OK, hello, everyone. In this talk, we'll be discussing glaucoma. I can call the talk glaucoma my nemesis cause it is really a very, very frustrating disease to diagnose and to treat as you probably know.
I also call the talk so much pressure, I guess that pertains both to the eye, which is under pressure and to the veterinarian who experiences lots of pressure when diagnosing glaucoma. But hopefully, by the end of the talk, you'll have a better idea of what to do with your glaucoma patients. As always, I start with a couple of slides reminding us of the underlying anatomy and physiology of the disease we'll be talking about.
So, just to take us quickly through the dynamics of aqueous humour. Aqueous humour is produced actually from the blood that flows through the ciliary body here. It's extracted from the blood by filtration.
A process that is mediated by carbonic anhydraz enzyme. This is an important point. We'll come back to when we discuss treatment.
Diffusion and active transport also take part in the production of aqueous. Then it clicks into this very small space between the ciliary body and the iris, we call it the posterior chamber. And through the pupil.
Diffuses into the interior chamber where it circulates providing metabolic support to the lens and to the inner cornea to tissues with no vascular supply, they depend on the aquiumal for metabolic support. And eventually it exits the eye through the iridocorneal angle, the angle between the iris and the cornea. It undergoes some sort of filtration in a trabecular meshwork, getting rid of cells and, other stuff that, .
May be present in the aqueumor, you will see the mesh work in a few more slides and eventually makes its way into Venus circulation. However, as you can see here, what I've just described is the conventional outflow of aqueous, suggesting that there is also unconventional outflow. And indeed, this is what you are seeing here.
Again, we have the aqueI being produced in the ciliary body by the filtration, transport, and diffusion that I mentioned. I mentioned earlier, leaking into the posterior chamber through the pupil, but while some of it exits through the angle, the conventional outflow, some of it actually diffuses back through the ciliary body. You can see it's called the UVO scleral outflow through the ciliary body, through the sclera and out of the eye this way.
As you can see, this pathway, differs in significance between the different species. It's very insignificant in us people, more significant dogs, very significant in horses and cats, and this may actually explain why we see little glaucoma in horses and cats because even if their iridocorneal angle is clogged, they still have a safety valve which they can which significant amounts of aqueous can get out of the eye using the unconventional outflow pathway. I should say that the unconventional outflow is mediated by prostaglandins, which means that it increases in UVIT.
That explains why pressure is decreasing in UVitis cause there are lots of prostaglandins in the eye, and this is another important point that we'll come back to when we discuss treatment. So we have constant production of aqueous in the ciliary body. We have constant outflow for both the conventional and unconventional pathways and the equilibrium between the production and the drainage gives you a steady state, gives you intraocular pressure, which is usually 15 to 25 millimetres of mercury in most species.
So if IOP is the equilibrium between steady production and steady drainage, we can theorise that elevation in intraocular pressure is due either to increase production or to decrease drainage. Either one of these will increase the pressure. In fact, There are no cases of glaucoma due to increased production.
All glaucoma cases result from decreased outflow, and that is really the cause of glaucoma. Now, as clinicians, we can classify glaucoma in two different ways. The first way to classify glaucoma is based on the cause.
And based on the cause, we talk about primary glaucoma and secondary glaucoma. Primary glaucoma being genetic or inherited glaucoma. Here we have a table from my mentor Kurt Glat at the University of Florida, who published a huge survey looking at 267,000 dogs, more than a quarter of a million dogs.
We really rarely see this kind of large studies in veterinary medicine. So looking at the prevalence of glaucomonous dogs by breeds, you can see that in mixed breed dogs that theoretically don't suffer from primary glaucoma, the prevalence of the disease is about 0.71%.
Any breed that has a prevalence higher than this baseline of 0.71 should be suspected of having inherited glaucoma. Certainly when you get to breeds like the American Cocker Spaniel, the Basset hound, the Chow, the Chopei, the Boston Terrier, that have a prevalence 45678 times higher than this 0.71 baseline.
So these dogs would be suspected of having primary genetic glaucoma. Alternatively, as I said, glaucoma may be secondary, and when we say secondary, it means that it is caused by another intraocular disease, and I'll be giving a few examples in a couple of slides, and I am showing a picture of a glaucomus cat here cause in cats, most cases are indeed secondary rather than primary. An alternative way of classifying glaucoma is based on the state of the iridocorneal sorry, I, pardon me, I jumped ahead.
I, I should say that this division to primary and secondary glaucoma is not just a division for researchers or a. Edemics, it has very important clinical implications to you and it's important because if you are presented with a case of primary glaucoma, it means that the owners are looking at lifelong therapy cause like all inherited diseases, you are not gonna be able to cure the disease. And the second implication of the fact that it's primary glaucoma is that the second eye is also at risk.
It's a very important point. I'll come back to Again and again during my talk, but cases of primary inherited glaucoma don't necessarily present simultaneously with the disease in both eyes. One eye may be affected first, but if it's primary, the second one is at risk.
On the other hand, if it's a case of secondary glaucoma, it means that it may be cured if the primary problem is solved. Again, I'll give you some examples, but I can tell you, for example, we have glaucoma secondary to interior lens laxation. Remove the lens and the glaucoma has been resolved.
And more importantly or just as importantly, if it's secondary glaucoma, it means that the second eye is not at risk. So as I said, this is one way to classify glaucoma, deciding whether it's primary or secondary. The other way of classifying glaucoma is based on the state of the drainage angle.
The iridocorneal angle that I mentioned earlier, here you can see it histologically. Here is the cornea, here is the iris. So this would be the The angle between the iris and the cornea, the iridocorneal angle.
You can see that it's propped open by these ligaments here that you'll see in a minute in a living animal, and you can see here the meshwork, the filtering mesh trabecular meshwork that I mentioned earlier, that philtres the aqueous. And you can see that this is a nice open angle. There is a definite angle between the cornea and the iris, which means that if this eye developed glaucoma, it's probably due to an obstruction here in the mesh.
However, other patients may suffer from what we call angle closure glaucoma, and here you can see that the angle between the iris and the cornea is much narrower than it was here. And in this eye here, it's been completely obliterated. The iris is in contact with the cornea and there is no.
Angle. And again, this is not just an academic or a scientific or research classification. It's also very important for us as clinicians because as I'll show you in a minute, I can actually look at the angle and examine the angle in a living animal and I can see whether it's open, whether it's narrow, whether it's shut, and that would help me determine if the eye is in.
At risk or not. So here we have a diagram of the two types of glaucoma, again ciliary body where the aqueous is produced, flowing through the posterior chamber and the pupil and being drained through an open. And iridocorneal angle into the trabecular meshwork and here you can see angle closure glaucoma, the aqueous cannot drain out of the irido corneal angle which has narrowed significantly.
Now, it's important to realise that the Two classification methods, primary, secondary, open angle, close angle, they are not mutually exclusive, they are actually complementing each other so you can have all four possible combinations primary open, primary angle closure, secondary. Open secondary angle closure and here I'll give you just one example of probably the most common type of inherited glaucoma, primary angle closure glaucoma. So primary.
Means that we are looking at inherited glaucoma. Angle closure means that the angle between the iris and the cornea has significantly narrowed. And as I said, this is the most common type of inherited glaucoma in dogs, and people I should say it would be primary opening glaucoma, but in dogs, it's a disease.
We see many spaniel breeds, retriever breeds in the chow, and as I suggested earlier, the primary angle closure glaucoma are frequently unilateral. The disease frequently presents initially as a unilateral disease with the second eye affected an average of 8 months later. And another thing that characterises primary angle closure glaucoma is very, very acute and painful attacks.
And when I say acute and painful, the owners went to work in the morning, Everything was fine. They come back home in the evening and they find a com lethargic dog, extremely painful. Eye is shut.
They run to the vet who diagnoses an edematous and blind eye, as you can see here. The attack may be treated. We'll talk about treatment.
You may be able to lower the intraocular pressure and vision will be regained, but again, it's inherited disease, so the Animal is likely to suffer from repeated attacks and every time more and more of the retina gets damaged until eventually you are faced with a blind and painful eye, unresponsive to treatment. So this is one example of typical inherited glaucoma. Looking at secondary glaucoma, it may be due to lens taxation, as I mentioned earlier.
Obviously, if you have a case of interior lens taxation with The lens sitting in the interior chamber, you can imagine that such a large lens in the interior chamber obviously disrupts aqueous drainage and aqueous circulation in the interior chamber, but even If you have a case of posterior lens taxation, which is what we're seeing here, that could also cause glaucoma cause the lens when it's in s is actually a barrier preventing vitreous from migrating forward. Once the lens. Has shifted, we have what we call here an ahaic crescent, this crescent area through where there is no lens, and now through this area vitreous can diffuse from the back of the eye to the interior chamber and clog the angle.
So we've just explained how both. Anterior and posterior lens laxation may cause glaucoma, but look at the asterisks here. They may also be caused by glaucoma cause in glaucoma we have, if you're watching the camera with thalus, the eye stretches, the zonal stretch, and .
The soul tear leading to lens laxation. So when presented with a gluonto eye and lens fixation, sometimes you don't know which is the chicken and which is the egg. Did glaucoma cause lensation or did lens taxation cause glaucoma as we've just seen?
Another common cause of secondary glaucoma is Uveitis. Again, in uveitis, you have lots of inflammatory material in the A consumer, you've got cells and proteins and platelets and fibr and obviously that would obstruct the drainage angle, which would clog it up, it would clog up the trabecular meshwork that I mentioned earlier, but it can also promote posterior sinicia adhesions between the iris and the lens, and that's because the Inflammatory material in the aqueous humour is very sticky material. As I said, it's platelets and it's fibrine and if it covers the lens, the iris will stick to the lens thereby not allowing aqueous to drain from the posterior chamber into the interior chamber.
You can See that the Irish is really pushed forward in this picture, and you can see here, even though it's a two-dimensional picture, how this iris is being pushed forward, that's because the Irish margin here at the pupillary margin is adhered to the lens, posterior sychia and Iris Bombay leading to elevated pressure in the posterior part of the eye. And the third and final leading cause of secondary glaucoma is neoplasia. Here we have a cat with diffuse iris melanoma and you can see that it led to secondary glaucoma and in every elderly patient with secondary glaucoma or with sorry, with unilateral glaucoma or with unilateral uveitis, please consider neoplasia.
So how, now that we know what causes glaucoma, how do we actually diagnose the disease? Well, the gold standard is obviously tonometry or measurement of intraocular pressure. When measuring pressure, please make sure you pressure, you measure it in both eyes, because significant differences between eyes are suspicious.
I said earlier that the normal pressure would be 15 and 25, between 15 and 2. 5 millimetres of mercury, but suppose you measure a pressure of 12 in one eye, 24 in the other eye, they're both normal or close to normal, but you really need to ask yourself why is there a difference of 100% between the two eyes. And one reason for that may be UVI in the background.
I said earlier when I talked about the unconventional outflow that it increases in UVIis due to the secretion of Pro glandins to the aqueous humour and UVI, eyes with UVIis are characterised by low intraocular pressure. Typically we measure pressure of 456 millimetres of mercury in an I with uveitis. If you have an eye with active UVI and you measure a pressure of let's say, 2020 is theoretically normal, but not in an eye with UV.
As I said, in I with UVIs, the pressure should be about 5. So if you have a normal pressure of 20 in an I with UVI, it's suspicious cause maybe the hyper. A hypotensive effect of glow UVitis is masking the hypertensive effect of glaucoma.
A couple more points about tometry. Please make sure that your assistant or the owner or whoever is restraining the dog is not applying pressure to the jugular veins. As I mentioned earlier, aqueous eventually makes its way to Venous circulation when it gets out of the eye, so.
Pressure on the venous vein will elevate intraocular pressure and in fact, in, people, neck ties are a risk factor for glaucoma, which is a good excuse if you don't like wearing neckties, just say, oh, I'm protecting myself against glaucoma. And finally, please use an instrument to measure intraocular pressure. Don't use your fingers.
You can do lots of things with your fingers, but measuring intraocular pressure is not one of them. Believe me, I've been doing it for 30 some years. I still cannot put my fingers on an eye and tell you what is the pressure.
You do need some sort of instrument. The basic and cheapest one is the shields, indentation tonometer, sort of unfriendly instrument, large learning curve, and, . To use it, you need the animal to cooperate, you need to convert the readings, but with experience, you can get good readings with the shields and it's It costs $100 to $150 US dollars, so no reason, no excuse why any clinic out there won't have shields, but your life will be dramatically changed and improved if you can afford one of the more modern electronications.
Or rebound tonometers, which take much more accurate readings, very user friendly, and, take several readings, give you an average pressure with statistical error error if you can afford them, that would be great. So this is one way to confirm our diagnosis following measurement of intraocular pressure, but there is another important, diagnostic test, something I alluded to earlier, gonnoscopy. Gooscopy.
Examination of the iridocorneal angle. Scopy is to look like microscopy or teloscopy or ophthalmoscopy. You're looking goo is the angle, so examining the angle and .
Corneoscopy is done by mounting a special lens on the cornea, and this lens refracts the light, bends the light so that I get an image as if I was standing in the pupil and I can visualise the angle and that is very. Useful in patients with suspected hereditary glaucoma. I write, examine the state of the angle in the unaffected eye cause it's usually difficult to examine the affected eye, usually is already with severe corneal edoema, preventing me from, seeing the corneal angle.
But as I said, the unaffected eye, which may also be suffering from inherited glaucoma, but it's 8 months, into the future, you can examine its angle and know whether it's at risk or not, and here are two, pictures depicting that. So, This would be a normal angle. Again, I'm standing in the pupil.
Here is the iris. Here is the cornea, and here is the angle between them with those ligaments that I mentioned earlier. So again, you can see the analogy in the histology.
Here is the iris. Here is the cornea above it and here is a nice angle propped open by the pectinic ligaments while here I'm standing again in the pupil. He is the iris, here is the cornea and nothing, no angle.
In between them. So looking at an eye and seeing this sort of an angle can tell me that this eye is definitely at a risk for a future attack of primary open-angle glaucoma. Obviously, this is something you'd probably need to refer your patient to a veterinary ophthalmologist cause this is a kind of exam done by a referral centre and it's a very important referral.
We'll come back to that in a few minutes. Another The test that your ophthalmologist may be able to perform is high resolution ultrasound. And when I say high resolution, I'm talking about 50 megahertz or so, and you can see that with such a high resolution ultrasound, you can image a nice open.
Cleft, that's a part of the angle versus a closed cap in this one. So this is another test that we can do. But as medicine progresses, we are now at an age where in some breeds, we can actually offer DNA testing, but in some dog breeds suffering from primary glaucoma, we've actually Uncover the mutation that causes glaucoma.
So for example, a mutation in Adams 10 causes glaucoma in the Norwegian elkhound in Adam 17, the basset breeds. So yes, you can actually send a blood sample or a chick swab to a laboratory and they would tell you whether or not the dog is suffering from primary glaucoma. Where do you send it to?
Well, here are a couple of free online resources that can help you decide whether or not glaucoma is inherited. One of them is the ECBO website which has a special section devoted to hereditary eye diseases. Just go to ECBO.eu and look for hereditary eye diseases and there is a manual listing.
The suspected or diseases that are suspected or proven to be inherited in each and every breed. So, if presented with a dog and you're wondering, jeez, does that dog have primary glaucoma or not, you can know whether the breed is suspected of having primary glaucoma or not. And Very important.
It also lists, the laboratories that test for the inherited eye disease. So again, if you're presented with a basset or a Norwegian Lhound, you can go to the ECBO website, look up Norwegian Ekhound or Basset hound, and find out which lab actually does DNA testing for that breed. A second resource which is very useful is from the United States.
This is the website. It lets you download what we call the Blue Book, which actually lists the results of all the eye exams in the USA. You can see here, just for example, the Cavalier King Charles.
They've had 43,000 dogs examined between 91 and 2013, and another 15,000 dogs. Between 2014 and 2018, so altogether 60,000 dogs and it goes on to list the findings in 60,000 King Charles cavaliers, obviously a very useful tool to tell you whether or not the disease you're seeing in King Charles is inherited or not. Note that you need the VPN cause it doesn't let you download the book if it recognises that you are outside the United States.
So, we could diagnose glaucoma based on all the methods I just mentioned, tonometry and gonioscopy and high resolution ultrasound and these online resources and genetic testing, much like any other disease, we can also diagnose it based on clinical signs. And glaucoma is rather unique that it affects each and every tissue in the eye, starting with pain. And I want to talk about a bit about pain.
It's very, very important cause pain is very evident in acute glaucoma. As I said, the owners, went to work in the morning, all was fine. They came back in the evening, they found.
The dog in extreme pain, they realise it's in pain, and if you recommend a nucleation because you tell them that the eye is blind and painful, they will usually go along with your recommendation. However, pain is less noticeable in chronic cases and often in chronic glaucoma, we are faced with a situation where the Eyes irreversibly blind. We are unable to control the pressure medically.
We recommend creation, but the owner say, hey, my dog is not painful, it's OK. It eats, it plays, it goes on walks. -huh, it's not painful.
I'm not inuccleating my dog. And the analogy that I always give them and that you might wanna use is that of migraines. People with migraines also wake up in the morning, they brush your teeth, they go to work, they come back in the evening, they have dinner, they go to a pub or a movie.
With some friends, they function, yeah, just like the dog, you know, they're eating, they're going on a walk they're playing, but they are in constant pain. They are constantly suffering and so do dogs with chronic glaucoma and when. I win the argument and I usually win the argument and I convince the owners of nucleation.
They come back 14 days later for suture removal. The first thing they'll tell me is, wow. You are right.
The dog is 5, 10 years younger. It is so much more playful. It is so much more active.
And the reason for that is that, you know, chronic glaucoma, the onset of pain was gradual. They didn't notice the gradual decrease in the quality of life of the dog and therefore they think it is not painful. Try it, try the migraine and now.
Or if you wish, just quote these studies. Here is a study from the United Kingdom, 7 dogs with bilateral nucleation. Never mind, sometimes I have troubles or convincing owners to take out one eye.
Bilateral nucleation is really very emotionally difficult for owners to accept. 90% satisfaction rate, all owners report significantly improving pain levels, facial palpation activities as I said, and quality of lives. Another study from the UK comparing behaviour of dogs before and after nucleation.
96% of participants were happy with their decision to go ahead. No one regretted their decision. So, If you can't convince them with the migrant theory, please, you can cite these studies to convince them that yes, nucleation is the right thing to do.
As I said, we have clinical signs affecting all of the ocular tissues. So we spoke about pain. The globe is affected.
Balmus, it expands as you can see in the left eye in this picture, you can Regard it as a self-defense mechanism because if you have elevated pressure in the globe and now the globe, if you're watching the camera expands, then the same amount of pressure is now divided over a larger area, so per square millimetre you have less pressure. Bufanus is more noticeable in younger patients where the sclera is more elastic and therefore, if pressure would come down, the globe may even revert back to its original size. In elderly patient, where the sclera is less elastic, it may be less noticeable and less reversible.
Red-eye, due to epicleral congestion, I mentioned that aqueous drains to venous blood circulation. It eventually makes its way to the jugular veins, but it does go through the epicleral veins. These are the epicleral veins, not to be confused with conjunctial blood vessels, which are these ones.
You can see that conjunctibral vessels are far smaller and they are branching. And they are tortuous. The epistal vessels far larger, far straighter and not branching, OK?
And here are a couple of more examples of what I call epicleral congestion in association with glaucoma. Here you can see glaucoma associated with posterior lens taxation. Not only do patients present with a red eye, they also present with a blue eye due to corneal edoema, and that's because of trauma to the corneal endothelium, the elevated pressure in the eye traumatises the inner.
Most layer of the cornea, the endothelial layer, which is responsible for keeping the cornea in a dehydrated state. When you get endothelial dysfunction due to the elevated pressure, you will get corneal edoema. Another sign that you may see in the cornea is what we call striad keratopathy, which is these white lines that you are seeing on these corneas.
I mentioned earlier bualus, the eye. Expanding as the eye expands, the cornea is stretched and what you are seeing here is really fractures in the cornea, in the innermost layers of the cornea. It's like fractures in the ground in cases of an earthquake, literal fractures in the endothelial, .
Sorry, decimates membrane and inner structures of the cornea. And when you see these lines, the striatopathy, this is really pathognomonic for glaucoma. Nothing else would cause this lesion.
Glaucoma patients, especially those with acute glaucoma, present with a fixed dilated pupils. So we've got glaucoma in the left eye of this cat. Two reasons for the fixed dilated pupil.
Number one is damage to the iris constrictor. As you know, the iris has both a dilator muscle and constrictor muscle. This diagram shows you the, the dilator muscle is a radial.
Going 360 degrees all around. The constrictor is just a small flimsy ring at the pupillary margin, so it is much more susceptible to elevated pressure and therefore you have an efferent deficit. The pupil is unable to constrict, but because of damage to the retina and optic nerve, you also have an afferent deficit, so there is no PLR due to both afferent and efferent deficits.
That's why the patient presents with a fixed and dilated pupil. As I've said, we have all tissues affected. OK.
We spoke about the globe being metalic, we spoke about the cornea, we spoke about the iris. We mentioned the lens, that may be subluxated or luxated and we said that it may be the cause of glaucoma with the lens sitting here in the interior chamber, disrupting the dynamics of aquisumor or it may be the result of glaucoma due to the stretching of the souls. And perhaps the most devastating.
The effect of glaucoma is that on the retina and the optic nerve, the elevated pressure number one causes ischemia as it reduces blood flow to the retina and you can see here the fundus of a normal dog, the fundus of a glaucometous dog, you see how attenuated the blood vessels are literally because the blood vessels are being compressed by the elevated pressure. And there is also mechanical damage. The elevated pressure causes mechanical damage both to the retina and the optic nerve, which is why we are seeing here a nice healthy, pinkish myelinated optic nerve, and here we are seeing around.
Grey looking optic nerve with no blood vessels on its surface. That's because of a phenomenon called cupping that you're seeing here. Here is a normal optic nerve head histologically due to the elevated pressure.
Pressure on this area literally compresses the optic nerve away causing optic atrophy and the blood vessels that used to be here simply disappear from the surface of the optic disc. So this is what a glaucometous fundus may look like and obviously, this damage to the retina and to the optic nerve causes progressive loss of vision and blindness. Not just in our patients, also in people, OK.
Here is a study, a rather old, it's from 2005, but telling you that bilateral blindness will be present in 4.5 million people with open-angle glaucoma and 3.9 million people with angle closure glaucoma in 2010.
And it will be over 10 million, over 11 million people in 2020. 11 million people blind in both eyes due to glaucoma. That's like more than the population of New York being blinded by glaucoma.
I always, cite these numbers to my clients telling them, listen, it's not just me who's been who's got limited resources as a veterinary ophthalmologist, take. Your patient, your dog to the leading hospital in London or Paris or wherever you may be. They are often unable to save the patient's vision.
And eventually, if the pressure lasts long enough, then it also destroys the elevated pressure. It is long-lasting. It eventually also destroys the sidiary body where aqueous is produced, a production system.
The eye atrophies and we gets bulba or an atrophy of the eye, you can see a small shrunken eye in this dog and this horse. So the end stage of glaucoma is really loss of pressure in the eye due to atrophy. We've spoken so far about canine glaucoma, a couple of words about feline glaucoma.
In dogs, as I said, it may be primary or secondary, and actually, we know that it's about fifty-fifty. Half the cases are inherited, half the cases are secondary. In cats, it is nearly always secondary.
There are very few cases of Primary inherited glaucoma, in cats, so it's usually secondary to uveitis, neoplasia, as I mentioned in every case of unilateral glaucoma in elderly patients, spec neoplasia or lens taxation. In fact, glaucoma has been reported in 28 to 50% of feline UVIis cases, the implication is that if you are presented with a cat with glaucoma, please do systemic work up for causes of UVIis cause this may very well suggest that it has UVIis due to some sort of systemic disease. It's rather more challenging to diagnose glaucoma in our feline patients.
Number one, because the history is more subtle. As I said, they don't have the primary open angular acute glaucoma. It's usually more of a gradual onset, so the owners will not notice it.
And both owners and veterinarians may have a harder time recognising the clinical signs of feline glaucoma. . Because the.
Eyelids in a cat protect the globe so well you don't see too much of the sclera or the conjunctiva, so you're unable to detect bualmus, you're unable to detect the red eye, . The retina is more resistant to pressure, so vision is maintained longer. As I said, the history is not telling.
It's not just the retina that is More resistant to pressure, so is the corneal endothelium, so the corneal edoema is milder. And when looking at the fundus, it is also more difficult to recognise fundoscopic signs of glaucoma in cats because of the appearance of a normal feline fundus. We've seen these two pictures earlier.
Normal dog glaucometous dog, normal feline, and note how similar looking the normal feline optic nervehead is to a glaucometous optic nerve head. Again, it's round, grey, with no blood vessels on its surface, so it is more challenging to diagnose. So we've discussed the pathogenesis, we've discussed the causes, we've discussed the clinical signs, and now it's time to talk about treatment.
And actually, we're talking about treatment of glaucoma, you should remember that our treatment has two aims. Number one is reducing pain, and I said pain is always there regardless of whether it's acute or chronic and prevent further damage to the retina and the optic nerve. Please note that Damage that has already occurred to the optic nerve and retina is mostly irreversible.
OK. That's why people become blinded by glaucoma. So, again, if you're presented with a dog with acute glaucoma, you will lower the pressure, vision would be regained, but some of the retina has been damaged.
Second glaucoma attack 6 months down the road. Again, you lower the pressure. Visual will be regained, but more of the retina has been lost, and that's why I say that prognosis is bad cause you lose more and more of the retina.
Eventually, the eye will become blind, but hey, that doesn't mean that we stop treating it cause we still have to consider the pain of the animal. As I've said earlier, secondary glaucoma may be cured if the primary cause is resolved. UVIis, lens taxation, treat them, and, you may have resolved the glaucoma, but primary glaucoma does require lifelong therapy, be it medical or surgical, and carries for long-term prognosis.
I usually try to tell my students, if you are to remember just one slide from my entire lecture, please remember this one. This is the most important slide in my talk. I'm gonna say that this may very well be the most important slide of my talk.
If you remember just one thing, please remember the following. As I've said time and again, primary glaucoma patients may present with unilateral disease and therefore, when in doubt, please treat the Other eye. What does that mean?
You have just been presented with this patient. And obviously, you've diagnosed glaucoma in the right eye and you treat it with this drug and that drug and the other drug. We'll talk about treatment in a minute, but let me tell you, looking at this patient, this eye is probably gonna be irreversibly blind.
You might be able to lower pressure temporarily, but I bet you that a few months down the road, you are about to remove this eye. And then All is quiet for 8 months, but 8 months from now the owner will come back and the dog is blind with glaucoma in this eye, and the owner will look at you and say, Doctor. What happened?
Could this have been prevented and you will feel awfully bad. You'll feel awfully bad. It will ruin your day, it will ruin your week because you for when this dog presented with this glaucomaous eye, you forgot that it may be primary glaucoma.
You forgot to provide prophylactic treatment to this eye, OK? So, What I'm saying is when this dog came in with the comma in the right eye, first try to determine if it's primary or secondary. You know, for example, Is there UVitis in this eye?
That means it's secondary, wonderful. This eye is not at risk. Is there a neoplasia in this eye?
Great news, you know, it's funny to say that neoplasia is great news, but yes, it's great news cause that means that this eye is not at risk. But if you are unable to prove to yourself that this eye is affected with secondary glaucoma, then either refer it to a specialist who will do goneoscopy in this eye, look at the angle, maybe high resolution ultrasound, look at the angle, know whether this eye is at risk or not. And if you have any doubt, provide prophylactic treatment to this eye.
Now, prophylactic treatment is not going to prevent glaucoma in this left eye, OK? It's an inherited glaucoma, but it is going to delay the onset of the disease by about 2 years. Studies show us, so when the owner now comes back 32 months from now, rather than 8 months from now, with a blind left.
I and looks at you and says, Doctor, could this have been prevented with a clear conscience you can say, sorry, it's inherited. We did all we could. Life sucks, you know, but you will go to bed with a clear conscience.
So please, whenever in doubt, cases of unilateral glaucoma, treat the other eye. How do we treat? Well, we can reduce intraocular pressure either by reducing production of aqueous or increasing the outflow, .
Choice of the drugs will depend on the cause of the disease. For example, prostaglandin analogues are not given in cases of UVI. If the glaucoma is secondary to UVIis cause the eye is already flooded with prostaglandin analogues, it will be pouring oil on fire.
We also don't give prostaglandin analogues in cases of glaucoma associated with interior lens laxation because we don't want to trap the laxated lens in the interior chamber. So that, these are two examples of how the cause will dictate my choice of drugs. And as I've said, prognosis for long-term management is poor, especially in primary glaucoma.
So what are the actual drugs that we are using? Well, for emergency treatment, and again emergency is those cases of acute primary narrow angular glaucoma where the owners went to work in the morning and all was fine. They come back to a painful and blind dog.
They rush to the clinic and you hook them too. An IV catheter and treat them with many intravenous magnol like a dose of 1 to 2 grammes per kilo, administered slowly over 30 minutes and withhold the water, place them in a cage without water for 3 or 4 hours so they don't rehydrate themselves. Manitol being hyper osmotic sucks the fluid out of the eye and may lower the intraocular pressure.
Or You can definitely try parasynthesis, what you're seeing here, going with the needle into the eye at the limbus. Yes, please practise first if you've never done it. Practise it on a couple of cadavers.
Patient needs to be heavily sedated or anaesthetized, but go in with the needle. 25 gauge needle. Note that there is no syringe attached.
I don't aspirate aqueous. Just let two or three drops blob bloop, drip out of the hub, and that would be enough to lower intraocular pressure. However, these are emergency treatments.
We're not sending patients home with manitol or a needle in their eye. Eventually, they do have to be treated medically and I would say that medically today we are talking about two leading drugs. Drug of choice is prostaglandin analogues which are administered.
Once or twice daily, and lots of brands out there in different countries. As I said, they would be contraindicated in cases of UBI or lungs, lung or lens laxation, but for all other cases of canine glaucoma, they are definitely my drug of choice, and Because they're so effective, we can also give them every 1530 minutes as an emergency treatment. So again, if you have that dog with acute onset of glaucoma, before, going in with a needle, you may try giving a couple of drops of prostaglandin analogues and see what happens.
My second choice, and also very effective would be topical carbonic anraz inhibitors, dorzolamide, zolamide, given 3 times daily. So the advantages actually of both of these drugs is that you can give them regardless of the state of the angle, OK? A person landing analogues who said increase the Non-conventional outflows.
So even if the angle is clogged or narrowed, they would still work. Likewise, topical carbonic anitrase inhibitors lower production cause you remember that carbonic anras is one of the key enzymes in production. So again, it will be effective regardless of the state of the angle.
And they also come in preparations that contain a beta blocker. Beta blocker reduces blood flow to the ciliary body. As I said, blood is a substrate from which aqueous is produced.
So if you give one of these combos, you're actually both lowering the amount of available substrate and inhibiting the production and really lowering intraocular pressure. In glaucom to cats. PG analogues are have more limited efficacy and therefore the topical carbonic anitras inhibitors are more commonly used, but beware that they have been associated with hypokalemia in feline species.
One drug you don't wanna give in glaucoma is atropine cause obviously atropine, narrows the angle and the way I tell my students they should remember this is atropine in glaucoma, no diploma, and this became so popular with my students that in the days of the corona, they actually made corona face masks out of it. Consider adding anti-inflammatory therapy. There are lots of indications that, inflammation also plays a role in, glaucometous damage or in the pathogenesis of.
Glaucoma in our canine patients. So start with prednisolone acetate, which has better intraocular penetration than dexamethasone. Sometimes it may cause coronal dystrophy and then you should switch to non-steroidal anti-inflammatories.
Another thing that, another group of drugs that you may consider adding is neuroprotective treatment. Neuroprotective treatment is treatment aimed not at lowering intraocular pressure as the name implies, it protects the neuronal tissue, which protects the optic nerve and protects the retina, . Lots of mechanisms out there.
I won't go into them, but basically preventing apoptosis and cell death in the retina. Here is a survey among veterinary ophthalmologists showing that 40% of respondents to the survey, do use some sort of neuroprotective, . Therapy, amlodipine, which we use to lower systemic blood pressure, is probably the most commonly used drug, as you can see here in this table, and that's because it's a calcium channel blocker and calcium channels play a role in the apoptosis of cells.
Ocuglow is also used by many of my colleagues. And as I said, most importantly, do not forget to treat the unaffected eye. What do we treat it with?
Well, you can see that different people use different drugs, to treat, the unaffected eye. There really is no consensus about it. I treat mine with a drop of topical carbonic anitraze inhibitors, but as I tell my students, you know, Have the owners even put a drop of saline or tap water?
I don't care. One of the more important aspects of this preventive treatment is that once a day, the owners really walk up to the animal and place a drop in the unaffected eye. That makes them take a close look at the unaffected eye.
They will see early corneal edoema, they will see early signs of retinal of a dilated pupil. They will come to you much earlier. Couple of work, it's about the feline glaucoma.
As I said, most cases are secondary to UVIT, so, diagnose and treat the primary cause of UVIT again, because UVIis is in the background here, you definitely want to add top systemic anti-inflammatory drugs. And you do need to consider breaking down the adhesions of the pupil in cases of Iris Bombay, maybe by tissue plasmic and activator and in this case, maybe using atropine despite what I said about it taking away the diploma. We've said earlier that Latanopo and proglandin analogues are ineffective in normal cats, maybe slightly effective in glaucoma cats, but for a short while.
Therefore, use carbonic anhydras with or without a beta blocker. If you are using beta blockers, monitor your filling patients for cardiac side effect. If you are using the carbonic anase inhibitor, be on the lookout for hypokalemia.
But eventually, many cases may have to be referred to surgery cause especially in primary glaucoma, drug medical treatment will eventually fail. You can refer to specialists and specialists also use the two approaches, either lower production or increased drainage. We can lower production by destroying partially the ciliary body using a laser.
Here you can see a laser probe, we're doing it in our, one of our patients, a laser probe applied around the eye and the energy penetrates the sclera and the Destroys the ciliary body. We go 360 degrees around the eye, applying 30 to 40 burns or some veterinary ophthalmologists even have a endolaser. You go into the eye, you actually see the ciliary processes and you shoot them as if they were dogs, ducks in a fair ground.
Or we can also increase the drainage from the eye by implanting shunts to increase out. You can see that this dog has been implanted. There is a tube sticking in the interior chamber.
Here beneath the conjunta, there is a one-way valve so aques can exit the eye but cannot flow back and actually it has very good results. Here is a paper out of Japan recording, reporting mint preservation of 58 months. Wow, that is amazing.
You wouldn't get . 5 years of successful treat medical treatment, but yes, drainage may be a highly recommended surgery. But Eventually, even with surgery, we sometimes fail and then we are faced with a blind eye and a painful eye, in which case a nucleation is the best option.
However, as you know, some owners really faint when you tell them the word nucleation. They want their pet to have two eyes, never mind that one eye is blind, that one eye is painful. They insist cause.
Metically on the dog having two eyes. So a couple of options you can offer them. One is intrascleral prosthesis whereby we open the globe at the sclera, we remove all the intraocular contents, the vitreous, the lens, the urea, inject a silicon ball, suture it back, and you can see the result.
Yeah, obviously, there is a difference between the two eyes cause this is just really An empty shell of the sclera cornea, which maintains its volume with the silicon ball, but the owners are usually happy. This is something we do only in eyes that have been blinded by primary glaucoma, obviously not if there is neoplasia or infection. There is severe post-op inflammation, but as you can see here, good long-term results, but please remember, this is a cosmetic solution for the owner.
This is not a treatment of choice for patients. This is a treatment of choice for patients. Here, we're really treating the owners.
Another way to treat the owners, sorry. Is what we call pharmacologic ablation of the ciliary body. We inject gentamicin or cidofovi into the eye.
These are cytotoxic substances, so they destroy the ciliary body. And thereby lower production. So, as I said earlier, it's the same effect as a long-term glaucoma causing disease.
Here, you're inducing disease by injecting a, a cytotoxic substance, gentamicin or ciophobia. Again, only in blind and painful eyes, only in primary glaucoma, less short-term inflammation, but There is failure contraindicated in young cats because it has been associated with sarcoid formation of a very nasty intraocular tumour. And again, remember, it's a cosmetic solution for owners, not a Treatment of choice for the patients.
But, you know, owners do care about cosmetics. The most dramatic example I've seen of that is the owner of this dog who really wanted his dog to have two eyes. So take home messages, as I've said, unless proven otherwise, inherited glaucoma should be suspected in unilateral disease and you should treat prophylactically the unaffected eye or refer it to an ophthalmologist for gononoscopy.
Remember that no matter what the owners say, chronic glaucoma is painful and the blind eye should be removed. Prostaglandin analogues, and carbonic drug inhibitors are the drugs of choice for canine glaucoma. I'm not sure about bovine glaucoma and cats with glaucoma should be worked up for cause of UVitis and treated with carbonic anitras.
So I'm going to leave you with these take home messages. Thank you very much for watching and I bid you a good day wherever you may be. Goodbye.