OK, thank you, Anthony and Good morning, everyone. I don't know what part of the world you're at, but it's 8:20 in the morning where I am, so I'll just say good morning. As Anthony mentioned, I've spoken in quite a few webinars.

I think this is my 8th 1, but it is a very special one as it is honouring, a dear friend, Poyel, and I really feel honoured, to be invited to talk in this particular webinar. So the title of my talk is UVitis. It's a clinical sign, not a diagnosis.

It's a point I'll keep making again and again. When you diagnose. UVIT, you have to ask yourself what caused UVIT.

That's like haemorrhage. It's not a diagnosis, it's a sign. You see haemorrhage, you ask yourself what caused the haemorrhage, and that's a point we'll be making throughout my talk.

I want to thank Aro, the sponsor of this, meeting. I've been asked to say that I have no financial relationship with any product or service except one, so I call it financial disclosure or shameless advertising. As I mentioned, I am a co-author of this textbook alongside David Max from UC Davis and Paul Miller from Madison, Wisconsin, and many of the pictures I'll be showing today are from this text.

So our topic is UVIT, so I'll begin with just one slide of anatomy to remind us what the UVI is. The UVI is the intermediate code of the eye. Here you have the three tunics of the eye.

The outermost in blue is the connective tissue composed of cornea. The innermost one is in red is the retina, and in between them in yellow, you see the uvea consisting of the iris ciliary body and choroid, so it's really the vascular and muscular layers layer of the eye. We tend to divide the UVI into two components.

The interior UVA is composed of iris ancillary body which are intimately connected here. And then the posterior UVA, the back coat of the eye, providing blood supply to the outer retina. And therefore, when we talk about uVal inflammation or UVI, we properly speaking mean inflammation of all three components.

We're talking about inflammation of the iris ciliary body and choid. So when you say UVITs in the strictest sense of the word, we are talking about pan-UVITs or interior and posterior VITs. However, in everyday talk and everyday use, when we say UVITs, we usually talk and refer to inflammations of the iris and ciliary body.

So when we say UVITs, it's really short for anterior UVIis and you'll catch me today in my talk. Also frequently saying UVIT when they should be saying interiorities, but the point I'm trying to make is that the iris ancillary body can be inflamed together as one entity. On the other hand, the choroid is really Separate entity, in many ways, and when it, and when it is inflamed, it frequently is inflamed together with the retina simply because they are so close to one another as I showed in the previous slide.

So when we have posterior uveitis, we are really talking about poo retinitis or retina poets, inflammation involving both the retina and the. Now, as I said, VII is a clinical sign, not a diagnosis, and this is a slide that really makes a point. I always try to tell my students, this is the most important slide of my lecture, forget everything else.

In many ways, this is really the most important slide of my talk, because what it says here is that UVIT is really an immune reaction. And it involves sensitised lymphocytes and plasma cells which enter the eye, forming antibodies and cell-mediated immune reaction. And therefore, the important point to realise is that the eye is inflamed.

It's not infected in cases of uveitis, even if the primary cause of the systemic infectious disease, . We have different causes of UVIis in different parts of the world. I'll come back to that later, but for example, in my country, Ehrlichiosis, Erlichiaannis is a very common cause of UVIis.

So when we have UVIis due to Ehrlichia, it doesn't mean that the Ehrlichia reached the E, it means that the eye is inflamed as a result of a systemic response to infection with Ehrlichia. So really, if you want to think about it, UVI is really just a fancy name for lymphadenopathy. The eye is inflamed just like your pocky tail or submandibular lymph nodes.

We are seeing ocular lymph adenopathy and the The lesson to be taken here is that because we're talking about inflammation rather than infection, we should be using. Non-steroidal drugs, steroids or non-steroidals, as Alison was just talking about, rather than antibiotics. So again, uveitis may be caused by Ehrlichia, but in the eye, we do not have infection with Erlikia.

We have an inflammatory response. Therefore, the eye will not be treated for lithia. The eye will be treated for the secondary inflammation.

So if we are saying that the I or UVI is really an ocular lymph adenopathy. Stop to think about possible causes, and you'll realise that just about any disease can cause UVitis, whether it's a new plastic disease, a new mediated, any sort of infectious disease, including bacterial and protosol and fungal and viral and parasitic, and a drug toxicity, etc. Etc.

Cause again, UVIT is a lymphadenopathy and anything that causes lymphadenopathy anywhere in the body can cause UVI in the eye as well. So you're not really expected to remember every disease listed here, but realise that really just about any systemic canine disease will, may cause UVI. In cats, the list is somewhat shorter and in cats when we have UVITs, our four primary suspects are three viral diseases FIV, FELV, and FIP as well as toxoplasmosis.

If you're in North America, fungal diseases are also very high on your list. I'll come back to really what is endemic in your area. But unfortunately, in both dogs and cats, many, many cases go undiagnosed, many, many cases are reallyathic UVIT, and only 40 to 70% of cases do we actually find the primary systemic disease causing UVIT and obviously that affects the prognosis and .

The chances for successful treatment, if we didn't identify the primary cause, we are unable to treat it. Looking at some specific causes, bilateral UVITs is frequently caused by systemic infectious diseases and as I said, always ask yourself what's Endemic in your area, so it may be early, it may be fungal disease, it may be Imania, all depends on what parts of the world you're practising in. So here is a paper from Greece that I co-authored, showing the prevalence of Early chiosis as a cause of UBIT and we'll get back to this other paper later, always think of what's endemic as a possible cause and inh as I said, think about, toxoplasma, FIP, FELV, and FIV.

However, as I said, it's a lymph adenopathy, so it's not necessarily always a systemic infectious disease. Any disease that breaks down the blood aqueous barrier will may has a potential of causing uveitis, be, be it a metabolic disease such as diabetes or hyper. Or inflammation or infection of distant organs.

Here is a paper on pyometra as a cause of UBI. Then please remember this sentence here. UVitis is really a lymphhadenopathy, especially when talking about bilateral UVIT.

In cases of unilateral UVI, we have to think about a few specific causes. First and foremost, corneal ulcer. That's because there is a neuronal feedback loop leading from the trigeminal sensory nerve in the cornea back to the ciliary body, and every trauma to the cornea can result in incessant spasms of the ciliary body muscle and the iris and that results in rather painful UVI because the Unending spasms of the ciliary body really cause lots of lactate acid buildup in the tissue and a very painful inflammation.

You can see an example here. You've got a very small corneal ulcer. You'd see the marked meiosis as The response of what we call this reflex uveitis due to a corneal ulcer.

In fact, any corneal trauma, be the perforating wound, cat claw thorns, or you as surgeons, anyone touching the cornea will cause this reflex uveitis. Another important differential for unilateral UVITs is neoplasia, and I want you to consider UVITs in any unilateral, sorry, consider neoplasia as a cause in any cases of unilateral UVITs or unilate. From glaucoma in an elderly patient.

That's what we are seeing here, a cat with lymphoma. You can see that the iris is obviously abnormal. You can see that the pupil shape is distorted.

This is a case of UV lymphoma. So again, unilateral UVis in an elderly patient is considered a neoplasia. So corneal ulcers may cause unilateral UVI neoplasia may cause unilateral UVI.

And another important entity that I'll mention very briefly is lens-induced UVIT, which is an immune reaction against lens protein. We have mature. Or high premature or rupture of the lens capsule.

The pathogenesis here is that when you look back at embryological development, the capsule of the lens forms before the immune system is formed in dogs, and therefore, the canine immune system never gets exposed to the lens protein. And as a result, when lens protein leak out, and you see some leakage here from the capsule and background of the iris, when such leakage occurs, really this protein is a foreign body as far as the immune system is concerned because it was never exposed to it and you get severe UVitis as a result, greatly complicating our lives when we Cataract surgery. Thankfully in humans it is not a problem because the immune system is formed before lens capsule is formed.

Therefore, in humans, lens protein is not considered a foreign body, and if you or anyone in your family has to go undergo cataract surgery, it's a much simpler procedure because there is less secondary UVIs. Moving on from causes to clinical signs of UVITs, a very important sign is reduced intraocular pressure. And this is a sign that surprises people because when you think that there is UVI or inflammation, you obviously think there is leakage from blood vessels and you'd expect the pressure in the eye to go up.

And you are correct, there is leakage. And I'll come back to this point very soon. There is leakage of fluid and cells from blood vessels in the UVA during UVI test, but at the same time, there is also increased drainage of aqueas from the eye.

Alison in her previous talk mentioned the unconventional outflow pathway and indeed, there is an increase in unconventional outflow in UVI because of the prostaglandins that you mentioned in your talk. And as a result, yes, there is some leakage into the eye, but there is also increased drainage and therefore, the end result is that pressure is reduced. UVI also causes discomfort which may be expresses the first spasm or elevation of the third eyelid as you are seeing here, and this discomfort or pain is due to the spasms of the sidiary body that I mentioned earlier.

As I said, UBI is associated with spasms of the iris and ancillary body, so it does cause pain and discomfort due to buildup of lactate, and it causes meiosis, another prominent sign that you can see here in the left eye of this dog. Another very common sign that we see in interior is the so-called red eye. The red eye is due not to congestion of quantumival blood vessels, which is a mistake that students often make.

The vessels, as you can see. Here are very superficial. The red eye in uveitis is due to congestion of deeper blood vessels, be they the epicleral blood vessels or the interior ciliary vessels, and you get this diffused red flash or the famous red eye.

The red eye is a sign of uveitis and obviously blue eye is a sign of uveitis. Blue eye caused by corneal edoema. The corneal edoema is due to dysfunction of the inner layer of the cornea, the corneal endothelium, which is responsible for maintaining the cornea in a dehydrated state.

Unfortunately, during UVITs, the composition of the aqueous humour changes as you'll see in a minute, and when that changes, the corneal endothelium loses its metabolic support cause the aqueous humour is responsible for metabolic support of the inner or of the inner cornea and corneal endothelium. Furthermore, in UVI, you have lots of inflammatory debris and material. Floating in the interior chamber and a lot of it causes trauma to the endothelium, so be it from loss of metabolic support or trauma to the endothelium, both will result in endothelial dysfunction and the famous blue eye due to corneal edoema.

UVI, the iris is inflamed, so just like any other inflamed organ, you'll see a swollen iris, a dark iris, such as you're seeing in this picture, you'll see congested blood vessels on surface of the iris, such as you're seeing here. And again, just like in And inflammation, they may leak, so you may see here on the surface of the iris, which is what you're seeing on this picture, or if the bleeding is more massive, you actually get hyema. This picture here showing the presence of blood in the interior chamber.

And we always tend to talk about dogs, so just to remind us that all of the signs that I just mentioned and also being seen in cats. So here we have obvious UVITs in the left eye. You can see how much darker the left eye is as a result of the inflammation.

Here we can see the red eye that I mentioned. Here we can see the the blue eye that I mentioned. And these two pictures go back to what I said that really UVI is a lymph adenopathy, and if you take a close look at both these eyes, you can actually see the lymphatic nodules on the surface of the iris.

Here they are on this eye, here they are on this eye. So again, UVIis is a lymphopathy. I've mentioned several times that during UVIis we have leakage of inflammatory material into the into the aqueous tumour, the inflammatory material may be platelets, it may be green, it may be white blood cells, and we can see this inflammatory material in the aqueous tumour.

As a quiz flare, which is another very sensitive sign for your VITs, and the analogy that I like to give, to help people understand what aquez flare is when think of driving in your car at night. Now, if you're driving at night and you're Turn on your headlights. The headlights, our beams are very well focused.

They are very well defined, and they illuminate the road in front of you. However, if you're driving in a foggy night or a rainy night, then the car headlights become diffused because the beams of light are striking the water droplets in the fog or in the rain, and they are scattered and therefore your car headlights are unfocused, they are diffused. The exact same thing happens in the eye.

This eye here is a normal eye. Non-inflamed eye. We are shining a narrow slit of light on the eye, and we can see it here on the corneal surface.

We can see it here reflected on structures inside the eye on the lens and on the face of the iris. And in between these two reflections. We have the interior chamber between the cornea and the iris.

Here is the interior chamber. It is clear and therefore it is dark. Move on to this eye, which is an inflamed eye, and again, you have the.

Lit the beam of light on the cornea and here even on the surface of the third eyelid. You have the reflection of the beam inside the eye once again on the surface of the lens and the iris, but everything here is scattered. This is the aqueous humour.

It's inflamed aqueous humour and therefore then all the inflammatory. Particles, platelets and the white blood cells are causing scattering of this beam of light just like your car headlights scattered in foggy night. So a non-inflamed eye, the aqueous humour is transparent and therefore this is dark, inflamed eye, the aqueous humour is full of inflammatory components and therefore you get this infused material.

Even if you don't have a slit lamp, you may get the same effect with your directophthalmoscope using the smallest aperture on your direct ophthalmoscope, you will see a transparent interior chamber an aquium or a non-inflamed eye, and you will see the foggy or murky, interior chamber in the inflamed eye due to scattering of light. Mhm. I gave this talk in China a few months ago, and after talking about UVI, we went to have dinner and we had beer, and one of us was having filtered beer and the other person was having unfiltered beer, and then my Chinese host looks at me and says, Well, here is your aqueous humour.

You've got Filtered beer here on the left, which is transparent. There is no particles. The unfiltered beer obviously full of particles, it's much more pure.

So, this may be an easier analogy for you to remember, transparent aqueous humour and I'll just to philtre beer and the inflamed aqueous humour analogous to the unfiltered beer. All the inflammatory material that's floating in your ear or in your eye, or in your patient's eye can eventually sink. It may sink on the interior lens capsule, and that's what we're seeing here in this picture of the horse.

You see that the pupil here is fully dilated and there is really just a small area up here of transparent lens. All the rest of the lens looks very dirty, and that's because all of the inflammatory material has stuck onto the interior lens capsule. A very important picture I'll come back to later, because it may result in a.

Of UVITs, it may adhere to the inner aspect of the cornea, which is what we're seeing here. We call it curatic precipitates or if there is enough of it, it will sink to the bottom of the interior chamber, forming a hypopion in this raptor that you are seeing here. And again some pictures showing various degrees of inflammatory materials.

So here are two large clots of fibrin on top. Both of them have some blood in it as well as you can see. There is a large blood clot or a femur here in both of these pictures.

We have inflammatory material adhered to the inner surface of the cornea. So whenever you see a dirty looking cornea, think that it may be carot precipitates. Here we have both carotic precipitates and inflammatory material on the lens capsule as well.

This inflammatory material on the lens capsule really is a potential cause of one of the greatest dangers of UVITs, and that is posterior sinicia or adhesions between the iris and the interior capsule of the lens. And to explain interior yicia, I take you back to this picture I showed a couple of minutes ago. Again, this is an inflamed equine eye.

There is a bit of clear lens. Here, all of the rest of the lens is coated with inflammatory material. It's coated with platelets, with fibrine, with white blood cells.

It's really coated with glue. This is sticky material covering the interior aspect of the lens. And as I mentioned earlier, UVitis is characterised by meiosis.

These pupil may constrict, and if it constricts, you have iris come in contact with glue on the interior lens capsule. The two will stick to each other, and this is a consequence. Here we have an iris that was adhered to the lens.

It was eventually pulled off the lens, but you can see how much iris tissue is left on the surface of the lens. And thisation between the iris and the lens terrifies us ophthalmologists because it may lead to secondary glaucoma. Here we go back to the physiology of aqueous sums.

Produced in the ciliary processes back here. It's supposed to flow from the back of the eye through the pupil to the interior chamber, but if the iris isn't here to the lens, then the aqueous cannot make its way through the pupil. It builds up in the back part of the eye.

Causing really the Irish to bow forward. That's what you're seeing here, even though it's a two dimensional picture, you can see how the Irish is Iris is pushed forward due to pressure in the back of the eye. It's here and here.

We call this Irish Bombay leading to elevated intraocular pressure and glaucoma and of course we can get glaucoma due to UVITs or also because of obstruction of the dra er the corneal drainage angle, by white blood cells. Additional complications of UVITs include cataracts. That's because the lens relies on, aquiumal for metabolic support.

So cataract is a complication. There is some difference between dogs and cats. As I mentioned, in dogs, cataracts is a common cause of you.

Due to the lensing UVITs. On the other hand, in cats, cataracts are a common complication of UVITs due to, the loss of metabolic support by the equium or, so there is a chicken or egg, question here different for the different species. And indeed in feline UVITs, we see lots of complications, cataracts, as I said, in 20 up to 1/3 of cases, secondary glaucoma in up to 50% of cases, retinal atrophy in 70% or more of the cases.

So really, whenever you see cataract, glaucoma, or retinal atrophy in cats, please think UVITs, please do the required workup. While in dogs, if you think about it, cataracts, glaucoma, and rectal atrophy are really retinal disease, inherited diseases. So a very important difference between dogs and cats.

And another example of the sentence we say a cat is not a small dog. Our clinical approach to many diseases in cats and dogs should be completely different. And here is an example.

These are secondary complications of UTI in cats. I work up, these are primary inherited disease diseases in many dogs. And in the inflammation lasts long enough, then eventually the eye will undergo atrophy and we have what's called fissbbie.

You can see here the obviously small cornea and the third eyelid conduct passively cover the shrunken. I've spoken about signs of interior uveitis, a bit about posterior uveitis. Again, people, tend to forget that the, choroid may also be inflamed and choroid is also a part of the UVR, but as I said, choroidal inflammations often go hand in hand with retinal inflammations such as you're seeing here, which is why posterior veitis is also called poo retinitis.

And the eye is a unique organ in that you can see signs of inflammation non-invasively, and nowhere is it more obvious than in the retina or the fundus. So just like any other organ when you have an inflammation of the retina, you will have leakage of exudate or transudate from blood. Vessels in the eye you can actually see it surrounding blood vessels.

You can see this here we call it revascular cuffing. It's really a puff around blood vessels. You can also see how if you follow these blood vessels, it is prominent here and then you lose it here because there is exudate leaking at this spot.

All this leakage of material makes the tapetum hyporeflective because if there is inflammatory material or transodate or exudate or edoema in the inflamed retina, then the epitum behind the retina is less reflective, so you have a large area of hyporeflectivity here, a smaller area of hyper hyporeflectivity in this eye. Not only do we have leakage of transodate and exudate, we may also have leakage of blood, so we will have massive bleeding that you are seeing here or smaller era that you are seeing here, rettal haemorrhage is another sign. Most of this leakage, be it of blood or inflammatory material, or transodate or exudate originates in the thyroid and it may.

Cause retinal detachment because this fluid leaking out of the choroid actually pushes the retina away from the surface of the choroid. So retinal detachment, which we are seeing here is this grey curtain floating behind the iris with blood vessels on it, some bleeding here as well. Here is a smaller detachment, but you can Understand that leakage from underlying tissue from the choroid into the subvertin space would cause this clinical picture.

Inflammations subside and in the choroid, we can actually see the scars resulting from retinal inflammations, and that's what you are seeing with these lesions here. Note that we have areas of focal hyper reflectivity in these pictures. And these focal areas of hyperreflectivity, tell us that there used to be rein.

Inflammation here and when the inflammation subsided, we had retinal atrophy in formerly inflamed areas and these seem as areas of hyper reflectivity. Note that in the centre of each lesion we have a dark lump. This lump is Actually a clump of RPD cells like pigment of cells that act as fibrocytes in the eye.

So whenever you have inflammation, these the retinal pigmented migrates to the area and performing its role to take care of the inflammatory debris. And here is a dog where we were actually able to catch in the same dog. You can see it's the same dog due to the vascular pattern.

We were able to document an active inflammation and an inactive inflammation or retinal scar. So here is the active stage. You can see that the borders are fuzzy, still defined, and there is an area of hypo reflectivity here.

Once the inflammation subsided, this formerly inflamed area is now atrophied and hyporeflectivity became hyperreflectivity and in both cases, you have the clump of hagocytic retinal pigment epithelium. Picture, with a more massive scar, a huge scar here, large area of hyper activity with lots of RPE clamping. The RPE migrated from the, non-type area and therefore in the non-typetal area we may get this appearance of what we call a mottled non-typetal sort of resembling marble, if you will, and that's because the RPE migrated from here, to here.

So now that we know what are the clinical signs of UVITs, we can move on to. The diagnosis and the point that I made in the first slide is that again UVIT is a clinical sign. It's not a diagnosis.

So when you determine that an eye has UVIT. We have to look for what we have to ask ourselves what caused the UVIT. So look for a systemic cause by taking a thorough history, performing a comprehensive physical exam, do your basic blood work, complete blood count, chemistry, and depending on the results, you may do serology or molecular testing for infectious organisms, urin analysis, imaging in some cases.

You, if you're really desperate, you may consider even aqueous par synthesis, which should be done by a specialist and submitting the samples for serology or cytology, because again, you do have to look for a systemic cause. And here are two papers demonstrating this. This is a paper out of Purdue University looking at 55 cases of UVI.

Look at the number of idiopathic cases of UVITs. I said previously, 30 to 60% of them may be idiopathic. Here it was even a larger proportion, so large number of idiopathic cases despite the comprehensive workup that was done if you read the paper.

14 or 55 were infectious. 111 of these were blastomycosis. Again, it goes back to the question of what's endemic in your area.

Maybe you don't have blastomycosis for me it would be Elikia. We have different diseases. Countries, 5 cases, so, of VKH or Uval dermatological syndrome and 2 cases of lymphoma, so it's supposed to obviously 55 here, not 44.

In cats, they said your main culprits are toxoplasma. FIP FIV FLV and this was shown in this study from North Carolina State University looking at 120 cats with UVITs, neoplasia again, something you have to consider in every animal with the elderly animal with unilateral UVITs and look at a large number of cases of UVITs. So going back to treatment, as I said, we don't treat, we first try to diagnose the primary cause and if we were fortunate enough to find one, we treat the primary cause and then because the eye is inflamed, we provide it with anti-inflammatory treatment.

Alison Gro, my previous, the previous speaker, gave a very nice. Introduction so I can be brief here, but we're talking about topical and or systemic anti-inflammatory drugs. It all depends on the severity of UVIT.

Some of them may be treated topically. If it's more severe, you have to go, with the systemic crowd, but obviously when talking about systemic medications, you have to consider the systemic condition of the patient. As I said, this may be, Cat with FIP or FLV or a dog with blastomycosis.

So obviously you have to take that into consideration. If you are seeing posterioritis, topical treatment probably will not suffice. The drugs will not and topical drugs will not reach the posterior segment.

You do have to go with systemic drugs as long as it is safe. But the point here, again, anti-inflammatory treatment is symptomatic treatment. Please try to find.

So people often know that yes, we have to give anti-inflammatory drugs in cases with UVITs, unfortunately, many people forget a critical component of treatment and that's atropine. And really I think I'd be a very rich person if, I had $10 for every UVI case I saw that was treated successfully, but the eye was lost because the vet who got to give atrophy. Why do we give atropy?

Number one, it's very analgesic. I mentioned that UV, has, is characterised by spasms of the ciliary body. These are very painful.

Give a drop of atropine, you paralyse this muscle and you bring immediate relief. My patients usually don't come to me with feedback about the treatment I gave them. They don't tell me it helped or didn't help, but talk to a person who had UVIs and they will tell you that atropine is really very, very energetic, bringing immediate relief from pain.

So analgesia is important, but second critical, reason for giving atropine is metriassis. Going back a third time to this picture here, we have a lens covered with lots of inflammatory debris. We have the interior lens capsule really smeared with glue, with platelets, with white blood cells, with fibrin.

The iris is meiotic. The iris will adhere. To the lens causing serious initia and secondary glaucoma unless you dilate the pupil.

So you will lose this eye if you don't dilate the pupil, you will lose it to secondary glaucoma. How much atropine do we give? Well, the eye is a wonderful organ, because the pupil will tell you exactly how much atropine to give and whether you're given enough or not.

So I usually begin with twice daily and I check the, whether the pupil is dilated or not. If it didn't, I'll go. Up to 3 times daily or 4 times daily.

I'll do whatever it takes to dilate these pupil and get the iris away from, the surface of the lens. If the pupil dilated, then you can decrease the atropy into once daily or every other day. The pupil will tell you whether or not you're given enough.

Please, won't give atropine. Remember the side effects. Colic, more concerned if you're an equine practitioners, always amazes me that I can kill a 500 kg horse with a few drops of atropine.

So do your colic watch. Remember we are talking about the parasy pathholytic drug that may reduce tear production. So if it's a dog, from that is susceptible to dry eye, check your production before starting, treatment.

You may also get other parasympathholytics toxicity, vomiting, diarrhoea, etc. Etc. And surprising side effect in cats, this massive salivation that you're seeing here, and I think it's a surprising complication because I just said that.

Atropine is parasympathlytic and which reduces secretion, so we don't expect to see salvation as a result of . Atropine, but in fact it's not a neurogenic effect. It's a reaction of the cat to the bitter taste of atropine.

You put a drop of atropine in the eye, it makes its way down the nasolacrimal duct to the mouth, and the cats react to the bitter taste of atropine with massive salvation. And when I say massive, I mean that. Whenever I want to send a cat home with atropine, I would always put a drop of the drug in the clinic so the cat salivates and tell the owners, see, that's OK, nothing to worry about.

It's normal reaction to taste. If you don't do this demonstration, you send the cat home on top atropine. I guarantee that.

Guarantee you that within 2 hours you'll get the first phone call from the owner who will claim that you're killing his cat with the drug that you gave him. It's really very, very scary. If you have access to atropine ointment, that may be a preferable option or tropekommide and other powers is weaker than, atropine.

And a final component again and again I go of treatment is injections of tissue plasmic and activator. I go back to the fibrine that's floating in the chamber that always scares me because it may cause the posterior sinicia. It is possible to break down the fibrine with an intraocular injection of tissue plasminogen activator going back to your clotting cascade.

So plasmigen activator producing plas. Mean which breaks down the brain. This is usually found in specialty practises and you may wish to refer the patient for that.

Here is, here are two pictures showing the wonderful, effect of TPA injection. Here is a very inflamed eye in a hat. You barely see the iris, the pupil is invisible.

There is a large clot here. 4 hours, same I, 4 hours after TPA injection. Look at the difference.

It's a wonderful drug because as I said, it works within a few hours. There's no need to send the patient home and think about, and hope that it works. And finally, in the way of treatment.

If it's, if the UVitis is caused by lensing UVIis, you may consider referring the patient for cataract surgery. And as I said, glaucoma is a frequent complication of UVITs, so in some cases you may consider prophylactic glaucoma treatment. Prognosis guarded due to the large percentage of idiopathic cases.

I'm going back here to the study I showed you earlier from Purdue University. There was no improvement or deterioration in 28% of cases early. 5% of dogs lost eye lost vision in one or both eyes.

You may remember that they had a huge proportion of idiopathic cases, and again, the numbers I showed you before of the high prevalence of cataracts, secondary glaucoma in blood. So to wrap up my talk, please consider UVITs in every case of corneal edoema, loss of aqueous humour transparency, or change of colour in the iris, your symbol of that in the left eye of this kitty here. Consider UVIis as the primary cause of blindness or glaucoma in cats.

Search for a systemic cause, consider neoplasia in unilateral UVIis in elderly patients, but remember that often you will not find a primary cause. Many cases are idiopathic. Treat the primary cause if you find, found it.

And treat the eye with topical and systemic, anti-inflammatory drugs. Please, please don't forget your atropine. And finally, please remember that these red eyes, yes, they may be UVI, but they may also be glaucoma, they may also be conjunctivitis.

Here are three red eyes, each of them a different disease. I'll give you a couple of seconds to look at them. But they are glaucoma, uitis, and conjunctiviti, so you have to think of this ruleouts.

Again, I thank the sponsors of this meeting, and again, I am honoured to take part in this memorial to Doctor Mel. I glad to take your questions. Thank you, Ron, that was really excellent.

UVI is obviously, you know, a big, big problem. In ophthalmology practise. Just interested with the neoplasia is it in the cat is that mainly lymphoma and melanoma or what what tumours do you tend to see in the eye?

OK, just like a new organ, that that's a very good question. Thank you. You know, just like any organ, the eye may be affected by primary tumours or secondary tumours, and primary, as you pointed out, would be melanoma, and melanoma, diffuse iris melanoma is very bad news in a cat, not so bad in a dog, where it's a far less aggressive tumour.

And if it's a Secondary tumour metastasizing from other systems and organs, and yes, you are right, lymphoma is the most common intraocular secondary secondary intraocular tumour that we see in our patients. And in fact, the eye is the most common target organ of lymphatic tumours outside the lymphatic system. More of them arrive in the eye than in any other organ.

That's great, thanks, Ron. Just to obviously let people know, we're gonna have a break after this, but come back at 8 o'clock British time. I know many of you listening in different parts of the world.

And there'll be a nursing stream, there'll be a stream on exotics and also a stream on orthopaedics, which is case related on the the falling. So do, you know, come back for that. Obviously, we've run this conference for about 6 years now.

I think the number, I was just looking at the number yesterday, so it may have gone up slightly, but we've got over 6000 delegates registered from 97 countries. So, Ron, Israel as well, a few people from Israel, which is great to see. It's really about this session is, is, you know, for the vets in, in Australia and New Zealand, and also in America and Canada.

Is this something that you want us to do again? Are these sessions useful? There will be a survey at the end.

You know, do leave your comments there, but also feel free to email me at Antony at the webinar vet with any comments. Do add in things in social media and, and tag us in those so that we can continue the conversation. And, you know, hopefully we'll we'll continue to see you on the webinars.

I think I will be going off to bed shortly for a few hours, cos I've not really been to bed. But I will be coming back on, for the keynote that we're doing today, Ron, is all about, . The scourge of plastic in the oceans.

Obviously it's become a real topical thing with one of our famous presenters, David Attenborough was, was doing a lot on Blue Planet about the, the effects of plastic, enormous amount of getting thrown in. The ocean, you know, obviously that's government responsibility, but we have our own personal responsibility for that, you know, how often do we use plastic bottles? Can we reduce that, you know, all the things that we can do.

You were talking to someone who's very fanatic about recycling. Mm, no, it's, well, it's just so important, isn't it, Ron, and I, I'm probably the same, so we, we, no doubt when we meet next time, we can, we can discuss how we can. Save the planet, but it is, it, it's such an important topic, isn't it?

So, and I think if vets aren't interested in it, you know, the fact that animals are dying in the oceans because they're swallowing plastic bags, whales or getting caught in, you know, beer cans or whatever, or beer can holders. It's a real responsibility and, and if vets aren't leading the way, then, then who is going to. So I hope that many of you will come to that special session, which is going to be at 11 o'clock, and all being well, if I wake up, I will be, I will be chairing that as well.

So do go over to the webinar vet site. Obviously there's a link for the virtual congress. You can see what the programme is.

Some of you may be going off to bed if you're in Australia or New Zealand, so, you know, we'll get to those, but everything is recorded. You do get access to the programme for a year. So you've got plenty of time to have a look at at stuff.

But . Have we got any questions for, for Ron, I think there's a couple that have come through. I also just mentioning the virtual goody bag.

So if you look in the chat box, we've put in, a link to the virtual goody bag where there are some offers from the various sponsors. Obviously, thank you to the sponsor today for sponsoring this, this session. And, let me just see on the questions and answers.

No questions, oh, now let me just see, there might be just . Oh, Mink is saying, thank you so much, oh God bless Doctor Pip. We will all miss him, but the good memories will stay with us forever, .

Minka, I know, I used to listen to quite a lot of the webinars that Pip did as well, and it's based over in California, but she said er great presentation, to you, Ron. Thank you. OK.

So, there doesn't seem to be any more questions there. Ron, as always, I always love listening to you speak. The, the slides are amazing as well.

And I think ophthalmology is one of those very, visual. Subjects, if you don't teach with slides, it becomes incredibly difficult. I, I remember when I was at university that the professor used to just draw pictures on the board, which I never really knew was he talking about corneas, retinas or lenses or whatever, and it left me rather confused at the end of my, at the end of my training.

These pictures were amazing, and I've, I, I feel that I've grown in my understanding of what is a very challenging area, that you're dealing with, presumably most days it is a condition that you see commonly, isn't it? Oh, yes, definitely. So Ron, thanks again.

Hopefully I might see you at the at the Plastics, but otherwise do have a look at that recording when it comes through and looking forward to seeing everybody else on the webinars shortly. Take care. Good morning.

Good morning, good afternoon, good night or whatever, Ron, you're quite right, thanks again and thanks everyone. Bye bye, thank you.