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TRANSCRIPTION CITY TYPING SERVICES
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TITLE: Presentation 2 Mr I Massood
DATE: 18th February 2017
NUMBER OF SPEAKERS: 1 Numbers Speakers
TRANSCRIPT STYLE: Intelligent Verbatim
FILE DURATION: 27 Minutes 3 Sec
TRANSCRIPTIONIST: Marg Searing
SPEAKERS
IM: Mr I Massood
FS: Female speaker
DS: Dr Strange
Audience
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GP Eye Health Network: Glaucoma, Mr I
Massood
IM: What I’m gonna talk about is what is glaucoma? What is this
disease that blinds people? I’m gonna talk about referrals and demand
management cos again that’s a huge issue with respect to glaucoma in
the NHS. And, then I wanna talk about treatment modalities that we are
currently using, sort of state of the art to treat glaucoma.
So, what is glaucoma? Glaucoma is a progressive optic neuropathy
where you get characteristic visual field changes and optic nerve
changes so that you get this cupping. And the major risk factor for
glaucoma is raised intraocular pressure.
So, that’s a normal optic disc and this optic disc has got 1 million nerve
fibre layers. So, these are these neurons and …
[interruption re lights 00:00:55]
FS: Mr Massood do you want the lights dimmed [unclear 00:00:57]
IM: Down a bit, yeah, that’s perfect.
FS: Good.
IM: Yeah, yeah.
So, there are a million retinal nerve fibre layers that come through here
and they go through the optic nerve to the brain. And the size of this
optic nerve is only the size of the O on the one p piece here. Okay. So,
that’s … it’s about a millimetre. So, these two tiny one millimetre cables
from both eyes is what allows you to see and interpret and process all
the visual information. It’s really, quite amazing.
And this is what happens to the optic nerve in glaucoma. And this is
probably the saddest sight in clinics that I do, when you see patients with
optic nerves like this: pale, with no neural rim. And this patient, this is
terminal glaucoma.
And because of the kind of population we deal with in Birmingham, often
these are young people. So, people in their 30s and 40s, particularly if
they’re Afro Caribbean.
And so, that’s a normal optic nerve and you get progressive loss of the
neural tissue and it ends up looking like that.
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So, why does the pressure in the eye go up? Okay. So, the major risk
factor is raised intraocular pressure. So, we have to try and understand
why the pressure goes up. The pressure goes … So, this is a … this is
what we call open-angle glaucoma. There are essentially two types of
glaucoma, open-angle glaucoma and angle-closure glaucoma.
So, in open-angle glaucoma, so, let me show you here. This is a cross
section of the eye. A bit like the kind of diagram you’d see in a GCSE
biology text book, so you should remember that. And in, essence,
you’ve got the ciliary body here which is the bit that makes the fluid in
the eye.
Okay, the fluid then circulates around the eye, nourishes the eye and
creates a pressure within the eye. Because you need that pressure to
keep all the optical elements in their correct position.
If you puncture the eye, the eye collapses. So, it’s under pressure. And
this fluid then drains in to the angle here, through this sieve-like area
called the trabecular meshwork into Schlemm’s canal and then is
drained away.
So, this is a sort of a histological cross section of the angle. There’s
Schlemm’s canal, this is the trabecular meshwork. So, essentially, what
happens is, for reasons that we don’t fully understand, you get this
meshwork, essentially, it’s the drain of the eye, it gets clogged up. And
so, as it gets clogged up, the pressure that is required to put the fluid
back in to the canal goes up. So, you need more pressure to bypass
this resistance and that’s why that pressure goes up.
But one of the side effects of having that pressure going up is that it puts
stress on the optic nerve and the optic nerve gradually begins to die.
This is what angle-closure looks like. So, in angle-closure, there is
actually, an obstruction of the trabecular meshwork in the canal because
of the iris. So, can see here, this is the iris, this is the trabecular
meshwork, this is the canal. And in this cross-sectional ultrasound
image, you can see that the iris is bowed forward and it’s actually,
making contact.
This is a ciliary body. It’s actually, making contact with the angle. So,
the angle here is closed. And this patient has then undergone, laser
iridotomy, that’s to make a hole in the iris. And after the laser iridotomy,
you can see that the angle has opened up. So, what the iridotomy does,
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is by making a hole there, you equalise the pressure either side of the
iris and the iris falls back.
So, again, just to you know summarise what I’ve said already. The eye
with glaucoma, the pressure builds up gradually causes the optic nerve
to die. And this is what it, you know, it looks like, so, to speak from the
patient’s perspective. This is normal vision and then, as you gradually
lose vision, you end up with an extreme glaucoma with tunnel vision.
So, this is one of the issues around diagnosis of glaucoma. Primary
open-angle glaucoma is asymptomatic. Okay. So, patients will not
come to us saying that their vision is blurred or that there’s a problem
and unfortunately in glaucoma by the time the patient says, I have a
problem, I can’t see very well, it’s actually, too late. We can’t do
anything then.
So, how do you diagnose glaucoma? These are the tests that we do in
clinic to diagnose glaucoma. Gonioscopy, this is technique we use to
look at the angle which allows us to decide whether the glaucoma is of
angle-closure type or an open-angle type. We examine the optic nerve
to look for cupping.
We assess intraocular pressure using Goldmann acclimation tonometry.
We look at the corneal thickness. This is quite an important thing,
because the way we measure pressure is by essentially, pressing on the
cornea. If the cornea is very thin, you’ll get an artificially low pressure. If
the cornea is very thick, you’ll get an artificially high pressure. And a
thick cornea is often a cause for a lot of false positive referrals. And
then we look at the visual field and then we look at the nerve fibre layer
analysis and I’ll show you some images to do that a bit later.
So, the signs of glaucoma, as I have said, are cupping of optic discs,
visual field defects and in very advanced disease that’s when the visual
acuity actually, goes down.
So, this is the type of thing you would see on a visual field defect on a
visual field plot. And basically, there are areas here where the patient
has lost field. Now, the patient will not be able to identify and say to you,
I can’t see here or there, I’m missing patches here. This is something
that’s picked up on a test. So, the patient will not be aware of these
necessarily. Some patients are, but most of them aren’t. And the other
important thing is, we’ve got to be careful that when we get patients
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referred to us as visual field defects, that we don’t miss other causes for
visual field defects. Okay.
So, this an optic nerve, which you know if you looked at it, you’d say,
yeah, that looks like glaucoma. It’s cupped. Okay, you can see that the
rim’s missing. The patient has got a temporal defect here and in the
other eye there’s a temporal defect as well. So, what do you think the
diagnosis here is?
[unclear mumbling in audience 00:07:09]
IM: Yeah, so you can see here this is the pituitary tumour. And you’ve
got this chiasm which is splayed over it. So, whenever I see someone
with a temporal defect, I’ll always think about you know examining them
fully to exclude neuro-ophthalmic disease. And there are instances of
patients where pituitary tumours have been missed in glaucoma clinics
and that results in big pay outs.
Okay, so, this is the retinal nerve fibre layer. So, the optic nerve is made
up of all these nerve fibres which are coming from all over the retina.
And we can actually, measure these. We can measure the thickness of
the nerve fibre layer using scanning.
Now the interesting this is that often we find that the optic nerve changes
before you get visual field defects. So, there is a lot of redundancy in
the optic nerve. You need 40% of the optic nerve to be damaged before
you’re gonna feel defect. So, again, the problem is that the disease is
asymptomatic in its early stages.
So, this is how we scan the optic layer using optical coherence
tomography and basically, the laser scans and looks at the thickness of
this retinal nerve fibral layer which is the surface layer of the retina. And
these are just some examples of cases. So, this is a patient who we
saw some years with advanced glaucoma and then the optic nerve is
very, very cupped here and the retinal nerve fibre layer analysis is
showing us that it’s very, very thin.
This was a patient who was referred with cupped discs. So, remember
we get a lot of false positive referrals. So, these diagnostic modalities
help us to discharge people. So, his visual fields are full and his
pressures are normal. We scan his optic nerves and, yes, you can see
that the disc look a bit cupped but actually, the scan is completely
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normal. Okay. So, I am … I can confidently discharge this patient and I
don’t have to keep monitoring them in the hospital eye service.
Okay, let’s talk a little bit more about demand management. Now this is
the kind of graph that I think, most people when they’re lecturing about
any disease I’m talking about. You know, the big explosion in our
patients.
Now, there is also a big increase in glaucoma incidence because age is
a big risk factor for glaucoma. So, in all racial groups these are the
predictive numbers. This is date from America but probably very similar
for the UK.
And this is a very important diagram. This is what I think of every day,
when I manage a patient. This line represents functional blindness.
This is a patient with glaucoma who if you leave them untreated they will
hit that functional blindness line in their lifetime. If you treat them, they
will still get worse, cos a lot of glaucoma patients still progress but the
progression is massively reduced. And our aim, when we treat
glaucoma patients is to prevent them becoming functionally blind in their
lifetime.
And unfortunately, this is the problem … well, fortunately or
unfortunately, however you want to look at it, this line, okay, we’re
looking at 90, 100, 110 and the problem is I’ve got 80, 90 year olds who
are extremely fit. And so, the question then is, what do I do. Do I
operate on them or do I leave them? And it becomes a difficult dilemma.
And I have started now doing glaucoma surgery on 90 year olds. So,
you know, that’s way we’re heading.
In order, for me to understand whether a patient is at high risk of going
blind, I risk stratify. So, I look at the age. So, obviously, a 90-year old
patient with a bit of pressure is unlikely to go blind in their lifetime.
And we look at the race, particularly in our multi-ethnic population in
Birmingham, we see a lot of Afro Caribbean patients and they tend to
get glaucoma earlier and it’s more aggressive. So, that is a risk factor in
my mind for blindness.
Family history, extremely important. If you have a family member who
has glaucoma, the risk of you having glaucoma is tenfold higher. So,
that’s quite an important thing. And in the family history it’s always
important to identify whether a family member went blind. So, if a family
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member has gone blind, the risk of your patient going blind is higher as
opposed to if the family member just had a bit of pressure.
Refractive error is important. So, patients who are … people who are
very short-sighted are at increased risk of glaucoma. Patients who are
very long-sighted are at increased risk of glaucoma. The corneal
thickness I’ve talked about and then these are sort of slightly softer risk
factors, and steroids. Steroids is very important. And this is not just
topical steroids in the eye. These are patients who apply steroids
around the eyelids. So, that’s quite important. So, if you’ve got patients
with eczema or any other periocular skin condition where they’re
applying topical steroid, you know, you’ve got to be careful that the
steroid may be being absorbed in to the eye and their pressure may be
going up. So, these patients do need to be checked out at the
optometrists.
The same goes for inhaled steroids and systemic steroids. Although
with inhaled and systemic the risk is lower, they do need to have their
pressure assessed from time to time
Just another graph showing the prevalence of the disease in Afro
Caribbeans versus Caucasians. So, at any given pressure level Afro
Caribbean patients are more likely to get optic nerve damage than
Caucasians. We don’t fully understand why that is but it may be
because the optic nerve is inherently more sensitive to pressure, or it
may be because of the optic nerve size. We know in Afro Caribbeans
optic nerves are bigger. So, perhaps bigger nerves mean mechanically
they’re under more stress with similar levels of pressure.
I’ve talked about the family risk already. So, what’s the scale of the
problem in the UK? Well, it’ a big problem because it’s a massive
workload of all eye departments up and down the country. So, there are
1.2 million glaucoma patient appointments times 2 a year. So, that’s
almost 2 million appointments in the hospital eye service that are
glaucoma related. And studies have shown that 23% of all hospital eye
service appointments are glaucoma related.
Now that doesn’t mean that they’re … that all these patients have
glaucoma but they may be glaucoma suspects, they may ocular
hypertension. And obviously, there’s this spectre of reduction in real
terms spending in the NHS which is the background against which we
have to work.
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And why is this demand going up? Well it’s, age, increased screening,
raised awareness. There’s literal supporting more aggressive treatment
of glaucoma and the NICE guidelines. The NICE guidelines for
glaucoma that were released in 2009 had a huge impact. And I’ll just
show you what that impact was.
So, in March 2009, this is the way glaucoma patients were referred. An
optometrist examined the eye, they measured the pressure, did a visual
field. Sorry, this is a pressure measurement device. Did the visual field.
Used their brain and made a decision about whether to refer the patient
or not. Okay.
What happened in April 2009, was these guidelines came out. And then
the association of optometrists, this then came out with this statement.
‘The AOP believes strongly that optometrists have no choice other than
to refer a patient who has sign of ocular hypertension, e.g. pressures
measured at over 21 using whatever tonometer that they choose’. And
let me show you what the impact was.
So, NHS, this was a study done in 2013, but basically, the NHS units
were flooded with false positive referrals. I mean you can see that there.
That was April, and you can see, that is one eye unit in the west of
England and look at that. That’s that particular year. It just, you know,
doubled or tripled the referral rates.
So, how do we improve referral quality? Well, in some … in some
studies the false positive rates are as high as 65%. So, yes, we want to
see the patients who are at risk of going blind but we don’t want to see
the patients who have got nothing wrong with them. And, you know, it’s
all about how can we improve referral quality. And I think that the
bottom line is to collect good quality data at the outset. I think the
intraocular pressure needs to be repeated. And there are schemes
around Birmingham now, where certain optometrists are trained to do
applanation tonometry and so we’re getting slightly less false positives
but I’ll show you some examples of referrals which we still get,
unfortunately.
If you can measure the corneal thickness in the community then that
allows you to say, that this cornea is thick and that’s why we’re getting a
falsely elevated pressure. We don’t want to send this patient in. And
perhaps imaging of the discs if that’s more readily available, that will
reduce false positives as well.
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So, there’s this concept of specialist optometrists. You know, it can
reduce the false positive rates.
Okay, so this is an example of a referral. So, pressures are normal.
Healthy coloured disc margins. So, basically, this patient doesn’t have
glaucoma. I can tell you that already and you can probably tell that from
looking at this now. Visual fields abnormal. Okay. Now, please note
the family history of glaucoma. Now this abnormal visual field, mostly
likely is spurious. I don’t know if any of you have done visual field tests.
Anyone? Put your hands up if you’ve done a visual field test. Okay.
Some of you. Is it an easy test to do?
[audience mumbles – no 00:16:55]
IM: No. I’ve done it myself. It’s absolutely awful. Right. So, I can
imagine, that you know if you’ve got an 80-year old patient who’s a bit
tired and hasn’t slept well, they’re gonna do a bad field on that day aren’t
they. So, this is another reason why we get a lot of false positive
referrals.
Another example of a very poor referral. Okay. So, optic nerves are
healthy. Pressures are 20 and 21. They’re not higher than 21, they’re
21. But look at the referral. Her, IOPs have increased from 15 last year
to 20 and 21. They haven’t increased. You get fluctuation in pressure.
Pressure fluctuates, okay, it’s like your blood pressure, it fluctuates
throughout the day. So … and even if they have gone up a bit, you
know, they’re 20 and 21, they’re within normal limits. So, why has the
patient been sent in? It’s cos people are not engaging their brain.
They’re just following you know, blindly, what the kind of guidelines are
saying. And even, actually, that’s against the guidelines actually, cos it’s
more than 21, so.
[laughing]
IM: Okay, so a little bit about referrals and things like that. Now let me
talk about glaucoma therapy. Dr Strange, how much time have I got
left?
DS: You have left, 10 minutes.
IM: Okay. alright. So, this is very relevant cos you will be seeing
patients on these different medications. So, I’ll talk you through the
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various classes of medications we have in glaucoma. So, all of these
drugs work by lowering the intraocular pressure. Okay.
So, the first group of drugs are the prostaglandin analogues. Okay. So,
these drugs work by increasing flow of fluid out of the eye. Okay. And
the drugs are: Latanoprost which is a generic drug now; Travoprost and
Bimatoprost. So, these are our first line drugs for the treatment of raised
intraocular pressure.
Second or third, second line, probably Beta-blockers or sometimes we
use these carbonic anhydrase inhibitors. So, Beta-blockers, the
commonest one used is Timolol. Carbonic anhydrase inhibitors, these
are drugs we apply topically. So, we have Brinzolamide and
Dorzolamide and then some patients need Acetazolamide which is an
oral carbonic anhydrase inhibitor. And these are the patients that need
to have their Us and Es monitored and full blood count monitored
probably every two or three … about three or four months if they’re on
them long term.
Then you have Alpha agonists: Brimondine; Apraclondine. And these
are the Miotics, the drugs like Pilocarpine which are cholinergic agonists
and they constrict the pupil as well as lowering the pressure. But we
don’t use these very often nowadays. And then there are combination
drugs which are combinations of Latanoprost and Timolol or Azopt and
Timolol. So, you can get combination drops as well. But this is the sort
of the armamentarium therapy, sort of medical armamentarium we have
to lower intraocular pressure.
Now this is something that, you know, is a real bugbear of mine because
I’ve been to numerous drug and therapeutic committee meetings about
preservative free medication and why are we prescribing so many
preservative free medication, they’re expensive and so on?
Now, and I keep getting told that we should only use preservative free
medication if a patient has preservative allergy. Okay. But actually, a lot
of the preservatives cause ocular surface toxicity. That’s different from
allergy and I’ll show you what I mean by that.
An ocular surface disease, that means, red eye, sore eye, is very, very
prevalent in glaucoma patients. So, a lot of these people are in our
clinics. They don’t really have a problem as far as they perceive
because the disease is asymptomatic. Yet, we’re putting them on drops
that make their eyes red and sore. It affects the equality of life. It affects
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the quality of your vision. It affects, you know, you get symptoms of dry
eye. And you know, it does affect surgical success.
So, if patients need operations for glaucoma which are reliant on the
conjunctiva, this is the lining of the eye, being healthy. If the eyes look
like this, they’re not going to do very well. So, this is someone, this is a
patient. This is just something I’ve taken off the internet. But you know
have seen a patient … I have seen numerous patients like this where
the eyes are extremely red. The patients are, you know, extremely
uncomfortable yet they keep persisting with their drops cos they don’t
wanna go blind. And this is not allergy. This is preservative toxicity.
So, what we do in these patients is we switch them to preservative free
medication and they are very happy. And sometimes their intraocular
pressure comes down as well. Because there’s some evidence now,
that the more red your eyes are, the more likely your intraocular
pressure is to be unstable.
So, that’s why we want preservative free medication. In the longer term,
it benefits these patients. So, it’s particularly, if I see young patients
now, I will put them straightaway on preservative free medication.
Because younger patients are more likely to need surgery in their
lifetime. And so, you want their ocular health to be better.
I’m gonna … time?
DS: Six minutes.
IM: Six minutes. Okay. I’ll probably talk for another couple of minutes
on state of the art sort of surgical techniques now.
So, this is, I’ve sort of gone through this already. Basically, flow goes
through the trabecular meshwork into Schlemm’s canal. This is
Schlemm’s canal with all the sort of aqueous veins coming off it. And
really, quite a dynamic system. And in the past, a lot of glaucoma
surgery was based around making, very crudely, a hole in the eye and
letting the fluid out. Okay.
What we do and what we can do now is use these new lasers and new
stent devices to treat glaucoma. So, this is an SLT laser and you apply
laser directly to the trabecular meshwork and it alters the biology of the
meshwork improving the outflow. And some of the results we get with
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SLT laser are very, very impressive. So, it can delay … at times it can
delay surgery by two, three, four years, so, very, very useful.
I always like to show this example. Again, this is creating a new conduit.
Okay. This is what we do with conventional glaucoma surgery. We
make a hole in the eye, we bypass the natural physiological system.
When we do angioplasty we are reinflating, we’re allowing the vessel
that has become diseased where we’re essentially, treating it so that the
flow can improve. And that’s what we’re doing with these new stents
that we put in to the canal.
So, this is a tiny … this is called an eye stent. It’s the smallest implant
that goes in to the human body. It’s made of titanium. It’s a millimetre
across, 250 microns in diameter and it goes directly in to Schlemm’s
canal. So, the fluid, the aqueous humour can then go through that
snorkel back in to the canal. So, this has been a big advance in
glaucoma surgery. It’s very, very safe and it’s very efficacious.
So, now with these, kind of techniques we can intervene earlier in
disease, okay, before you get irreversible damage to the outflow
pathways. And it may reduce the need for more aggressive surgical
options in the future.
Okay, this is just an example of a patient with treated with this kind of
technology. He had very, very high pressures. He had cataract and
he’s been … he’s had stents put in. This is his fields, so, you can see,
pretty much blind in one eye. The other eye has got a little bit of field
left. And we operated on both eyes and he’s remained pretty stable over
about three or four years. And we didn’t … most people, around the
country would have done conventional surgery. We actually, put stents
in and he’s done very well.
I’ll just see if this video works. Just so I can show you how we pop these
stents in. So, this is a little lens on the eye called a Gonio lens. It allows
us to look at the angle. This is the drainage canal. Okay, and we
popped this little stent in there and you’ll see this is probably the nicest
videos that I’ve manage to get of this procedure. Cos, you’ll actually see
a little bit of blood coming out of the little snorkel there. There. Okay.
So, we know we’re in the right place.
Okay, this is another stent that we’ve been using. It’s a slightly longer
stent and you can see again. And you know it’s very … this is made of
the same material that coronary stents are made of. So, it goes in to the
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canal, it dilates the canal and it improves the outflow of fluid in to the
canal. I wanted to show you that.
So, this a study that was done in America and it’s actually, shown that
over the last sort of 30 or 40 years, there’s been a measurable reduction
in glaucoma blindness. So, all the work that we are doing, it is having a
positive impact on patients in terms of functional blindness, so that the
rates of functional blindness are going down. Clearly, there’s still more
to be done. And the key really is early detection.
Now, what, you know the patients that I sort of want to see are routine
and complex glaucoma, laser, patients who need laser; patients who
need surgery and so we see a lot of patients for second, third and fourth
opinions.
So, I think there’s been a real revolution in diagnostics in glaucoma. I
think we’re now able to prevent blindness in a, large number of people.
But it’s ultimately down to successful case detection. And unfortunately,
I still see patients with very advanced glaucoma. And that is as real
concern. And there was a study done in Australia, where they said that
50% of patients who are diagnosed with glaucoma had actually, seen an
eye care healthcare professional in the preceding 12 months. So, we
still need to sort of educate people and we need to train people better to
be able to detect glaucoma. And I’m very proud that in Birmingham we
are able to offer state of the art therapies and we’re very much leading
the way nationally in these, sort of new innovations.
Thank you very much.
[applause]
END OF TRANSCRIPT
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