Hello, everyone, and welcome to my lecture on the diagnosis and treatment of the red eye. My name is Ron Offrey. I'm a professor of phthalmology at the Veterinary School of the Hebrew University of Jerusalem in Israel.

Now, I think we all know that red eye is a very common, perhaps the most common ophthalmic complaint with which patients may present in your clinic. However, not all red eyes are created equally. There are subtle differences.

Between red eyes, depending on what causes the red eye, which is why I call this lecture 50 shades of red. And hopefully, by the time we are done, you'll be able to diagnose the different causes of red eye and treat them properly. I should note that this lecture is part of the ophthalmology stream of VC 2021.

The other speaker at the stream is Professor David Maggs from UC Davis, who is my co-author on Slatter's Fundamentals of Veterinary Ophthalmology along with Paul Miller from Madison, Wisconsin. We've co-authored the 4th, 5th, and 6th editions of the book. I should also note on a sadder note that this talk is dedicated to the memory of Pip Boydell, a fellow phthalmologist from Britain who passed away a few years ago.

PIP actually sat with me for the first ECVO board exam back in '96. . And I miss him terribly.

This talk, in fact, this entire session is dedicated to his memory. So, as I said, the topic of the talk is red eye, and here we have 3 different red eyes due to 3 different ophthalmic diseases. And this lecture is being recorded, but if we were doing a live stream, then I would stop for a poll question asking you for your thoughts on the diagnosis and the causes of each of these red eyes, since this is a recorded lecture, you can actually press the pause button and take a moment to think.

I'll jump in and say that actually, well, if you don't want the differentials, pause now. If you want the differentials, I can tell you that we are looking at eyes with conjunctivitis, glaucoma, and UVI, which are the most common diagnosis for red eye. So you can pause the recording to take a minute and think about it.

And if you are back, here is your answer. We have a red eye due to glaucoma, TUVitis, and to conjunctivitis. And as I said, these are the three most common and important differentials for red eye, but there are other differentials that you have to consider, including deep keatitis.

Oops, sorry for the spelling mistake here, superficial keratiti and an orbital disease. So actually, we are looking at 6 diseases that we want to consider that when we are presented with a red eye, and the question is how do we go about differentiating between these 6 causes. So really, with every red eye that presents in your clinic, you want to consider the following diagnostics and the following things that you wanna look out for.

We'll go through them one by one, starting with the depth of the blood vessels. Actually, red eye can be caused by two types of blood vessels. It may be due to congestion of superficial blood vessels, and superficial blood vessels are congested in cases of conjunctivitis or in cases of superficial keatitis.

Deep vessels, on the other hand, are associated with uveitis, glaucoma, deep keratiti, and orbital disease, so the other four differentials that I mentioned previously. The question is obviously, how can you tell by looking at the blood vessel whether it's a superficial blood vessel or whether it's a deep blood vessel. Well, Superficial blood vessels.

Originate in the conjunctiva and we frequently invade the cornea and are individually identifiable as you can see here in this picture, I am pointing towards this conjunctivi blood vessels which is invading the. Cornea and so is this one and this one. You can see individual blood vessels and I stress the word individual cause in the next slide, I'll show you invasion of blood vessels that cannot be seen individually.

They branch frequently as you can see here, sort of like roots or branches of a tree. Often they present with camosis, which is a fancy word for edoema of the conjunctiva. So you see a really congested conjunctiva with branching surface, branching vessels on the surface.

The superficial vessels are of smaller diameter than the deep ones we should be discussing in a minute. They are mobile unlike the Deeper vessels, and if you're unsure, you can always take a drop of 1% epinephrine drops and place them on the conjunctival surface or on the ocular surface. Superficial vessels being superficial will blanch very rapidly as opposed to the deeper vessels which will take more time to blanch when topical epinephrine is applied.

Deep vessels can originate in two places. We can get a red eye due to congestion of the epicleral blood vessels, which are large diameter vessels that are shown here in this diagram. This is the epicleral blood vessels.

You can see. That indeed they are deeper than the conjunctival vessels that I just spoke about in the previous slide. And here is a picture showing congested epistcleral vessels.

So you can certainly see that they are much larger in diameter than the previous vessels that I have shown. And the second possible source for the red eye due to deep vessels is congestion of anterior ciliary or circumcorneal vessels shown here, so really deep vessels that are actually from the ciliary body and congestion of these vessels cause they are located inside the eye underneath the sclera will cause more of a diffuse. Red flash, you can't really tell many of the individual blood vessels here.

It is sort of a diffused red flash and when it invades the cornea, it looks like a paintbrush or bristles on your toothbrush. You can't identify the individual blood vessels as you could in the case of the supervision conjunctive vessels shown previously. Branching is rare.

Again, it's impossible for me to see branching here and here, in the case of the epial blood vessels, they don't really branch and they are immobile because they are beneath the conjunctiva. OK, if the conjunctiva is up here, this Blood vessels as are here. So yeah, I can move the conjunctiva and the conta blood vessels with a swab or even with forceps if I apply topical anaesthesia, but even if I move the conjunctiva, I hope you're looking at the camera screen with my hands, these ones will remain immobile.

And here is a close up of the two blood vessels, conjunctival superficial ones on the left, and you can see the individual vessels branching like roots or branches of a tree, so they are on on the conjunctiva and these are the large diameter episcleral vessels associated with glaucoma, I might add at this stage. You see that they hardly branch and you can see the difference in diameter between these epicleral blood vessels and the conjunctival vessels, which are what you are seeing here. So, an obvious difference in diameter, also differences, as I said in the response to epinephrine and whether or not you can lift them.

So, really, just by looking at the blood vessels and determining whether they are superficial or whether they are deep, you can already get an indication of whether you're looking at superficial disease, primarily conjunctivitis and KCS or whether you are looking at deep disease process, glaucoma, uveitis, datitis, and orbital disease. Next thing you want to check in each and every patient presenting with dry eye is do the Schmer tear test. In some cases, it's obvious that you have to do a Schermer tear test cause you see here the secretions, the purulent.

Secretions, suggesting dry eye, you also see the dull reflection of the camera flash. Many of the KCS patients will present with a dry looking cornea, but even if you don't see These signs really, there is no excuse for not doing the Schirmer tier test, which takes just 60 seconds. Normal values are 15 millimetres wetting per minute in the dog, 9 millimetres of wetting per minute in the cat, and as I said, in every case of red eye, please do.

Schmert test. You'll, number one, it takes only 60 seconds per eye or 120 seconds for both eyes, and you'll be surprised at how many cases of dry eye you may have missed if you didn't perform the test. And number 2, it's a very visual test.

You remove the test strip, you show the owners the amount of wetting, and you tell them, you see, the wetting was supposed to reach all the way here to 15. Your dog has only 4 or 5 millimetres. It has dry eye.

It's a very visually striking test which owners can always relate to. So, with the Shimmer test, we can really narrow down and finalise our list of diagnosis. This patient has a dry eye.

The next thing you want to consider is the pupillary light reflex and or I should say the pupil size and its reaction to light, the pupillary light reflex, that would also help us differentiate between some of the diseases. The pupil is meiotic in cases of UVIis. You can see that in the left eye of this dog.

You see that it has a red eye, you see that the iris is more congested and it has a meiotic pupil cause UVitis, and again, I hope you're looking at the camera, is characterised by spasms of the ciliary muscle and the iris causing constriction and because the pupil is meiotic, PLR may be minimal. Because the pupil is already constricted. So even when we shine strong light at the eye, there won't be much of a response because the pupil is already constricted.

A good indication, something you want to do at this point is maybe check the consensual or indirect constriction in the other eye. If we're talking about the pupil in UVITs, remember that it may be distorted due to adhesions, of the iris to the lens, adhesions that are made possible due to the presence of fibrin and platelets and other adhesive factors in the anterior chamber. We'll talk about that in a minute.

Do keep in mind there's another differential that the people can also be meiotic in cases of acute keraitis and corneal ulceration because there is a neuronal feedback from the trigeminal nerve, the sensory nerve of the cornea to the ciliary muscle, and any stimulation of the trigeminal nerve will cause the spasms, secondary uveitis and meiosis. Glaucoma, on the other hand, patients will present with a fixed dilated pupil. It is non-responsive to light.

It can be non-responsive due to loss of afferent input because of damage to the retina and optic nerve and can be Non-responsive because of lack of efferent input if in case the iris sphincter has been damaged. So again, you may wanna check the consensual PLR in order to determine whether you're looking at lack of afferent or efferent input. Fixed dilated pupil is also possible in orbital disease if there is a retrobulbar abscess or retrobulbar tumour compressing on the optic nerve, then again, you have loss of afferent input and you will have a fixed dilated pupil.

On the other hand, conjunctivitis and dry eye will present with a normal pupil. So, again, by looking at the pupil and its reaction to light, we can get an indication of whether we are looking at glaucoma, fixed dilated pupil, UVI. Myotic pupil or conjunctivitis, a normal pupil, even though, as I said, it may also be affected in a secondary fashion with the other diseases.

The next thing you will want to check is aqueous flare and loss of transparency in the aqueous humour due to presence of inflammatory material. I'm talking about platelets, about white blood cells, about fibrine, about proteins that leak in. To the anterior chamber in cases of UVIT.

So aqueous flare is really an indication of UVITs. How do we detect aqueous flare? Here are a couple of slides showing you how to best do it.

On the left, we have an eye of a normal patient. We are shining a fine beam or a fine slit of light onto the eye and you see the beam of light reflected on the cornea and we see it reflected on the surface of the iris and the lens. In between the two, we have this dark gap.

This is the interior chamber and the aquiumor in this animal is transparent, which is why this is dark. On the other hand, on the right-hand side, we have an inflamed eye, and again, we shine a slit or a beam of light on this eye. You see it reflected on the cornea and even a bit on the eyelids here.

You see it internally reflected on the iris and the lens, but you see this area, the interior chamber, which was previously dark, it is all lit up. And it is lit up because the light is scattered by all of the inflammatory material that is floating in the interior chamber, the platelets and the fibrine and the white blood cells that I mentioned earlier. The analogy I'd give here is, if you are driving at night and you turn your car headlights on, if it's a dry night, then the car lights are well focused, illuminating the road in front of you.

However, if it's a foggy or a rainy night, then the headlights are scattered. They are diffused cause the light beams strike the water droplets in the rain or in the fog, and they are scattered. This is exactly what happens here.

These particles in the aquium or are scattering the light beam. So, as I said, you can do it with a, a fine slit of light or you can use the smallest aperture on your direct ophthalmoscope and looking through it, you can also visualise a transparent aqueous, transparent aquiumor or foggy aquiumor as shown here on the right. If you need another analogy, I once gave this lecture in China, and after the talk, we went to a restaurant and obviously, we had some beer, after a long day of lecture, and then the guy sit next to me looks at me and says, Well, here is your Aquez flair, filtered beer, unfiltered beer, OK?

So, here is the transparent aquiumor, and here is the aquisumor with all the particles or the beer with all the particles since it's unfiltered, floating. So you may wish to remember this analogy. But going back from beer to the eye, we are talking about Inflammatory material which may float in the equiumor and cause loss of transparency or it can actually form all sorts of clots and adhesion.

So here we see a large fibrine clot with some blood in it. Here we see another clot of fibrine, we see hyema cause we can also get blood leaking into the aqueous humour. We see the particles settling on the inner aspect of the cornea, we call it craic precipitates.

Here in this picture, we see a setting on the inner aspect of the cornea and on the anterior lens capsule. So if you see a dirty cornea, or a dirty lens that may also indicate the inflammatory material. So all of that, the aquiumor, the fibrin in the interior chamber, the hyfema, the hypopion, excuse me, are indications that you are looking at the red eye caused by UVIT.

Obviously, another important diagnostic test that you want to do is tonometry or measurement of intraocular pressure. As we know, pressure is elevated in glaucoma, that's the very definition of, glaucoma, elevation in intraocular pressure. Pressure is normal in UVIs, sorry, it's lower.

In UVIs and that's because of increased drainage of aqueous su or from the eye. It comes as a surprise, to people that pressure is lower in Uveitis cause UVIT, as I just explained a few slides ago, we're talking about leakage, of inflammatory material and exudate and transodate, from blood vessels of the UVI into the interior chamber. So if there is leakage, you'd expect pressure to go up.

Yes, there is leakage and there is theoretical elevation of pressure, but it is offset by the increased drainage of aquereas from the eye, and I'm talking mainly about the unconventional outflow, through diffusion from the UVA and sclera and not through the iridocornea. And finally, pressure is normal in cases of Conjunctivitis, so really measuring of measurement of intraocular pressure is very important for distinguishing between the three diseases. It's very important to measure pressure in both eyes, because, significant differences between eyes are suspicious, even if both are within normal range.

We usually say That the normal pressure in dogs is 15 to 25 millimetres of mercury, but if you are measuring pressure of, let's say 24 in one eye and 1213 in the other eye, you definitely have to ask yourself, why is there a 100% difference in pressure between the two eyes you want it to be within 20% of each other. In this context, I should note that normal to borderline high pressure in UVITs is also suspicious because I just said in the previous slide that in UVITs, you would expect pressure to be low. Some cases of UVITs that have intraocular pressure of 567 millimetres of mercury.

If I see an I with UVI and pressure of 20, for example, I would definitely be worried that the hypotensive effect of UVITs, the lowering of pressure in UVITs, is actually masking glaucoma, and if it wasn't for the hypotensive effect of UVIT, I'd be measuring pressure much higher than 20. So again, if there is A patient with UVI and pressure of 7 in one eye and 20 in the other eye, significant differences between both eyes, you definitely should be worried. When measuring pressure, please remember not to press on the jugular veins while taking readings cause that would decrease outflow actually in Men wearing a necktie is a risk factor for glaucoma, which is why I'm not wearing a necktie today.

And a very important point, please use an instrument to measure pressure, not your fingers. I've been doing it for 25 years or more, and I still cannot place my fingers on the eye and measure pressure. You need an instrument.

I strongly recommend the modern electronic applation tunnel pen or rebound tone of that, which take accurate readings, no matter the position of the eye, they take several readings and provide you with a Mean reading and statistical error. If you can't afford them, then the least you should buy is an indentation, Shistonometer, less friendly to use, takes more practise, less patient friendly, but you do want some sort of an instrument that will provide you with pressure reading, you can't use your fingers as I said. And with a tonne of vet or a tunnel pen or a shields, you can distinguish whether you, you can determine whether the red eye is caused by glaucoma or by UVIT.

Next, we want to check retropulsion. Retropulsion is shown here. I am placing my fingers on both globes through the eyelids and I am applying pressure.

Now, I'm not measuring intraocular. Pressure. I just said two slides ago that you need an instrument to measure intraocular pressure.

You can't do it with your fingers. What we're doing here is trying to push the eye into the orbit and determine whether there is something behind the globe. Such as you see here, resisting this pressing or this retropulsion test, OK.

So if there is a retrobulbar abscess or a retrobulbar tumour such as you were seeing here, obviously, you'll not be able to push the globe back into the eye and this would indicate that you are looking at a retro bulbar disease. Now, I know that it sounds kind of challenging, putting your fingers and trying to determine, is this a normal tensive eye that will not be pushed back into the orbit or is this an eye with elevated pressure that is being pushed back into the orbit, but if you do compare both eyes and with some practise, you can tell the difference and the retropulsion test is a very Easy test to determine whether or not you've got orbital disease. Of course, if you suspect an orbital disease, then your next diagnostic step would be imaging, either an ultrasound or a CT MRI as you saw in the previous slide.

And finally, of course, we must stain each and every red eye to determine whether or not you have a corneal ulcer. So this would be the final test you perform and that would help you determine whether it's just simple conjunctivitis or whether you have ulceration causing deep parotitis or maybe secondary to dry eye. Besides all of the tests that I have mentioned, there are additional unique signs for each of the leading differentials that I have listed.

Conjunctivitis has unique signs. Number one, it's the only disease listed that, in which a patient will present with mucroid or purulent discharge, and that's because we do have infection or inflammation of the conjunctiva. It's the only one where the 3rd eyelid will be involved in other words, it will be congested and it will be red.

Note that the 3rd eyelid may be elevated in retro bulbar disease in orbital disease. If you have a disease process behind the eye, pushing the eye forward, it will also push the 3rd eyelid forward, but the presentation of the eyelid, 3rd eye. It will be normal looking.

You won't see the congestion that you are seeing here in this conjunctivitis patient. Chemosis, as I said, characterises conjunctivitis. As you can see in this picture, we have a congestion of the conjunctiva both on the 3rd dili on the globe, and on the palpibr conjunctiva.

And finally, Lymphatic follicles, you see these follicles here on the conjunctiva of the lower eyelid. You will see more of them if you invert the third eyelid and look on its inner surface. If you have hypertrophy.

Of lymphatic follicles and note their clinical presentation. They look like grapes. And as I said, if you flip the third eyelid, you'll really see clusters of grapes that tells you that this is a case of conjunctivitis.

Glaucoma also has unique signs. Number one is almus as the pressure increases, then you have expansion of the globe and the patient presents with this thalmic or enlarged eye. Stride keratopathy is another sign that is pathognomonic to glaucoma.

You see this white line here? This is really, I would say a fracture or a fissure in the cornea. As the eye stretches to become buthalmic, you get fractures or fissures in the inner.

Cornea in decimates membrane, almost like cracks appearing in the ground in cases of earthquake, and this can only be caused by elevated intraocular pressure and by glaucoma, and that's a sign, that will Remain even if the balmus is gone and is resolved. Another sign that's unique to glaucoma is cupping of the optic nerve, which is what you are seeing here as the eye expands, there is one focal point where it is extremely weak, which is the optic nerve head and more pressure is applied to the optic nerve. It is sort of like a tyre or I'd say a balloon with one weak point, you inflate the balloon and it expands symmetrically, but then you get one bump there at a point where the balloon may have been weak.

This is what we're seeing here. This area of the optic nervehead. Is more depressed, we call it an optic nerve cupping.

Notice that all the blood vessels come to the edge of the cup and they dive into it cause it's literally diving into a cup. So, these are the signs that are unique to glaucoma and finally, UVIis will also have unique signs in that. There is a dark congested iris such as you see in the left eye of this cat.

Not surprising. We're talking about UVI, we're talking about increased blood flow to the UVA, more blood flow in the iris, more pigments, so it's darker. We'll get posterior synichia, as I mentioned earlier and as in here, adhesion of the iris to the anterior lens made possible by all of the.

Inflammatory material that is floating in the interior chamber leading to this misshapen pupil. You can see here the iris being adhered to the lens. And if you can look at the posterior segment, then you will see often posterior uveitis, cho retinitis, signs of posterior segment inflammation, including retinal edoema, retinal detachment, retinal haemorrhage, .

All of these indicate that you're looking at posterior UVITs, which goes hand in hand, often with anterior UVITs. So we have all of the signs that we've discussed earlier that we look for in order to try and distinguish between our differentials, and we have the unique signs of conjunctivitis, glaucoma, and UVitis that I just described. Put them all together and now you know you're 50 shades of red and you know which is which.

As I've said, we are talking primarily about three diseases, about, glaucoma, uveitis, and conjunctivitis. So, I want to conclude my talk by telling you, at least in my opinion, what is the most important thing you have to remember about each of these diseases. The most important thing I want you to remember about UVIis is that bilateral UVIis is most often due to a systemic disease.

My friend David Mags whom I mentioned earlier, really calls it an ocular lymphadenopathy. Just like a systemic disease will cause a lymphadenopathy with the poll and the submandibular and scapular lymph nodes, it also causes lymph adenopathy in the eye, and that's uveitis. And therefore, just like lymphadenopathy, UVI is not a diagnosis, it's a clinical sign.

When you find enlarged submandibular lymph nodes, you don't go, aha, I have a diagnosis. You begin working up the patient asking yourself, what causes. Is lymphadenopathy, and that's what you should be doing in cases of bilateral UVITs.

Systemic workup is mandatory in order to determine or identify the systemic disease causing the UVITs, but please keep in the back of your mind that many of them are UVITs. Here are bi or idiopathic. Here are a couple of examples.

Here is a study from Purdue University in the United States looking at the causes of canine UVI. 55 dogs, 14 of the 55 were diagnosed with infectious agents, and here I would say it depends on what's endemic in your area. So in Indiana, you can see that mycotic and fungal infection are a common cause of uveitis.

For people in Meterranean area, it may be Erlichia or Lismania. In other places, it may be Babezia, whatever. Is endemic in your area.

They had cases of VKH or uo dermatological syndrome and autoimmune disease. They had lymphoma and I am sorry here, it should be, definitely, you can see that I made a mistake, it should be 34 rather than 4. I, I dropped the 3 here, cases which are idiopathic.

120 cats with UVI is a study from North Carolina State University, and you can see the leading causes of cats, with UVITs. Toxoplasmosis is a leading cause FIP. FIV FELV againnioplasia, and idiopathic UVitis is a leading cause.

So in both dogs and cats, you have to do systemic workup cause you want to know if the cat has toxo or you want to know if the The dog has blasto, you do have to diagnose these systemic diseases and treat them, but be prepared, for the possibility that despite extensive workup, you will find nothing and the disease will be idiopathic. David Maggs, my colleague is going to talk extensively about feline conjunctivitis, so I won't talk, I won't devote too many slides to it. The most important point I want you to remember is that conjunctivitis is really a classic example of the famous sentence, a dog is not a big cat or a cat is not a small dog in that our clinical approach to conjunctivitis in cats and in dogs is completely different.

In dogs, conjunctivitis is usually a secondary infection or inflammation in that there is something causing chronic irritation of the eye. Maybe the eye is overly exposed in brachycephalic breed, maybe it's irritated by abnormal eyelashes such as tracheasis or dysticiasis. Maybe it's irritated by entropion or exposed you to ectropion.

Maybe there is dry eye. I hope everyone is seeing the dull camera flash here on the cornea. So something is irritating the eye causing a secondary infection and therefore, when you are presented with a dog suffering from conjunctivitis, and I hope by now you have You know how to determine the conjunctivitis and not other causes of red eye.

You need to devote your energy to identifying and treating the primary cause. So do a comprehensive ophthalmic exam, checking the anatomy of the globe of the eyelashes, of the eyelids. The tumours, as I said, do everything you can in order to identify and treat the primary cause, and then you can treat the infection or inflammation with both broad spectrum antibiotics or steroids as the case may be.

But the important point is that if you treat a patient with conjunctive without reaching a primary diagnosis and treating the primary diagnosis, in most cases, the infection will return once treatment has stopped. So in dogs, it's a secondary disease and we concentrate on diagnosing it and then treat the secondary inflammation. In cats, it is a primary disease usually caused by herpes, herpes, and herpes, sometimes by chlamydophila, and as I said, David Mags is going to talk about it in greater detail in his talk.

And the most important thing I want you to remember about glaucoma is that it may be a glaucoma may be a primary or secondary disease, meaning it may be inherited or it may be secondary to another ocular problem. But the really important point here is that Even patients with inherited glaucoma, with primary glaucoma may present with unilateral disease. In fact, the literature teaches us that most cases, most patients with primary inherited glaucoma will present with glaucoma in one eye and the second eye will be affected only 8 months later.

And therefore, when you are presented with a patient with unilateral glaucoma, please ask yourself, is it a primary disease or secondary disease? And if there is any doubt, treat the other eye. And that's an important point I'm trying to make, and let me repeat it by way of discussing this slide here.

So we have this dog here presenting with glaucoma in the right eye. The left eye looks to be normal, and we attempt to treat, the glaucoma here with prostaglandin analogues and with carbonic chondrase inhibitors, and we throw every drug in the book at this eye, but Looking at this eye, I think it's the goner, and if it's not gone now, you'll probably lose the fight with the battle within a few months and you'll have to nucleate the other eye, to nucleate the eye. But then 8 months from now, the owner will come back and the dog will be blind in this eye.

And the owner will look at you and will ask you, Doctor, what happened? And you'll tell him it's glaucoma, and he'll ask you, could this have been prevented? And you will feel like crap, pardon my expression, you will feel very, very bad because what happened is when this dog showed up with unilateral glaucoma and you began treating the right eye, you forgot that it could be a primary glaucoma and that you should also provide prophylactic preventive treatment to this eye.

So what I'm saying is, what I'm trying to say is that when this patient presents with unilateral glaucoma, please try to determine whether it is primary or secondary. For example, are there, is there a sign of uveitis? If there is a sign of uveitis in this eye, then glaucoma in this eye was called by uveitis, hooray, you know.

No, if you see a tumour in this eye, hooray. I mean, it's fine to say hooray about the tumour in the eye, but if there is a tumour in this eye, it means that the tumour caused secondary glaucoma. It means that this eye is not at risk.

But if you perform an exhaustive evaluation of this eye and you can't find any reason for the glaucoma, please consider the possibility that it's primary glaucoma and either refer the patient to a specialist who can examine the angle of this eye through a test we call goneoscopy and determine whether it's, it is at risk to glau of glaucoma or if you can't refer. Please provide prophylactic preventive treatment to this eye. Now, obviously, it's just prophylactic treatment.

You are going to delay the onset of glaucoma. You're not going to prevent it. Our literature teaches us that if you begin preventive treatment today, you will delay the onset of glaucoma by 2 years.

So instead of this Becoming glaucoma test in 8 months, it's going to become glaucoma test in 32 months, which is great. You bought the dog another 2 years. And more importantly, when the owner comes back in 32 months with a glaucomatous blind left eye, and he'll ask you, could this have been prevented, you can look at them and say, we did everything we could and The dog was unfortunately blinded by hereditary glaucoma.

So, the most important lesson for glaucoma is when in doubt, treat the other eye. So to summarise my talk about the red-eye, please, when presented with a patient with red-eye, determine whether the blood vessels are superficial or deep, superficially indicating superficial keatitis or conjunctivitis, deep vessels, all of the other disease. Do the shimmer tear test to determine whether or not you have dry eye.

Look at the pupil size and PLR if it's meiotic think youveitis. If it's Or a secondary constriction due to keratiti. If it's fixed, dilated, it's probably glaucoma, though it may be retrovular disease.

Normal pupil, you are looking at conjunctivitis, aqueous flaring opacities of the aqueous tumour will indicate UVI. Elevation of intraocular pressure will indicate g global coma while hypoteny. Will indicate UVI, do the retropulsion test to determine if there is a retropulbar disease, stain every red eye for the presence of a corneal ulcer and look for the unique signs of conjunctivitis, of uveitis, and of glaucoma.

I am going to Bid you farewell by showing you this chart developed by my colleague Karen Plummer from the University of Florida. You can find it online if you go to the NABC clinicians brief website, showing you how to work up the red eye. According to the guidelines we have just discussed.

And since this is a recorded lecture and I will not be able to see or hear you, I have brought my own applause. Thank you very much. It's been a pleasure and I hope to see you at the live recording February 26th.

Thank you.