Good evening everybody, and welcome to the latest webinar vet webinar tonight. It's my pleasure to introduce Ron Ofri, who is a member of the charter class of the Coret School of Veterinary Medicine, Hebrew University of Jerusalem, Israel. After his graduation, he travelled to the University of Florida, where he spent the next 4 years undergoing clinical training in veterinary ophthalmology and obtaining his PhDD.
During this time, Ron developed an interest in the physiology of vision, focusing on retinal electrophysiology and animal models of retinal diseases. Upon his graduation, Ron returned to Israel and joined the faculty of his alma mater, where he's currently a professor in veterinary ophthalmology and winner of numerous Teacher of the Year awards. He's expanded his research interests at the university to include comparative visual physiology and wildlife species and gene therapy of retinal diseases, and to date has published more than 90 refereed papers.
So Ron, over to you. OK, thank you, Andy. Good evening, everyone.
I'd say nice seeing you again, except that I'm sorry I can't see you, but it's always a pleasure to come back and speak at these webinars. Subject for tonight is dry eye, diseases of the lacrimal system, beyond Schermer Tear test, and cyclosporin. I am always asked to disclose any financial relationship with products that I have and I have nothing to disclose, but those of you who've been to my previous seminars know that they use the opportunity for partial disclosure or what some may call shameless advertising, noting a book here that I've co-authored letters Fundamentals of Veterinaryphology, 6th edition, and many of the pictures will be seeing today are from this textbook.
So we shall be talking about diseases of the lacrimal system and by way of introduction to slides, quick reminder of what tiers are and why do we need tears. So basically the tier film is composed of three layers. The outermost layer is an oily layer that's and its role is to prevent evaporation because obviously, Especially in these days of global warming, if there was no outer out of oil on your tier film, then it would quickly evaporate.
This oily layer is, produced by the malbomin glands that are located on the eyelid margins and you can see here mybomin being extracted from the myboin gland openings of the upper eyelid of the cat. The innermost layer is a min layer that allows binding and even spreading of the tear film. What I always like it to is taking your car to a car wash and having the Windshield waxed.
Now you know that before waxing the windshield, if there is water on it, it would throw away, but after waxing it, the water beads and stays on the car windshield, and that is really what the museum does. It allows the tear film to stay on the corneal surface. You can see these two layers here, in this diagram depicting the tier film.
We have the lip layer that I mentioned previously as the outermost layer, event. Evaporation and we have the inner mucin layer here and you can see the corneal surface is actually reticulated. It's not as smooth as we think it is.
The mucin fills in these gaps and allows, as I said, the main component of the tear film, the aqueous layer to bid on the corneal surface. This aqueous layer is produced both in the main tear gland in 30% of it is produced in the tear gland of the third eyelid. This is really the main layer of the tear film function layer, and its functions include flushing way of foreign bodies.
We all experienced that when an eyelash or something gets into. To our eye, we tear until we flush it away. It's responsible for corneal metabolism because the cornea, as we all know, is transparent.
It has no blood vessels, which really depends on the tears to supply it with oxygen, nutrients and carry away waste. Lubrication, it allows our eyelids to slide over the cornea smoothly. We all know that when we wake up in the morning, our eyelids stick to the eye because they're not lubricated, refracting light and immunology with enzymes.
In the aqui. So that's what the tiers are and talking about diseases of the lacrimal system, I'm really going to divide my talk into two parts. The first one has to do with diseases of production and the second part with diseases of drainage.
And speaking of diseases of production, the main and most common disease as we all know is KCS standing for lerato conjunctivitisika, lerato being the cornea, conjunctiva, so inflammation of the cornea and the conjunctiva due to a deficiency usually of the aqueous layer of the curling. There are other deficiencies. So what causes dry eye?
What causes KCS in dogs? The most common cause is really primary disease or inherited disease, whereby we get an immune-mediated inflammation of the ear glands. You can see that it's a lymphocytic plasmocytic inflammation, so we're talking about a humidated inflammation.
It's not. Infection, and in fact, it's an autoimmune inflammation of the tear gland. The body produces autoantibodies against the tear gland, causing progressive atrophy and the process of the lacrimal gland, ending up with the dry eye.
And because we're talking about the primary disease and inherited disease, it's obviously more common in some breeds than others. In Europe, most commonly in the West Highland white terrier, in North America, in the bulldog breeds, but it's common in many other popular breeds such as the cocker spaniel, the King Charles cavalier, and in many brackets phallic breeds, Boston terrier, Shih Tzu Pug, Pekine, etc. These breeds, as you know, have Anatomical problems with the orbit being so shallow, the eyelids barely closing on them, the eyes are not well protected by the eyelids, and then on top of that, they have their tear film problems to really, really complicate the health of their ocular surface, but we're really talking about an inherited disease in many, many others.
So inherited disease is the most common cause, autoimmune inflammation of the tear gland, but we do have other causes of dry eye. One common cause is neurological, dry eye, and the neurological dry eye, neurological dry eye is due to parasympathetic denervation of the ear gland. This parasympathetic denervation.
May present with additional clinical signs depending on where is the lesion to the parasympathetic nervation of veer gland. So if the lesion is proximal to the terriopalatine ganglion that you see here, the animal will also present with a dry nostril, what we call a zerobacteria, ipsilateral dry nostril. If The parasympathetic innervation is proximal to the philomastoid foramen that you're seeing here, then it will present with ipsilateral facial paralysis.
So these signs together with dry eye may clue you into the fact that you are looking at neurological dry eye and both of these. Structures, the ganglion and the steomastoid foramen are close to the inner ear and therefore whenever you have neurogenic dry eye, you should always suspect it is in turn up as the primary cause of the disease, inflammation spreading to the person that inva period time and we'll come back to that later. So we may have primary dry eye, we may have neurological dry eye, we may have neurological, we may have dry eye due to other systemic diseases.
There are infectious agents, Age. Gland, we're talking in dogs mostly about distemper virus and there are some very nice studies showing the significant decrease in tear production in distemper. Dogs present with dry eye, very common sign besides the neurological signs.
This meiosis is another infectious agent that targets the tear gland in dogs, and feline herpes virus targets in cats will come back to cats later. There is also low tier production in many endocrinological diseases. We're talking mainly about hyperthyroidism, diabetes, and Cushing's.
All of these diseases have been shown to, cause reduced tear production. Not all patients develop a clinical dry eye such as this dog here, but you do have to monitor your endocrinological, patients for to measure their tear production. Dry eye may also be caused by drugs or toxicity, so you should measure tear production before beginning treatment with some of these, these drugs.
Sulfa is very well known, it is toxic to the lacrimal glands which. Cause acute dry eye. Usually in the first week of treatment, if you pass the first week, you're probably on safe ground.
A dry eye caused by sulfa treatment may be transient, but usually it's not usually it causes irreversible dry eye. Ketodolac, a non-steroidal anti-inflammatory drug, also causes dry eye in dogs, very severe dry eye, and again, many cases are non-responsive to treatment and are irreversible. Atropine, it's a parasympathholytic agent and we mentioned that we have parasympathetic innervation of the tear glands.
So obviously treatment with atropine will lower tear production. However, this would be transient as would the effect of anaesthesia. Everyone knows that anaesthesia Lowest tier production, most anaesthetic agents with lower tier production and in addition, the patient doesn't link.
So obviously you have to keep the cornea lubricated. It's, we've learned it in vet school and it's been proven in many. And finally, in the list of causes, we have ocular diseases, any inflammation of the eyelids or the or the conjunctiva may be associated with, dry eye.
Obviously, if you take a look at this dog here and you see the inflamed lids, you realise that the ducts, leading from the tears. And onto the ocular surface would be destroyed. Maybe there is even destruction of the actual tear gland itself, so any inflammation in the surrounding area may cause dry eye, as would removal of the tear gland of the third eyelid.
I mentioned earlier, it provides about 1/3 of the aqueous portion of the tear film. And studies have shown us that if you remove this tear gland in cases of cherry eye, about 50% of the dogs will develop dry eye within 5 years, so 50%, significant number of patients. That's why we always insist that you replace collapsed gland and do not.
So we know what causes dry eye. How do these patients present? Well, usually they present with bilateral disease, but what is really typical of the disease when they present is the history that the owner gives you.
And the history will go something like that. My dog had an inflammation, so I went to this vet and gave this Drops that worked wonderfully. They really helped.
But then after 10 days, I stopped treatment and the inflammation came back. So obviously this vet didn't know what he was doing, so I went to a second vet and he gave me a second type of drops, which were just as great for another 2 weeks. And then when treatment ended, The inflammation came back.
So I went to a 3rd vet and the story repeats itself. And that's a history you hear. These people always treat their dogs and it doesn't matter with what, it may be antibiotics, it may be steroids, it may be non-steroidals, but the inflammation goes away and it comes back as soon as treatment is stopped cause it doesn't matter what they were treating with, what matters is that the drugs actually.
Lubricated the cornea. So it could be, as I said, antibiotics or steroids. It could have been tap water matter.
They were lubricating the cornea. They were moistening the cornea and as soon as treatment stopped, the dry eye came back. It's really a very classic history of many, many patients.
Looking at clinical signs of inflammation of a dry eye, they're really divided into acute and chronic. In acute dry eye, it's a very painful disease. As I said, you wake up, you feel your eyes sticking to your cornea, you're sort of In pain is you're tearing your eyelids away from cornea first thing in the morning.
So yes, painful disease, there is inflammation of the conjunctiva so conjunctiva hyperemia, and to start noticing all of the pictures I'm showing, I'll go back one. Look at the cornea. You see that it's not bright, you see it's a dull looking, it lacks lustre.
It's really a dull looking cornea, so that is something else that's typical appearance. There is obvious discharge. And because as I said earlier, the tear film is essential for corneal metabolism.
If there is efficiency in tier film, you can get cornea necrosis, ulceration, and e perforation. I've sometimes seen in acute cases going from a completely normal cornea, corneal perforation in 48 hours, really, really scary. However, if the cornea manages to overcome this acute stage and move into the chronic stage, then the eye adjusts.
And when I say adjusts, it means really that Blood vessels move into the cornea. They, infiltrate the cornea and these blood vessels provide the cornea with the metabolic support that was formerly provided by the tear film. So the blood vessels take over the role of the tearil providing metabolic support.
Yeah. And at the same time, the cornea undergoes histopathological changes, hyperplasia, fibrosis, etc. Thickening, it really becomes like skin, OK?
You have a thickened cornea, hyperplastic epithelium, vascularization, progressive pigmentation that you are seeing here. May cause loss of vision. Here you can see it totally of a cornea due to severe pigmentation.
Obviously this patient is not seen. So really vascularization, hyperplasia pigmentation, it's just like skin, discharges and pure and but this stage there is less pain. So just as with any other patient.
Based on the history. I said there is a classic history. We can diagnose dry eye based on the clinical signs I've just described for the acute cases and the chronic cases, but really the golden standard for diagnosing dry eye is a Schumer tear test.
And really this is a test you must perform in each and every eye for presenting with discharge or hyperemia. There is just no excuse for not performing this test. It takes all of 120 seconds to perform it in both eyes, and you'll be surprised by how many cases you diagnosed.
And I also like this test because Once you perform it, you can take the tear strip out, show the owner, see, this is the amount of wetting that your dog has. This is the amount of wetting that the dog is supposed to have. Your dog has dry eye.
It's a very visual test that the owners can easily appreciate. So what are the values that we are looking for? Well, Anything below 5 millimetres of wetting per minute is diagnostic of dry eye.
Anything above 150 millimetres per minute is normal, and 5 to 15 is this grey area where we say the patient is. May have dry eye, we suspect dry eye and in these cases will confirm diagnosis based on the presence of other clinical signs, meaning some dogs will present with 7 or 8 millicher material test values of 7 or 8 millimetres and signs of severe inflammation such as you're seeing here, that dog obviously has dry eye. However, some of them may present with 9 or 10 millet .
Per minute and they'll have completely normal looking cornea, that may be that odd dog where 9 or 10 millimetres are sufficient. So anything between 5 and 15, look for the presence of additional clinical signs before deciding whether to treat or not. So moving on to treatment, basically, I always tell the owners that the prognosis for treatment depends on the results of the Schirmer tier test, meaning that If we diagnose schmer when they're, if we diagnose dry eye when a dog had cher values of 7 or 18 mm per minute, we're in relatively good shape because it implies that there is some latin gland left.
We have something to fight over. We have something to protect, so the prognosis is much better than cases that present with 0 or 1, which implies that the tear gland is mostly destroyed. Prognosis is better in acute cases before we see the chronic changes in the cornea or when the cause is reversible.
So for example, some of the endocrinologic diseases I mentioned or the Leishmannia that I mentioned, if you manage to cure them, and the dry eye may, be cured, but unfortunately, most chronic cases usually require lifelong treatment. This is a very important point in client education, and I'll come back to that in a couple of times. So really, talking about treatment, there is lots of supporting treatment that you can provide.
You can instruct the owner to use wipes or Lead, some sort of lead wipes to clean the discharge. We can give them artificial tears, many preparations reach in hyaluronic, just to increase patient comfort to lubricate the moist in the cornea until we manage to increase tear production. And if there is secondary bacterial infection such as we're seeing here based on the purulent discharge and or corneal ulceration, obviously we have to treat those, so you should consider adding topical antibiotics.
I put here in parenthesis ointment cause dry eye corneal ulcers caused by Dry eye is one case where I could consider treatment with antibiotic ointments. As ophthalmologists usually we prefer eye drops to ointment because ointments, ointments tend to delay healing of corneal ulcers. Corneal ulcers tend to heal by having epithelium migrate from the peripheral.
Of the ulcer towards the centre covering the defect, but if you put a glob of ointment on the ulcer then it physically prevents the migration of epithelium. So usually we prefer drops to ointment, but the ulcers caused by dry eye are one case where we prefer ointment for extra lubrication. If there is a deep ulcer, we may require, surgery, mainly conjuntale flap.
However, please keep in mind that without tears, corneal healing will be much more complicated. However, as the title of the slide here says, all of this is supporting therapy, artificial tears, the antibiotics, etc. Etc.
The real aim of treatment is to increase tear production and here the drug of choice is cyclosporin. And usually I don't like putting pictures of animals that have been dressed up as people, but actually, this dog has a very important role in the history of treatment of dry eye. Those of you familiar with American college sports may recognise that the G here stands for Georgia.
This is the University of Georgia. And the bulldog and the team is called the Georgia Bulldogs. So this is a bulldog and if you remember a bulldog is a breed predisposed to inherited dry eye.
And back in the late 1980s at the University of Georgia, the coach of the football team came to the local ophthalmologists at the school. Doctor Rene has one and told her, Listen, our mascot has this eye inflammation and gosh, we may lose games because our mascot has this problem. You must solve it for us.
And anyone who's been to America in American college knows that always the sports department is the richest. You can have as much money as you want, just solve it for me. And Doctor Kasan put 2 and 2 together.
She remembered it's an autoimmune disease, so she said, let's try cyclosporin based because it's an immunosuppressive or I should say immunomodulating drug used for example to treat mophilia patients or used after transplantation in patients and lo and behold it worked and Dr. Kasan still makes 1 or $2 million per year. Year in royalties from sending Optimon so that in the University of Georgia earns another 1 or $2 million per year.
So really a very interesting story there. As I said, it takes over 120 seconds to diagnose dry eye, 60 seconds of measuring tear production in each eye. So I have a diagnosis within 2 minutes, but then I spent another 15 minutes on client education.
Part of the treatment. I always explain to them that, gosh, this is going to be a lifelong treatment because actually we're not curing the disease. OK.
Remember this is an autoimmune inflammation. We're controlling the inflammation with immunomodulating drugs. We're not curing the dog.
It's an autoimmune disease for life. I was given the analogy of insulin and diabetes. With insulin, you're not curing diabetes, you're just controlling diabetes, same with cyclosporin and dry eye.
But they have to realise that they will be treating for the. Lifelong treatment. They should always realise that the effect of cytosporin may take up to 2 months to build up.
People always come to you expecting that within a week or 10 days at most, the inflammation will go away. So, they should have realistic expectations. It's going to take 2 months, so it builds up very gradually, but stop treatment for 3 or 4 days and production will fall back to 0 and the inflammation will come back, which means they always need to have a spa tube or a spare bottle at home, never ever run out of it.
But if they keep these guidelines in mind with time, we can get regeneration of the land and we can get regression of the clinical signs, including the pigmentation. So yes, persistence in therapy will pay off. We have other therapies, other immune modulating drugs in new generation, many I'm talking about the rolimus and chemic rolimus.
They're more potent than cyclosporin shown here in one study that we did. So, there is an advantage to using them, but I draw your attention to this black box of the dermatological preparations of the rolymus and rolymus as you can be seeing, as you can see here, these dermatological preparations have been associated with neoplasia in people, so they are still approved for use, but it should be used with caution, and that's why I keep them only for sacros or any resistant dose. They are not my line.
And if you have a neurological case, then your treatment of choice would be pylocarpine, parasympathomimetic drug. We give it most commonly orally, not topically cause topically it may irritate. So more commonly we give it orally at this dose 2 drops of 2% polycarbon for 1010 kg body weight every 2, every 12 hours.
So it's 22, 102. Or makes it easy to remember. It is slightly bitter, so you should give it with this on a spoon, calculate how many drops the dog needs and put it on a spoon of edible food.
I mean, don't have the owner sprinkle it on the dry food cause they will not eat it. You should warn the owners that long term use may cause some parasympathomimetic, . Toxicity like diarrhoea or vomiting, to get those signs, stop treatment for 4 days and then renew at the lower dose and take one drop off and another drop off until you reach dose.
And as I said, many neurological cases are due to Oitti Interna, causing the parasympathetic nervation and therefore is do work up for Oitti Internna and I know some very respected ophthalmologists who whenever they see a case of Neurological dry eye would empirically treat the dog with antibiotics for 6 weeks. In half the cases, it, that may resolve the neurologic dry eye. So we can try these immunomodulating drugs, we can try pylocarpine, and if nothing else works, then we take the dog into surgery.
Surgery usually involves transposition of the parotid duct from the mouth into the eye that's shown here. We're cannulating the papilla of the parotid duct in the mouth. We are Isolating the duct, freeing it up, and then transposing it to the eye here, the hemostat is inserted, inserted through the fornx of the lower eyelid.
We grab. The papilla with the duct and pull it up, tur it in the forenix, and now you have saliva, moistening the cornea. Used to be a very popular surgery.
I was training in Florida right, right around the time when Rene has one discovered cyclosporin. Before she came her discovery, we used to do 150 of these surgeries every year. The osporin came out, we went down to 1 or 2 surgeries per year.
So many dogs do respond, but occasionally you are forced to do the surgery, not an ideal surgery cause the saliva is not, tears and sometimes you may have build up of oxalate or calcium on the corneal surface which can be very irritating. Sometimes you may cause the reverse problem, too much saliva. Every time the dog sees food, he would start crying, if you will, using too many tears and causing opposite problem, but sometimes there is no choice.
So, We have spoken at length about quantitative dry eye. I remind you that is the deficiency of the aqueous part of the tier film. However, the tier film, as you may recall, has two more components.
It has the oily layer and the mucin layer, and deficiencies in these may cause what we call qualitative dry eye. OK, the quantity of the aques. Part of the tear film is OK, but there is a problem in the quality of the tear film.
There may be loss of the lipid layer and that will be due to destruction of the myboing glands where the lipid is produced. That's that drain these glands. So cases of chroniclephritis such as I showed you earlier or inflammation of the gland will cause loss of the lipid layer and on the other hand, we may get loss of the mucin, the inner mucin layer if We have loss of goblet cells in conjunctivitis.
The goblet cells producing the mucin layers are in the conjunctiva, so cases of infectious or new conjunctivitis will cause loss of. How do we diagnose qualitative dry eye? Not very easy.
If you suspect lipid deficiency, look carefully at the margins, look invert the io margins, look at my boing glands, see if they're healthy or not, squeeze the eyelids in order to express them and see whether you get clear viscous oily secretion or not. And there was an instrument called the myboter. We published a paper about it some 12 years ago, but actually it was a promise that never panned out.
So it's more of close examination, using layer. We can evaluate it using what's called the tin breakup time shown here. It says fluorescine stain in the cornea in the dog one, so we have fluorescin covering all of the cornea surface.
And then keep the eyelids open, prevent the dog from blinking. Start looking at your watch and wait to see these breaks in the fluoresce showing up. That tells you that the tear film is breaking up.
Normal dogs, the tear film should stay intact for 10 seconds or more. It breaks up in less than 10 seconds. You may have using deficiency, you can confirm it by taking a biopsy of the.
OK. The go. How do we treat qualitative dry eye?
Well, if we suspect inflammation of the my boing glands, we can treat those with antibiotics, steroids, and compressors, and we try to replace the missing lipid layer or the missing mucin layer with preparations as shown here and in this table here that are specially made to replace. A few words about dry eye in cats. As I said, in dogs, the most common cause of dry eye is autoimmune inflammation.
In cats, the most common cause of the disease is feline herpes inflammation. And really feline herpes causes dry eye by lots of mechanisms. As I mentioned earlier, the virus is destructive to the tear gland.
It causes inflammation of the tear gland, so that's one mechanism. Then the severe inflammation also causes scarring of the ducts, draining tears from the gland to the eye. The virus, damages the trigeminal nerves, so there is less corneal sensitivity, meaning less blinking, so less spreading of the tear film and as if this wasn't enough, there is loss of the conjunctable gobat cells causing loss of mucin.
So really lots of ways in which the herpes virus causes dry eye in cats. And here you can see people dry eye in cat and again I point out the dry, dull looking, flash of the camera. However, it is more difficult to diagnose dry eye in cats than it is in dogs due to huge variation in the normal production values.
You can see the range of normal tear production in cats is measured with a shimmer tear test. With a red tier test and with a tier film breakup time that I showed you earlier, huge variation. So basically we diagnose it based on history of herpes, infection and on the clinical signs as I've shown you here.
And sadly, because it's not an autoimmune inflammation, it's a viral inflammation. Treatment is less effective. Basically, what we can offer them is hyaluronic-based artificial tears to replace the loss of public cells.
We can try some of the drugs that we give in dogs, cyclosporin, tacrolimus, andarine, and the broad deduct transposition that I mentioned, but we really have no effective, we are not sure whether or not. So that brings to an end the first half of my lecture, as I said, production problems, but I won't go on and talk about drainage problems and excessive tearing, what we call epiphara as shown in this picture of excessive tearing on the face of this. Barrier do.
And when you have excessive tearing or epiphera, it may be due to one of two reasons. Either there is something irritating the eye causing more production or maybe production is normal, but this picture is caused cause tears are not drained. So when presented with the clinical pictures such as this one.
You want to first rule out excessive production by looking carefully for causes of irritation. Check the eyelid margins. Is there entropion irritating the eye?
Check the eyelashes. You can see here in this picture, in this picture thisitia coming out of the my bonela openings. Obviously they're irritating the cornea.
Maybe there is a foreign body, so. First, look to see whether there is something irritating. Once you've ruled out irritation and excessive production, you have to start considering drainage problems.
That We need to remember the anatomy of the drainage pathway. So here we have again the main tear gland and the tear gland of the third eyed producing tears, drainage. It begins through two small openings called punctas at the eyelid margin, about 1 or 2 millimetres from the medial cans.
I'll show you a picture in a minute. Each puncta is connected to a short canalliculi as shown here. The two canalliquili come together in a larymal sack, and this sac.
Leads into the nasolacrimal duct which as the name implies, nasolarymal leads to the nose. Obstruction of drainage may occur anywhere along this pathway. From the puncta to the distal opening, it may be congenital or acquired.
We'll talk about that in a minute and it may be internal, something plug obstructing the pathway from the inside or it may be external such as this cyst here pressing on the nasallaal duct from the. So if we've ruled out that something is irritating the eye and causes causing excessive production and we are suspecting drainage problems, we have to confirm it and what the easiest way of confirming it is with the fluoresce passage test, the Jones test, put a drop of fluorescine in the cornea and wait for it to appear in. The nostril may take up to 10 minutes for the dye to show up in the nostril as you were seeing here, and please remember to check the mouth because many of them have ectopic openings in the mouth, rather than in the nose.
This is a picture I love showing cause it really shows the power of this fluorescent passage test. Here is a poodle presenting with severe epiphari. You can see both.
It stained with excessive tearing, so we put fluorescine in both eyes and look what happened. Here in the right eye, the fluorescine didn't arrive in the nostril. Indeed, it drained or spilled over the eyelids and is moistening the cheek, so staining the cheek, sorry.
So obviously here in the right eye you have blockage of the nasolacrimal duct. Left eye, however, you see that the fluorine has arrived in the nostril and then we take a close look at this eye and we see that this dog had entropion in the lower left leg. So both eyes with identical clinical presentation, one of them due to obstruction, the other one due to irritation, fluorescine gives you the answer.
You can confirm this by cannulating the system and flashing it, . Angulation is usually done through the upper puncta, which you can see here, you insert a catheter, this flushing may be diagnostic and may also be therapeutic as you are flushing it with saline, maybe be a bloodline. Or a type of secretions or a foreign body may come flying out and you've resolved the inflammation.
If something does come out, you may collect samples for culture and sensitivity and instead of flushing with saline, you can also flush with drugs, antibiotics. It so Therapeutic You can also cannulate without a flash, so we can cannulate the system with a 20 nylon suture passing again through the upper puncta coming out the nose, and if you think there is a chronic inflammation in the eye and you think that gosh maybe. The mesolaal duct is going to scar or the nose.
You can thread the tube over the suture and then leave it in place to prevent stenosis. This is what you're seeing here in this horse. The tube went through the puncta out the nose, tie them together, keep it in place for a few weeks.
Cases of inflammation. And a final way of confirming the diagnosis is through imaging, with contrast material, Dareo cysto rhinography, Dacreo is tears, cyst, so the tear sac, rhino is the nose, really a very long word, but what it says is that you are imaging the system by injecting. The die at the puncta and trying to follow the pathway.
Here we have a patent pathway. He pathway is blocked. So what are the most common causes of obstruction?
Well, in some dog breeds we will have an imperforate punkta. The punkta didn't form or it's a very small punkta. If it affects the upper punkta, we'll probably lower puncta.
But if there is a lower puncta, then yeah, we'll get a Piphora, we'll cannulate the upper puncta, we will flush it and then we'll see this small bulging where the lower puncta is supposed to be like and forming there and then you can take your scissors, remove this tissue that is covering the lower puncta, the imperforate puncta, so create an opening or widen an opening and you've resolve the problem. Another common cause of, of obstruction is inflammation of the nasollamal system. So, patients with acreocystitis will present with signs of inflammation limited usually to the medial part of the eye, so medial discharge, conjunctivitis, dermatitis, andsation all limited to this area.
Again, cannulation and imaging will give you a diagnosis and as I said. Said earlier you can treat them by cannulation with an indwelling tube such as you are seeing here or maybe refer them to surgery. This is tricky surgery.
You do have to go open the cyst and drill through the bone to expose the nasolachal, the lamal sac, remove a foreign body, for example, and then again put in a tube prevent scarring. If that didn't work, well, sometimes some people may contemplate surgery to create new drainage pathways. You can see here a drainage pathway drilled into the nose.
You can see here a drainage pathway created in. To the mouth and here is an example in a, a dog, but here I would say you have to pause for a minute and ask yourself with these types of surgeries, are you helping the animals or are you helping the owners? I mean, when you are seeing this type of dog.
Gosh, OK, yeah, it's not very cosmetic, but the dog is not terribly bothered by it. This is not severe enough to justify such a dramatic and drastic surgeries treating into the nasal cavity. Maybe it can just be treated with frequent cleaning and treatment of avoiding surgery.
Which really brings me to the last topic I wanna quickly mention the tear stain, tear stain that so frequently bothers the owners. What causes this tears pain? Well, if there is, if this tear stain is present in miniature dog or placephalic dog, it is often caused by medial entropion.
So there is entropion right here in the medial part of the lower lid, right where the punkta is supposed to be. The lower lid is rolled inwards and thereby the puncta is shut off because it's rolled inwards and furthermore, you have hairs from the Inverted eyelid irritating the cornea and causing excessive irritation. So there is irritation of the cornea and obstruction of the junta.
Lacephalic cats will also present with a tear film stain, but here it is caused by clinking of the nasal. Bromal duct, in this b cephalic cats, this is, the duct in a normal cat and this is the duct in a bachphalic cat and you can see the severe kinking that causes this, obstruction. So in cats can't do much about them.
In dogs, yes, if there is a middle entropion, you may resolve the problem by doing a. A hot Celsius repair of the medial entropion. However, remember that many of these bracephalic dogs have other anatomical factors that I mentioned earlier asiasis to her, the facial folds, the etc.
Etc. So. Before promising the owners that this simple surgery will solve problems, maybe you want to confirm that temporary measures such as staples or skin surgerys will in fact solve the problem, or else you may be looking at a more, radical surgery to this entire complex of an.
And finally, people always ask why is it brown? Well, it's brown because of lack of rain in the tears. There is iron in it and with lots of tears, you will get iron stains.
That's what causes it to be brown. Nowadays on the internet you can buy many magical proportions that promise to remove this. Stains here it says I stain, eye tear stain remover.
That's the wonderful thing about the internet. You can sell anything you want without furnishing any proof. We don't really have any, clinical studies showing that any of these preparations work.
Some people claim that thylacine, tetracycline, or metronitazole may work, but again, studies are lacking. So we've spoken about production problems, we've spoken about drainage problems. If you were asleep for most of my talk, that's OK.
Please remember just one a whole message and that is that in every red-eyed patient, please measure tear production. You'll be surprised by how many cases of KCS you can diagnose. I thank you very much for your attention and we'll be glad to take any questions you may have.
Great, thank you very much for that tour de force, Ron. We have noticed there have been some sound issues and apologies if anybody's been struggling with that, but I think Ron's slides were very comprehensive, so you should have been able to, make out the, the message he was trying to get across if that was the case. We have got one question so far, just to remind everybody, there is the Q&A box if you want to ask one.
So it was, earlier on in the talk, really enjoying the webinar, Ron, in cases where owners are having real trouble with topical treatment for KCS like dog bites, is it worth giving oral pylocarpine a try? You, well, yes and no. Oral pylocarpine is usually reserved for neurogenic cases, so you may get some additional.
Production if you stimulate production of tears with hylocarpen, but in most cases, we are talking about an immune autoimmune inflammation of the tear gland and therefore really yosporin is a drug of choice. If the owners can't medicate the dog publicly, I have another option for you. And that is cyclosporin implants.
You can buy them, from the veterinary school at North Carolina State University. They'll ship them anywhere in the world. They are very simple to insert, you insert them subconjunctively, which means just one snip of the scissors, here.
The pocket in the conjunctiva, throw in the implant, place a couple of sutures, and the implants will provide sustained samples or release for 12 months according to the manufacturer or even longer in some cases. So owners who can't medicate, that may be a solution for them. OK, fantastic.
OK, we've got another one comes through. If non-responsive to optimune, do you use a stronger cyclosporine topically before opting for tacrolimus? Frankly, well, I know that in England you may have some, regulatory issues with whether you are allowed or not allowed to use compounded drugs.
Personally, I nearly always use topical solutions, that are usually 1.5 to 2% of cyclosporin, so about 8 to 10 times stronger than the ointment. Usually that is my drug of choice, the solution.
I reserve the ointment for those cases in which the dog is irritated by the olive oil or the corn oil in which the cyclosporin is diluted. So yes, definitely, if you should try the topical solutions. One thing you shouldn't try and thank you for bringing it up is human preparations.
I mentioned earlier that has one discovered cyclosporin, for us veterinarians. It took another 15 years or so until cyclosporin made its way from the veterinary market to the human market, and today there is a drug called reassis. Produced by our end for treatment of dry eye in humans, concentration of Ritai solution is 0.05%.
So one quarter of the, ointment that we're giving dogs. So do not be tempted to use rtais, that's probably too diluted, use compounded preparations 1.5 to 2%.
OK, great. We've had a response to your initial response, so the y exploring implant sounds very exciting, so they're gonna look into that. So thank you.
As I said, sorry for interrupting. The only place I'd say you have to, search for North Carolina State University, the pharmacy of the teaching hospital, and they have a page dedicated to cyclosporin implants. If you are going one.
Critical issue. They are also selling cyclosporin implants for horses. Those are intended to treat equine recurring UVIs, do not mix the two.
By canine implants for dogs, buy equine implants for equine recurring UVI. Excellent. Another question, can anything be done to remove pigmentation once present in chronic cases of KS?
OK, number one, as I said, persistent, therapy will cause some, . Regression of pigmentation. Tell the owners this is something that they'll begin to appreciating in 6 months from now, OK.
So again, an education is very important. You have to tell them 2 months until the inflammation is under control, 6 months until you start seeing improvement implementation. You'll not see it in all cases and especially not in these black cephalic dogs, that, as I said, have.
Sorry, where was that slide? . In the bracket cephalic grids where you have a host of anthropics such as the skin folds, etc.
Etc. Here, the pigmentation is also because of the shallow orbit because of the lack of talmus and the Nasal fold irritation. So here you may probably need a more dramatic surgery as shown here plus cyclosporin, before the pigmentation would resolve.
So many of the bracket phallic breeds, just cyclosporin will not be enough. And those who need to combine with surgery to treat the ocular bracketphalic syndrome. OK, great.
So there are no other questions at the moment. If anybody has any burning questions, if you can either post it in the Q&A or the chat. I'll give it about 10 seconds.
Yeah, and Dawn would send me questions, if she gets them at a later stage, so that's OK. I'm not going away. So, I'm always reply by email at a later stage.
If you think of anything, email Dawn, and she'll pass them on to Ron. So nothing else is coming through. So just again to say thank you very much, Ron.
That was an excellent presentation, very thorough. Thank you very much, Andy. Thank you everyone for coming.
Yeah, we'll see you again next time. Thanks, Ron. Good night.