Diabetes & General Endocrine ECHO: Diabetic Retinopathy – 1/17/19

Sorry doctor Klass, I had you on mute. Okay. So it
is now three or four minutes after the hour. I think we ought to get started. Here is Dr. Khanani. Perfect timing. Great, so without further ado, I’d like to
just introduce our guest for this morning Dr. Arshad
Kanani who is a vitreoretinal specialist in Reno. He has been a great ECHO partner
over the years and we’ve been able and lucky to call on him I think every year
that we’ve been doing this program for. Always happy to be here. For a discussion of
diabetic eye disease and it’s a topic that I think we all share
anxiety about. It’s the kind of thing that we’re all conscious of in our
patients and we work so hard to prevent. There are aggressive efforts at controlling our patients diabetes and we know that that’s effective. We have plenty of
evidence over the years to demonstrate that glycemic control impacts
development and progression of diabetic retinopathy, but despite our anxiety I
think we have trouble often times knowing what screening is appropriate. I
think all of us struggle using our ophthalmoscopes to get a good view of the
retina even though I’m a great proponent of the pan optic ophthalamoscope, not many of us are very good at using it and we refer our patients for eye evaluations
and then from those consultations the patients find their way to
vitreoretinal specialists. I can’t think of anybody who can do more to
enlighten us on this topic than Dr. Khanani so Arshad it’s all yours. Thank
you for the kind introduction. While we load up the slides, I’ll tell you this:
last year FDA approved the first artificial intelligence software to
detect diabetic retinopathy. It’s by a company called
IDx-DR and I think part of the problem has been getting patients in to anybody
whether it’s ophthalmologists and optometrists to try to screen for them. Part of it is that we we are so busy, but also because we just
just don’t show up. The idea is that how can we connect where you send us a
referral or somebody send us a referral and half of those patients don’t show up
and then there is really good real-world evidence that once we start treatment
majority of the diabetic patients who need treatment don’t follow up. There’s a big problem. We always have to think that the reason they’re in
this situation that they tend to be non-compliant and even though we educate
them head over first with it, I will tell you the communication
between us and the primary care doctor is not always perfect. We’re all busy so
we don’t think up the phone and say hey this is somebody who is in trouble, but I think artificial intelligence may play a role in the future. Now this
software was approved for a specific camera so I think in the future, within
the next five years, it may be where patients are in your office and they
need a diabetic screen so they have a photo right there and then the software
will just read it and then it will tell us what kind of retinopathy they have
and from that they can go into a specific referral clinic, because in my
clinic we always see the bad stuff like bad macular edema, bad peripheral
retinopathy, so I think as the numbers are growing there’s something to keep in mind. (inaudible) So today I’m just going to talk about some Anatomy, talk about
diabetic retinopathy and then also what we do in our clinic so everybody
here has a better idea about how these patients are managed when they come
complaining to you that I don’t want to get those injections in my eye you know
exactly what we are doing and why we are doing that. So let’s get started with the
normal anatomy. When you look at a fundus photo, obviously all of you are
familiar with this, but the yellow round thing is optic nerve this is a patient’s
right eye. The way you know whenever we have medical students or
even residents the question is: is this the right eye or the left eye? In the
right eye the macula is on the right, in the left eye the macula is on the on the
left and that’s from the patient’s perspective. Just to keep in mind
this is the right eye, the optic nerve you can see is normal. You can see the
fovea, that’s a dark pigmented area. That’s where the retina is a little thin
and you can really have good vision. (inaudible) Is where you have the best vision. The whole part here, do you have a pointer? (inaudible) so this is the soil
part is called macula. So if you get swelling in here you get what’s called
diabetic macular edema. The arteries are the thinner structures you can see. Then the veins are thicker than arteries. Sometimes we see patients
who are diabetic with artery or vein occlusion also. So this is just a normal
anatomy and then this is orientation I was talking about. When we talk about
superior arcade, this is the blood vessels going on top. Inferior is here. The
posterior pole involves the optic nerve, the macula, and the fovea and this is the right eye OD
if you see is right eye. OS is the left eye. Opthamology is made right because
we don’t want to tell anybody what we find so we use all
these acronyms in there just to confuse everybody. (laughter) This is the layers of the
retina. The retina is a really complicated tissue. It’s usually about 275
to 300 microns thick and the good news is that now with technology we can
actually look at all the layers, not specific cells, but all the layers of the
retina with technology called OCT which I will show you later
but basically what happens is the retina gets schemic because you know bad
glucose and high you know A1C and then what happens is that they should
start to have fluid leakage in the retina and then they get swollen and
it’s called diabetic macular edema. In terms of retinopathy, retinopathy also
affects the blood flow then you get what’s called neovascularization of the
retina and you end up in trouble in terms of itches, hemorrhage, and
proliferative disease. We’ll talk more about it, but you don’t need to know all
the layers, but what I wanted to show is it’s a very complicated tissue that
you’re dealing with, especially doing surgery you will see how fine the retina
is and I have a surgical video in there for you. In terms of the functions,
rods in retina periphery are dim light. Cones are concentrated in foveA for
color vision and high-resolution visual acuity. Then there’s three different
kinds of cones: red, green, and blue. In terms of diabetic retinopathy still is
the leading cause of blindness in age twenty to sixty five years old. The
duration of diabetes and the sugar control and even see as I said is
directly correlated with what we see. Then the classification of it is based
on how bad the retinal vascular change has been involved. In terms of diabetic
retinopathy we have two kinds we call it background or nonproliferate diabetic retinopathy where you see dot and blood hemorrhages. Here you also can see some “cotton-wool”
spot. When I start seeing “cotton-wool” spots, I also worry about
blood pressure. The second kind is proliferative diabetic retinopathy, where you get a normal blood vessel growth where there is an optic nerve
here or in the periphery and these are the patients who end up with bleeding
and then they still don’t come and see us and then they get what’s called
tractional retinal detachment and once they have that they end up losing most of
their vision and we’ll discuss a little bit more about that.
As of 2013, 382 million 8.3% in the world have diabetes and Evan probably
has better numbers for me . By 2030 the number is estimated to be about 600 million.
Duration of the diabetes correlates with retinopathy 84% to 90%at diabetic
retinopathy with a duration of 10 to 15 years. If somebody comes to me and
they have diabetic retinopathy I know that they just didn’t get diabetes six
months or a year ago. Usually, I tell them you have had it for you know at least
five if not ten years and most of these patients because you know are walking
around being diabetic cannot be diagnosed and sometimes they come to us
and we diagnose them and send them back. A third of patients above forty
years of age have diabetic retinopathy. These are the patients with diabetes. Thirteen percent of patients with DR have DME. Every 1% increase in
A1c corresponds to 50% increased risk of DME. That’s something we follow
closely. If we don’t worry about any medical problem, the main thing we ask is
A1c and what I’ve seen lately is that I think the primary care teams have done
a good job in terms of educating the patient. Eight nine years ago
most patients didn’t know they’re A1c and now I’m seeing more and more of
my patients that actually know their a1c. I think that’s good,
you guys get all the credit for educating the patients telling them what A1c is and how A!c is managed. Most of my patients will come and
tell me you know my A1c 8.5 or 9 or 10 and you know we
see a lot of patients about 13 and 15 sometimes and they’re in real trouble,
but the good thing is in terms of education, I think patients are more
aware of their their A1c so these are the new guidelines so that were
published in 2017. Some of my friends were also on this paper. Basically
what they say, I’m just gonna read it so it’s easy and Troy has the slides in
case it becomes a little confusing. Screening via dilated eye exam by an eye
specialist should begin within five years after onset of type one diabetes
and at the time of diagnosis of type 2 diabetes. Obviously we know the reason
for type 2 diabetes that diagnoses it because you don’t know how long people
can still live and function even though they have symptoms. Sometimes you’re always
surprised at how they live with symptoms for that long but they could have had
diabetes for 5 or 10 years so that’s why you need to send them for a
dilated eye exam once they’re diagnosed with Type 2 formation. Either type of
diabetes, if no evidence of retinopathy is found, follow-up eye exams can be scheduled about every two years. This was a change in guidelines in 2017 because in
the past and even now some of us will bring these patients in one year if you
feel like they are going to have retinopathy but the real guidelines are from
American diabetic Association. If there is no retinopathy in somebody who just
had a dilated eye exam, they don’t need to need to be seen on a yearly basis.
They can go about every two years If any retinopathy is
identified, subsequent dilated eye exams are advise at least annually, and more
frequently for those in whom the retinopathy is progressing or sight-threatening. What we do here is that we look at the eye and if
they’re non diabetic retinopathy and if it’s mild, we usually bring them in about
nine months. If they’re moderate, about six months. If they’re severe, about
three to four months. If they have macular oedema then obviously they need
to be treated. If they have proliferative diabetic retinopathy, they need
to be treated. Women with pre-existing diabetes who are planning pregnancy should
be screened prior to becoming pregnant or if that does not occur, during the
first trimester. I think that’s a really high risk population. I’ve seen patients
with moderate retinopathy going to really bad proliferate retinopathy with hemorrhaging during pregnancy but I think that’s something to keep in mind. A lot of time
you don’t think about that but I think if they’re planning to get pregnant or
they’re pregnant they need to see and have a dilating exam as soon as possible
because and then they are followed very closely. Any questions here from anybody
before we go into more of otology? Anything about diabetic screening my
question is: what guidelines are you guys using? Are you using the newer ones or how are we managing patients? I have a question this is Jan Boyer in Elko. Can you hear me? I didn’t realize and I’m just wondering because I work at a
federal Indian Health Services Clinic. I think that our, what we call our GPRA, our measurements of outcome, are asking for exams every year. This
would be something for me to look into because that I think we want to go with
the ADA guidelines in general for standards. No, I agree with you. I
think with the newer ACOs and insurance companies even they actually
will ding you if you don’t do the exam every year. That’s why I was wondering have
these guidelines been implemented in your clinics or they’re still new
enough that seems like again in your clinic they have not been implemented. I think it’s every year in our clinic right now, I believe. Yeah. I would think that is probably the norm. Although, I do think that, you
know, I think that these guidelines are really much more sensible and also much
more achievable. They are reality-based I mean
where there is so little opportunity and availability of manpower. Tthis is I think
a fairly prudent guideline. I agree. I think that’s why they’re probably
changed because it seems like people have to go every year and then it goes
at least we can commit them to go every two years if they don’t have any
retinopathy. I think that’s the only change. Once they have retinopathy, then
it’s always the same it’s just that the screening in terms of not having any
retinopathy is every two years. I mean this was something new for us too
and you know and I think I agree with you. I think they’re more sensible and
more real-world instead of forcing patients to go more often and they’ll
say oh well they didn’t find anything why should they go again next year. This is a graph that shows direct correlation of retinopathy with
A1c and we talked about and again you know most of my patients who have
retinopathy, obviously pretty much all of them have neuropathy and you know a lot
of them also have naturopathy and you know protein in their urine so they’re
all correlated, but if you look at this graph, one thing that stands out in terms
of you know retinopathy it has a really severe relative risk as A1c goes up. When I’m treating a patient with diabetes obviously we have to understand
that it’s a team sport you know and yeah I can do all the treatments, but if
they’re not controling their retinopathy, you’re not gonna go anywhere. They’re
gonna come in here and get a shot in their eye every month and still not be
able to see because they’re not doing their job. That’s something we tell
the patients and you’ll be surprised that a lot of them still don’t listen
and their A1c’s are still high and sometimes you know because the systemic
disorder you know I tell my fellow in residence that you know we get
frustrated because we are treating them and they’re
not getting better and their patients will actually control their sugars and
they’re still are not getting better. I met several patients where they went
on dialysis or they had a bypass or they had some other intervention and it
always looks like they’re macular edema retinopathy got better. It’s kind of
like a systemic disease that you know as ophthalmologists we are kind of thinking
about the eye but you know I try to educate my trainee that we
have to think about the whole body. I’ve had several cases where patients
got treated for a couple years and no improvement. They went on dialysis and
then now they don’t need improvement because there are fluid overloaded in their body
and they were you know leaking the fluid in their macula. I think
something we tell the patients but unfortunately as all of you know we can
educate so much. We try our best but majority of these patients still have a
high A1c’s, still don’t show up to their appointment as as recommended and
it can get frustrating in time but you know all of us are here because we want
to work as a team and we do our best. In terms of background or nonproliferative diabetic retinopathy, I already told you it divided into different categories but
here you have a picture. This is a left eye. You can see the optic nerve looks
good. There is no proliferative disease. This is the fovea. There’s a micro aneurysm. So
these are the ones that will leak and cause swelling. There’s some exudate here. There’s some aneurysms here that are leaking protein. There’s a spot of cotton-wool spot right there. There’s some more hemorrhages. So this patient you know
obviously has non-proliferative diabetic retinopathy. What has changed over the last few years
is now what we do is called white field imaging. This is the picture of the
posterior pole but now we have technology where we can get images of
far periphery in these diabetics and what we are doing is we’re actually
picking up more diseases because a lot of ischemia and non perfusion of the retina
starts in the periphery. Imaging has really helped to revolutionize what we do and things are improving in terms of diagnosis and
intervention but the only problem is obviously bringing these patients in
when they’re supposed to. Neovascularization.
Now this is the patient that now we’ll call PDR or Proliferative Diabetic
retinopathy. This is the fluorescein angiogram. You can see there’s abnormal
vessels here you can see them very nicely here. It looks like these three
branches coming out. They tend to be much thinner than the regular vessels and
they tend to be more fragile. That’s why they believe there’s a little bleed
going on here from this optic nerve you can see there’s a majority of vessels
are abnormal. So these vessels grow into the vitreous cavity and then they bleed
and cause you know vision loss and problems This is somebody with a
boat-shaped hemorrhage we call it and this is a bleed between the retina and
the vitreous. When you look at hemorrhages in the retina you either
have what’s called a pre-retinal hemorrhage or a sub-retinal hemorrhage. Usually diabetics get pre retinal vitreous hemorrhage. Remember this
is the back of the eye and now you have vitreous all in front of it and the
light is going straight there so you can’t see any vessels of the retina so
you can easily tell that this is a pre retinal, meaning hemorrhage in front of
the retina, because the blood is blocking the vessels, because you see this
vessel here you can see because there is bleeding. This person also has exudates in the macula so they also have diabetic
macular edema and then they also have a lot of hemorrhages. So this patient is in
trouble they need injections in their eye they need some laser to control
their disease. What happens is because patients tend to be younger, their blood
gets trapped between the vitreous and the retina and over time this will cost
some fibrosis. So patients keep leaving, they still don’t come in, they do see
their vision is going down, and then they end up with a tractional detachment
which we’ll see later. This is a tractional detachment. This was the same
patient, you can see the optic nerve was supposed to be here. This is all
fibrosis all around. You have a traction band. So what happens is the traction
starts, and then it goes into the macula, and then it pulls on the macula, and then
that’s how patients go blind, and we can surgically remove the scar tissue, but
it’s too late. Most of these patients have already done permanent damage and
they can’t see again. I just saw a patient yesterday that went blind in one eye
from neovascular glaucoma. The other eye at tractional detachment. We fixed it about
two or three years ago put oil and removed the oil and I’ve not seen
her for one year and yesterday she came in and she could only count fingers
here and her complaint is I can’t see and you know my partner who was a glaucoma
specialist managing what is called her neovascular glaucoma told her that this is
how good it’s going to be and then she still came to me and she said I
really can’t see and those are tough situations because now I can’t help her.
There’s nothing surgical I can do. I already fixed the tractional detachment but
she has photoreceptor loss and she can’t see anymore. She did have a little bit of
a cataract which we were gonna get out but really it’s frustrating and
she’s only in her 40s and she only has one eye that can only count
fingers and unfortunately the disease has done the toll on her. She’s obviously
on dialysis she was on a wheel chair and she’s in real trouble, but it can get
frustrating when visions reach this stage. So I think the whole goal of this
program is how we can as a team communicate with each other and get
these patients in sooner than later so that we can avoid all these bad
complications because this is something real. I’m sure all of you see that
when somebody with bad diabetes or long term diabetes comes to your clinic, they have amputations, they are on dialysis and they’re blind. So in terms of the macular edema,
you can see that this white stuff, as I was calling exudates or lipids are
leaking so macula is all of this and then this is the fovea. So this is
somebody. So you can have mild non proliferative retinopathy but you can still have macular edema with it. So if you look at the codes that
we use now ICD-10, mild moderate or severe with or without macular oedema. So
if somebody has macular oedema but they have mild proliferative diabetic
retinopathy, they still need to be treated because what happens is the
macular edema will damage their photoreceptors and they’ll still end up
with vision loss even though the retinopathy is still mild and don’t need
intervention. So when you look at clinical significant macular oedema this
is the classic definition. You guys don’t need to worry about it but it’s
basically thickening in or around the center of the macula. So sometimes you
will see the word CME or CSME, clinical significant macular edema on the nodes
and sometimes you will see DME or diabetic macular edema on the nodes. So
CSME is a clinical diagnosis that we have to look at the patient and you
know it has to fit certain criterias. DME could also be diagnosed just from
imaging where you can see that in the macula so they’re used interchangeably. Usually, lately we’ve been using just DME. So you’ll see that diabetic macular
edema meaning there is swelling from diabetes in the macula. So this is
somebody with pretty bad diabetic macular edema. Their vision is probably
like 2200 or 2400, probably the legal blindness range, because of all these
exudates and you can see right here there’s some pigment changes so what
happens is the vessels leak because they’re damaged from high sugars and the
protein builds up and then over time the photoreceptors get damaged and then
patients can’t do anything. So these patients would come to us and say hey doc I can’t see but my sugars are better. My A1c is 6.5, how come I need to get
injections and the reason is that this is a long-standing chronic disease and
they’ve already done the damage and I tell these patients your vessels have
been damaged and they continue to leak, your retina has been damaged because you have had it for a long time so we can try to get you better and control the
disease but unfortunately sometimes the vision doesn’t move because they already
have the damage and sometimes once the vision doesn’t move, they stop coming
because they say well the treatments don’t help me and why should I go, but
unfortunately if they don’t come then they get worse. That’s why you know they’ll
come to you and say oh I got tired. I got a note from PCP yesterday there was a
patient we were treating like for one year or two years and hasn’t shown up for nine months and goes on and says I can’t see and the PCP said patient got
tired of injections and they were not helping. So sometimes the patient
perception is different even though we educate them with with these photos and
imaging but sometimes they don’t understand the fact that the damage has
been done and what we’re trying to do is prevent further damage. Cotton-wool spots, these are right here. You can see them from diabetic retinopathy but as I said
earlier most of the time when we see them this is mostly hypertension and
obviously most of these patients will have bad kidneys or have hypertension
with it. We just saw a new patient a couple days ago with pretty
bad looking retina and I asked him if he has high blood pressure he said no I just have
diabetes, but clearly he had pretty bad hypertensive retinopathy so I told him
to call his PCP, go back and get an evaluation and control hypertension. So
if you’re controlling diabetes, but not hypertension it’s kind of like having
two bad things at the same time. You’re still not gonna have improvement in your
retinopathy. Something to keep in mind from our standpoint is you know to
make sure that patients are not hypertensive. In terms of diagnostic
tools and things we use fluorescein angiography still is very helpful. What we
put a dye in their vein and it goes to their eye and we can see the
blood vessel damage and we usually inject this in clinic. The test is
usually you know it takes about ten minutes. If you see somebody who saw a retina specialist and they were all yellow and pale you know and
they cut down, they’re not anemic they probably got a fluorescein angiogram. So
they look you know they get a little yellow hue to their skin, they urinate
fluorescent dye for 24 hours. We usually don’t do the tests if their kidneys are
not right. Not because that it damages the kidney like radiology die or anything,
but it takes it much longer to get it out of their system,
but if patients are on dialysis it’s not a problem. So the majority of our patients
will get the dye test. It does have a risk of anaphylaxis and luckily I haven’t
seen one for a while. A few years ago, we had couple in clinic where patients were just slumped over after the dye test and my assistant came in and I’m like wow I did injure medicine intrernship, but I don’t remember anything so call
911 and I took my EpiPen out and used it
couple times and then it was fine. So it sometimes because you’re injecting
something IV, you always have to be ready for it so like you Evan, you’re
very close to renown and REMSA is right there but we haven’t had any issues. I mean when you carry an EpiPen and benadryl some patients do have itching from it, so we treat them with benadryl. So it has several
different phases. The venous phase, the recirculation phase, and main phase, but
you don’t need to worry about it, but basically what it shows is that it shows
the vessels in the macula and it shows leakage. So you can see this is somebody
with damaged vasculature and the dye is leaking. The other thing I showed is the dead neovascularization, as I showed
earlier, it will light up. Now the technology is Whitefield
so we can actually see a lot of pathology in the periphery.
Hopefully next year I’ll have better photos for you. Troy. Okay. So OCT, this is a technology that shows us the layers of the retina. So this is the
fovea, these are the cells. Technology here is also much better in terms of
resolution so we’ll routinely do OCT on every single
diabetic and this will show us if they have swelling. This is somebody with
macular edema. You can see the fluid is leaking and they have lost their foveal
contour. This is somebody who has what’s called central involving diabetic
macular edema and they probably have vision issues from it. Focal laser
you still do it so if they have vessels away from the center where the dye is
leaking, we take the laser and we burn those vessels. The fluorescein
angiogram what it does is it helps take those vessels dow. and then we can do the laser and
then over time this protein will get absorbed by the retinal pigment
epithelium. Not for center involving macular edema. Usually we do injections
but sometimes if they have stuff next to the fovea we will still use the laser. Pan-retinal photo-coagulation is done for proliferative diabetic retinopathy. So the
idea is that the retina is ischemic and is growing new abnormal blood vessels, so we
have to basically kill that part of the retina so it stopped asking for this
growth factor called vascular endothelial growth factor, so then their
proliferative disease gets better. The problem is when we do the laser, they
obviously have peripheral vision loss because you’re basically burning the
peripheral retina. They seem to have problems with their pupillary
dilation and you know light sensitivity because the ciliary nerves also go
through the peripheral retina in to the interior chambers and the people’s
don’t work very well. They can also have color vision issues. Laser is used but
FDA has approved injections especially lucentis and there’s another injection
eylea and it’s also going to get approved for it. Now we can treat diabetic retinopathy just with injections. The problem is patients tend to be young
and they don’t follow up on a routine basis. If you just do injections, you
have to come in initially every month and then every two or every three months.
Now obviously you’re not doing any damage to the retina by just giving them
injections, but the problem is they all commit to it they say oh yea I promise I’m
going to be here every two months and then they’ve disappeared for nine months
and then they have a bleed and then you ask them what happened they’re like I
really wanted to come, but I got a toe infection, then my toe got amputated, then I went into renal failure, I’m on dialysis, and I had a stroke. So it becomes really complicated. So we still use a lot of laser but a lot
of patients prefer actually, believe it or not, injections because they don’t
really hurt much. Laser does hurt and it does do permanent structural
damage. That’s something to keep in mind that we can do either injection
only or do injection plus laser or just the laser. There’s no guarantees that if
you do this Pan-retinal laser they’re not going to bleed because the disease
can still activate later. Again sugar control is the key for anything we do. So
this is an intravitreal injection. We inject 0.05 cc of anti-VEGF agent we call it.
There are different names: Avastin, Lucentis Eylea and what they do is they blow out the VEGF that’s secreted in the eye
that’s causing the leakage and abnormal blood vessel growth, but again the
medicine cycle out of the eye and patients have to come back and get
repeated injections, but most studies show that if you have diabetic macular
edema, if you treat it aggressively in the first year, if they control their sugars,
a number of injections over time will go down and there is a good number of
patients after two or three years they will be injection free. So my talk
to them is control your sugars, make sure you know you see your PCP
routinely and then we can help you maintain or improve your vision. Patients
they will go how come I have to go back for an injection? I say we don’t have a
cure but we do have a treatment. So the injection that really revolutionized
what we do, 13-14 years ago we just used lazer, a lot of people went blind. With
injections, not only can we restore vision but we can also maintain it
long-term. These are different injections we can
use. Kenalog is an off-label steroid. Whenever you get steroid in the eye, you
have risk of high pressure and cataract formation, so we tend not to use steroids
as first line of treatment. Kenalog, ozurdex, and iluvein, these are all –
your steroids. Ozurdex is FDA approved. Iluvein is FDA approved. Kenalog is not
FDA approved, but obviously it’s very, very cheap. Macugen was the original
anti-VEGF agent that nobody uses. It really did work but it started this
revolution of injecting things in the eye. Avastin is actually a drug for colon
cancer. It’s also used off-label in the eye because it’s cheap it still holds
about 50% of the market. It is not FDA approved. Lucentis is the first
FDA-approved medicine for diabetic macular edema, as well as diabetic
retinopathy and you know it’s really it’s a great drug and it’s
basically a small fragment of Avastin as you can see, they’re both
made by Genentech and Ilia is by Regeneron, also a fusion protein. also an anti-VEGF. Either we treat them it was for an anti-VEGF where shut
down the vascular growth factor or with the steroid. Steroids also lower the anti-VEGF but there is enough studies showing that in diabetic macular edema
it’s just not because of anti-VEGF So about a third of patients will not respond to eylea or lucentis, then we have to consider steroids, but again since steroids come with side effects of high pressures and cataract, we usually use them as second line
agents. So talking about VEGF, we already talked about it. It has a role in leakage
and neovascularization and abnormal blood vessel growth. So this is somebody,
in fact that lady I was talking about that came yesterday, this is how she looked
when she came into my clinic. This is all fibrosis. So basically this patient has
advanced PDR with fibrosis and traction to the whole macula. So we can go in surgically and remove the membranes, but again most
of the time the damage has been done and this patient probably will see the
big E or count fingers. So that’s why our goal is to avoid this. Our goal is to
intervene early, see these patients early on, because we have really good
treatments. If they come in and have mild macular oedema or early proliferative
disease, they can maintain their 20/20 vision for a long time, as long as
they’re in our clinic and they continue to follow up. So what we do in surgery.
Surgeries are the fun part. What we do is we make three tiny incisions and we go
to the back of the eye and we peel these membranes off. So this is the case where
there was somebody with proliferative disease, we were able to remove all the fibrous
membranes and make the retina relatively look normal, but again as I said if their
their macula is pulled, even if we remove the membranes theres still screa and
damage to the cells so they may not see ever as good as they used to see, but
there will be some improvement or stabilization. Sometimes it’s hard
because you do this great surgery and patients don’t see any better because of
the damage and even though you tell them in advance they just don’t understand the fact
that oh I can’t see and it’s like well we told you that the damage is already
there and this is just always further damage, but I think you know it’s very
difficult sometimes to educate these patients. So this is a surgical case of
at tractional detachment. This is what’s called a retractor. This instrument
cuts and removes gel and membrane. This is a light bite and then there’s
another line in there that maintains pressure in the eye. Should I click to run the video or, here we go. So what I’m doing here is that I’m removing the gel and
this is basically all the membranes covering the macula. So you can see that
we can actually remove them and then this retractor can cut and remove these membranes, but we have to lift it
very, very carefully because I assure you the structure of the retina is only
about 275 microns thick. If you hit the retina, obviously you will have a
hole and you will have bleeding. So this surgery is to remove all these fibrous
membranes from the macula. So what we do is we have to lift him and you
know sometimes we use this tool or we use forceps to kind of this off. This
patient obviously looked great afterwards, but their vision was only
like 2400, still legally blind which is 2200 or worse. So again our goal is to
not get there, but we do have the technology to help them, but sometimes
the membranes are so fibrous in the retina that we are not able to remove
them and we just have to give up but in this patient the retina is right there
and these are all sitting, you can fast forward a little bit, yeah. So we were
able to remove this that he was lucky. Sorry about that glitch. Do you need me to go forward a little bit more? That’s fine. You can just run it again. Yea, right there. Right there is good? Yea. Okay. (inaudible) okay. Is it going to run? You can run it more. Oh okay. So you can see this fibrosis. So this is from old bleeding. This patient had multiple episodes of
bleeding between the vitreous and the retina and then the
vitreous is fibrosis to the retina and is pulling on it and what we’re doing is
we’re removing this tractional membrane here. A lot of times when you do that the
retina will have holes underneath or is going to be detached and we do more
laser and we put either gas or oils. If you see a patient with oil in the eye that
means that they had pretty bad tractional disease. This is the optic nerve. So you
can see that because of repeated bleeding the gel has been fibrosis on top
of the optic nerve and what you’re trying to do is peel that off
from the optic nerve. Then try to remove as much as you can. So this is after we removed all of that. We did laser and now we are putting air in the eye and we put oil. So unfortunately some of these surgeries
don’t go this well. So the goal is to diagnose these patients early,
communicate and we are the worst ones in terms of communicating, even though we
said now supposedly, but we get a lot of requests for it, but always if you have
any questions just pick up the phone and call us and we are always available. It’s always a pleasure being here every year and I’m open to any questions. So Arshad, from
the standpoint of us medical folks, I think we know what our job is. We
try to do it and it’s primarily prevention but should a patient call us,
what constitutes an emergency? What might a patient report that you know if
we didn’t intervene urgently there could be serious sequela you know? Are there
circumstances where we really do need to respond to a patient and get them
referred urgently as opposed to viewing this is as kind of a chronic and
progressive disorder. I think that is a great question. So obviously if I do surgery on a patient. They say I
had surgery three days ago and I can’t see anymore or I was able to see now I lost my vision obviously we worry about endophthalmitis and you know last
week I had a very nasty and awful endophthalmitis from a cataract surgery that we intervened at
night and you know it was a staph epi infection and patient is doing good. So the worst thing that can happen is an endophthalmitis, but that’s going to be somebody with some sort of eye surgery when he was
able to see and now lost vision, but if you’re talking about somebody who has
never seen us and he’s been a diabetic, most of the time they’ll say I woke up and
I can’t see anymore and more than likely in a diabetic that’s going to be a
vitreous hemorrhage. The day you tell a proliferative diabetic retinopathy that
vitreous hemorrhage, so in that case they need to be seen you know, it’s not
something they need to go now but it needs to be seen within the next day or
two so that’s more of an emergency. Somebody who has severe pain in the eye and
really bad headache or nausea and vomiting they can have neovascular
glaucoma, so that’s somebody that needs to go to
the ER right away or be seen because their pressure needs to be lowered,
otherwise they are going to have permanent optic nerve damage. So those are the two
scenarios that I’m sure you get a lot and you just have to intervene and
sometimes you try to get them to an ophthalmologist and you really all the
offices oh well they’re too busy the good news is that there is always somebody on call at Renown Northern Nevada and st. Mary’s so you just have the patient go to the ER. The ER
doctor will see them and then call the ophthalmologist on call for it,
but here you have my cell phone number so you always can get your patients in. I can’t guarantee about everybody else. (laughter) Any other questions? (inaudible) Wells, can you take
yourself off mute? Or were you, oh yeah. You have some audio issues
today right? Hi there. So we have the new in office retina scans with an iris that we send off to John Hopkins to read and what typically try to do is do that once a year and then do a comprehensive
ophthalmologic exam every other year. I understand now that the guidelines have
changed and there is no retinopathy; however, I just wanted to ask you
clinically how useful because we will refer, if there is
anything abnormal, we will refer to you and your colleagues if there is anything
that’s found. So I just actually wanted to ask you how useful our scans are the
reports are in terms of a baseline for all. So I don’t think they’re too useful
at times. A lot of times they’ll say go see an ophthalmologist, there’s a concern
and sometimes they’re concerned that the patient has a cataract and they didn’t
have a good photo versus a vitreous hemorrhage from diabetes. So I think
telemedicine is good if you don’t have access in terms of or locations don’t
want to see somebody or you don’t have access to get their eye exams done. So I
think it’s good to have photos than have nothing, but again the gold standard
still is the dilated eye exam and I don’t need the photos or the report
that was done by Johns Hopkins or whoever is doing telemedicine if they’re
in my clinic and they’re waiting to see see me, but as I said you know the artificial
intelligence will be much better in terms of reading those photos. The
specificity is as good as having somebody read it but you can have better
photos with certain cameras and so I think the way to the future will be that
people will have access to these cameras in clinic. Patients will come see you,
you’ll have a photo, the software will tell you right away
how much retinopathy they have and then whether they need to be referred or not,
but to me screening is crucial. So if photos are the first basis of screening,
I’m happy with that versus no screening. So I just checked the 2019 ADA guidelines
and it’s actually you know initial screening as you had mentioned you know,
but follow-up is sort of I think a compromise because they say follow up
every one to two years I think (inaudible) I’ve got a lot of feedback from insurance companies and
health authorities so one to two years exactly. One to two years. So they published the pivotal paper in 17 did they publish this or they just put
it on their website? Well the ADA guidelines come out every
December. So these are the 2019 guidelines that came out in December of
18. Okay. Sounds good. Can you, this is jan, can you comment briefly on the JVN process. We do that at the clinic and
just what is a JVN and how useful is it. I don’t know. You said JVN? JVN. You’re not familiar with that, okay.
All right well you know in our clinic we have a, I don’t do it but one of
our technicians has it, is trained to use the machine that and I’ve had it done to
me so I know it’s very simple about 15 minutes and she looks in the eyes and
does some kind of report that’s sent out she sends out and gets a report that
tells them whether they need to go further with screening with that. That is very
interesting what tool are they using? Are they using a camera or… It’s, I don’t know, it’s JVN equipment. I don’t know if it’s, it’s something that takes a picture. I know that at the Owyhee Tribal Heath Center Of course this is in Elko that I’m talking about. Yeah so I know that
IHS has installed retina cameras in many many sites around the country and I
believe that’s what they have at Owyhee. Yes. They’re just like imaging telemedicine
camera that sends the photos out. So I think that’s why you know FDA was excited
to approve the software that you won’t have to telemedicine anymore. You can get
a picture and then the software will read the photo on the spot and you
have an answer versus uploading or sending the photos. So it’s
interesting how it’s gonna change things for everybody in the future. It’s not
going to affect us. It’s going to be mainly for screening where the machine can tell
you whether they have retinopathy or not So JVN, and I would think that as Evan said, maybe it’s
just a kind of a telemedicine camera, probably some company that and you know
all these big sensors have partnered with these companies to read these
photos. I believe that there are some iPhone camera adapted tools that we
will ultimately be using I suspect. Yeah there’s a company called Paxos out of DigiSight they changed their name now. We bought that camera just to see. They
were thinking about implementing it in ER and other places so they can take the
posterior pole photo and most of these cameras have done a good job with
interior segment but the photos of the back of the eye are still not very clear.
You still have to dilate them and have the right person to do it, but I agree
with you that instead of these big $50,000 camera, if you can have an add-on
to an iPhone with good quality pictures and then the software can read
it on the spot, then you’re all set. You don’t have to worry about all this telemedicine. So I think technology is going in that direction. We’re not there yet,
butI suspect within the next three to five years we will be there. Yeah. Arshad, thanks a million. Anybody else have any questions for Dr. Khanani? I think it’s very impressive what he’s told us. I wish everybody could see this because it really bringing this to reality what
the complications are of high blood sugar. Yeah that’s the bottom line.
Thanks everybody. Okay. Thats good. Thank you.

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