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TRANSCRIPTION CITY TYPING SERVICES
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TITLE: Presentation 1 Mr A Sharma
DATE: 14th February 2017
NUMBER OF SPEAKERS: 1 Numbers Speakers
TRANSCRIPT STYLE: Intelligent Verbatim
FILE DURATION: 20 Minutes 45 Sec
TRANSCRIPTIONIST: Marg Searing
SPEAKERS
AS: Mr A Sharma
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GP Eye Health Network: Diabetic
Retinopathy, Mr A Sharma
AS: So, my remit is to talk very briefly on diabetic retinopathy which I
don’t want to bore people to death. But, it’s a very, very important topic.
Yes, we need to make sure we’re getting our disease registers up to
date, monitoring the patients, checking all the parameters. And we do
know that controlling all the parameters including blood pressure and
lipids is a very important part of managing the retinopathy and not just
controlling their long term diabetic control.
We do know that studies have been done, published some years ago,
now, in 2007 to show that managing the lipids using fibrates. And the
studies were the field study and the Accord study published in the
Lancet some years ago, even combined with a statin, it reduces
progression of retinopathy. Particularly, the lipid exudates in the
macular. So, all those yellow areas that we’ll look at in the macular are
very, very difficult to control. Reducing your cholesterol with statins and
fibrates as a combined therapy, obviously, if medically tolerated can be
beneficial for the patient over a period of four years.
However, screening is very, very important and I know the disease
registers are all being used to make sure screening is as widely
encompassing as possible for all patients with a diagnosis of diabetes.
So, the epidemiology? Well, the figures just get worse and worse. The
latest data that I’ve got from the office of National Statistics, shows a
prevalence of around about 5%. But if you look at all the borderline
cases and the impaired glucose tolerance cases, I think the figure can
be a lot, lot higher. The 5% figure comes from this publication from the
National Statistics, but also patients from South East Asian origin or
African origin the prevalence can be three to six times higher. So, it’s
incredibly important that we’ve got the resources in place to make sure
we can screen all these patients.
Now, the National Screening Committee from 2005 recommended a new
way of classifying retinopathy. I don’t want to bore you to death with all,
of these, but basically, proliferate retinopathy is now R3 and
maculopathy can be either there or not, zero or one. P just basically,
means the patient has had laser treatment. So, if it’s R3 or R3 M1, here,
that means I’ve got proliferate retinopathy and its sight threatening and
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that is urgent treatment. So, you might see letters from
Ophthalmologists or particularly optometrists who will use that
classification nomenclature.
R2 can be seen routinely as normal and R1 background retinopathy can
be monitored in the community with regular screening.
So, this is moderate, what we call R2 type retinopathy and as you know
from medical school days, using the ophthalmoscope and trying to spot
these haemorrhages in exudate. And basically, when they say, ‘cotton
wool spots’ that’s just a description of pre-proliferative changes. So,
when you get haemorrhages in exudate it doesn’t necessarily mean that
they are gonna need urgent treatment unless they’re within one disc
diameter of the fovea. But if you’ve got cotton wool spots they are
pre-proliferative. They are patients who within a few months will develop
proliferative retinopathy.
And proliferative retinopathy, well we can see what exudates will look
like. Scattered lipid exudates throughout the macular. That’s a cracking
case of diabetic maculopathy and they’re called ‘circinate exudates’
because they appear in a circular fashion predominantly because
somewhere in the centre is a leaking microaneurysm.
So, that’s maculopathy and macular oedema which is what we used to
call retinal thickening, can, actually, be detected now very, very
accurately using what’s called optical coherence tomography and I’ll go
on that in a minute. But basically, it produces a laser reflected image of
this … of the retina. It’s not a thermal laser. It’s a non-thermal laser that
shows up pockets of fluid within the actual macular region itself. In the
old days, we used to, well even now even to detect this at a subtle level,
you’d have to inject fluorescein dye in to the blood stream and that
circulates around the body. And within about 15 maybe 30 seconds, you
get leakage and pooling of dye in the macular region. And that’s very,
very important cos that’s sight threatening. Nowadays we can do it
relatively non-invasively using optical coherence tomography.
We’ve mentioned about lipids and about controlling macrovascular
disease which is a risk for all our diabetics. Considering statins apart
from in pregnancy and fenofibrates what we’ve already mentioned as
per the studies published in 2007 and 2010.
Childhood diabetes that also, is a risk factor for retinopathy. And the
figure goes up the older the child presents with diabetes. So, if they
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have diabetes diagnosed at the age of 10, there’s 1% prevalence but
that goes up to about 17% if they’ve had it picked up later on.
So, the general thing is that within four years of diagnosis, everybody
including children have, to be within a screening programme. And we
know from the older studies such as the DCCT and the UKPDS, that
controlling the diabetes itself reduces your risk of developing proliferated
diabetic retinopathy by about 47%. So, metabolic control is highly
important, I don’t want … I do want to just re-emphasise that. And for
the none dia … the type 2 diabetics, the risk reductions are pretty,
similar, about the order of 32% reduction in proliferation.
Neovascular chances can lead to sight loss. And neovascular changes
in type 1 diabetes are predominantly due to … will cause sight loss in
about 20% of patients. Macular oedema is responsible for sight loss in
about 25% of patients. So, a fair proportion of sight threatening
retinopathy is due to treatable causes.
What we know that after a long history of diabetes, all patients, well after
20 years of type 1 diabetes, all patients will have some degree of
retinopathy. Some of that is unavoidable.
Type 2 patients about the order of 60% of patients after 20 years will
have retinopathy. And when type 2 patients go on to start insulin, the
proliferation, the rates of proliferation do go up but that’s partly due to
the severity of the disease process not that the fact they’re actually
taking insulin.
We’ve mentioned the diabetic macular oedema and we know that the
diabetic macular oedema can be made worse by the diabetes affecting
the blood vessels. Also, the level of hypoxia can stimulate production of
this which is called, vascular endothelial growth factor. And that can
also exacerbate. Not just proliferation of vessels but leakage in to the
macular as well.
We know about the screening standards. Over the age of 12, obviously,
patients need to be screened. I mentioned four years, there was a figure
on that earlier on, but basically, as soon as they’re diagnosed, if they’re
over the age of 12, they need to be in to the screening programme very
early on, within three months of diagnosis.
The mechanisms of retinopathy, we’ve mentioned all about most of
these classifications. Laser treatment which is administered on a
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microscope like this with the patient having an anaesthetic and a lens on
the eye. And the laser can be targeted to those leaking area of blood
vessels, either in a focal pattern, or a grid pattern. But more commonly
what we try and do is utilise pan-retinol photocoagulation for proliferative
retinopathy still. That’s still the safest standard treatment that’s in
widespread use.
Now, you will certainly be aware of all the other modalities of treatment
of diabetic retinopathy, such as injections of drugs directly in to the eye.
Now there is an area of eyeball called the pars plana, just behind the
lens equator where if a needle is injected into the vitreous at a
perpendicular angle, there’s no damage to the retina and there’s no
damage to the lens and there’s no damage to the vascular structure, it’s
just through the ciliary body.
So, that area of the pars plana which is about three and a half, four
millimetres back from the corneal limbus is the only place to safely inject
a drug into the eye. And we can inject all manner of drugs such as
steroids of anti-VEGF drugs such as lucentis and also a new one called
Eylea.
We can go on to the patterns of laser. We’ve mentioned about focal
grid. This is panretinal photocoagulation which is quite a striking
aggressive but relatively well used mode of treatment that has reduced
proliferation at the optic disc of new vessels but shutting down
production of vascular endothelial growth factor. And it works by just
doing that, killing the cells that produce the molecule and it reduces sight
loss by about 30 to 40% and that’s been tried and tested for many, many
years.
We talked about injections and the molecule that we’re trying to block is
vascular endothelial growth factor secreted by multiple layers in the
retina. But what vascular endothelial growth factor does is it makes
blood vessels leak and also, causes the production of endothelial cells.
So, there are lots and lots of leaky vessels in the retina with VEGF.
And over the last five to six years, we’ve now changed our advice in that
laser in the macular region is predominantly for those areas where the
disease is just outside the foveal zone. Which is the central 400 microns
of the fovea. So, if it’s outside that zone, it’s safe to administer laser cos
laser is a destructive treatment modality. But if it’s right on the centre
and the centre is actually oedematous to about 400 microns thickness
then you are now licensed to give Lucentis or Ranibizumab.
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I put a question mark over Bevacizumab although the … it’s not a
licensed drug. It’s off licence. It therefore will have to be applied
separately but we have got funding now for Ranibizumab and that’s the
drug that we’re all using.
This is the machine that actually generates the scans that tells the
surgeon how the thick the retina is in the centre and it’s called the optical
coherence tomography. And the patient just puts their chin on the
chinrest, forehead against there, totally non-invasive with non-thermal
laser that causes laser interferometry and reflections from different
layers of the retina. And it generates a map, a thickness map, of the
retina such as this. And this is what a normal retinal profile should look
like with the centre around about 180 to 200 microns in thickness. If it
gets to more than 400 microns you are then eligible for treatment with
Lucentis.
So, a lot of patients now need scans, injections and a repeating cycle of
those fairly regularly, especially in the first year of treatment.
That shows another image of macular oedema. Now, macular oedema
can be due to all hosts of other things as well. But if they’ve got
diabetes and no other cause for it, then it’s generally the diabetic
retinopathy that causes it.
So, what are the results from using intravitreal therapy? So, that’s
intra-vitreous injections of drugs. Well, we know steroids will cause a
rise in pressure and also precipitate or accelerate the development of
cataract. So, we try to avoid giving steroids in those patients who have
got glaucoma or cataract. So, it rules out a fair proportion of patients
who have got clear lenses who don’t want to develop a cataract.
So, the first line treatment really, is intravitreal Lucentis. And you can
defer the laser or do the laser if it’s extra-foveal. It is now shown that
with the data, particularly over the last five-six years, that central
thickness of the retina is better treated with Lucentis and that leads to an
improvement in visual outcomes as is shown on this graph where the top
two lines which is the organ and the light blue are Ranibizumab with
prompt or deferred laser showing lines of vision gained. And the bottom
two lines are people who have had either a sham injection or just steroid
with laser.
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So, the data is out there that anti-VEGF injections are the best first line
treatment for macular oedema affecting the central part of the fovea.
And that’s what NICE have now recommended and the cut off they use
is 400 microns of retinal thickness as measured on the OCT.
The cost of the drug is substantial. The cost of Lucentis is around £700
per vial. And if you estimate giving that about eight times in a year, the
costs do add up. So, the manufacturers have provided the drug on an
agreed discount to the NHS as per a patient access scheme from 2012.
And they’ve done that for all other NICE accredited drugs as well.
So, the other manufacturers that are making a different type of drug
called Eylea, otherwise known as Aflibercept, which is another
endothelial growth factor blocker, so it blocks VEGF-A which is in a
different isoform such as VEGF-B and, also placental growth factor
which is another molecule which is also found in the eye that stimulates
the growth of endothelial cells.
At, the moment, the two are used almost to the same level of efficacy.
Aflibercept is also targeted at almost the same cost but it can be given
slightly less frequently after the first five injections. So, we give them
every two months, the Eylea. So, that allows a little bit of relief to the
patient from having injections every month.
And we’ve also mentioned steroid implants which can be used.
Dexamethasone or Fluocinolone. Dexamethasone is thought to be a
powerful drug but the effect is actually, much less than what’s stipulated
on the bottle. They say, about six months, we think it’s about a month or
two.
However, Iluvien which is the latest steroid implant is supposed to last a
lot longer but costs the same in total terms. So, the cost of Ozurdex is
£870 whereas the cost of one injection of Iluvien is 5,500. And what the
Iluvien manufacturers have done, they’ve basically taken three
Ozurdexes per … over three years, that’s about nine times 800 and said
right, well we’ll just come in at just a little bit above that. So, 5,400-5,500
that’s what Iluvien is costing now.
There is a patient access scheme for Iluvien but it’s all a commercial
confidential agreement which I don’t have information on unfortunately.
Okay, I’m just going to be presenting a little bit about surgical treatment
for these patients. So, what happens when the drugs don’t work, the
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macular oedemas got worse or the proliferative changes have led on to
vitreous haemorrhage or they need to have a vitrectomy basically.
Which is basically removal of the vitreous humour and any opacities and
membranes that are pulling on the retina. It also allows us to do further
laser treatment for the detached retina treatment and further treatment of
the macular oedema.
And this is what traction on the retina can look like on an OCT … ooh,
sorry. So, you’ve got membranes of the posterior hyaloid which is the
back surface of the vitreous still stuck to the retina no doubt
exacerbating the resolution and the improvement of the macular
oedema.
Can we dim the room lights a little bit because I might want to just give
you a bit better contrast? Thanks very much for the video which should
hopefully play.
Now, if you’ve got a lot of opacity in the vitreous of the eye, this is your
light, this is your vitrector instrument which sucks a small proportion of
clotted fibrin and cuts it like a guillotine and removes it.
So, we’re very, very gently trying to remove old vitreous haemorrhage
that’s now looking very white. There’s a bit of a haemorrhagic, fresh
haemorrhagic change there. And you’re basically working down an
operating microscope looking at this in high resolution and high mag.
There’s healthy or relatively healthy retina there and there’s clotted fibrin
sitting on the retina that’s obviously, blocking the view for the patient
which he obviously, can’t see very well through. And we’ve developed
much, much, better instruments now that allows us to do bi-manual
surgery. So, one hand actually, picks up the membrane, the other hand
can cut it. That means you’ve got a chandelier that’s self-retaining in the
eye which allows one hand to be used for dual function surgery.
And basically, when you’ve got membranes on the retina you want to try
and lift and cut them in the interface between the membrane and the
slightly elevated retinas. You wanna be very, very careful not to damage
the retina and not to leave too much behind. So, there is a fine balance
in getting this appearance to look like that which improves the vision to
about half way down the chart. Whereas previously they were
obviously, just seeing the top letter.
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And this treatment where the retina is detaching because the
membranes can quite easily pull and lift-up the retina, which will cause a
profound drop in vision. And what that refers to is tractional and
rhegmatogenous retinal detachment. Which is the break in the retina
that causes the retinal detachment.
And that’s the post-op appearance where the disc is rather pale, the
vessels are a little big occluded. So, the blood supply to the retina isn’t
going to be very much improved but the vision does improve by
removing the opacity and detachment.
Okay, so just to summarise:
It’s the leading cause of blinding in the working population.
Early detection is no doubt very important and treatment with laser
and with all different intravitreal drugs and adjuncts does lead to a
prevent … improvement in vision.
But we do still need to make sure our targets for screening all
patients are being met. Because that’s the simplest, easiest way to
prevent them getting to the end stage of the disease.
Great. Put the lights on now. Thanks very much.
END OF TRANSCRIPT
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