Hello, everyone, and welcome to this lecture about acute blindness in dogs. By the way, this picture you're seeing here with a collie wearing a vest saying, I am blind. It's not just a gimmick, actually, it's a very important accessory for blind dogs cause a blind dog cannot see a person approaching to pet it or does not see.

Child come to play with it and they can easily get startled if someone unexpectedly pets them and pets them and therefore they may bite. And actually, this is a very good way of letting people know that a patient is blind. It's a vest that you can find on the internet like everything else nowadays, and recommend to owners of blind dogs.

Right. So actually, this talk means that we are halfway through a blindness series. If you go back to the webinar vet archives, you'll see that back in August, I spoke about applied anatomy of the FAI and obviously you have to understand the fundus anatomy if you want to understand blindness.

In October, we spoke about examining your Your ophthalmic patient and examining your blind patient. Today we'll be talking about acquired causes of blindness and next year we'll be talking about blindness caused by diseases of the optic nerve. We'll be talking about blindness in cats and later next year, later in 2021, we'll be talking about Inherited causes of blindness, the data is yet to be set, so it's not up here.

So, as with any patient that comes into your clinic, when a blind patient is presented, you begin by taking the history. And besides the general questions you'll be asking, there are a few specific questions that you want to ask the owner of each and every blind patient. The first question you wanna ask is whether the blindness was sudden or gradual.

Cause with this one simple question, you can get a very good idea of whether it's of whether the blindness is due to an acquired cause or due to an inherited cause. Most causes of acquired blindness are characterised by sudden blindness, such as this case of retinal detachment in this eye, and we'll be talking about retinal detachment later today. Most inherited causes of blindness are characterised.

By gradual progressive blindness. So with one simple question, was it sudden or was it gradual? You can get a very good idea of whether it is acquired or inherited.

Here, as I said, is written detachment characterised by acute blindness. Here is a case of regeneration, inherited retinal degeneration characterised by progressive blindness. The second question you want to ask is whether loss of vision started with preferential loss of nighttime vision.

And that's because most of the inherited causes, such as the one you're seeing here are characterised by preferential loss of nighttime vision as the rods in the retina are affected before the cones are affected. Now please be very, very careful when asking this question. You want to phrase it in a neutral way.

Do not lead the owners, do not indicate what type of answer you're expecting by saying, did your dog, Did the loss of vision in your dog begin with loss of nighttime vision? Cause as you know, owners will always want to make you happy, and often they'll say yes, no matter what you ask them, yes. Does the sun rise in the west?

Yes, it does. Is Liverpool the capital of England? Yes, it is, you know, no matter what you ask them, they'll say yes, because they won't make you happy.

So don't lead them into Suggesting that you're looking into preferential loss of nighttime vision, phrase your question in a neutral sort of way. Ask them, was there a difference between nighttime vision and daytime vision? And you'd be surprised to see how often they say, you know what, you're right, my dog sees much better at day than at night.

And then once again, you can suspect an inherited blindness such as this threating degeneration. And finally, even though the patient presented you to an ophthalmic problem, due to blindness, you wanna ask whether the animal is healthy, whether it's showing any signs of neurological diseases or systemic diseases, cause as you'll see today, many causes of acute blindness are due to systemic or Neurological diseases and that is why following the history, you wanna continue your exam by doing a complete physical exam looking for signs of systemic disease and you want to follow it up with a neurological or a neuropthalmic exam as the case may be. Now, as I said in an earlier talk, I described a comprehensive ophthalmic examination.

I just want to repeat a couple of very important things you want to check in the case of a blind patient. First and foremost, the pupillary light reflex, the PLR, and as you know, We check both the direct and the consensual PLR, the direct PLR being the constriction of the pupil that is being illuminated or stimulated, and the consensual or the indirect PLR is the constriction of the unstimulated pupil such as shown here. Another important subcortical reflex that you want to check in blind patient is a dazzle reflex, taking a bright source of light, placing it next to the eye, and watching the animals squint or blink in response.

Note this is. A reflex, a subcortical reflex, this blinking doesn't mean that the patient is necessarily visual, but it's a very important component of the ophthalmic exam and the workup of blind patients as you'll see in a moment. Now, it's very important, as I just indicated, to remember that a normal PLR and a normal das reflex do not imply vision.

One reason is that, as I mentioned, they are subcortical reflexes and therefore in an animal with cortical blindness, the PLR and dazzle will be normal. Here is a simple diagram showing the optic nerve, leaving the both eyes splitting in the opticciasm forming. The two optic tracts leading into the visual cortex, but right at this point you have the afferent fibres responsible for the PLR diverging midway through the optic tract and going to the thalamus, providing afferent input to the PLR and therefore, If there is cortical bla disease.

Localised here, the PLR will be normal cause the afferent fibres for the PLR have already diverged from the visual pathways. So again, animal with cortical blindness, PLR and dazzle will be normal. Another very, very important point to remember is that minimal input is needed for these reflexes, and they are also present in animals with advanced cataract, such as the one you're seeing here.

Obviously this eye is blind for all practical purposes and not enough. Light is penetrating this dense cataract to enable vision, but a few photons can still penetrate, reach the retina, and trigger the PLR. So yes, the eye is functioning blind, but because you need so little input for the PLR, the little light that does penetrate this caract will, Facilitate a PLR and also in advanced retinal degeneration, even if 95% or so of the retina has degenerated, the remaining 5% will be enough to facilitate a PLR.

So remember that the reflexes are present in these animals and that minimal stimulation is needed for these reflexes. Nonetheless, they are very, very important for the workup of blind patients, as you'll see in a minute. Now, talking, after, sorry, after checking the PLR and the dazzle reflex, as I said, you want to continue your ophthalmic exam.

Checking to see number one, whether the retina is healthy and even before that, asking yourself, can light actually reach the retina? Obviously, in all these three pictures, light does not reach the retina due to excessive facial. Falls in the shar pei, advanced cataract here, Iema here, and if flight doesn't reach the retina, then the animal is blind.

This is actually a picture of a patient I had not, just a few months ago, came in with a complaint of blindness, and I said, Yeah, I can fix it with eyelid surgery. Obviously, the owners thought I was mad, suggesting eyelid surgery to resolve blindness, but taking look at this picture, obviously, light cannot reach the retina cause of the excessive facial falls and the lera spasm, the pain caused by these falls, and therefore, the animal is blind, blindness that can be fixed by eyelid surgery. Now, if you go to textbooks discussing blindness, obviously the question will be how do we localise the lesion causing blindness, and you'll find lots and lots of these complex diagrams that frankly They often confuse me even though I'm guilty of generating one of them.

Sometimes I say it looks like the electric circuits on the back of a refrigerator, all these squiggly lines that you are seeing here. So instead of all these complex diagrams, I like to keep it simple and easy and when faced with a blind patient, I usually construct a 2 by 2 table that you are seeing here. The 2x2 table is based on whether the ophthalmic examination was normal or abnormal and whether the PLR was present or absent.

So really a 2x2 box and each and every case of blindness that comes into your clinic will. In one of these 4 boxes. So really a very, very simple diagram to localise the lesion causing blindness.

Keeping in mind two things. One is the diagram that I discussed earlier that the Pathways for cortical vision and for the PLR are a common pathway up to this point, halfway through the middle of the optic tract where the afferent fibres for the PLR diverge from the fibres providing afferent input for cortical vision. And as I said, little afferent input is required for the PLR.

Again, two cases. Of blind patients due to advanced Care Act and advanced retinal degeneration, but in both cases, there will be PLR here because some photons penetrate the denseA Act and trigger the PLR and here because 95, 98% of the retina is gone, but the remaining 5%, 2% are enough to trigger a PLR. So let's go back to the 2x2 box and see how each and every case of blindness falls into this box and how do we localise the lesion that's causing blindness.

The first box here is. Abnormal examination, yet a normal PLR. An abnormal examination and a normal PLR in a blind animal can be due to one of two reasons.

The first one is light doesn't reach the retina. As I've said, the case of the Sharpei with a viro spasm due to excessive facial folds, severe corneal edoema, hypo hyfema, the cataract I've shown you earlier, here is another case of cataract in a bush baby, in case you're wondering what this creature is vitreous opacities. So an opacity somewhere.

In the pathway of light between the cornea and the retina, something obstructing the light, so obviously it's an abnormal examination because you are. Supposed to identify these these obstructions or these lesions that prevent light from reaching the retina, but as I said, the PLR would be normal even in the face of a severe edoema or hypopion or cataracts. If you can't see the PLR in the affected eye due to edoema or hyfema, look for the consensual PLR in the other eye, it will be present.

The second reason for an abnormal examination and a normal or diminished PLR would be. Retinal diseases, in other words, the retina is not normal looking. Here we have an example of a atrophied retina due to out retinal degeneration, so-called PRA progressive retinal atrophy, so completely atrophied retina, you don't see any blood vessels, you see significant hyperreflectivity of the tapetum.

Or alternatively, choreo retinitis, we'll be talking about choreo retinitis, inflammation of the retina, in this talk today. You can see the significant edoema, affecting the dorsal 2/3 of the fundus here. So in both of these cases, there are obvious.

Abnormalities in your funduscopic exam, which is why the exam is abnormal. However, once again, as I said earlier, not the entire retina is affected and therefore you will have a normal PLR so we are still with this box. So two possible reasons for an abnormal exam in a normal PLR are, as I said, opacities preventing light from reaching the retina or signs of retinal disease.

So we've moved in this chart from opacities in this part of the eye to diseases of the retina, choo retinitis, and PRA affecting the retina here. The second box is abnormal examination and no PLR. Abnormal examination and no PLR may be due to three diseases you want to consider.

One is glaucoma and in the webinar archives, you will find my talk about glaucoma. There are lots of clinical signs associated with glaucoma, so the exam is abnormal, but the patient presents with fixed dilated pupil, no PLR. The second cause is retinal detachment seen here.

As I said, we'll be discussing it later today in my talk, but you can see that the exam is obviously abnormal, so abnormal exam, and because the retina is detached, there will be no PLR. And the third possible cause is proximal optic neuritis, inflammation of the proximal part of the optic nerve, and I stress the word proximal because a proximal inflammation of the optic nerve would involve the optic nerve head. We will see signs of optic nerve.

Inflammation in our funduscopic exam and therefore, the exam will be abnormal, but when there is an inflammation of the optic nerve, there is no pupillary light reflex and as I said, my next stop in the series of blindness in our patients will address diseases of the optic nerve. So, going back to this diagram, we are gradually moving from the retina through the proximal optic nerve, OK. We've started by talking about loss of opacity in the pathway of the light, diseases of the retina, proximal optic neuritis.

Causing an abnormal exam with no PLR. The third box in this 2x2 diagram is normal exam but no PLR. Normal exam but no PLR could be due to one of two possible reasons.

Number one, we are talking about diseases of the more distal parts of the visual pathways, because they are distal. Diseases, the optic nerve head is not involved and therefore the ophthalmic exam will be normal. But as long as the disease is localised before this point where the afferent fibres of the PLR diverge, there will be no PLR.

So really, we are talking about diseases of the The optic nerve shown here, diseases of the optic chiasm and diseases of the proximal optic tract up to this point here, because this dictates the fact that this patient has no PLR and again, we'll be talking about all of these diseases in my next talk in this series and another disease we shall be discussing today, SARS, sudden acquired retinal degeneration syndrome. The patient presents with a normal looking fundus but no PLR and therefore SARS patients also fall into this box. And the last and final box here is a normal exam and a normal PLR.

If there is a normal PLR then by default, the lesion is located to this part of the visual pathway after the afferent fibres to the PLR have diverged. So we are talking about diseases of the distal optic tract, the LGN, the optic radiation of, or the visual cortex. Actually, we are talking about neurological.

Diseases, be they congenital metabolic, infectious, inflammatory, etc. Etc. We are talking about neurological diseases, so, put on, take off your ophthalmic hat, put on your neurology thinking hat or refer this case to a neurologist in cases where you are in a multi-specialty practise.

So, as I said, we'll be discussing these diseases of the optic nerve pathways in my next talk. Right now, I want to talk about acquired causes, acquired diseases, sorry, of the retina. In this next part of my talk, and we will be talking about blindness due to retinal haemorrhage, retinal inflammation, retinal detachment, and SARS.

Here is another dog with this vest advertising the fact that it is blind. And let's start things off by talking about retinal haemorrhage. And the important thing to remember is that really retinal haemorrhage is a clinical sign.

It's not a diagnosis. . You will diagnose retinal haemorrhage for the same reasons that you will be diagnosed in haemorrhage in other organs and tissues of the body.

The only difference being that in the retina, you can actually visualise the haemorrhage using an ophthalmoscope. So you may be looking at haemorrhage due to a platelet disease such as caused by earlyannis or immune-mediated thrombocytopenia. You will be looking at.

Systemic hypertension, we'll be talking about it in the summer when we talk about blindness in cats, anticoagulant poisoning, coagulation disease, vascular diseases, posterioritis, which we'll be talking about today, trauma. So any disease that can cause bleeding anywhere in the body can also cause blindness in, sorry, will also be causing haemorrhage in the retina. Here is a study coming out of Cornell University looking at 83 dogs presented with presented with retinal haemorrhage and the cause of haemorrhage in these dogs.

As you can see, in many cases, it was due to diabetes. Systemic hypertension, hypothyroidism, chronic renal failure, Cushing and multiple myeloma. So altogether 50 of the 83 dogs were diagnosed with a systemic disease that caused the retinal haemorrhage.

In 33 of the dogs it. Was secondary to ocular disease or a cause could not be found despite the extensive workup. OK.

So these are some of the diseases you wanna keep in mind you, when presented with rectal haemorrhage. What does retinal haemorrhage look like? Well, here are a few pictures depending on the causes that I just mentioned in the previous slide.

You can see small peteria due to thrombocytopenia. You can see more massive haemorrhage due to systemic hypertension and even more significant haemorrhage due to trauma in this eye. So what this tells us is that because it's a clinical sign, not a diagnosis, then any patient presenting with retinal haemorrhage, you really should be performing systemic workup, complete blood count, consider serology for infectious agents common in your area, PT, PTT to check the coagulation.

A cycle. If it's an elderly patient, measure blood pressure, do the appropriate workup for the, the signalment of the patient, for the additional clinical signs that you uncovered in your physical examination and uncover hopefully the cause of blindness, even though as you saw in the study from Cornell, often, it is idiopathic and no systemic causes is found. If you were fortunate enough to find a primary cause, for example, blood pressure, then by all means go ahead and treat it and vision will be restored.

Again, we'll talk about it when we talk about, blindness in cats and for the eye, please. The systemic steroids cause this blood here in the retina may lead to inflammation and I stress systemic steroids, to drugs will not reach the retina, so they are ineffective for these patients. The second disease I want to talk about is retinal inflammation.

And actually, when talking about retinal inflammation, we should use a more proper name. Corio retinitis, inflammation of both the choroid and the retina, and that's because it is very rare to see inflammations just rest just of the retina restricted to the retina. Distemper may be.

One of those rare exceptions. Usually we are talking about inflammations of the choroid which spread to the retina and therefore we're talking about choo retinitis or about posterior uveitis. What can cause Corioretinitis or posterior uveitis?

In dogs, the list of potential causes for UVIis is really endless. It is virtually every systemic disease, be it neoplastic or metabolic or immune mediated or infectious or toxic. However, when we're talking about posterior uveitis, then we tend to concentrate more on the infectious causes of uveitis, be they algae or bacterial, protozoal, fungal, viral or parasitic causes, OK.

So non-infectious causes are more characteristic of the interioruve. The infectious causes may cause either anterior or posterior uveitis. Again, another study looking at cases of causes of UVITs.

This one coming out of Purdue, Indiana, in the United States, looking at causes of UVIis in 55 canine patients. As you can see, 14 of 55 of the dogs were diagnosed with infectious diseases. And the type of infectious diseases really would depend on what's endemic in your area.

This study comes out of the American Midwest, so you can see that fungal disease is a leading cause of UVIT in the American Midwest, in other countries in the Mediterranean region. For example, it may be Leishmannia or likia. So it all depends on what's endemic in your area.

5 dogs were, had UVitis due to VKH, uo dermatological syndrome and autoimmune disease affecting both the skin and the eye. 2 cases of lymphoma, and what is most distressing. 34 of 55 cases were idiopathic, despite all the extensive workup done in Purdue, no cause was found in a majority of patients.

So that's causes of UVIities in dogs. What about cats? In cats, the list of potential causes is shorter than the table I showed earlier in dogs, and yes, we may get non-infectious or infectious, causes of UVIis, but both lists are much shorter.

In cats and typically in cats when we're talking about infectious UVIis and posterior uveitis, we have to consider FIV FLV, FIP, toxoplasmosis, and depending on what's endemic in your area, also fungal diseases. Another study, this time in CATs, showing you what to expect when you're working up patients with UVITs. So a study out of North Carolina State University looking at 120 cats with UVITs.

As you can see, toxoplasmosis, FIP, FIV, FELV are the leading causes, just as I indicated in the former slide, neoplasia was the cause in some of these patients. And again, idiopathic is a leading cause maybe the leading cause in both species. So really in both dogs and cats, 30 to 60% of cases of poster uveitis are idiopathic UVI.

Systemic disease such as this case of cryptococ is found only in 40 to 70% of The patients, and obviously this has great prognostic implications because if you can't find the primary disease, you are much more challenged, in treating the patient. What are the signs of posterior uveitis? Well, the signs are similar to that of any other inflamed organ, but once again, just as I said for the cases of retinal haemorrhage, the difference in the retina is that the signs become visible with an ophthalmoscope.

So as you know, in any organ or any tissue, when you have an inflammation, you have exudate and transudate leaking from blood vessels. You can see it histopathologically in other organs. In the retina, you can actually see it with an ophthalmoscope, and that's what you see in all of these pictures.

You see this opacity around the blood vessels and because it's around blood vessels, we call it perivascular coughing, and these cuffs around blood vessels are inflammatory exudate or transudate leaking from the vessels due to. The inflammation, obviously the leakage doesn't necessarily stop here and it's not restricted to the area of the blood vessels. If it's more significant and more massive, it can leak into the vitreous and will cause a vitreous haze, just like leakage of inflammatory material into the interior chamber will cause.

Aqueous flare, here, the leakage in cases of posterior viitis will cause a vitreous ha haze and you see, note that you cannot see details of the fundus. There is also leakage not just from the retinal blood vessels that I showed in the former slide. There is also leakage from the choroid into the sub-retinal space, so you will get subretinal edoema, which is what you are seeing here.

Note how this rein blood vessel is literally elevated by the sub-retinal edoema. Sometimes the edoema will be in the retina due to leakage of vessels in the mid retina and note in these two cases how the edoema is really obstructing the view of the rein blood vessels. And the result in both cases is a hyporeflective tepitum because if there is fluid in the retina or beneath the retina, then the reflection of the tepitum becomes more obscure and you cannot see it as well.

Another sign of inflammation of the retina is obviously retinal haemorrhage. We've already discussed it previously and note the different presentations of a massive or more punctate retinal haemorrhage depending on which blood vessels it originated from. As a result of the haemorrhage or the transoate or the exudate leaking into the subretinal space, we may get retinal detachment.

Which is what you are seeing here. We're seeing a completely detached retina through the pupil of this patient. We are seeing a partially detached retina, in the fundus of this patient, and we will be talking about retina detachment next.

As with many inflammations, the, once the inflammation subsides, you will get scarring of the tissue. Again, it holds true for most tissues and organs, but in most tissues and organs to see the scars, you really need to have a histopathological sample. In the eye, you can see the scarring of the retina, the post-inflammatory scarring of the retina using your almoscope and that's the lesions you are seeing in these two pictures.

You are seeing a. Focal area of hyper reflectivity with a clump of black pigmented cells in the middle, the clump of Pigmented cells that you're seeing here is actually retinal macrophages that came to clean up the inflammatory debris and as a result of the inflammation, the retina that was involved in the inflammation has atrophied, which is why we are seeing a hyperreflective tepitum. And here are Two pictures from the same dog.

You can tell it's the same dog looking at the revasculature, where we were able to catch signs of active inflammation and post-inflammatory scarring. You will note the clump of phagocytic cells in both pictures cleaning up the inflammation. For debris here we have an active inflammation.

There is edoema, there is transudate, which is why the borders of this lesion are fuzzy because of the edoema. The tapitium is hyporeflective. Once the inflammation has been controlled, then the.

Retina, which was previously inflamed, has atrophied and we are now seeing hyperref reflectivity. OK, so hyperreflectivity is a sign of active inflammation, hyperreflectivity as postoperative scarring, post-inflammatory scarring, and in both cases, you're seeing the clump of phagocytic cells. So, In order to treat the patients with posterior uveitis, as I've said, most of the cases are due to a systemic disease and therefore, before treating, we look for a systemic cause by taking a comprehensive history, performing a comprehensive systemic examination based on the results and what's of the systemic examination and the ophthalmic examination, you may be submitting blood work, CBC, chemistry, serology, depending on what's endemic in your area, molecular testing for infectious agent, you.

Analysis, imaging. Sometimes we even do vitreous synthesis looking for the agents in the vitreous. You wanna do everything that you can to identify the causative agent of the inflammation.

If you found it, treat it, and maybe the inflammation would be resolved and in any case, regardless of the cause, depending on the patient's systemic condition, you wanna treat it with systemic steroids or non-steroidal drugs because as I Said topical drugs do not reach posterior segment. However, you do have an inflammation in the posterior segment, so you do wanna treat it with systemic steroids NSAs, or sometimes even severe cases such as this one, you may even consider intravitreal injections either of antibiotics, antiphagy agents, or cannalog long-acting, steroids in order to control the inflammation and treat the primary cause. And if you are going with the needle into the in order to inject these agents, you will be aspirating some vitreous in order to make room for whatever it is you're injecting.

Please submit this vitreous sample to pathology or serology as the case may be indicated. The third cause of acquired blind cause of acquired blindness that I want to talk about is retinal detachment. Retinal detachment, as the name implies, is a detachment between the retina and the underlying choroid, or more precisely between the retina and the retina pigment epithelium.

Here you can see it histologically as you We know the retina is usually supposed to be adhered to the posterior wall of the eye. Here it has detached and it remains attached to the globe in just three places at the aura serata, at the very periphery of the retina, where the retina ends and the ciliary body begins, and at the optic nerve head. Here are a few more pictures.

So again, histological picture showing a detached retina attached at the aura errata and the optic nerve head. Here you can see it. Actually, in a macroscopic view of the eye and again you can see the detached retina and in both of these patients, you can see the massive subretinal inflammation transodate that caused the rein detachment and here another picture is Histological picture showing you the actual point of retinal separation.

Here we have the choroid with the choroidal blood vessels. Here we have the retina. Here it's attached to the retinal pigment epithelium and the choroid, and at this point it has become detached from the underlying RPE and the choroid.

So what causes retinal detachment? There are actually 3 mechanisms by which the retina may become detached. First is due to accumulation of subretinal fluid, as I hinted previously, it may be exudate or transudate or blood, some sort of fluid that leaks from the choroid into the subrein space and pushes the retina of the choroid surface.

You can see two examples here. Here is a massive. Transudate really almost a granuloma causing focal retinal separation.

Once again you can see the elevated blood vessel due to the retinal separation, the retinal detachment, and here a more massive retinal subretinal haemorrhage causing a massive or significant retinal detachment. So this would be the first. Mechanism, accumulation of some sort of fluid in the subrein space pushing the retina away from the choroid.

An alternative mechanism would be something pulling the retina off of the choroid. That may happen if the vitreous body moves forward and as it moves forward, it pulls the retina with it. Why would the vitreous moves forward?

Well, it may move forward in cases of luxation such as you're seeing here, if the lens moves into the interior chamber, it pulls the virus with it and the virus pulls the retina along with it. Maybe you did cataract surgery. There are tears in the posterior lens capsule through which the vitres moves into the anterior chamber.

So forward movement of the vitreouss is one possible cause. A second possible cause is inflammation of the posterior segment. During the inflammation, we have formation of vitreal bands or epireum bands that you can see here.

It's really . Fibrine, and just like any fibrine anywhere else in the body, eventually it will contract and if this contracts, it pulls the retina off of the choroid. So traction or pulling of the retina of the choroid is the second mechanism.

The third mechanism called rhematogenous detachment sounds a bit complex but actually may be the most common type of rein detachment. Ah, rhematogenous detachment requires two separate events. Number one is Partial vitreous liquefacation, it becomes a more fluid, the vitreous, and number 2, it requires a formation of a hole in the retina and if there is a hole in the retina, then the liquefied vitreous penetrates the subreal space and causes a retinal separation.

As I said, this may be the most common type of detachment in dogs. It may be acquired. If the virus is liquefied during inflammation, trauma, cataract surgery, glaucoma, then it can penetrate through small retinal holes into the subretinal space and it can be inherited in, many retinal diseases called the anomaly, retin dysplasia, or simply inherited dis predisposition to rheumatogenous.

Retinal detachment shih-tzus are definitely predisposed to this sort of detachment. Here are two retrospective studies of patients undergoing retinal reattachment surgery following retinal detachment, and you can see that 45 of 135 patients in this study were shih-tzus, 44 of 275 in this study were shih-tzus, so really shih-tzus are. Represent a significant number of patients with retina detachment due to genetic predisposition to maogenous detachment, consider it whenever you have a Shihzu presenting with acute blindness.

But it may also be seen in other breeds such as listed here. So now that we know the causes, what are the clinical signs of retinal detachment? We are talking about acute blindness, that's the overall topic of this talk, acute or required causes of blindness.

If there is a focal detachment, Such as shown here, it may be an incidental finding cause yes, there is a blind spot in the visual field of this patient, but it will compensate with the other eye and the owner will not have any idea that there is a Problem and you'll not be aware of a problem unless you take an ophthalmoscope and actually examine the fundus of this patient, but a complete detachment will present with acute blindness and with a fixed dilated pupil. Remember my 2x2 chart to identify and localise the causes of blindness. If you stimulate the affected eye, the unaffected eye will not, the pupil in the unaffected eye will not constrict.

However, if you stimulate the, the unaffected eye, the pupil in the affected eye will constrict. That tells you that there is an afferent deficit and again, the Consensual PLR looking at what's happening in the other eye is very, very important in cases where you cannot visualise the pupil cause as I said, sometimes these detachments are associated with inflammation or haemorrhage. So checking the consensual PLR is very important when you can't visualise people in the affected eye.

And the first and foremost sign probably is actually seeing the detached retina. The retina is out of focus, as you can see in this and the previous pictures that I showed you, you're unable to focus it within anharmoscope because it moved from its normal position. And often it will move so far forward that it will really move up against the lens and then you can get this picture here.

Note that this picture is not taken with an ophthal through an ophthalmoscope, it's actually taken through the pupil. You're just looking at the eye through the pupil and you see these blood vessels come up again. The posterior aspect of the lens, these blood vessels can originate only in one place.

They are retinal blood vessels. When you see them, it means that this patient has retinal detachment. In this case, it was caused by fungal infection, which is why you're seeing all these granulomas in the detached retina.

Some more pictures and again note that all of them are taken through the pupils, so you don't need your thermoscope for them. You actually see this whitish greyish looking veil or curtain sort of floating behind the lens. You'll see blood vessels on this curtain or veil.

Sometimes you'll see the haemorrhage or you'll see the granulomas as I showed you in the former picture, you can really visualise the detached retina. However, as I said, many of the cases may be associated with inflammation or haemorrhage, in which case you cannot see the pupil and the detached retina, in which case, the ultrasound is a very useful diagnostic modality and an ultrasound will show the detached retina. As you can see here in this ultrasound image, note how it resembles the histopathological picture with the retina attached at the aura errata and at the optic nerve head.

We call it the seagull sign because it reminds you of the wings of a seagull. Here they are, here is the body of the seagull, and here are the tips of the wing. How do we treat these patients?

Well, if it's a non-rheumatogenous detachment, you can treat that primary cause depending on what you found. So if it's hemorrhagic, do the blood count, measure blood pressure, coagulation workup, etc. Etc.

And treat the primary cause. If it's inflammatory, you wanna try and Identify the infectious agents by serology, chest X-ray, vitrey synthesis I mentioned earlier. If it's traction detachment, you want to remove refer the patient for removal of the lax lens, perhaps do a vitrectomy.

So these are some of your options in non-rheumatogenous detachment and if it's a rheat detachment, there are some veterinary ophthalmologists to whom you could refer the patient for reattaching the retina, which is what you can see in these pictures. Here, here is a completely detached retina which has been reattached in by a vitreal retinal surgeon. The last disease that I want to talk about today is SARS.

SARS, as I said, stands for SA acquired retinal degeneration syndrome. And if you want to know more about SARS, I refer you to this wonderful review paper. It's actually now 4 or 5 years old, still an oldie but goody summarising everything that we know about SARS.

The disease is actually defined by 5 parameters. First, as the name implies, we are talking about acute blindness caused by loss of photoreceptor function, and this can be confirmed by an extinguished electroretinogram. We try to record rein function using the ERG and we see a flat line.

Initially, in the When the patient presents, it will present with a normal looking fundus. Signs of retinal degeneration will appear months or years later. Patient will present with midriatic pupils that are slowly responsive to white light, non-responsive to red, and responsive to blue.

I'll touch on that in a few minutes, and the patients frequently have systemic abnormalities suggestive of Cushing. So who's your typical SARS patient? Here she is, and I say she because a majority are females, usually spayed, middle-aged females, moderately overweight.

So I mentioned earlier that frequently you have a systemic abnormalities suggestive on Cushing. You can see that the patient presentation is also Very suggestive of Cushing as shown here. Most dogs are mixed breed, but those who are not, not mixed breed are usually the small breeds that are listed here.

However, the disease, as the name suggests, sudden acquired rein degeneration, means that there is no genetic predisposition. Not only is the presentation suggestive of Cushing, the history is also just suggestive of Cushing. The owner will report weight gain, lethargy, polyphagia, polyuria, and polydipsia in many cases, and, this may precede the onset of blindness by several weeks or months or appear at the same time.

If you follow the patients, you will see that with time, the polyphagia will increase in severity. However, other signs like the lethargy, the polyuria, and the polydipsia will decrease and disappear in the coming months, which will become relevant in a few minutes when I discuss causes. So frequently you're left only with the polyphagia and the blindness in the long term.

As far as ophthalmic exam goes, well, we're talking about acute blindness that is not associated with any neurological deficits. The fundus examination is completely normal. So, and please remember this for our talk, .

In the spring, when we talk about diseases of the optic nerve, we are talking about acute blindness with a normal looking fundus. In some cases it does resemble, cases of distal optic neuritis. Signs of rein and optic nerve head involvement will appear months or years later.

As far as the pupillary light reflex goes, if you're using the white light, which is what most of us have in our clinics, you'll see that the pupils are fixed dilated or very, very sluggish. However, in recent years, we have what's known as the chromatic PLR test whereby you can test the responses to blue light and to red light and SARS patients have no response to red light because we're talking about outer retinal degeneration, but they are responsive to blue light, so chromatic PLR testing may help you establish a diagnosis of SARS in this patient. As I said, the presentation, the history of these patients resembles Cushing, and so does the blood work of these patients.

In 75% of the dose you'll find elevations in ALP, AST ALT, you'll find elevated cholesterol and triglycerides, you'll find inopenia and neutrophilia, reduced urine specific gravity. So really, It screams Cushing. Many dogs even have an abnormal ACTH stimulation test or low dose dexamethasone suppression test.

So really, this dog screams, I have Cushing, but In fact, when you continue the workup, classic Cushing is diagnosed only in 20% of these patients. As I said earlier, polyuria, polydipsia, lethargy and other signs of Cushing will disappear with time in these patients. And as you know, these signs never disappear in Cushing patients.

And if you look in the literature, you'll find that there were actually to date, there have been only 2 cases of SARS diagnosed in dogs with preexisting Cushing. So, despite our inclination to suggest that SARS is due to an endocrinological dis disorder, the evidence suggests otherwise. Another theory as to the cause of SARS that you may have heard about is that it is an autoimmune inflammation of the retina and this is based on a similar disease in people called autoimmune retinopathy.

Human patients with autoimmune retinopathy. Present with acute vision loss with a normal looking fundus. You're talking about middle aged women, you're talking about patients having an extinguished ERG such as you're seeing here, really identical presentation to these dogs with SARS.

Many of these human patients have a history of autoimmune disease, and many of them have cancer, neoplasia, other non-ocular cancer or melanoma, which is why it's called cancer associated retinopathy or melanoma associated. Retinopathy and the theory in these human patients is that the new the tumour produces autoantibodies for retin proteins, especially antibodies against these two retin proteins and because you have autoantibodies against retin proteins, this will induce an autoimmune inflammation of the retina characterised by apoptosis of the retinal photoreceptors. However, when we look for these autoantibodies in SARS dogs, we have found them only in a small number of dogs.

And if you go back to the review paper that I presented in the first slide, really the most authoritative review of SARS, it says that the connection between SARS and cancer has been ruled out in dogs. How do we treat these patients? Well, it's a problem because if we don't know the cause of the degeneration, we really have problems treating them.

If you believe that it's an endocrinological disease, then glucocorticoid and hormonal replacement theory, therapy have been suggested, . However, I, I warn you that no controlled or peer reviewed studies have been published on the subject, and I say I warn you because at this day and age your clients will go to the internet to look for therapy, and they may come across this website by Dr. Fletcher who says that my Treatment protocol does work and patients will have sight returned in 85 to 90% of cases.

If treatment is started within a week, if started within 1 to 4 months, vision will be retained in 60 to 65% of patients. Excuse me for my language, but this is a whole lot of baloney, our SARS. Patients do not regain vision, certainly not in these numbers, and that's what you should tell your clients if they come across this website.

There is no study to prove this. In fact, many of the therapist suggested at this website are downright dangerous when you look at the dosages suggested. If you believe it's an autoimmune disease, then some people suggest treating with intravenous immunoglobulins, cyclosporin, mycophenolate, azathioprine.

Again, these are protocols that clients may find on the internet. They originate from some studies in Iowa State University, but again, no controlled or peer-reviewed studies and the results have not been to. Implicated by others and therefore I'm very sad to say that as shown in these two quotes, currently there are no proven safe and effective treatment for SARS and the loss of vision is permanent.

No treatment can prevent or reverse blindness. This concludes my talk about, acquired causes of blindness. I just want to take the opportunity to invite you all to a very exciting event taking place next month, the virtual congress of 2021, where actually, we have an ophthalmology stream consisting of yours truly together with David Maggs and Paul Miller, my two co-authors on stats.

Mentals of veterinary ophthalmology. Here we are on stage in Finland. David was, celebrating his birthday, which is why we're dressed like that.

This was actually the first time, we lectured together last summer in Finland, and Virtual Congress, 2021 will be the second time you can catch us all together in the same symposium. So I look forward to seeing you then. Thank you very much for listening and have a good day.

See you next month.