Hello, everyone. My name is Ron Offrey. I'm a professor of veteraninthalmology at the Hebrew University of Jerusalem in Israel, and I am here to talk to you today about why cats go blind.

Don't worry, I'm not going to be talking about the big and exotic cats. They're fun to work with, but maybe less relevant to our work, we will be concentrating on the Domestic cat that we see in our clinics. Actually, those of you who've been following me know that this lecture is part of an ongoing series on blindness.

I've already given 4 talks which you can find in the webinar vet archives beginning back in August of last year on applied anatomy of the funders. Then we spoke in October about the. Examination of blind patients, acute blindness in dogs, central blindness, and as I said today, we'll be talking about blindness in our feline patients, which means actually that we have just one lecture left, and I hope to see you all on September 23rd in the final lecture about inherited retinal diseases in dogs.

As always, I should declare that I have no relevant financial relationship with any product that I will be mentioning, but as always, I should disclose that I have a financial relationship with some of the pictures I'll be showing as many of them have been borrowed from Slatter's veterinary, Slatter's Fundamentals of Veterinary Oophthalmology, a book I've co-authored with David Maggs and Paul Miller, the last three editions of the text. So, what should we be talking about today? We'll be talking about feline uveitis.

We'll be briefly talking about cataract and glaucoma in cats, two leading causes of blindness in dogs, but may be a bit less common in cats. We'll be talking extensively about hypertensive retinopathy and we'll wrap up by talking about other feline retinopathies, retinopathies that are unique to cats and actually retinopathies that may be avoided. And as I said, we'll start things off by talking about feline UVITs.

Now, this is not a UVIT lecture. I've already given a talk about UVITs to the webinar vet and you can find it in the archives of the company. Instead, today we'll be concentrating on those aspects of UVITs that are unique to cats.

So those of you who remember my talk about canine UVIT may remember this table, which shows you the causes of UVITs in dogs, and actually some of you may be complaining about the small print and the fact that you can't really see much in this table, and that's true cause the aim of this table here is to show you that in dogs, virtually any systemic disease can cause uveitis, be it neoplastic or metabolic or immune mediated or any sort of infectious disease, be it algae or bacteria or fungal or viral or parasitic, toxic diseases, etc. Etc. Really.

Any systemic disease may cause Uveitis, especially in dogs, and that's why we tend to think of UVIis really as an ocular lymph adenopathy, just like, any systemic disease may cause lymph adenopathy in, the lymph nodes of the body. It can also cause lymph adenopathy in the uVal tract of the eye. So that's the way I tend to think about UVIis.

In cats, the list, as you can see, is much shorter. Yes, we're still talking about infectious and neoplastic and immuniated diseases, but really, when we're talking about blindness, which implies that we're talking about poster. Uveitis, then the list is even shorter.

We have 4 main culprits that can cause posterior UVIis in a cat leading to blindness. We're talking about FIV, FELV, FIP, so 3 viral diseases and toxoplasmosis. If you're in regions, parts of the world where you have fungal diseases, then cryptococcus, blasto, and other fungal agents may also cause posterior uveitis.

And in elderly patients presenting with unilateral UVI, please consider tumour as a cause, as a possible cause of UVIT. So these are really the main suspects, the leading suspects in feline posterior uveitis or choriorotinitis. And just to underline that point, here is a study published by my colleagues at North Carolina State University, looking at 120 cats with UVITs.

And as I said before leading culprits or suspects were toxoplasma with one quarter of the cases, FIP 15 or 16%, FIV FELV 10% each, and neoplasia, 5% each. Now, I know that for the last few seconds, none of you have been listening to me cause you've been doing some mental math in your head and totaling this up and saying, hey, we've got a speaker who doesn't know math cause this doesn't total 100%. Well, that's because the most common cause of UVIis in cats and in dogs is really idiopathic.

Despite the extensive workup, which I'll talk about in a few minutes, done to all these patients in North Carolina State University, in 40% of the cases, no a primary agent was found. And again, if you're doing the mental addition and arithmetic in your head, now you're coming up with a total of more than 100, but that's OK, you know that Some cats may be infected with more than one agent. As you know, for example, toxoplasmosis will often present with FIV or FELV.

But really, the main point here is that 40% of the cats suffered from idiopathic UVITs and the same findings have been demonstrated. In other studies, really in feline uveitis and in canine uveitis, I might add 30 to 60% of cases are considered to be idiopathic. A systemic cause is found only in 40 to 70% of cases.

Which obviously has a bearing on the prognosis and the treatment, which I'll talk about in a minute. I should note at this point that some people have suggested that many of these idiopathic cases in the cat are actually due to Bartonella infection, . And if you are ever in a boring meeting of ophthalmologists and you want to liven things up, you can always ask, what do you think about Bartonella as a potential cause of fela uveitis and you'll have people starting screaming at each other and throwing punches at each other.

It's really a very controversial subject. Some people believe it strongly and actually treat, these patients for Bartonella. Most people do not, do not believe it is a cause and in fact, I'm not aware of any study that has shown a correlation between UVIs and serology or titers for Bartonella.

As I said, I gave a lengthy talk about UVITs previously in the webinar vet, so I'm going to just skip the clinical signs of UVITs and move from causes on to treatment and as I implied, many of the UVIT's cases are due to a systemic cause and therefore, before treating cats that have been diagnosed with UVI, you really have to look for a systemic cause, keeping in the back of your mind that many of the systemic agents that I mentioned may also cause neoplasia. I'm talking about FLV and FIV or they may cause neurological disease. I'm talking about FIP and toxoplasmosis.

So you may want to add Neurological workup or oncological workup to your usual systemic workup. But basically, any cat that presents for UVIs, you should sit down with the owners and take a comprehensive history, status of vaccination, has the cat been travelling to endemic areas with fungal diseases, etc. Etc.

A thorough. Systemic and possibly a neurological exam, basic blood workup, CBC and biochemistry, and depending on your findings and what you suggest, you may start doing serology, PCR IFA, ELISA, etc. For some of the infectious agents that I mentioned, urinalysis, imaging, if you suspect the fungal agents, and As I said, often you'll come up empty-handed.

It may be an idiopathic case or the answer may lie elsewhere, it may lie in the aquiumor and you may consider tapping the interior chamber and taking a sample of. With you more or maybe you want to refer it to a specialist who will take a sample and submit it to serology and cytology. Here is a number of papers showing you how samples taken from, collected from the aqueous tumour via aqueous synthesis can be used to work up.

Dogs and cats with UVIT, especially useful in cases of coronavirus, as you can see here, and in toxoplasmosis and in neoplastic diseases of the eye. So this is another diagnostic modality that you may consider. Moving on to treatment, well, if you were fortunate enough to find a primary cause for the UVIT such as toxoplasma, for example, then obviously you want to treat it, but again, keep in mind that you will find it only in 40 to 70% of cases and that in 1/3 to 1.

And therefore, only 1/3 to 1/5 of all your VIT's cases are responsive to treatment because obviously, if you haven't found the primary cause, you've got nothing to treat and the cases will not respond to treatment. Besides treating the primary cause, again, for example, if you diagnose toxoplasmosis, you'll obviously wanna treat it with clindamycin, but subject to the systemic condition, you may also wanna add systemic And topical steroids or non-steroidal anti-inflammatory drugs. Again, obviously only if the systemic condition permits it.

Please keep in mind that topical treatment is ineffective in cases of posterior uveitis because the drugs do not Reach the back of the eye and therefore, when I say add, consider adding topical drugs, it's only to prevent the spread of the disease from the posterior uvea to the anterior uvea. In order to actually reach the posterior uvea, you really need to provide systemic treatment. We all know that systemic topical steroids, excuse me, are contraindicated in cases of corneal ulceration and because we are talking about cats, please remember that steroids, be they systemic or topical, may cause shedding of feline herpes virus and they May cause recurrence of herpetic disease.

So, you may want to consider adding prophylactic antiviral treatment to the anti-inflammatory treatment. But really, the main point to remember here is that this anti-inflammatory treatment is symptomatic. Hopefully, you were able to find the primary cause and provide appropriate primary treatment.

Another very, very important component of the treatment besides the anti-inflammatory treatment is atropine. We give atropine to our UVitis patients for two reasons. One is analgesia.

The atropine paralyses the muscles of the iris and the ciliary body, what we call cyclopplegia, and that gives an analgesic effect because of these muscles which result in meiosis, a classic sign of uveitis, spasms of these muscles are very painful and paralysing the muscle brings immediate relief. My patients usually don't come back to me and report on the effect of medication, but talk to people who've had UVITs and they will tell you that, atropine brought immediate relief to their pain and suffering. The second reason we want to give atropine is to dilate the pupil, and that is in order to reduce the risk of posterior sicia, the adhesions of the iris to the interior lens capsule.

I know we're talking about cats and this is a picture of a horse eye, but it really demonstrates beautifully, I think, the importance of giving atropine to these patients. This horse suffers from uveitis. As you know, uveitis is characterised by the presence of lots of inflammatory material in the interior chamber, be it in the shape of aqueous flare or a hypopion if it's more severe, but you get lots of fibrine, which I'll show in a minute.

And platelets and white blood cells in the interior chamber. Some of it is deposited on the interior lens capsule, which is what you can see in this source. You can see that really 90% of the interior lens capsule here is.

Semi-transparent because of all the inflammatory debris that's accumulated on the lens capsule. We really have a very small area here which is clear of these deposits and these inflammatory deposits serve like glue. They are adhesive and they facilitate the adhesion of the iris to the lens and obviously, when we have meiosis, and again, remember the spasms of the ciliary body and the iris, when we have meiosis, we have lots of contact with the, between the iris and the interior lens capsule, thereby increasing the risk of Posterior sinicia, if you dilate the pupil, you minimise the contact area between the interior lens capsule and the iris and thereby reducing the risk of these adhesions and secondary glaucoma.

How much atropine do we give? Well, that's an easy one cause the pupil. Tells you whether you've given enough or not.

Remember, your aim is to dilate the pupil. So really, you want to achieve a fixed and dilated pupil, and the people will tell you whether you are giving enough or not. So I usually tend to begin with twice daily.

If I get my fixed dilated pupil, I can decrease it once daily, once every 2 or 3 days. If twice daily wasn't enough, you may go up to 3 or 4 times daily, you Really want to get that pupil dilated, a point I cannot overemphasise because it's quite possible that you'll treat your VI successfully, you will overcome the inflammation, but you lose the eye due to these adhesions and the secondary glaucoma in which they result. Since we are talking about cats, please remember that atropine will cause salivation in these cats and I know that some people are right now scratching their heads cause we know that atropine is actually a parasympathholytic agent.

It's supposed to reduce secretions, for example, it reduces the secretion of tears and causes dry eye, so we don't accept, expect a parasympathholytic agent to cause salivation. But in fact, it does so in these cats cause they react to the bitter taste of atropine. You put a drop of atropine in the cat's eye, it makes its way down the nasallacrimal duct to the nose and the oral cavity, and these finicky cats will react to the bitter taste of atropine with this massive salivation.

It is really quite scary, the amount of saliva they can produce and therefore, a small tip, if you are going to discharge a cat with atropine, I suggest you put one drop in the clinic as a demonstration so that the owners can see the resulting salivation, and then you can tell them, you see. That's OK. It's nothing dangerous.

The cat is just reacting to the taste of the atropine, cause if you don't do this demonstration in the clinic and send them home with atropine, I guarantee you that later that evening, you'll get a frantic call from the owners. What are you doing? What have you done?

Your drug is killing my cat. It is really very, very scary. So please remember, atropine, as I said, both for analgesia and to reduce the risk of posterior sinicia.

However, if there are massive amounts of fibrin in the. Chamber, another treatment modality you should consider is the injection of tissue plasminogen activator into the anterior chamber. The tissue plasmic and activator breaks down the fibrin, actually, if you remember your basic cascade.

Of coagulation, the plasmingen activator is activated into plasmin which breaks the fibrbrine into fibrinogen. And actually, this procedure may serve a secondary purpose in that when you go with your needle into the interior chamber to inject the tissue plasmic and activator, you can also aspirate some aqueous humour and submit it to serology and cytology as I have shown you previously. Again, it is something, going into the interior chamber with the needle is something that You may want to consider referring the, to a specialist, especially because tissue placement and activator tends to be quite expensive and not, not every general practise keeps it in storage, but I will tell you that it works, it works wonderfully.

It works very fast. It's not something that where you send the cat home and tell the owner to come back in 10 days. See whether it worked or not.

Wait a couple of hours and you can see an almost immediate effect here is the same cat before and after injection. Before injection, you can't really see the pupil. All of the interior chamber is full of the fibrrin you're seeing it, and you're seeing here, and 2 hours later, it's like completely different eye, all of the fibrine has been dissolved.

A final word about you filling UVI and that is the complications. Yes, there are lots of potential complications, some of which we'll be discussing later in this talk. .

15th to 1/3 of all UVI cases end up with cataract, and that's because the lens depends on aqueous tumour for metabolic support. You remember that the lens, just like the cornea has no blood vessels and therefore, both of these tissues, the cornea and the lens depend on aqueous humour for metabolic support. Uveitis, the composition of the aqueous.

The tumour is altered and therefore, the metabolic support is disrupted and these cats end up with cataract. A lot of them up to 50% end up with secondary glaucoma. That may be because all of the inflam inflammatory material that I mentioned earlier obstructs the drainage angle and because of the that I mentioned earlier between the iris and the interior lens, if posterior ya has formed, there is no flow of aqueous from the posterior chamber where it is formed to the interior chamber from which it's supposed to be drained and you'll get elevation of intraocular pressure in the posterior segment, what we call iris bombay.

And up to 72% of cases may be blind due to reckon detachment or more commonly due to reckon degeneration. Sorry about the spelling mistake, that's what happens when you add a word just 5 minutes before the lecture, but it is, is a very common complication in feline uveitis. And actually, this is a very interesting slide here, cause it traces a point I'll come back to again and again.

In dogs, these three diseases, cataracts, glaucoma, and retinal degeneration are often inherited, OK? Inheritance, is the most common cause of canine cataracts along with diabetes, it's a common cause of glaucoma, and it's a the common cause of retin degeneration. In cats, these are secondary diseases, secondary to uveitis.

So another proof that a cat is not a small dog, which is the title of a talk I'll be giving in December. Hope to see you for that one as well. So moving on from UVI on to cataracts and glaucoma.

So, as I've just said, in dogs, inheritance accounts for about 50% of glaucoma cases. Here is a huge study published by my mentor from the University of Florida, Kirk Gillette, looking at a quarter of a million dogs, 267,000 dogs. You can see that the overall prevalence of glaucoma.

In this huge population of dogs is about 0.9%, but you can see many dog breeds with a prevalence that is much higher than the baseline. Obviously these breeds such as the American Cocker Spaniel, the Basset, the chow, the Sharpei, etc.

Etc. All suffer from inherited glaucoma. In cats, inherited primary glaucoma is very rare.

In fact, we're aware just of one colony of Siamese cats with inherited glaucoma, which is maintained by my friend Jim McClellan, originally from Scotland, now practising in Madison, Wisconsin, which is where she's studying this colony of cats. Usually, as I've said, in cats, glaucoma is secondary either to UVIis as we've discussed at length or to neoplasia and therefore, when you see a cat with glaucoma such as this little kitty here, it Require systemic workup to find the potential cause of UVITs and if it's an elderly cat presenting with unilateral glaucoma, then you should consider neoplasia as the cause of this unilateral glaucoma. Again, I've given the talk about glaucoma, you can find in the archives of the webinar vet, but a few things to point out about the clinical signs in cats.

I should say that the history in clinical signs of glaucoma are much more subtle in a cat than in a dog. Several reasons. Number one, Acute attacks which are characteristic of the inherited primary narrow angular glaucoma that is so common in dogs are very rare in cats.

Most of the cases are really insidious. You have a gradual buildup of pressure, gradual progression of the disease, so you won't have The owners coming, running to the clinic with a case of acute glaucoma where they left the dog at home in the morning and all was fine and they came back from work in the evening and they have an acute glaucoma attack. Yes, it happens in dogs, it doesn't happen in cats.

So the history will be different. Thankfully, vision is preserved much longer, so also something you will not get in the history that the owners provide you they not come complaining of blindness in these cats, and that's because the feline retina is more resistant to the adverse effects of elevated pressure than the canine retina. Because of the orbital anatomy and the way that the eyelids protect the globe, it is more difficult to detect the almus in the cat and more difficult to detect the red eye cause you don't see much of the episclera and the conjunctiva.

So two signs that are typical in cats, dogs, sorry, are more. To detect in cats, corneal edoema, blue eye, another very common sign of dogs is also less common in cats cause just like I said that the retina of the cat is more resistant to elevated pressure, the corneal endothelium of the cat is also more resistant to elevated intraocular. Pressure and therefore they get much milder corneal edoema.

But of course, you all know that there is an exception to every rule. Here is a cat with obvious corneal edoema and obvious buftalmus. So yes, they get mfalmus, they get corneal edoema, but it is less common and less noticeable than it is in dogs.

And finally, changes to the optic nerve. Are difficult to diagnose in glaucomotous cats because of the anatomy and the clinical presentation of the optic nerve head in a cat. Here is a normal fundus of a dog.

Here is a fundus of a glaucometous dog, and you see that the optic nerve head is now more drown. Grey as opposed to the whitish pink optic nervehead of the dog, of the normal dog, and you see that the blood vessels stop at the margin of the optic disc. They do not cross the surface and that's because of the phenomenon we call optic nerve cupping, the increased intraocular pressure actually causes a depression of the optic nervehead, it is pushed towards the back of the eye and therefore, when the blood vessels get to the edge of the optic disc, they dive in and they are lost because the optic disc has been pushed backwards.

So this is what a glaucometous dog looks like. This is what a normal feline fundus looks like and not the similarity to a glaucometous dog. The optic disc again is greyish brownish, and the blood vessels stop at the edge, so it would be more difficult to diagnose the cupping of the optic nerve.

And therefore, because clinical signs are less obvious. Obviously, you have to resort to tonometry to diagnose your glaucoma cases, just like you would in dogs, you have to measure intraocular pressure. We do not diagnose glaucoma based on clinical signs.

We suspect it based on clinical signs, but then we confirm the diagnosis based on measuring intraocular pressure. Every clinic must have a shield tonometer, and I say mask cause it's a very cheap instrument, you can buy it on eBay or Amazon for $150 or so. .

It's a reliable instrument in the sense that it's mechanical, so it's hard to break. However, it is not very user-friendly cause the head must be held vertical, as you can see here, and therefore, the third eyelid often gets in the way. It's affected by corneal anatomy and pathology.

It really requires both patient cooperation and lots of experience to use properly. And therefore, your life will dramatically change if you can buy one of the modern tonometers that are out there, either the applation toninometer known as a tonopen or the rebound tonometer known as the tonove. Note that each instrument produces a slightly different normal baseline reading in a CAT 18 versus.

21 and Jim McClellan, whom I mentioned earlier, says that both of them provide reproducible IOP readings, though the tone of it provides readings that are closer to the true IOP so you may want to prefer the tone of it. Another advantage is that it requires no topical anaesthetic, unlike the tonal pen where topical anaesthesia is required. Moving on to treatment of feline glaucoma.

Well, if glaucoma is secondary to UVI, then, as I said earlier, you want to diagnose and treat the primary cause of UVI. So maybe I should backtrack here. As I've said earlier, if you see a cat with glaucoma, you should suspect that it is secondary to your VI.

You wanna do the workup that we discussed earlier in order to diagnose the primary cause. Again, perhaps it's toxic toxoplasmosis, perhaps it's a tumour, and you wanna treat that primary cause. As I've said earlier, you wanna give the topical and systemic anti-inflammatory treatment that we forgot, and we wanna break down the adhesions of the pupil, the posterior sinicia, the adhesions of the iris to the interior lens capsule.

We can do it either with TPA or with atropine, as I mentioned earlier. You all know, I hope that we do not give atropine in, usually in, we do not give atropine in glaucoma because atropine and the dilation of the pupil will close the iridocorneal angle and will actually elevate intraocular pressure. So usually, atropine is contraindicated in glaucoma.

In fact, the way I tell my students they choose, remember it is acropin glaucoma means no diploma. It became such a popular sentence with them that they actually made COVID-19 face mask with this sentence really a good way to remember it if everyone in the clinic walks around with this face mask. But when the UVITs Is the primary cause of glaucoma.

When the glaucoma is secondary to UVI, then you should consider giving atropine in order to break down the adhesions or prevent posterior ya. Other treatments that we can provide to our glaucomatose feline patients? Well, I think that it's fair to say that in dogs, Latanarost and other prostaglandin analogues are, are drug of choice.

However, they are ineffective in normal cats and in glaucoma. Cats, they produce only a short effect, so really, we can use them briefly, but we can't get long-term management of the disease with Latarost and other proglandin analogues. Also, please remember that Latanaro and these prostaglandin analogues.

Excuse me, are contraindicated in UVITs cause in UVITs, there are enough prostaglandins in the interior chamber anyhow. You don't want to pour oil on fire by adding more prostaglandin analogues. So really, the most commonly used drug in canine glaucoma is Not used or used briefly in glaucomus cats.

Instead, our go to drug is the topical carbonic nirase inhibitor dorzolamide. With or without timolol depending on the patient's cardiac status. Sometimes we resort to systemic carbonic rise inhibitors such as metazolamide or acetazolamide.

Keep in mind that in cats, they are more toxic than a dog, and if we are talking toxicity, another treatment modality that we use in dogs that should be carefully considered in cats is intraocular injection of gentamicin. You know that in end-stage glaucoma in dogs, if the owner refuses a nucleation for one reason or another, usually cosmetics, then we could offer them an intraocular injection of gentamicin. Gentamicin is cytotoxic, it destroys the epithelium of the ciliary body.

And thereby reduces aquiumal production. However, in cats, these injections have been associated with intraocular sarcoma, a lethal tumour, so really they should be avoided, except perhaps in elderly cats, that's because the time, the average time for onset of these tumours is about. 5 years.

So, if it's a, 15 year old cat, yeah, you could consider an intraocular injection of gentamicin cause the cat is likely to die of chronic renal failure of old age before it develops sarcoma. But if it's a 2 or 3 year old patient, I definitely would avoid these intraocular gentamicin injections. Moving on from glaucoma into cataracts, as I've said earlier, in dogs, the most common causes of cataracts are diabetes.

This is a diabetic cataract with the vacuoles that you see here or Inheritance, this would be the two leading causes. However, once again, as I've said, in the cat, cataracts are usually secondary to UVI and 15 to 1/3 of feline uveitis patients develop cataract due to The dependence of the lens on aussum or for metabolic support. Inherited cataracts are very rare in cats, as are diabetic cataracts, that may be slightly surprising because we do have lots of diabetic cats.

However, you may recall that Aldos reductase is an enzyme that plays a key role in the pathogenesis of diabetic cataracts in dogs. Cats lose the activity of aldos reductass by the time they turn 4. And as you know, most cats develop diabetes at an older age.

So yes, we do have diabetic cats, but by the time they develop diabetes, all those reductas is no longer active and therefore, we don't get diabetic cataracts in our feline patients. Instead, as I've said, about glaucoma and as I've said time again, cats presented with cataract must be worked up for UVitis as a primary cause of this cataract. And again, note a significant difference between cats and dogs in cats.

As we've said, UVI causes cataracts. In dogs, the reverse is true and cataracts, especially mature and hypermature cataracts, cause uveitis. OK.

So which is the chicken, which is the egg depends on whether you are a pet or a dog. However, treatment is the same. If you have a cataract cataract in your feline patient, you can certainly refer it to surgery.

We do, We do cataract surgery on our feline patients. Here is a paper out of England. In fact, I'd say the prognosis is even better because cats don't get the secondary lens-induced to it that is so destructive and so prevalent in our canine patients.

Moving on to the next cause of blindness in cats, hypertensive retinopathy. Hyper hypertensive retinopathy should be suspected in elderly cats that present with acute blindness and fixed and dilated pupils. You take a look at the eye and you see retinal detachment with or without.

Retinal haemorrhage. Here are two pictures demonstrating what a detached retina looks like. Note that these pictures have been taken through the pupil.

Here is the iris and here is the iris. So these pictures were not taken with the fundest camera. You can actually visualise the detached retina with or without the haemorrhage through the pupil.

You don't need almoscope for that. You see. This white grey veil floating in the posterior back of the eye, sometimes, as I said with haemorrhage, as you can see here on the right, and you see blood vessels on this grey veil.

These blood vessels in behind the lens can come from only one tissue. They are retinal blood vessels that have moved forward from their natural location to the back of the lens cause the retina has. And if you do take an ophthalmoscope, you'll discover that you are unable to focus on the retina simply because it's not in its true location and you can get a sense here.

For example, this picture, note that all of this retina is out of focus cause it has moved from its natural location. I can focus on the optic disc here, but everything else is blurry, blurry, blurry with the Blood vessels on this grey veil that has moved towards the pupil. Sometimes you're unsure whether these patients have, whether these patients have retinal detachment, maybe they also have high femur.

So a good way to diagnose it would be using an ultrasound. This is what retinal detachment looks like histologically. The detached retina is usually fixated to the globe only in 3 locations in the optic nerve head and In the very periphery in the or errata, we call it the seagull sign cause it looks like the wings of a seagull, and here is the ultrasound image and you can see the seagull wings that are shown here histologically.

So ultrasound very useful to image a detached retina. So we've got A detached retina causing blindness, however, the disease is called hypertensive retinopathy, which implies that it is due to elevated blood pressure and indeed we do measure elevated blood pressure in these in these patients, . So we consider values of 180/100 to be abnormally high, by values of 200/110 to be clinically significant and as blood pressure increases, you get more and more severe signs.

I'll show that to you in a minute. So with Borderline elevated pressure, you may see some retinal edoema as you're seeing here, maybe a couple of bacteria and the more severe signs that you've seen here will present when the pressure is higher. However, as you know, hypertension is also not a primary disease.

It is also secondary disease and these cats with hypertension must be worked up for a systemic disease. This is presented in another study from North Carolina State University, looking at 69 cats with systemic hypertension, 68. Of the cats, 2/3 of these cats whose primary problem is systemic hypertension, I shouldn't say primary, whose systemic problem is hypertension, actually presented to the ophthalmology clinic with blood.

Blindness usually due to complete or part to complete retinal detachment, as I've said, it's bilaterally in half cases. Others have haemorrhage or aema or glaucoma, all of them are due to blindness. They are due to systemic hypertension.

However, as I've said, the systemic hypertension is also not a primary problem. It's a secondary problem to another systemic disease. So here is a table from that study.

Looking at the 69 cats, note the mean age of 15 years of age. Here is a clinical diagnosis, number of cats, systolic blood pressure, serum creatinine, urea, and the specific gravity of the urine. You will note that 22K cats had chronic renal failure as their primary cause of hypertension with elevated creatinine and BUN.

There were, however, 8 more cats with endocrinological diseases, most commonly hyperthyroidism, some of them diabetes or hyperaldosterinism. So really, You have sort of a cascade here, a primary systemic disease such as CRF causing systemic hypertension, causing retinal detachment and blindness. However, the presentation is reverse.

The owners come to the clinic with blindness. You look at the eye, you diagnose the retinal detachment, you put on the cuff and you measure blood pressure, you get systemic hypertension and then you do the workup to diagnose one of the systemic diseases that has caused the hypertension that has caused the retinal detachment that has caused the blindness. So really a snowball effect here.

However, A surprising fact to come out of this paper is that a significant number of cats actually have only mild azotemia or even normal renal function. So no, not all of them have this CRF as a primary disease. That paper was published, I think, around 2000.

It took North Carolina State University another 18 years to publish a paper about the outcome and the prognosis of these cats with hypertensive retinopathy. This study looks at 88 cats, so 176 eyes, 132 of which were blind eyes, 54 of the 88 cats were blind. And thanks to treatment, we are now talking about the outcome.

You can see that Half or just over half the cats regained vision, 76 eyes out of 132 regained vision, and of these 76 eyes that regained vision, half of them, 39 or 76, did so in less than 3 weeks. Just under 1/3 did it within 3 weeks to 2 months, and a fair number of them, 1/50, regained menace after more than 2 months thanks to reattachment enabled usually by Amlodipine. I'm sure you don't need me to tell you that this is the.

Of choice for treating systemic hypertension in our feline patients. So really, the prognosis is more than fair, more than 50% regained vision, but even if vision is not regained after 2 months, tell the owners not to give up. It's still possible that the cats will regain vision.

And the point also brought home by another more recent study, from a group of Italian colleagues looking at 225 cats with systemic hypertension. Again, the, remember, systemic hypertension is not a primary disease. You had to continue the workup and in this, of these 225 cats, 60% had chronic renal failure.

Hyperthyroidism in 29% and 8% had both. They graded the ophthalmoscopic signs in these 225 cats and they were present in 59 cats. So 41% of cats with systemic hypertension had a normal looking fundus and no ophthalmic signs, but 59 of them.

Head signs that were graded 123, and 4, you can see, as I said again, just mild edematous changes in the low grade, more severe edoema, more severe bleeding and total retin detachment as blood pressure elevates and indeed, this is an important point to come out of this study. This is stoic, though not the diastolic blood pressure is correlated with severity of signs and age. So here you can see the systolic blood pressure and the grade of the clinical signs I showed you in the previous slide and you can see how with the higher systolic blood pressure, you get more of the grade 4.

Clinical signs, and yes, all cats were treated with amlodipine and similar to the North Carolina State University study, 50% of cats regained vision within 21 days, but Others took much longer, as much as 1 year, 2.7% of the cats actually regained vision after one year, so again, not all is lost. So to summarise, hypertensive retinopathy, a very important disease in elderly cats, please consider systemic hypertension in all elderly cats presenting for acute blindness.

Measure their blood pressure, consider CKD or hyperthyroidism as the primary cause, treat them with amlodipine and vision will be regained in more than half the patient. I'm very quickly going to review some other retinopathies. Inherited retinal degeneration, as I said, is a very common cause of blindness in dogs.

Inherited retinal degeneration is rare in cats, even though we do see it in some cats, including the Abyssinian, Persian, and Bengal cat breeds. Usually it's very early onset, we get these neuropthalmic signs at 2 months of age. We get the classic signs of PRA that we see in dogs.

Such as the petal hyperreflectivity and attenuation of blood vessels at 8 to 12 weeks of age, and most cats with inherited retinal degeneration will be blind by 1 year of age. Here is a study that yours truly published in a colony of Bengal cats with inherited retinal degeneration. Yes, fundus is normal at 8 weeks of age, you can see some hyperreflectivity by 25 weeks of age, advanced retinal degeneration, and complete retinal degeneration at 1 year of age, all of them correlated with histological changes in the retina.

So you can diagnose it with the ophthalmoscopic examination or using the ERG electroretinography, you record the electrophysiological responses of the retina to flashes of light. Here we are doing it in a Bengal CAT, . Between the age of 5 and 14 weeks, and you can see the progressive decline in the amplitude.

5 and 7 weeks, the amplitudes were more or less the same, but then it started decreasing red, green, and pink at 14 weeks of age. The responses are severely attenuated. Thankfully, in some breeds, the mutation has already been diagnosed, so, there may be genetic testing that is available to diagnose, send a DNA sample and diagnose inherited.

Reckon degeneration in these cats. But again, please remember inherited re degeneration is a rare entity in cats. Most of them are due to UVITs, so most cats that present with retinal degeneration should be worked up for UVIT.

Then there is a bunch of other feline retinopathies which can be avoided. Hooray, hooray. Not often can we avoid retinopathy, but yes, some of them can be avoided.

The first one is tau ring deficiency. Felines are unique in that they cannot synthesise tau ring. They depend on dietary intake of taurine, which is an essential amino acid, and if they get an improper diet, then lack of dietary taurine will cause retinal degeneration and dilated cardiomyopathy.

The retinal degeneration begins as cone degeneration, so behaviorally we get signs of cone degeneration, which means loss of daytime vision, and indeed we see the pathognomonic lesions in the central retina where most of the cones are concentrated and this pathognomonic lesion is this hyperreflective horizontal streak just above the optic disc. If you diagnose this lesion, number one, you have to send the cat for cardiological workup for dilated cardiomyopathy, and obviously, you must supplement the diet of the cat with touring. If you start touring supplementation, you will reverse dilated cardio cardiomyopathy, you will stop the progression of rectal degeneration.

Unfortunately. You know, we cannot restore vision to, that has been lost to due to wrecking degeneration. So yes, we can stop it, but we cannot reverse it.

Most canine food companies will now add taurine to canine diets, to canine commercial food, not because dogs need taurine, simply because some people give. Canine, commercial food to their cats cause it's cheaper than the cat food. So the food companies have learned that and will supplement canine, diets with towering, but still, you do get cats that are given only scraps from the table, perhaps hunting dogs, and, these may develop tourine deficiency, something that can be avoided.

Another retinopathy that can and should be avoided is afluoxin toxicity, an antibiotic that causes acute blindness. Patients will present with fixed dilated pupils and classic signs of retinal degeneration and total retinal dysfunction, a flat ERG. For a long time, we didn't know why cats get.

It and why some cats get it and other cats don't get it, but then we discovered the cause of this toxicity or the pathogenesis of this toxicity, which is a mutation in this protein. This protein is a constituent in the endothelium of the blood vessels or the capillaries I should say in the retina and if there is a mutation, then The auro fluoxetine can leak from the blood vessels into the retina, and fluquinolones are a photoreactive molecules. So next time the cat goes outdoor or next time that you shine a bright light into the cat's eye, you will get production of oxygen radicals and you'll get destruction of the retina.

So this is why some cats get it if they carry the mutations, others don't get it if they Don't carry the mutation. Usually, we don't test for it before, go for treating our patients with Arofloxacin. So the recommendation of ophthalmologists is never give more than 2.5 migs per kg per day, which is far less than the 5 to 10 migs per kg recommended by the manufacturer, and if it's an elderly cat, even consider dividing it into smaller doses.

Some other floquinrons, notably orbifluoxetine, has also been implicated in this toxicity, but not the marble fluetine. Another cause of blindness you may get is if you do dental work on your feline patient and you use a spring-loaded mouth gag, and that's because the spring-loaded mouth gag will lead to wide opening of the jaw and the mandible, the epicondyle of the mandible will press on the maxillary artery, which supplies blood to the cortex and to the visual pathways and you will get post-anesthetic, cortical blindness in cats that underwent dental work with a spring-loaded mouth gag, which is why in cats, you should consider taking a syringe, cutting it to the appropriate length, and using that as a gag rather than the spring-loaded one. And a last and final cause of blindness that you should avoid is in cases of nucleation.

A cat comes with one eye that needs to be nucleated. You take it into surgery, you nucleate the affected eye and it wakes up blind in its only remaining eye. And the reason that's happened is because the retro.

Are part of the optic nerve, part of the optic nerve between the globe and the optic chiasm is very, very short in a dog, a cat, sorry. So, as you're nucleating, if you're trying to grab the optic nerve to clump it with your hemostat, during a nucleation and if you tag on it and pull on it, then you may very well end up Clumping on the opticia or you may end up traumatising the opticia in another way. And as I said, you've taken one eye out, but the cat will wake up blind in the other eye because of damage and trauma to the opticia.

Definitely something you want to avoid, that would be a very, very bad day in your life. So, this has been a brief review of blindness in our domestic felines. As I've said, I hope you get a chance to work with some of the big and exotic felines because they are lots of fun.

I thank you for your attention and look forward to seeing you in September, on the last lecture of the series on inherited causes of blindness in dogs. Thank you very much. Have a good day and stay healthy.