GP Eye Health Network: Glaucoma, Mr I Massood
TRANSCRIPTION CITY TYPING SERVICEShttPD://transcriptioncity.co.ukinfo@transcriptioncity.co.uk0208 816 8584TITLE: Presentation 2 Mr I MassoodDATE: 18th February 2017NUMBER OF SPEAKERS: 1 Numbers SpeakersTRANSCRIPT STYLE: Intelligent VerbatimFILE DURATION: 27 Minutes 3 SecTRANSCRIPTIONIST: Marg Searing SPEAKERSIM:Mr I MassoodFS:Female speakerDS:Dr StrangeAudienceGP 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.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 openangle glaucoma. There are essentially two types of glaucoma, openangle glaucoma and angleclosure glaucoma.So, in openangle 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 angleclosure looks like. So, in angleclosure, 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, 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 openangle 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 angleclosure type or an openangle 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 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 neuroophthalmic 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 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 90year 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 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 shortsighted are at increased risk of glaucoma. Patients who are very longsighted 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 timeJust 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.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.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 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 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 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 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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