the the retinal veins
coming out, the retinal veins are a little bit bigger than the arteries, so
that’s the trick. Is like which one is vein which one is artery? You can see the
arteries are, you know, the diameter is smaller and you can see kinda the sheeting in there and the way it’s- really I mean, it’s very hard you know unless you’re Doctor Klass, to see retinopathy with your (inaudible) scope. I really could’nt. So that’s why, you know, in clinic we
obviously dilate these patients. So again the orientations I said MOOM, macula, optic nerve, optic nerve, macula. So you can kind of see OD is the right eye, OS is
the left eye. And you can see you know the vessels coming out, and then you get
into the peripheral retina which is very hard to
examine you know. So basically this is probably what you can see if you
really have a very good exam, and if you dilate the patients, you know you can get
really a much better exam. And there’s some panoptic scopes, I don’t know if the medical students are using that now. They give you a little bit bigger view- I
started using it about three or four years ago and it changed my whole
experience- Yeah it’s much better but again you know, we do indirect opthalmoscope in clinic, which we get a much better view. But yeah you know for
screening I think panoptic or regular scope is good as long as you have a
good patient. Layers of the retina, I won’t bore you with it, but basically this is
the inner retina and then it goes all the way down. And now we have imaging that we can actually see each layer of the retina in our clinic using what’s called OCT.
So we know about rods and cones. Just keeping it simple, rods are in periphery
used for dim light, cones are mostly in the center for color and high resolution
visual acuity. There’s three different kind of cones: red, green and blue. So
diabetic retinopathy is the leading cause of blindness between age 20 and 65
years. And remember you will not go blind if you get your exams done, and I’m
surprised hearing patients who have insurance who live and were educated
they actually end up running into trouble because they don’t go to
their screening visits. So if you get a retinopathy and you watch it, if you get
into trouble we can actually treat it and save the patients from
going blind. So you know initially we call it background or non prolferative
diabetic retinopathy, where you get the hemorrhages, cotton wool spots can come from retinopathy or mostly from hypertension, there’s a little nerve fiber layer
infarcts in there. And then you know you get proliferative stage where you grow
abnormal blood vessels. So when I think of diabetes
I think of diabetes as a disease of blood vessels. So I tell the patient, first
time I see them, is your blood vessels are getting damaged in your feet, you know,
they usually have- all of them have neuropathy by that time. They have
retinopathy then they go into you know nephropathy
then heart disease and whatnot. So I tell them your retina is running out of blood,
your vessels are getting damaged, and we see signs of hemorrhaging. And after the
hemorrhages are gone, you know or get worse, you get leakage and then you get
proliferative disease where you get abnormal blood vessels flowing into the
vitreous and then they bleed and then that’s how they go blind. So this
perception that “hey, I’m gonna go blind anyways because I have diabetes”
obviously is not true. We have mutual patients that have been diabetic for 40
years and they have no retinopathy, and then we have patients who just got diagnosed a year ago and they’re blind. So really screening is the number one thing, getting them to go to
their screening exams and if there’s any pathology we’ll be able to treat that in
advance. Duration correlates with retinopathy and obviously we classify
the diseases that we will talk about. These are some recent numbers. So as of 2013 382 million people in the world have diabetes. I don’t know if you agree with
those numbers close enough. Seems like 382 million in Reno (laughter). By 2035 estimated to be 592 million and
obviously duration of diabetes correlates with retinopathy. 84 to 90
percent of diabetic retinopathy with the duration of 10 to 15 years. So if
somebody comes in and they’re retinopathy they say I just got diagnosed with diabetes, I usually say well you’ve been diabetic for a long time now, you just didn’t know
about it. 28.5% of patients above forty years of age
with diabetic have DR. That’s a big number so a quarter of your patients will
have diabetes if they’re above forty and 13.6 percent of those
patients have diabetic macular edema, which causes you know vision loss. So
those are big numbers when you’re looking at population in general. And
you know, when I moved from Dallas we had a lot of bad diabetics, and I came to
Reno and I thought it’s going to be you know, much less. But on a daily basis I
see tractional retinal detachment in 20 year old, 30 year old, who are blind
from it we have to do surgery to save whatever we
can. So again it’s a big epidemic even, as Ellen said, in Reno because
we have so many patients here even though they have insurance they still
have not gone and gotten their eye exam. And how many times they’ll come
in and say “yeah my PCP wanted me to do it, and I just didn’t have time, and I
delayed it for five years”. And then they come in with diabetic macular edema on their first exam with retinal detachment. Another big number is controlling the
A1c. I’m surprised that most of my diabetic patients in Reno actually know
their A1c. We ask them “Hey what was your A1c?” and most of them will remember it was seven something or eight something. And you know, our goal obviously, the lower the better you know if I can get close to six point five first or six
I’m happy. But you know on a daily basis again, we have patients with A1c
of 14 and 15. And they say “Well I’m doing my best”, and then you know they’ll
have a big doughnut in their hand and a coke can (laughter). So, you know, first time I see
the patient I really scare them in terms of the eye and obviously the whole body.
I said this is something we can see in your eyes, show them the images and
this is what’s happening in your kidneys probably in your heart, in your brain, in your feet, everywhere, and you just can’t see it and this is how it
looks. Imagine that in your heart you’re probably gonna have a heart attack or a
stroke, so we talk to them in detail but again, you know, communicating with the
PCP is a goal because, you know, you are the ones who are actually managing the
overall disease and, you know, we can try to be involved but again the focus
obviously is to try to, you know, prevent vision loss. And sometimes I have seen
that once they start treatments for diabetic macular edema or retinopathy,
which we’ll talk about, the sugars get better, because they are really really
scared. But the unfortunate part is that the compliance rate for diabetics to
come to retina clinic is very poor because there are so many appointments,
they tend to be working, they tend to be younger, they tend to have commercial
insurances with big co-pays and and no matter how we do I have enough patients who will just disappear for six months or a year and then come back with a
hemorrhage and be blind with it. So compliance is always an issue but we do our best to keep them on track, and you thank them for all their appointments and
undergo treatment most of them do not go blind. So these are the new screening
guidelines by American diabetic Association.
So basically screening right dilated eye exam should begin within five years
after onset of type one diabetes. So type one diabetic within five years
but type two diabetes, just for the reasons I mentioned, sometimes they have it much
longer and they don’t know it, it should happen at the time of diagnosis. For
patients with either type of diabetes if there’s no evidence of retinopathy,
follow-up can be scheduled about every two years. So this was a change from the
old guidelines, that you have to go in every year for it, and I always wondered
if they don’t have any retinopathy it’s very hard to just suddenly get it
in one year. So I think it’s good to know that hey you can tell the patient,
go for your exam and if it’s all nice and clean you probably don’t have to go
back for two years. If there’s any retinopathy obviously, then we
decide based on the extent of the retinopathy, how often a patient needs to
be seen. If it’s just mild non proliferative retinopathy, maybe 9 to
12 months, if it’s moderate or severe maybe 6 months or 3 months depending on
what you plan to do with them. And this is very interesting about women with
pre-existing diabetes who are planning pregnancy, should be screened prior to
becoming pregnant or if that doesn’t occur during the first trimester. Because
I’ve seen, I remember, from my training there was a young girl who got pregnant
and boy she went from nothing to proliferative diabetic retinopathy and we had to do a lot of lasers and whatnot to to make sure she doesn’t go blind. So that’s another
key point from this guideline, is that if you have somebody who has
diabetes and who wants to get pregnant please kind of counsel them in advance and we’ll have to watch your eyes carefully. And usually
you follow them every trimester if they are high risk because if they go
proliferative you can actually treat them so that they don’t go blind. So a
correlation of A1c, you know, it’s basically higher valency as it
correlates with higher risk of retinopathy so primary care physician’s,
you know, goal is to really control the sugars and keep the A1c as low as
possible. I tell my patient that, hey you’re coming in and you’re getting
lasers or injections in your eye, if you control your A1c and lower it down,
you may be able to stop that. A lot of times it’s pretty obvious that patients
who really take care of their A1c’s and blood sugars they actually do
very well long-term, they don’t have to be on treatment for a very long time. On
the flip side, their are patients no matter what you do they keep getting worse
because they’re not controlling their underlining diabetes. So background
diabetic retinopathy or non proliferative diabetic retinopathy, we have mild, moderate, severe, and very severe. These are dot-and-block hemorrhages right here, these are
some exudates. So what happens is the blood vessels get damaged and you get
what’s called micro aneurysms and then they leak protein into the retina. So
this was, right here, this patient’s vision will be much worse. So this is a
cotton-wool spot again it’s usually from hypertension but
you can see it from diabetes, it usually goes away if you control your blood
pressure and sugars. The hemorrhages usually stay there they don’t really
regress there’s some new coming treatments to stop and reverse
retinopathy which we’ll talk about later. The exudates will go away, it will take
several months, as long as you can figure out which aneurysm is leaking and you
can treat it either with an injection or with a laser. Then you get what’s called
the neovascularization, so if you look in somebody’s eye and the nerve looks
really really like this, these are abnormal vessels growing into the vitreous. So now they have proliferative diabetic retinopathy. This is a flourishing (inaudible), which is shining up those abnormal vessels here and also shining up some
microaneurysms here in the macula. So what happens is these proliferative
vessels grow into the vitreous and then they start to bleed, so they’ll bleed
under the vitreous or into the vitreous and patients will just go blind. And
I’m surprised, a lot of times patients will not come in when they have that, because the
other is fine and then over time they get membrane formation on top and the
retina gets full and then that’s how they go blind from this disease. So if I can
just interject, so I think it’s important on this picture to recognize that although
you’re looking at a two dimensional image and those new vessels look as if
they’re kind of pancake flat -they’re actually- it’s a three-dimensional event
so that those vessels are growing actually towards you. When you’re looking
in the eye they’re extending upwards from the surface of the retina almost
like a little palm tree, you know, of vessels. That’s why they’re so fragile. Absolutely,
and then they tend to bleed very quickly. We have a question. Yes? Yeah it’s on your screen. So their question is “We have an optometrist in town, is it okay for optometrists to do dilated diabetic eye screening or must I refer to
out-of-town ophthalmologists?” No I think, you know, as long as the optometrist
is dilating the patient, they should be able to do the screening for you and
again, the ophthalmologist or the retinal specialist usually get involved when
things start to go in the wrong direction with diabetic macular edema
and proliferaive diabetic retinopathy. That being said, you know going forward
hopefully we have some treatments that as soon as you have retinopathy you can stop or reverse it. Currently we are kind of putting a patch
on the wound. We don’t have anything, you know, for the eye to stop the disease
from getting worse other than giving them injections or lasers. But absolutely,
I think it’s an easy enough exam for an optometrist to dilate the patient and do
it. Just make sure the patient gets dilated. A lot of these patients will go to optometrists, will just say “Oh yeah I got my glasses”, and they don’t get dilated. So a dilated eye exam is crucial. With fundus
photography? Photography is actually not necessary, exam would be the key. So if
you don’t, you know, a lot of these people are doing remotes,
I know Renown is doing some remote photos. I think that’s great if you don’t have a
practitioner in town. A lot of these patients will go in and get photos and
get an exam, and the question is what’s the point? Some of it becomes a business
matter for other things but I usually don’t do any photos on my
patients unless, you know, I’m doing fluorescein angiogram or something. You can usually rate the retinopathy based on your exams. But if you don’t
have a practitioner and you have some remote facility to do photo, absolutely.
Main thing is that they get their exam done you know it doesn’t matter how,
somebody needs to look at their fungus. So a proliferative diabetic retinopathy, this is somebody with what’s called a pre-retinal hemorrhage. The way you seeit’s a pre-retinal
hemorrhage, you can’t see the underlining vessels. So in younger patients with
diabetes, this happens quite a bit because their vitreous is stuck very
tightly to the retina so these blood vessels will just bleed and the blood
will get stuck between the vitreous and the retina. And what happens is this causes fibrosis and then starts pulling it. So if this was right here, the
patient would be completely blind. They will come in and say “Hey I can’t see anything, I
have a big black spot”, and most of that becomes surgical because since their
vitreous is so tightly adhered to the retina the blood cannot get into the
vitreous and then you have to go surgically and you have to remove the
blood and clean it out. And these are some exudates so this is diabetic
macular edema, there’s some microaneurysms here and
this is all the protein leaking. So this person, you know, obviously needs
to be treated ASAP. And what I’ve seen is the younger the patient, the better the
response to treatment, whether it’s laser or inter (inaudible) injections, they’re very
ischemic, so if you try to cut the ischemia down I think they do
very well. So again sooner the better to treat this patient. This is how
patients go blind, and we have a cool surgical video at the end, but basically
they get these fibrous bands from bleeding and you can see this is a
fibrous band. And what happens is it sits on top of the macula and pulls
everything, then they get what’s called tractional retinal detachment, and what
we need to do is we need to go in and trim and remove these membranes. But a
lot of time the damage is already done to the center, so even if you do surgery
and the anatomy looks much better, their vision is still nowhere close to
perfect. So again, if they came in on time you would avoid all these things and we can treat them early. Macular edema, so as I was talking about this is lipids right
here, swelling of the retinas is hard to see, it’s a 2-D photo. There’s an old
definition of clinically significant macular edema, you don’t need to worry
about it. When you see our notes, now we call it diabetic macular edema so
even if it was not close to the center we’ll call it diabetic macular edema. Now,
the treatments have changed. Before we just had laser to treat all these areas
and the patient will lose some vision because of the burning of the retina. Now
if it’s central involving macular edema, we can have endometrial injections,
which we’ll talk, about to stop the leakage. So this is somebody who’s a bad
diabetic, their vision is probably legally blind range 2,200 2,400 you can
see just exudates everywhere and this is from all these vessels that are damaged
right all around the macula and the protein is actually being leaked into
into the macula. So the protein comes after just fluid. First we’ll just have
serous fluid leaking in the retina and if it’s not controlled then you get more
protein leakage based on the damage. So this is somebody, even if you will treat,
you will probably not end up with good vision because by the time they’re not
in here there was a lot of damage all around their macula. Cotton wool spots that we talked about earlier. This is somebody who looks more like hypertensive retinopathy. You can see the cotton wool spots, you
can see these hemorrhages that go linear and these are called nerve fiber layer
hemorrhages. So the nerve fiber layer on the retina goes like this, you can see these
hemorrhages in linear direction. So this is somebody I would worry a lot about
hypertension, and luckily all of this will resolve if they control their
blood pressure. So again all these findings in the eye, hypertensive retinopathy can be very acute but once you control the blood pressure over three to six
months, all of these findings can resolve. So I would call it optic nerve edema.
So the difference between optic nerve edema and papilledema, is that optic
nerve edema can happen because of diabetes because, of hypertension, because of violent tension. Papilledema, we usually call it, that there is an
intracranial thing that’s happening, that’s causing the optic nerve to be swollen. So
if you hypertensive retinopathy you will get that. So the the difference
between papilledema and optic nerve edema, the other thing, you see these
vessels right here? In papilledema they might be all blunted. In this case,
so I would agree you know they’re kinda interchangeable at times, but I would call
that optic nerve edema, and you may see that in your clinic. And obviously
sometimes it’s hard to distinguish. You see somebody like that, they need an
urgent referral to make sure there is no intracranial legion causing it. So, we use
fluorescein angiography. We put a dye intravenous and then it goes to their
eye and we take pictures, you saw some of those pictures earlier. The technology is
getting better and better now you can get good peripheral images and a lot of
ischemia will start in peripheral retina and we can catch a proliferative disease
early to treat it these days. So this is a fluorescein angiogram, early phase and
then late phase. So you can see the dye is going into the vessels, there’s something
going on right there, and then over time you can see there’s a leak right there.
So this is clinically significant macular edema,
it’s very close to the center and this patient probably needs intravitreal
injections to control the leakage. So if you have a patient coming in, they put a
dye, and I became all yellow and I was being fluorescent this is what they
had done. OCT, this is this an older image but OCT is showing the layers of the
retina and this is the foveal contour here, since it’s somebody with diabetic macular
edema, it will be swollen. So really OCT has been the go-to test. Now we’re doing less
and less fluorescein angiograms, because we can see even very small cysts or leakage in it. So this is somebody with macular edema. You can see all the protein and serous fluid
has leaked into the center, so the light is hitting the center and the vision is
going to be blurry because it’s not getting to the cells at the bottom. So
older treatments, we still do it sometimes if the leakage is not
into the center. What we do is we take a little laser and you burn these
microaneurysms all around, and then over time this leakage will go away
because the (inaudible) cells of the retina will start absorbing the fluid.
Pan-Retinal Photo-Coagulation, we still do quite a bit of this because the
diabetics tend to be unreliable most of the time if they don’t follow up. These are
burns that you perform on the peripheral retina. So they have ischemia and they grow those NVD or neovascul vessels that we saw earlier here or in the retina and
we burn all the ischemic retina so that those vessels go away so they don’t
bleed anymore. So obviously this is the macula, you’re using it 90 percent or 95
percent of the time, but you also use your peripheral retina. So once you have
this laser you are gonna lose some peripheral vision. This is an older photo,
so now we are not doing as tight laser as weused to because you know, the
technology is much better. But again, they will lose the peripheral vision. They may say “Hey I had laser surgery in my eye”, and it could be the focal laser we talked about for the
center, which does not hurt. This one hurts. And they say “Oh my god, my eye hurt really really bad during the laser procedure”, they probably had this Pan-Retinal Photo-Coagulation. Usually we have to do it in one or two sessions. Now the
intravitreal injections, MDA just approved for any kind of retinopathy. So you can
do the injections in the eye every month, but you can do it every two
or three months if you’re a reliable patient, and you can avoid the laser. So
somebody is a pilot or a truck driver, they don’t want to lose their peripheral vision. This also affects their pupils because what happens is the nerves are
coming horizontally and vertically and you’re doing the lasers so they may also
have a difficult time for light adaptation going from dark to light, because their
pupil doesn’t really move too much because of the laser. So these are
the intravitreal injections. I now say the retinal specialists are like human
syringes (laughter). Every other patient in our clinic gets an injection whether it’s
macular degeneration, diabetes, retinal vein occlusion…
and if you don’t know what it is we still inject (laughter). So what we do is we do
tons of these. These are done on the local or topical anesthetic, we numb the
area with some, you know, some type of lidocaine, or drops, or jelly
everybody has a different approach. We inject the needle at what’s called the
pars plana, which is the area there is no retina. So the retina starts six
millimeter behind what we call the limbus right here. So this is the area
where we do all the surgery from and this is area where we inject things in the eye without causing too many trauma. I have patients who have been getting it
for, you know, eight years every year, so these are really really safe, but again
there’s always the risk of infection with anything sticking in the eye.
Luckily the rate is very low, it’s at three to five thousand, so very very low.
But we have to be careful to keep the lashes away so this is a speculum you’re
using, and the injection is going into the eye. So if I have a reliable diabetic with proliferative disease. So proliferative disease, we treat with Pan-Retinal laser as I said, if they don’t want to lose their peripheral vision.
Most of the time they don’t even notice it, because that area is dead
already from ischemia but if they will lose some, and if they don’t want to do
it, and they’re reliable and they really want to keep the peripheral vision, then
they’ll have to commit to getting these injections every one to two or three
months so that they can not have progression of their disease. If they have
diabetic macular edema in the center, this is the go to therapy and we’ll talk
a little bit about it. So these are the agents we use in our clinic. Kenalog is an old steroid, and if we didn’t have any other treatment, if you look at the
Kenalog box, it says do not inject in the eye.
So rapid guys do a lot of off-label treatments because we are kind of
desperate and anything works we try to use it. Macugen was an old treatment, it’s now gone. It’s not available because it really didn’t work. Avastin is, so if
you hear the word Avastin, it was actually a colon cancer medication that’s made by Genentech. So it’s a big, big deal. It’s also used in breast cancer
and because we were so desperate, especially with macular degeneration,
because lasers really didn’t work in that disease other than you know
blinding the patient because the leakage is in the center, people start injecting
in the eye and they saw great results in terms of stopping the leakage. So, these
drugs, these three, are what’s called anti-VEGF agents are these four. So
what happens is you get ischemia in your retina, and so body secretes less for the
endothelial growth factor to grow new vessels. But as we saw, those new vessels
are abnormal and also the VEGF tend to leakage into the retina, so these drugs
actually brought that VEGF and really revolutionized how we treat our patients.
You know, macular degeneration is number one cause of blindness in this country
above 65. There’s a paper out, after the advent of these, overall in the world 75
percent of blindness had been cut because of these injections. But unfortunately it’s not something that you do once, you have to get it every month or every other month
based on your disease, so we don’t really have a cure we just have a treatment to
stabilize their vision. Lucentis was the first FDA approved drug for
macular degeneration and also for diabetes. It’s basically Avastin, but it’s a small fragment. The reason they made
Lucentis was, that it’s not a full antibody. The idea was that anything
you inject in the eye goes to your blood circulation, so Lucentis was a
smaller molecule, and that’s why it didn’t recycle in your body and it didn’t stay
in your system more than two hours. Eylea was the newest one approved in 2011 for macular degeneration. So all of these words you see, I just want to mention it
so that you know, that these are all injected in the eye. Ozurdex is a
dexamethasone implant, so we are really not injecting steroids. Some of these
diabetics will not respond to just the anti-VEGF agents, so you have to put
steroids in the eye. Obviously, you try to avoid steroids especially in young patients,
because they end up in cataract formation, and also 30% risk of
intraocular pressure spike. So these are the second line agent, and Iluvein came
out about two or three years ago. It’s a three year implant, so actually you
inject this, and it can last for up to three years. The problem is the efficacy is
not as good as all the other agents. so it can more become like a chronic
therapy for baseline control. So, this is what I was talking about what VEGF is, you know it’s was triggering all these
things and our goal is to inhibit the VEGF and stop their normal vessels. So
this is somebody who had advanced PDR. This is all membrane formation, you can
see actually the optic nerve is right here, and this is all covered with scar
tissue. Soyou’re going surgically to remove all this, but again the damage
underneath may be the problem but you can maybe get
this patient from seeing count fingers to maybe 2400. So right now, you know, what do we do is our goal is to save
whatever we can. And that’s why a lot of ophthalmologists don’t go in the retina because it can be frustrating at times. It’s like managing diabetes, you know. You do your best and sometimes, still it’s not, you know, it’s patient dependent at times too.
So it can be challenging, but you know we do our best to, so again the goal is to
get these patients early for their screening and treatment. And this is just a cool
video I wanted to show right after this. So this is not the same patient, but the
patient underwent surgery to remove all the membranes, and I just put this video
that I did the surgery a few a few months ago. So you can see this
was a young patient with diabetes there’s some lasers in the periphery, but
the center is all covered with membranes. And what we do is, these are the instruments we put in the eye. This is called a retractor and there’s a light. But so
again we are going through those, that pars plana when I talked about where we go to do the injections. And we’re actually now, the instruments are so good that these,
there’s a new retractor, thats why I made the video, this has a bevel edge. And what
we can do, is we can actually slice and go under these membranes and remove them. But again this is what’s called a macula involving tractional retinal detachment.
So you know, even not for fixing it, the patient’s vision improved but not
significantly because of the underlying ischemic damage. But so that’s all the
retina here- keeps stopping- and this is a macular right there, so you have to be
really gentle peeling this off that you don’t want to tear the retina. A lot of
these cases you will have tears, but that’s not a big deal you can treat them
with laser, and put either a gas fill an oil fill in the eye to start with
detachment. But these are the membranes that form when they keep bleeding, and
the vitreous, the posterior hyaloid, we call it, which is the posterior edge of
the vitreous. So this is somebody who had that
hemorrhage right in the center, didn’t come in on time and they end up, you know, coming up with these membranes. I usually make sure I don’t have my coffee (laughter). So no robots for this surgery? No robots, actually they’re working in Belgium but the problem is the pathology is so wide spread and it’s not the same thing
with every patient, it’s very hard to train a robot to do it. And you know, I
think I may need a robot once I turn 60 (laughter) but at this point I think I’m okay, but
they’re working on it. But you can see that we are, so now you can see the optic
nerve, and the goal is to remove this traction because if you leave the
traction you can end up with tears. So this is after all the removal. I did the laser,
I’m now putting some gas in the eye, there’s the hole in the retina there
underneath. Any questions? That thing you just showed us is amazing.
What type of vision correction resulted from that, approximately? So I
think the patient went from seeing just shadows to about 2,400. So they’re still in
the legally blind range, but now they can see instead of just being shadows they
can see kind of this room here, or a little bit. So you know our goal is, that
vision is very functional, and you know our goal is to save whatever we can. But
when we all come as a team here to prevent that from happening, and
unfortunately it happens on a daily basis in our clinic. But that’s where the
first time you see the diabetic, that’s where the disease education comes into
play. If this could have been all avoided, the patient would be much better if we
caught them when they were in proliferative, and just do the laser and we are done. Other questions? Otherwise I’m going to…yes? So, we have, here at Wells, we have the ability to do our IRIS, which is a retina screening. And we do it at least annually, but not every six months, if its determined, you know depending on what the read is. If it’s red, I now decide a
specialist. And sometimes you know typically what we do is, we’ll do it
annually and then if it’s abnormal we send them to someone locally. I know that
the recommendations now are every two years, but I feel like again for our patient
population, annually is still probably most appropriate because most of our diabetics have adherence issues with their regimen. What would you- does that seem appropriate? Well I think the problem is the recommendations are for dilated eye exam. So if you’re just sending the photos out- We dilate before the retina scan. For those yes. But a lot of times the retina scan, the problem- what system are you using, in terms of photos? The IRIS, is what it’s called. I’m familiar with the IRIS registry that is by AAO, but I’m not familiar with the IRIS system. So it depends how wide your photos are. That’s why exam is crucial, because a lot of
times the disease will start in the periphery. And these cameras, and we
have a struggle every day, I mean even if you have certified photographers we just
can’t get the photos that we want. So I think if you are doing the photos it’s
not a bad idea to be more aggressive, maybe every six months or every year at
minimum, you know, because it cannot replace the exam but it’s a good supplement. So if you don’t have the manpower to do the good fundus dilated
exam, then I would at least do photos every year even though you don’t see
the pathology. Because there’s clearly some peripheral pathology that can be
missed from those photos. I’m going to jump in for one second. There was a paper in the
New England Journal about four weeks ago, from the EDIC group, the folks who
follow the DCCT. And what they actually looked at were individualizing screening
regimens, based on duration of disease and A1c. And so there was some
interest in that, and then there was some pushback. There was an editorial
that said, you know, that’s great but you know, if this is so important maybe we
shouldn’t relax our vigilance because catching this disease early is just too
important. So if anybody wants to check that news, I mean it was an interesting article and editorial. I totally agree. I mean it’s, remember you
sometimes you say come back in two and they’ll come back in five. Right.
That’s that’s the problem is the reliability is an issue with diabetics.
So you know, the guidelines are something we can use, but again you have to look at the patient. If their A1c is 14 and they have no retinopathy this year, I mean this is
somebody who’s (inaudible) exactly, sooner than later. The other thing is artificial intelligence, you know. There was a paper
out a few months ago, and I forget the journal it was.They were actually
using computers to look at these photos and about 75,000 photos they look
at, and the computer was able to pick retinopathy in about 85 to 90
percent of the cases. So that may be the way of the future because, you know,
the lack of manpower with this disease is exploding, that there is no way everybody can get their dilated eye exam when they’re supposed to. Arshad, thank you so very much. You’re welcome.

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