Hello, everyone. My name is Ron Offrey. I'm a professor of veterinary phalmology at the Hebrew University of Jerusalem in Israel, and I'm happy to welcome you to my second webinar lecture on common eye diseases in horses.

I always start these webinars by saying that I have no relevant financial relationship with any product I'll be mentioning. This time I really mean it because I actually will be mentioning some specific products, made by specific companies, but no, I have no relationship with any of these companies and of course, I wanna thank the sponsors of this session, Bailey's Horse Feeds. So those of you who attended my previous lecture on the examination of the equine horse may remember this quote from my teacher and mentor at the University of Florida, Dennis Brooks, and you can see here, who says that horses really have only 3 ophthalmic diseases.

They have corneal ulcers, they have UVITs and they have everything else. But really, if you're looking at diseases of the equine eye, corneal ulcers, and UVITs are more than 80% of your work and since we've only got one hour today, we shall concentrate on these two topics, maybe leave everything else for another meeting. So, starting with corneal ulcers, I tend to divide them into simple and complicated and starting with simple corneal ulcers, well, as I said, they are uncomplicated, but basically, Here is a simple ulcer.

It's superficial, even though this is a two-dimensional picture, you get a sense that it's not a deep lesion like some of the other pictures that are coming up later in today's talk, and there are no signs of infection or cellular infiltration. Again, we'll see plenty of pictures of those, however, they refuse to heal. And in a way, when you, we look at this picture and the history of a superficial ulcer with no infection, no cellular infection, the infiltration that refuses to heal, We are talking about something that resembles the so-called boxer ulcers or, or scads in dogs, if you remember your companion animal ophthalmology back from vet school.

And one of the defining features of these ulcers is, besides the fact that they are superficial and have no signs of infection or cellular infiltration, is that there They have a loose epithelial lip that can be easily deprided with a swab. You can see the lip here, actually see it and you can see a bit of edoema. Under the lip, under the epithelial lip, and if you take a swab, you can actually, as you see here.

See the epithelium coming off right here? We are expanding the size of the ulcer, or I should say theoretically expanding it cause we're just removing loose epithelium that wasn't adherent. Here is a, here's another picture.

Another movie I should say. And again you can see it going ventrally. See how the size of the ulcer is expanding and Here is what the horse looked like before we deprided it, and here is the size of the ulcer after we deprided it.

So you could say that the ulcer has expanded, but really this was just loose epithelium sitting there on the stroma and . Therefore, the ulcer seemed small, but it was easily bred and its size expanded, and that's a giveaway that this is a boxer ulcer in dogs or a simple ulcer in horses. How do we handle these simple ulcers?

Well, as the name implies, it's rather simple treatment. Again, if you remember your companion animal ophthalmology, and if you're as old as I am, you may remember that we treat them with multi-grid keratotomy or multipunctic keratotomy where we take a needle and we literally, literally scratch the surface of the cornea to Remove abnormal tissue that's adhere that's preventing the pithidium from adhering to the stroma. However, recently, we have, progressed into the 21st century when the diamond bur came along, which is This brush you are seeing here that is literally covered with diamond dust, and this diamond dust, as the brush is burning along, actually debrides the abnormal tissue that's preventing the epithelium from.

Adhering to the stroma. So again, a couple of movies that you can see here. Here is the Diamond.

Rush a diamond burr being applied onto the cornea. We are sometimes washing to saline so that the cornea doesn't eat as we're doing it. And you just move it along the surface of the ulcer.

You see the borders of the ulcer cause its floor in stained. Don't worry about it no matter how hard you press, you will not be able to cause any damage. You will not make the ulcer any deeper than.

It is the diamond dust is simply moving the abnormal tissue. So that was one movie, here is another movie. You can tell by the movement of the horse is completely awake, maybe use a twitch, maybe some mild sedation, but it really works wonders as we can see in this paper, .

Treatment of 60 horses with diamond bird debridement, a paper published in at the vet school in Pennsylvania. So, as I said, they were looking at 60 horses with these simple ulcers that were non-healing, that were characterised by the presence of this loose epithelial lip that I mentioned earlier. And they had a duration of at least 7 days.

So we're talking about middle aged horses for some reason, much more frequent in males than in females. You can see that 80% of the horses, they were truly simple. There was no other corneal disease.

They were present prior to the procedure for 29 days. They were treated with diamond burr and 92% of them have healed within two weeks after the procedure. So highly recommended cause, yeah, and also that's been present for a month now can heal within 15 days after treatment.

As it says here, we don't really know what causes it and dogs really a genetic mutation is suspected, but whatever the cause is, we can treat them rather easily. With the diamond bur procedure. And if we perform diamond bur, then I also recommend that you place a contact lens in, on the cornea afterwards.

It doesn't speed up the healing. There is no evidence that it makes it faster, but definitely increases patient. Comfort as it protects the cornea from further irritation.

That's a contact lens that's specially designed for horses as far as curvature and size go. You can buy it at Unvision. Again, I have no commercial interest with them.

You'll notice that The contact lens has two black dots on its surface, and that's for the owner to monitor whether the contact lens is still in place or whether it is falling out. And here is a diagram showing how it's very easily applied. Wash your hands first, make sure they're clean, remove the contact lens from the bottle, take it in your fingers, and simply place it on the cornea.

Make sure it's adhering to the cornea. Make sure that the third eyelid covers, the. And the contact lens that the contact lens is not over the third eye that it's beneath it, and that's what it looks like.

It's something you can do in an alert or, maybe with a twitch. As I said, it may have been sedated for the DVD procedure, so, you can easily place it now. So simple ulcers, simple treatment, confirm the diagnosis by deriding them with a swab, treat them with a DVD and place a contact lens, they will heal within 15 days.

As opposed to the complicated ulcers, which are indeed much more complicated and challenging to treat, many of them are traumatic in origin, foreign bodies, hay, bedding, getting into the eye, maybe . Maybe whiplash, etc. Etc.

The problem is, and what makes them complicated is that they become infected, they may become infected with bacteria, in which case, Pseudomonas is the organism we fear the most, or they may be infected by a fungal agent, in which case, Aspergillus is the agent we fear the most, and these Infective agents may lead to the formation of a corneal abscess or, sorry for the span mistake here, a so-called melting cornea. What do I mean by melting cornea? Well, we have here a problem of cascade and enzymatic cascade that's actually degrading the cornea, when it also develops, there is obviously increased tear production.

And the tearin contains proteinases. They're supposed to protect the cornea, but here proteina is secreted by the tearin by the corneal cells, cells themselves. Start degrading the cornea, their activity increases during ulceration.

Obviously, there is also proteinases secreted by the aspergillus or by the pseudomonas or whatever infectious agent you have. White blood cells come to the area, they die, they secrete their enzymes, so you really have a cascade, the Presence of infectious organisms increases tail and its enzymatic activity, increases cellular infiltration and each enzymatic and . Activity and all of these enzymes degrade the cornea in a sort of a snowball effect, which is why we call it a melting ulcer.

And here is a picture of one, and you can see the whitish mushy appearance at the margins of the ulcer. That's a giveaway. Also, its depth, again, I'm sure you can tell it's much deeper than the ulcers we've seen previously.

And yes, the cornea literally melts before your eyes. This ulcer gets deeper and deeper by the hour or by the day. And we have to remember that the thickness of the cornea is only 0.5 millimetre, OK?

Not half. Centimetre. We're talking about 0.5 millimetre, 500 microns, maybe a bit more in the horse, but that's what we're talking about, less than a millimetre.

So when we are talking about such a deep ulcer in a cornea that's less than a millimetre thick, we are in trouble. As I said, these ulcers are infected and therefore, as you can see here, the cornea is much more colourful. Again, we can see the whitish yellowish appearance of the cornea, that tells us there is white cells infiltration, maybe the formation of a corneal abscess.

As I said, it is also mushy looking, it's not as healthy looking as a cornea here. There is lots of blood vessels that you are seeing here at the surface. Notice that they are, they start as individual blood vessels in the periphery, but as they approach the lesion, they dive in cause it's a deep ulcer, and then they get this paintbrush appearance.

You can no longer tell the vessels. It's like the bristles of a paintbrush and note that the iris is very Very dark because there is secondary UVIis here. We'll be talking about that later.

Here is another picture of a complicated ulcer again, the white yellowish cornea, definitely an abscess here, bluish cornea symbolising the edoema cause of the keatitis. Blood vessels here are much further away from the lesion than they were in the Previous slide and note that unlike the previous slide where I could see some details of the interior chamber here, everything is hazy. That's an indication that we have secondary UVITs, lots of cellular infiltration in the interior chamber, and something you should always keep in the back of your mind is that every corneal ulcer.

Triggers a secondary UVitis. That's why we have the dark iris in the previous slide. That's why we have the hazy interior chamber here.

Yes, there is secondary UVIis and we have to remember its presence when deciding on our treatment plan. As I said, these enzymes or the enzymes secreted by these organisms and by these white blood cells degrade the cornea, and if it keeps on degrading, we get what's called a dematocele, where all of the corneal stroma is really gone, and the eye is literally hanging on decimate's membrane. And the endothelial monolayer, so really just one layer of cells in its basement membrane, that's all the eye is hanging on.

I have these plastic bags here cause really now the cornea is as thick as just one plastic bag. That's how thin it is. .

Note that when the ulcer has reached the endothelium when we have thismiocele, it will not stain with fluorescine cause fluorescine binds to the corneal stroma, it doesn't bind to endothelium. So as you can see in this picture here, if you stand with fluorescine, The walls of the ulcer, the walls of the crater, if you will, will stain, but the centre of the crater will not stain, and that's a giveaway when you have an ulcer that the walls are staining but not its centre. You are looking to dismantle seal.

The eye is literally hanging by a thread and if it progresses just a little more. Excuse me, you'll get this iris prolapse. Whenever you see this.

Bulge on the surface of the cornea, that's give away that yes, now we have an iris prolapse. Sometimes it doesn't look like much of an iris. I mean, it's more brown, grey brown gelatin rather than the firm dark iris we're used to seeing in the eye, but that's cause it's becoming very irritated when it's exposed to the air, to the outside environment, and it quickly becomes covered with fibrbrin.

Some more colours here are a couple of pictures of corneal abscesses. You can literally see, the yellow cellular infiltration in both of them. Not that they may be intrastromal, so this won't necessarily sting with fluorescine.

Maybe the horse got a thorn in the eye. The thorn allowed the seeding of bacteria or aspergillosis in the stroma. Then that hole sealed up.

So these corneas may very well be floy negative, but you can see by the colour that there is serious disease going on in the cornea. Again, lots of corneal edoema. In this eye, lots of vascularization, vascularization here too.

And so we've got corneal abscesses and in both eyes, we have evidence of secondary uveitis that I mentioned. In this picture, again, you cannot really see any details of the intraocular structures. Because there is lots of inflammatory material floating in the aqueous chamber.

Here, it has sunk to the bottom of the interior chamber. That's the straight line here. That's what we call a hypopion.

All the cells that were floating here have now sunk to the bottom. Maybe we can see a bit more details, but definitely. A sign of secondary UVIs.

So, what should you do when presented with a With a complicated ulcer, always look for a foreign body cause as I said, it may be a common cause. So look under the eyelids, don't forget to look under the third eyelid for a foreign body that may trigger it. In horses because we are so terrified of the infectious microorganisms, it's always a good idea to take culture.

And sensitivity, including mycology, but you are not gonna wait around for results of cultural insensitivity or mycology to come back. You should also take a cytological scrape from this area. How do we collect cytological scrape here is a nice paper from the University of Florida.

Comparing three collection methods for equine ulcerative keraitis, they used either a cytobbrush, a spatula, or the handle of a scalpel blade to collect their samples. And what I like about this paper is that the simplest, instrument, the cheapest instrument was the best scalpel blade provided. The most diagnostic samples, even though all three sampling techniques are adequate.

So what you do is you restrain the horse, put a drop of topical anaesthetic in the eye, take the distal end of the scalpel blade and vigorously scrape the cornea. I know it sounds scary, but then you're working with. The distal end of the blade.

I don't think you are going to damage it, but really, you should vigorously scrape the cornea. Just lightly touching it means you will not get any cellular samples. You need a good scrape in order to detect the bacteria or the fungal hyphae that are involved.

How do we treat these guys? Well, number one, we must install a lavage system. As you'll see in a minute, this horse is going to require plenty of eye drops and if a horse is in each eyedrop has to be administered several times a day.

So overall, we may be talking about 1520 applications. Of eye drops per day, or various eye drops per day. No way is a horse with a painful eye gonna let the owner or the student or anyone treated so frequently.

I always, smile in scepticism when the owner tells me, yeah, I've been treating the horse. With everything and if I see there is no lava, I know it's not happening. So here is what a lavage system, looks like.

Basically, we are talking about atrocar tied, connected to a tube. You can pass it from the inside of the eyelid outside. It can be either the upper eyelid or the lower lid.

There is no paper showing which is better, and you just pull it through the eyelid until it gets arrested by this foot plate and then the owner can take the distal. End of the tube as shown here and use it to flash medicine onto the cornea. You can look at the MIA website for this paper or maybe I think even a YouTube movie by Andwire on how to insert it.

Really, every horse. With a complicated ulcer must have a supplepilaage system installed in order to properly and effectively deliver the medication. Don't let the owner talk you out of it.

Don't let the owner convinced you that, yeah, I can administer medications. They cannot. So, after, what does therapy include after installing the lavage system, we wanna give broad spectrum antibiotics, both topical and systemic.

So make it broad spectrum until you have the result of your, culture, coming back. Definitely if you have Pseudomonas in your area or If you're worried about sodomonas, consider adding gentamicin in, in addition to the broad spectrum antibiotics. Don't automatically give gentamicin cause it's cytotoxic, so it may delay corneal healing, but if it's melting cornea in you, you are worried about sodomonas, definitely give gentamicin.

If you're concerned about fungal agents, give a topical antifungal drug, and don't forget, as I said, to treat the secondary UVITs with systemic NSAIDs and perhaps with topical NSAs, we'll talk about it soon when speaking about UVITs, but don't forget to treat the secondary UVITs. Besides the antibiotics and the non-steroidal drugs, 2 more, . Topical solutions that you must give.

The first one is serum or plasma and the aim of serum or plasma is to inhibit the proteolytic. Activity of the enzymes, the proteases, the colegenases that I described earlier. There are some commercial products out there, but really plasma or serum containing alpha 2 microglobulin is just as effective as any commercial product.

It's great cause there are no contraindications, you took it from the horse itself. So obviously there is no possibility of overdosing or toxicity and therefore, when we do have a melting cornea, we literally have a student or a technician sit with the horse and apply a drop every 30 minutes or every 1 hour constant serum until you see the melting stop. Serum gets contaminated easily, so if you prescribe serum to the owner, They should discard it after 8 days and get a new bottle.

If I'm giving this lecture to companion animal doctors, then we have to talk about the problems of getting enough serums from a small chihuahua or a Pekinese dog. In a horse, it's no problem, discarded after 8 days and get a bottle of fresh serum, obviously a very cheap drug, but very, very effective. And one last thing that you must administer is atropine.

Two reasons that we give atropine. Number one is that it is very analgesic, and that's because Every UVI is characterised by spasms of the sidiary body, spasms of the iris, and these become very painful over time. Just take your hand and twitch your fingers for five minutes and you see what I mean by pain.

The horses I treat you. Usually don't come back to tell me how effective my drugs were, but talk to a person who had UVIis and they would tell you that atropine is actually a wonderful and energetic one drop brings immediate pain relief. And the other reason that we give Atropine, perhaps more important is in order to dilate the pupil and reduce the chances of what we call posterior synia or adhesions of the iris to the lens.

This picture in this diagram shows you. While it's important, as I've said before, during UVI, the interior chamber fills up with lots of inflammatory material. It may be platelets, protein, fibrin, white blood cells.

We are talking about very sticky stuff. And as you can see in the eye of this horse, a lot of it has sunk on the interior lens capsule. In fact, only this region here is still transparent.

All of this lens capsule is really hazy looking cause there is all the inflammatory material sticking onto it. So, if you take a horse with your VIS, the interior lens is covered with sticky material and the iris is in spasms and meiotic pupil, as we'll see on later. So lots of contact area between the iris and the lens, potential for adhesions.

You want to give atropine to dilate. The pupil to decrease the contact area between the iris and the lens and prevent these adhesions cause they will cause glaucoma. I wish I had 10 pounds for every horse I see or every dog I see where the UVI was treated successfully, but the clinician forgot to give atropine and they lost the eye to secondary glaucoma.

How much atropine should we give? Well, your aim is a fixed dilated pupil, and the horse will tell you, the eye will tell you whether you're giving enough or not. I usually start with twice daily.

If the pupil is fixed dilated, I can decrease it once daily or once every other day, because after all, we do one. Prevent colic. Don't forget that entropy may cause colic.

On the other hand, if twice daily did not get me a fixed dilated pupil, I will go up to 3 or 4 times daily, at least for 2 or 3 days, while maintaining a colic watch cause we must get a fixed dilated pupil. And a final very important component in treatment is an eye shield. Make sure that the horse is not able to rub on its, painful eye, so it must be an eye shield made of sturdy plastic material, not some flimsy cloth.

We're not talking about mosquito. We are talking about an eye shield. So just to recap, install a lavage, give the topul and systemic antibiotics, perhaps antifungal, treat the secondary UVIs with systemic anides, maybe with topical anads, definitely with atropine, and definitely with lots and lots of serum.

Unfortunately, some horses will not recover or will not respond to treatment fast enough, in which case we have to take them into surgery in order to save the eye. The aims of the surgery are really to clean up the abscess, to protect the cornea from further damage, to promote healing by bringing blood vessels, . And lymph vessels to the lesion feel the defect, and I stress this because I know that some people think that they can surgically treat corneal ulcers by doing a third eyelid flap or a temporary dorsoy.

These procedures do not meet these aims. Yeah, maybe you're protecting the cornea from further trauma, but you're definitely not feeling the defect. You're definitely Not promoting healing by bringing in blood vessels and worse, you are limiting the ability of the owner to give top medications and does not allow monitoring of the eye and therefore the surgery of choice for these horses is a conjunctival flap as you are seeing here.

It provides great corneal support. It's tissue is incorporated. Into the cornea.

It brings blood vessels and lymph vessels and allows to medications and rejects, but of course, this is something that usually should be referred to a specialist. Here is an example of one horse, Ben, with a very, very nasty looking ulcer here, a definite melting cornea with all The signs that I've described earlier, we've performed a conjunctial flap, as you can see here covering the defect with this nice tissues. So you see what I mean by bringing blood vessels that at this stage were quite far from the lesion.

Now they're over the lesions. Now it's able to heal. We did make a mistake here by leaving this harvesting the conjunctava with a small piece of pigmented tissue.

So when it was all said and done, we did have some pigmentation on our scar. So some visual deficits here, but it's in the periphery. It's not in the centre of the visual axis, so we're definitely OK, especially when you're comparing the preoperative to the long term outcome of this surgery.

So that's my talk about corneal ulcers very briefly. Let's move on to talk about UVI. So just remind us what is the UVI.

The eye may be regarded as a globe consisting of three layers. In blue, we have the outermost layer, the connective tissue that's holding the eye together composed of the cornea and the sclera. The innermost layer in red is the retina, what the eye is all about, allowing us vision, and in yellow, we have the intermediate layer which is the UVA consisting of the iris is the anteriormost part, continued more posteriorly by the ciliary body and then by the choroid.

So we're really talking both about the muscular layer and the vascular layer of the eye, the iris being more muscular, controlling the size of the pupil, the ciliary body is also muscular, lots of vessels here, but especially in the choroid cause the choroid is responsible for blood supply to the photoreceptors of the retina. Because of anatomical proximity, the iris and the ciliary body are considered to be the interior UVA. The choroid, which is more to the back of the eye, is considered to be the posterior uvea and here you can see what I mean by a rich vascular bed of the choroid wrapping around the eye 360 degrees in order to supply the photoreceptors.

So when we're talking about UVITs, we're really talking about inflammation of all three parts. We're talking about anterior and posterior uveitis, inflammation of the iris ciliary body and choroid. But in everyday language, actually, when I say UVITs, it's usually used to describe just information of the Irish ancillary body, which means that Pro, if I were to talk properly, I should say interior UVITs every time, but we're sort of lazy and skip over the interior and we just say UVITs, you will catch me saying UVITs when they should be saying interior UVITs plenty of times.

But I'm stressing the point that the iris and the ciliary body because of their anatomical proximity are inflamed together, so that's interior realities. The choroid, as I said, is geographically or anatomically, . Placed next to the retina and therefore inflammation of the choroid or posterior viitis is usually combined with retinitis, inflammation of the retina.

So another word for posterior viitis would be choreoettinitis, inflammation of both the choroid and the retina, which is what we are seeing here. So if we're talking about UVITs or more specifically equine recurrent UVITs, formerly known as moon blindness or periodic ophthalmia. You get the sense in all of these names, recurrent UVIs, moon blindness, cause it's been in old days, it's been associated with the cycles of the moon, periodic ophthalmia.

We are talking about recurrent inflammation. Recurrent immune-mediated inflammation and in between these periodic episodic attacks, you do have quite some periods. But basically, we are talking about an immune-mediated inflammation, so we are talking about Some sort of in trigger, which we'll discuss in a minute, causing activation of T cells, production of cytokines and anti-rein antibodies destroying the retina.

The uveitis, the bout of uveitis will. Be treated and may be resolved so we have a quiescent period, but then the immunological memory predisposes the animal to repeated bouts of uveitis due to repeated exposure to the inflammatory trigger. Prevalence of UVITs, you can see that it affects up to one quarter of the horses in the United States and may cause blindness in up to 2, 2% of horses in the US.

So we are talking about the leading cause of blindness. I mean 2% of all horses become blind with ER ERU, also very figures in Central Europe may be a bit less common in the United Kingdom, because perhaps there is less lepto, which is one of the triggering agents, but basically it can affect any horse at any age, breed, or sex, though mostly we see it in Aalusas, as you'll see in a minute it may be unilateral or bilateral in both eyes. So, as I've just said, really, one of the triggers for the immune response for the immune-mediated inflammation is leptospira.

It's been recognised since the 1940s as being a trigger for ERU. As you know, there are many several variants for Leptospira. Interrogan's pulmona is probably the most common one, and UVIis will occur.

A year or months, 2 years after exposure to leptospira, it leads to the initial inflammation, to the initial blood ocular barrier breakdown, triggering activation of T cells, the production of cytokines and antibodies as I described, and the formation of immunological memory, meaning. That repeated exposures to leptospira will trigger repeated inflammation, but we must know that you probably know that the picture is not that simple and positive or negative cell activity does not rule in on or out lepto as a contributing factor to ERU. As I said, it's an immune-mediated inflammatory response, so lepto is definitely not the only trigger.

Lots of other bacterial diseases, viral and viral diseases and parasitic diseases can trigger these attacks of recurrentVI and again, Initial infection triggering an initial inflammation, forming the immunological memory and predisposing the horse to repeated attacks. Trauma will cause UVITs, hypermature cataract yho sarcoma, tumours. My friend UC Davis from UC Davis.

David Maggs calls it truly an ocular lymph adenopathy. So, just like any of these bacterial or viral or parasitic diseases can cause lymph adenopathy anywhere in the horse, it can also cause a lymphadenopathy in the eye. And what And, and therefore, the implication is that when you diagnose UVIS, it's not really a diagnosis, it's a clinical sign.

Just like enlarged lymph nodes are not a diagnosis, they are a clinical sign. Same with UVITs. It's really a clinical sign for many, a great number of diseases and when you establish a diagnosis of UVITs, you have to perform a comprehensive workup to determine what is the primary disease causing UVIT just like you would perform a workup in order to establish what what caused the lymph adenopathy.

As I've said, Appelusas are predisposed. Here is a classic paper again from Ewyer, the same doctor I referred you to who has the lay lavage system, instructions. She showed the Appalusas are more than 8 times more likely to have ERU than non-Appalusas in her study, 23.

Of all Appaloosas went blind as compared to just one quarter of non-apalusas. 80% of them had chances of bilateral, ERU, meaning they're gonna, good chance they'll be blind in both eyes versus 20% chance of bilateral UVITs in non-apalusa. So that's another predisposing factor.

How do we diagnose uveitis? Well, there is lots of clinical signs. The eye is painful, so you will see the spasm, you will see a red eye because we're talking about uveitis, so there is more blood flow in the UVR and it can be projected through the sclera and you'll see the red eye.

There is a corneal edoema because lots of inflammatory material in the aqueous humour, the anterior, the inner, sorry, the posterior cornea is dependent on aqueous humour for. It's metabolic support. So when the composition of aqueous tumour changes, there will be a loss of metabolic support for the posterior cornea and corneal edoema.

There is the aqueous flare, the haziness of the Andres more due to the presence of the inflammatory material, meiosis due to the spasms of the ciliary body that I mentioned earlier. Hypoteny. Decreased intraocular pressure, sometimes surprising people because I've just spoken about the leakage of inflammatory materials, so there should be more fluid in the eye.

Yes, there is, but there is at the same time increased drainage of aqueousas from the eye. The net result is hypoteny, so measuring intraocular pressure is a good idea. It's a very, very sensitive sign of UVI and sorry, and The inflammatory material as I've described earlier, can sink at the bottom of the interior chamber, causing a hypopion that you see in both of these cases or hyema.

A long list of complications as a result of UVITs, cataract, again, just like the Inner cornea is dependent on aus humour for metabolic support, so is the lens and therefore in UVI, the lens, it loses its metabolic support and you get cataracts secondary to uveitis. Indeed, any horse with cataracts, except for foes where cataract may be congenital, but adult horses cataract should be suspected of having UVITs. We can get the.

Poor synichia that I described earlier, the adhesions between the iris and the lens, atrophy of the corpro nigram, which is clearly seen here against the background of the caract. The inflammation may loosen the souls that are holding the lens in place, causing lens laxation. We can get vitreal degeneration, glaucoma.

And retinal detachment, and here are and as well as retinal atrophy, and here are a couple of pictures of the complications that you may see in the posterior. Section of the eye, so we are seeing the retinal atrophy around the optic nerve, especially these lesions here called the butterfly lesions which are really classic indicators of chorea retinitis. We see the hazy vitreous here.

Due to the presence of inflammatory material, not just in the aqueous, also in the vitreous, and we see this floating whitish grey sheet in the back of the eye that's a detached retina. If you're not sure that your a detached retina, you can do an ultrasound and here it is depicted very nicely. We call it a sea gull sign because it looks like the wings of a seagull, the retina, which is usually supposed to be here in the back of the eye, is now detached.

So, how do we treat these horses? Well, we should talk to the owner about the goals of treatment. We treat each and every episode in order to preserve vision, decrease pain, and prevent or minimise the chances of recurrence.

If we found a primary cause such as lepto or Bruce. Or something, that's great. However, often we don't and we just give non-specific anti-inflammatory treatment to control the inflammation.

You really, really must be very, very aggressive about treating these cases, and you must warn the owner that long term, maybe lifelong treatment is necessary. What does the treatment include? Well, we are talking about inflammation, so we need anti-inflammatory drugs.

These are given both systemically in the next slide and topically. During the attack, we may give 4 to 6 times a day. Again, you need a lavage system for that.

We prefer steroids and especially prednisolone, cause prednisolone is #1 more potent and #2 has better intraocular penetration. Dexamethasone, less intraocular penetration. And less potent, but it's available in ointment form which some owners may find easier to use.

Of course, we never give steroids if there is a concurrent corneal ulcer or abscess present. We also give Toy NSides, diclofenac, or more lately, nepofenac or Navinac. They're not as potent as prednisolone, but their advantage is that they may be used in cases of corneal ulceration, and I say may be used because they may also have a negative effect on ulcers and may worsen things, but you do have to give some sort of anti-inflammatory material and if there is no ulcer, then you should be able to give both topical steroids and NSAs together to get increased in anti-inflammatory effect.

As I said, we also want to give systemic anti-inflammatories, so we give fluoxine, we give ennibutisone, we give aspirin, and we may even give systemic corticosteroids, and here are the doses, but I'm sure you don't need me to tell you the doses of anti-inflammatory drugs in horses. Again, don't forget your atropine. Very, very important to get a fixed dilated pupil.

You may consider a subconjunctive injection of kenalog, a long-acting, anti-inflammatory drug, triamcinolone, which gives you 7 to 10 days of protection. As I said, if you found a primary cause such as leptospira, please try it. And I often that asks, should I vaccinate the horse?

Well, yeah, you should, but not when there is active UVIT, so wait until the inflammation is resolved and then you can consider vaccination, not when there is active UVIis. So this would be the conventional treatment, treating the primary cause, giving atropine, giving systemic and topical anti-inflammatories. Note that I am not giving antibiotics.

There is no need for antibiotics. It is not topically in these cases, maybe systemically if there is a systemic infectious disease. But the eye doesn't need topical antibiotics cause the eye is inflamed, not infected.

However, there are some other things that you may consider given. One of them is an intraocular injection of tissue plasminggen activator. As I've said, one of our greatest Complications in your VI is the presence of inflammatory material in the aqueous tumour which predisposes the horse to posterior yic and secondary glaucoma.

. Inject tissue plasm and activator into the interior chamber and that dissolves the clot. It's the same material that you would get if, God forbid you had a stroke, a coronary or a brain stroke, and you were to go to the emergency room, you'd be injected with tissue plaing and activator in order to dissolve the clot, very, very effective. But very expensive material.

Maybe a few of you should get together to buy one bottle. You can make hundreds of doses from it, place it in Eppendorf tubes, place it in a deep freezer, and it will keep for many, many months. The great thing about it is that it works immediately.

It's not, well, send the horse home on steroids. I'll see you again in 2 weeks. It works within hours.

OK. Here is the same horse before and after tissue has been an activator injection. No, there is no pupil here because of adhesions and a large clot that's visible and look how the clot is dissolved and the pupil is opened up within 6 hours after injection of TPA.

Some more treatments that you may try, in the last few years, we have begun trying intraocular intravitreal injections of low dose gentamicin to treat equine recurrent UVI. You can see here a couple of recent papers 2019 about it. We sedate the horse but no need for anaesthesia and inject 4 to 6 milligrammes.

Of gentamicin into the vitreous, and that's because we believe that so many of these cases are associated with Leptospira and as I've said previously, you won't always find the leptospira, but you may be treating it with this intravitre injection. In this paper by Fisher, 88% of horses with the follow-up. Of one month were controlled there was no repeated inflammation.

In the second paper here by Lanois, after 6 months, nearly all horses, 70 or 71, did not develop any repeated inflammation, though it is a phone survey, so it should be treated with caution. A couple of surgical options, I guess many of you have heard about sacrosporin implants. Sacrosporin is a wonderful anti-inflammatory drugs, but topical sacrosporin does not penetrate the eye.

So instead, we can Put it as a suprachoroidal implant here which releases cyclosporin into the eye. Yes, it does require anaesthesia in order to perform the surgery. We do need to add topical medications, but when there is no active inflammation, when you're in between bouts, that's a good time.

And supposedly, it gives you 36 months of protection from repeated bouts. Implants are available from one place and one place only, and that's a pharmacy of North Carolina State University. I don't have stocks in the North Carolina State University pharmacy, but you can look them up on the internet and order them.

Make sure you're buying the equine implants and not the canine implants. Surgery involves creating a flap in the sclera. In fact, the flap here is so deep that you can see the choroid poking through.

You place the implant and then you suture the sclera back. Here are a couple of studies showing us the outcome of these implants. Brian Giler followed 67 horses for 14 months and 85 of them remained visual and virtually no attacks point.

All 5 attacks per month, 80% of horses were visual after 2.5 years, which is absolutely great. Another study by the same Gilger, this time with double number of the eyes both in the US and Europe, because again, we may be talking different .

Different, strains here, but it was equally effective. Again, minimal number of attacks during the follow-up time, 78 or nearly 80% of the eyes were visual at the last follow-up. And finally, another surgical option for which you have to refer is what we call vitrectomy, where we go into the eye and remove the vitreous.

This is a treatment of choice mainly in Europe. We remove the vitreous and number one, it clears up the media. #2, it removes the inflammatory material that may be present in the that may be present in the, vitreous.

It will clear the infectious agents and basically decreases the frequency and the severity of the attacks. Obviously, this is a specialist surgery, so you do need a specialist performing it in a specialist clinic. But yes, it's a very popular procedure in Europe, mainly because you're removing leptospira and clear up the eye from it.

As I have said, in Europe, following the procedure, 90% of horses have less inflammation and only 25% develop cataracts. In the US it's less success. Only 70% success and 50% developed cataract, maybe because of differences in the variants of leptospira between Europe and the United States.

Here is what the procedure looks like and you can see the yellowish inflamed vitreous that was removed from the eye. But basically, you can try everything that I've just described, including the topical and systemic and surgical approaches. Still, the prognosis is not good.

Here is a study of 338 eyes. You can see Appalusas were one quarter of all cases, and of horses tested, not all of them were tested for lepto, but 40 of 88 horses tested for leptospira were positive. 28% of blind eyes were blinded presentation.

11 had glaucoma. Many of the horses were retired, reduced work load, euthanized, or sold. Yeah, it's a disease with very bad prognosis.

Lots of horses lose the eye or lose vision. And we should remember that in horses, if they lose vision in one eye, it becomes a very severe handicap due to their laterally placed eyes. If we look at the cat with frontal placed eyes, if it loses one eye, then it really loses just 30.

Degrees of the visual field of the right eye, the horse would lose 145 degrees of visual field, so it's a severe handicap if it loses vision, should definitely be ridden only by a very experienced horse, but nonetheless, . It is not a reason for euthanasia. We even have a very famous story of several horses, I think, that are one-eyed and placed well in the Kentucky Derby.

So with experienced riders, they can definitely cope. And even if the horse is totally blind, as long as you just need to manage the pain and it can live a happy life. You can refer owners to this website for some advice on horses with UVITs.

I thank you very much and hope I helped you cope with your next case of corneal ulcers or uveitis. Have a good evening.