Hello, everyone. Welcome to this webinar about non-ulcerative diseases of the cornea. Usually, when thinking about corneal diseases, we think about corneal ulcers and rightly so, cause they can be devastating and we can lose an eye due to nasty ulcers.
However, we should always remember. That the cornea may also be affected by numerous diseases, not necessarily causing ulcers, and that is the subject of today's webinar. Specifically, we'll be talking about these diseases.
The 1st 4 are really Corneal diseases, and I added scleriti and episcleritis cause they are diseases affecting the connective tissue of the eye and we really don't have an opportunity to talk about them in other webinars. As you will see, many of the diseases we'll be talking about today are inherited. So before I begin, I want to introduce you to a couple of free online resources that may help you determine whether disease you're seeing is inherited or not.
The first is the ECBO website, the European College of Veterinary Ophthalmology website, which has a section devoted to hereditary eye diseases. It has a manual listing about 200 and something dog breeds, 40 something cat breeds, and for each and every cat and dog breed, you'll find a list of Diseases that are suspected or proven to be inherited in that breed. The ECBO website also lists laboratories that perform DNA testing for those diseases if the mutation has been identified.
So if you have an older or a breeder wants to send a DNA sample, that will tell you which laboratory you can submit it to depending on the breed and disease that is under investigation. A second online resource is the so-called Blue Book put forward by the American College of Veterinary Ophthalmologists, and it actually lists the results of all of the eye exams conducted by ACBO diplomats in the United States. I have here one example, the Ker King Charles, and you can see that in between 91 and 2015.
They've had over 49,000 King Charles cavaliers examined by HBO diplomats, and another 15,000 between 2016 and 2020. So altogether more than 60,000 or sorry. More than 60,000 King Charles, really an astounding number.
We'll be talking today, here I've listed the findings in the cornea, and there are two diseases we'll be talking about today. Corneal endothelial degeneration, you can see is very rare in King Charles Cavalier, only a prevalence of only 0.1% in this time period and 0.1% in this time period.
So endothelial degeneration is probably not inherited in the King Charles Cavalier. However, corneal dystrophy, another disease we'll be talking about today, has a prevalence of over 8%, affecting thousands of dogs. So this one is definitely inherited.
So, If you have a King Charles presenting your clinic, you simply open the relevant topic, and the relevant breed, sorry, and you can see the prevalence of the disease in the United States. You can download the book for free at this website, but you do need the VPN connection disguising your origin if you're outside the United States. So, the first disease we are going to talk about or the first couple of diseases are congenital diseases.
Dermoid is they defined as normal cells or tissue in an abnormal location. And in the case of an eye, we are talking about abnormal skin tissue located in the eye. And you can see here.
Two examples of dermoids. You can see it is skin because of the hair follicles, but it really has all the hall markings of skin including retinypithelium, blood vessels, the hairs you're seeing here sweat glands, fat, smooth muscle, nerves, sometimes even cartilage and bone, and it is located, as you can see here. Either on the conjunctiva and or on the cornea.
Dermoids, as I said, are a congenital lesion. They are non-progressive, but obviously they may pose a clinical problem cause the hair that you are seeing here is naturally irritating, and rubbing on the cornea constantly and may even cause corneal ulceration. The only solution for that, the only remedy for that would be surgical removal, superficial cleatectomy shown here where you remove the superficial layers of the cornea containing the dermoid.
However, I should Note that the cornea underlying this dermoid is often thinner than normal, so you should consider referring these cases to an experienced veterinary ophthalmologist in order to perform the surgery. Another congenital disease that affects the cornea is persistent pupillary membrane, otherwise known as PPMs. Persistent pupillary membrane is the remains of embryonic vascular tissue that's responsible for providing metabolic support for the lens during embryonic development.
As we all know, after birth, the lens receives metabolic support from the aqueous humour. However, Prior to birth during embryonic development, there is no aquiumor and therefore, the lens receives, oops, sorry, metabolic support from this vascular network that originates in a blood vessel called the hyaloid artery originating in the optic nerve head down here, you'll see it in a minute. And this blood vessel really wraps all around the lens, forming a very, very dense vascular network that is supposed to provide metabolic support to the lens.
Usually, it regresses. Around birth, but sometimes it doesn't. And here is an ultrasound image showing you the hyaloid artery originating as I've said, at the optic nerve head and Forming a rich vascular network around the lens.
This is a postnatal ultrasound image, so it hasn't regressed as it's supposed to, and actually when we switch our Doppler on, you will see that it is still patent. I'm sorry about that. I think I need to.
Well, I did check it. OK, there you go. You can see the blood flow in a patent blood vessel.
So that is obviously a very serious clinical problem because we are unable to patch a patent blood vessel without causing severe bleeding inside the eye. However, this is a severe case of lack of regression of this embryonic blood supply. Usually, we have milder cases, again, persistent pupillary membranes which are seen as fine strands, almost like spider web strands.
Their base is always in. On the surface of the iris, as you can see here, here, you can see again fine strands here, here, here, the base is always. On the surface of the iris and the distal end may touch the lens, in which case it forms a caract.
It may cross the pupil from one side of the iris to another, as you're seeing in this case, or maybe the distal end is free-floating, as you can see in this albino dogs so hard to pick them out cause they are white strands or because we are talking about diseases of the cornea, and the distal end. May actually touch the inner aspect of the cornea, the endothelial aspect of the cornea, causing what we call a glaucoma or a white spot. OK.
And again, the telling sign is fine strands of iris tissue with a base in the iris and the distal end touching the cornea. Again, just like dermoid, it's a congenital lesion, non-progressive, but obviously it causes a corneal opacity. Nothing we can really do about it.
We can't treat it medically cause the Endothelial cells that come in contact with these membranes are dysfunctional and there is no way we can restore their function. The only treatment we can offer in cases of severe glaucoma is Corneal transplantation. If it's a myeloucoma such as what you're seeing here, then we just tell the owners to let it be.
It's like me having some fog or dirt on my glasses. The animal will manage quite fine. One dog breed in which, PPMs are a clinical con an inherited concern is the Basenji, where it is inherited in other breeds, it's developmental, but in Basenges breeding should be carefully considered cause as you can see, it can cause quite nasty lesions as in the case of this dog.
The second disease I want to talk about is corneal edoema, fluid inside the corneal stroma. And when talking about corneal edoema, we should keep in mind that there are two barriers for preventing fluid from entering the corneal stroma. One of them is the corneal epithelium, the outermost layer of the cornea, and if there is a corneal ulcer, if there is loss of this epithelial barrier, we will get flow of fluid usually tears into the stroma.
However, this would be focal edoema around the ulcer, as you're seeing in these two cases. The rest of the, of the cornea or the more distant cornea is really unaffected. The fluid is causing focal edoema around the corneal ulcer.
However, in cases of endothelial dysfunction, endothelium being the innermost layer of the retina, the layer that contains water pumps that are in charge of. Keeping the cornea in a dehydrated state, water pumps that constantly pump fluid out of the cornea, in case that these cells become dysfunctional, then we get more diffuse and a more severe edoema such as you are seeing here. And looking at this picture, you can understand why another name for corneal edoema is blue eye.
It certainly looks blue. Not only does it look blue, it also had a certain texture to it. We'll be seeing lots of corneal opacities today and sometimes people or my students ask me, well, how do you know this is corneal edoema and not corneal dystrophy?
Well, if you take a close look at this picture, you'll see that it's not homogeneous blue. It's not a homogeneous opacity. If you take a close look, you'll see that there is some sort of texture to it.
It sort of looks like the surface of an orange peel or a golf ball. It's made up of. Lots of small hexagons and the reason it's made up of lots of small hexagons is the shape of the endothelial cells.
This is a scanning electron microscopy picture of the endothelial cells, and you can see that they are in the shape of hexagons. So, if this endothelial cells, sorry, becomes dysfunctional, then you will have fluid accumulating in the sector for this, for which this cell is responsible, so you will have edoema in the shape of hexagon. If this one becomes dysfunctional, another hexagon, another hexagon, another hexagon, and that's why Corneal edoema, secondary to endothelial cellos, will have the shape of numerous small hexagons.
As I said, it looks like the surface of a golf ball or an orange peel. And here are a couple of more pictures showing it. Why would we lose endothelial cells?
Well, we can lose it due to intraocular diseases, chronic uveitis being one of them. I mentioned earlier that aquiumer is responsible for metabolic, providing metabolic support to the lens. It's also responsible for providing metabolic support to the inner.
Cornea, the cornea just like the lens is another vascular tissue, a tissue without blood vessels. Outer cornea gets its metabolic support from the tear fin. Inner cornea gets its metabolic support from the aqueous humour, and in cases of chronic uveitis when the composition of aqueous tumour changes, then These cells become dysfunctional and you will get corneal edoema, glaucoma, mechanical pressure being applied on the endothelial cells, and likewise interior lens taxation, bang the r lens banging against the cornea, and again traumatising the corneal endothelium.
All of them will cause loss of endothelial cell function and are associated. With corneal edoema. In fact, you know that blue eye is a classic clinical sign for UVitis and for glaucoma.
Yours truly may cause loss of endothelial cells during intraocular surgery, namely cataract surgery, if we don't take steps to protect the endothelium as we're extracting the lens. And unfortunately, We and our patients age and we lose endothelial cells with as we age and you can get corneal edoema in elderly patients. However, as I've said earlier, at the beginning of my talk, many of the diseases today we'll be talking about, are also inherited and we do have Primary corneal edoema inherited corneal edoema due to endothelial dystrophy.
You saw earlier that it is not common in the King Charles cavalier, but it is common in Boston terriers, in dachshund, and in German short haired pointer, and it is more common in elderly dogs because of the senile degeneration that I mentioned in the previous slide. In cases when it's inherited, the edoema will begin in both eyes, not necessarily in a symmetric manner, but it will begin in both eyes in the dorso temporal quadrant and slowly, slowly progress and. And invade or involve the entire cornea over 1 or 2 years.
Anyone interested in reading about it, here is a recently published study case series from the University of California Davis describing 99 cases of of an inherited endothelial dystrophy. And the final cause of endothelial dystrophy is Infection with canine adenovirus and that is one reason why infectious canine hepatitis is called blue eye. Again, you can see the orange peel texture in this affected cornea.
What happens in patients is that the virus infects endothelial cells. Triggering type 3 hypersensitivity reaction leading to endothelial cell death. You will see signs of uveitis because of the infection and a day or two later you will start seeing endothelial cell death and corneal edoema.
You may see during natural infection or as a result of vaccination, even though I should say that nowadays we rarely see it as a complication of vaccination because we've moved away from the live vaccination with CAV1 to the CAV-2 vaccine and therefore we see less and less cases as a result of vaccination. Why is endothelial cell loss such a clinical problem? Well, endothelium doesn't regenerate.
So At early stages of endothelial cell loss, adjacent cells can migrate and sort of fill in the defects and fill in for the lost cells, so you'll get reversible edoema that can be corrected by this migration if there's still enough viable cells. However, once you pass a certain Threshold, then the edoema becomes irreversible cause there are simply not enough cells to migrate and fill in the gaps. And then as you lose more and more cells, the edoema becomes more and more severe, and eventually, it is so severe that the cornea becomes almost like a sponge.
It soaks up so much fluid and Fluid forms pockets of fluid in the corneal stroma, and these pockets, or you could call them blisters, burst, and they would cause very, very painful corneal ulcers. We call these blisters bullae, and as I said, they would rupture causing painful and persistent corneal ulcers. How do we treat these patients?
Well, obviously, if there is an ulcer, we have to treat it medically and there are, there is a lecture I gave on medical and surgical treatment of corneal ulcer in the archives, so you can go and listen to those ulcers. We can attempt Treatment with hyper osmotic saline, 5% saline, and because it's a hyper-osmotic solution, it's supposed to suck fluid out of the cornea. However, as you can see, it gets 4 question marks because their effect is really debatable.
I call it grandma medication. As you know, you always get medical advice from your grandma, oh have some chickens. Soup or eat this or eat that.
And sometimes it works wonders, sometimes it doesn't work at all and there is no medical evidence for that other than grandma's wisdom. Same with the hypersmotic saline, sometimes it works great, sometimes it doesn't work at all. In the study from the University of California Davis that I mentioned earlier, it was used in 2/3 of the dogs with minimal efficacy.
Another treatment that we can try is transplanting your cornea. If the dog has lost all of its corneal endothelial cells, then we can transplant a fresh cornea, we call the procedure penetrating kerato. You can see here a study about it and you can see here a dog one year out after surgery.
This part of the cornea has been replaced and you can see it is much clearer than the part of the cornea that hasn't been replaced. So yeah, the dog has a small window through which it can see. Not a very pleasing results and therefore people have been trying to develop more effective surgical treatment.
One of them is instead of transplanting entire cornea, is transplanting only the endothelial layer. OK. You take, collect an endothelial cell layer from a donor and transplant it into a.
This is a case series out of Australia and you can see the wonderful effects it had on this dog. This is prior to surgery. You can see it's the same dog based on the pigmentation, and you can see how gradually it clears up.
However, I admit that this is Very challenging surgery. Not every veterinary ophthalmologist could perform this surgery. And therefore, as ophthalmologists who are less talented than this team in Australia would consider a Gunderson flap.
What we do in the Gunderson flap is we do superficial carrotectomy. We remove the very superficial layers of the cornea, and we place over them a very Thin conjunctival flap and the theory behind that is that the blood vessels in the conjunctival flap suck the fluid out of the cornea. As you can see, such a flap will cause a significant reduction in corneal thickness.
The edoema causes. An increasing thickness when it's reduced, the thickness is reduced, there is improvement in vision and in corneal cloudiness, or at least that's what's reported. Again, when you look at these pictures, you are, I'll forgive you if you are not very impressed by the results.
These two are the last couple of procedures I've presented, the corneal transplantation, the endothelial transplantation, the Anderson flap may require referral. This is something you can try on your own though I admit it is not for the faint of heart, thermokeratoplasty. Thermocytoplasty is shown here.
You actually take your cory unit and you Hover over the corneal surface. You don't actually touch the cornea, just hovering over the cornea and you make lots of small burns on the corneal surface as shown here. These burns would then form scar.
Tissue and like every scar tissue, it contracts. So it sort of squeezes the sponge that I mentioned earlier, decreasing the amount of fluid in the cornea and the scar tissue forms a barrier preventing the further fluid from entering the cornea. If you read this report, it works great.
All 13 cases had bull sclerotopathy, and those blistering ulcers that I told you about earlier. All 13 healed, but as I said, it is not for the faint of heart. If you are going to try it, I suggest you should practise on a couple of cadavers before taking your calery unit to a patient's cornea.
And because all of the surgeries I've mentioned are challenging and the results are sometimes questionable, the greatest promise may be this. Medication, which just came out a few years ago. It's a rock inhibitor, that promotes proliferation of endothelial cells and inhibits their apoptosis.
So medical treatment, that promotes proliferation or renewal of endothelial cells. It is a drug that's been developed in Japan, as treatment for glaucoma. In humans, unfortunately, it is not effective for canine glaucoma, but it may be effective in our endothelial degeneration patients.
You can see here, baseline results and 12 months later and you can see the increased . Density of endothelial cells, not, it doesn't prove 100% effective. When you look at these two pictures, you will see that actually there isn't much of a difference in the degree of edoema between the two, but, so there is no regression of the edoema, but there is no progression of the edoema, which is very important because as I Said this is an inherited disease and with time, over time, you'd expect things to get worse.
They didn't get worse. You can see that in this study here, 62% of eyes improved or stabilised, one third of them progressed. One problem with this drug is that it is only available in Japan, must be ordered online, costs about $70 or $80 per bottle and given 4 times daily, so.
Are recommended for clients with deep pockets. If your clients have financial limitations, this may not be something that they could use. The third disease I want to talk about is crystalline keratopathy.
And crystalline keratopathy is actually a syndrome that is a collective name for three different disorders. I'm talking about corneal dystrophy, which is inherited, lipid keratopathy, and corneal degeneration. Let's discuss them one by one.
So corneal dystrophy. We are talking about lipids that are deposited in the interior stroma, usually in the central stroma, of the cornea. You can see that depending on the breed, they have different appearances.
Sometimes it's a racetrack, sometimes it's a bull's eye, sometimes it is multifocal. And again, if you ask me how do I know it's a dystrophy and not edoema, well, we said edoema has the typical. Orange peel appearance.
Here, if you take a close look, you can actually see the individual crystals, the lipid crystals. It looks like a grain of salt that has been sprinkled on the cornea and that tells you you are looking at corneal dystrophy. It's an inherited disease.
It's usually non-progressive. It has minimal effect on vision. Again, it's like me having some dirt or fog on my glasses.
It is not painful cause the deposition is in the stroma, doesn't involve the epithelium. And here is a list of some of the breeds that are affected, the beagles, the husky, the Shetland Sheepdog, and as you saw earlier, the King Charles cavalier with a prevalence of over 8%. But again, no clinical significance.
So when an owner comes to me, and says, hey, there is something strange in the cornea. And we diagnose it as corneal dystrophy. We tell them that's OK, it's not painful, it's not gonna progress.
Learn to live with it. As opposed to lipid keratopathy, which definitely has clinical significance cause here we are talking about lipids deposited in the cornea due to a systemic disease, systemic hyperlipidemia or systemic hypertrigliermia, so we're talking about. Systemic diseases such as hypothyroidism, Cushing, pancreatitis, diabetic metitus, unbalanced diet, etc.
Etc. Here, the typical clinical appearance is what you are seeing in these two pictures. The deposits have the shape of a crescent or a banana or an arc, which is why another name for it is arcus lipodesis.
It's a peripheral crescent and if you look very closely, you will see that there is always an area of clear cornea, 1 or 2 millimetres of clear cornea between the limbus and between these deposits. Once you identify, lipid keratopathy, you obviously have to suspect a systemic disease, so you need to, diagnose the primary disease, treat the underlying disease, change the diet, . That have already been deposited in the cornea will not evaporate.
They will not leave the cornea, but if you have successfully treated the underlying cause, then you will not get any progression. And if there is severe, there are severe deposits prior to the diagnosis and treatment, then you could consider surgical removal after you've diagnosed and controlled the primary problem, because, most of the audience is from the United Kingdom. I wanna.
Pay tribute to Sheila Crispin, who was the ophthalmologist at the vet school in Bristol for many years, rose through the ranks, became head of the Royal College of Veterinary Surgeons. A few years back now, she's happily retired, but, she was, the leading authority on acoustic poids in our canine patients. And the third entity that can cause a crystalline keratopathy is corneal degeneration whereby we get these deposits due to Ocular disease, it may be secondary to uveitis, scleratitis, scleritis, something I'll be talking about at the end of my talk.
Maybe it's following trauma, sometimes due to systemic abnormalities, but Note that now we're talking about calcium rather than lipids. So these deposits and may be calcium may be lipid, but again, if you look closely, you can see the individual crystals forming the deposits. The problem here is that sometimes these deposits become so dense, so dense that they actually become like a chunk of calcium, like a stone really, which falls off, breaks off, and then it forms this.
Nasty looking ulcer, you see that here we in the centre, we really had a chunk or highly concentrated calcium that fell off, causing the smatocele, very challenging to treat because of the surrounding deposits that make it hard to treat. Another cause for corneal degeneration, I should say, is you when you prescribe topical steroids, when you prescribe prednisolone, for example, you can see that in humans it causes trauma calcification and also a recent paper out of Korea saying that, suggesting that topical corticosteroid is significantly associated with calcaneus corneal degeneration. How do we treat it?
Well, once again, look for the underlying cause if there is hypercalcemia or hyperphosphateemia, if there is scleritis, if there is tin disease, look for it and treat it. We can try another grandmother medicine, 2% EDTA, 2% EDTA is a chelating agent. It's supposed to bind the calcium and thereby reduce these deposits.
Again, grama medication, meaning sometimes it works, right, sometimes it doesn't work at all. We don't have any studies showing their efficacy. .
Here is a study out of Australia suggesting combining topical EDTA with diamond bird debridement, the instrument that we use to treat boxer ulcers by polishing the anterior, surface of the cornea, and they report great success with this treatment. We weren't so impressed with 2% EDTA. But a couple of years ago, we found a company out in Florida that sells 14% EDTA.
Here is their website. I'm not commercially affiliated with them. And 14% EDTA is no longer a grandma's medicine.
It provides us with excellent results. What we do with these patients is, soak their cornea. In 14% EDTA for 5 to 10 minutes, you can literally see the amount of deposits in the cornea reduced.
Afterwards, we bury it and we are very happy with the results. If you are unable to import it, to your country, then sorry, superficial curreectomy may be another medical option for you. Panos, the 4th disease that I want to talk about, has many names, chronic superficial caratitis is the proper clinical name for it, and Uberreiter's syndrome, named after the Austrian ophthalmologist who discovered it.
Panus is really an autoimmune disease with two, components. The first component is genetic predisposition. It is especially prevalent in German shepherds, Belgian shepherds, and related breeds, and the second component is ultraviolet radiation.
And what happens is that the ultraviolet light changes the antigenicity of corneas in susceptible dogs and now the cornea is a foreign body. You can see it also in this space. Here, the foreign cornea is a foreign body and you have an autoimmune inflammation characterised by lymphocytic plasmatictic infiltration plus to antigens and cell-mediated immunity.
As I said, two risk factors for the disease. One is genetic. Here is a study out of the Czech Republic, showing that out of 377 German shepherds presented at an ophthalmology clinic.
30% or almost 30% were affected by PAOS, no sex predisposition, median, middle aged dogs. Interesting to see that one third of them were hypothyroid, another disease with an autoimmune component. Yeah, so the immune system of these dogs may be malfunctioning.
It triggers anus, it triggers hypothyroidism. The second risk factor is ultraviolet radiation and therefore, the disease was is more prevalent in dogs living at high altitude where there is more ultraviolet radiation. That's why it was first discovered and described in Austria.
It's more prevalent if you're in the United States, in places like Colorado where they really have what, they call PAUS clinic days where you see 40 German shepherds lined up for PAUS treatment. Also very prevalent in the southern hemisphere, so places like Australia and South Africa, the whole world. They've lost the whole, the ozone layer, and there is a hole in the ozone.
Thankfully, it's now being repaired, but during the days of the hole in the ozone, they had lots and lots of panels because that was supplying protection from ultraviolet radiation. Clinically, we are talking about a bilateral inflammation cause it is inherited and it's progressive cause again, of the inherited component and cause the dog will always be exposed to sunlight. It begins in the temporal or ventral temporal quadrant cause if you look at the camera, that's the quadrant that is most exposed to sunlight, OK.
Sunlight from above will first hit the ventral or ventral temp. Quadrant of the cornea starts as a conjunctival lesion, but progressing to affect the temporal cornea with classic signs of keratiis, vascularization, pigmentation, a leading white edge which is the plasmocytic lymphocytic infiltration, but it slowly progresses, progresses to cover the entire cornea. So again, a couple of pictures showing how it starts.
As a moderate lesion in the temporal cornea. Sometimes, as you can see, the third dili is also affected if it is elevated, but it progresses and progressively more and more of the cornea is invaded by this inflammatory process, the vascularization, the cellular infiltration, the pigmentation until in very advanced stages you Get a complete loss of corneal transparency and the eye is basically blind in advanced cases. And as I've said before, you can get cases where it's really mostly the third eyelid being affected.
It is thickened and you have areas where it's circular areas usually where it loses its pigmentation. Treatment? Well, we're talking about an autoimmune disease, so the aim of the treatment is to control the disease.
We'll never cure it because it will always be a German shepherd. The prognosis depends on the age of onset. The disease is more severe in younger dogs and milder in elderly dogs.
It depends on the altitude. Prognosis is better if you're at sea level, it's worse if you're In high altitude, in my case, you know, often it's dogs, that, that run with their owners on the beach. That's another reason why their corneas would be exposed to sunlight.
So exposure to radiation is definitely a risk factor and therefore, one way to control the disease is to reduce ultraviolet radiation. Or exposure and where there is a need, there is a solution. So here is a website of a company called Goggles which fits dogs with goggles.
And these goggles actually have ultraviolet philtres, that, protect the cornea from exposure to ultraviolet light. Some dogs don't wear it. Other dogs, take to it, and yeah, #1, it helps.
#2, it makes for a great fashion statement, as you can see. And a few years ago, I was in Peru, in Machu Picchu, and I was impressed to see that the llamas there also walk around with protective goggles protecting them from radiation. But of course, that was not enough and that is not a solution that you can offer every dog cause some of them will, kick off the goggles within 5 minutes and therefore we do have to provide medical treatment.
We are talking about an autoimmune disease, so we're talking about anti-inflammatory treatment. You can try topical steroids, and if you can control the disease with that. I congratulate you.
Try to taper, but I doubt you'll be able to stop treatment. On the other hand, if it's not effective, then you may have to add additional drugs such as cyclosporin, tacrolimus, pincrolimus as shown here in this paper, and often in severe cases, we would do subconjunctable injection of long-acting steroids. Superficial keatectomy is another solution in advanced cases where really the eye is blinded due to advanced pigmentation.
Yes, I could remove the superficial keatectomy where all the pigment is located, but it would still be a German shepherd, it would still be exposed to radiation, so recurrence is likely. We can try and decrease it with supportive treatment, radiotherapy, cryotherapy, radiation, etc. Etc.
The 5th and final disease I want to talk about, scleritis and epistcleritis. As I said, it's not really a corneal disease, but it does affect the sclera, which is the connective tissue, the non-transparent connective tissue that is a continuation of the cornea. So just to remind us, here is the cornea with the nice arrangement of parallel collagen fibres keeping its transparency.
The more posterior continuation of the cornea is the non-transparent cornea and you can see that here there are more cells and the collagen fibres are not in a parallel manner, which is why the sclera is non-transparent. We know that overlying the sclera, we have the conjunctiva, but what we sometimes forget is that there are a couple of Thin connective tissue layers between the sclera and the conjunctiva, namely the epiclera, which is why we are going to talk about scleritis and episcleritis, inflammation of the sclera and the episclera. And once again, we are talking about an immune-mediated inflammation.
And when I say immune-mediated, it means that yes, it may be inherited in a number of diseases. And as you can see, we're talking about popular breeds like the collie, the cocker spaniel, the golden retriever. So, inherited in some disease by in some dog breeds, but in other dogs, it may be secondary to.
Systemic or ocular infection, be it fungal, bacterial, toxoplasma, lichia, etc. Etc. It may be secondary to systemic histiocytosis or secondary to other ocular disease as you are seen.
If we start talking about episcleritis, episcleritis may be nodular, which is what you're seeing here, or it may be more diffuse, which is the clinical picture that you are seeing here. When we're talking about nodular episcleritis, yes, it may be one mass. Or it can be multiple masses such as you're seeing in these two dogs.
It may be unilateral or bilateral, and as you can see, it is frequently at the limbus, frequently at the temporal limbus. However, episterittis will also have a more diffused appearance where you can see that really the entire globe is affected, frequently also involving the adjacent cornea causing edoema vascularization or degeneration. I go back to what we spoke about earlier.
Sorry, when we discussed corneal degeneration, we said it these crystals may be the result of episcleritis. Note again, in some of these pictures, yes, you are seeing masses. Here, it's very in the nodular case, it's very easy to recognise the fact that it's localised.
The rest of the conjunctiva is unaffected. Here it is more difficult. You see a huge mass, but look closely at this area of the conjunctiva.
Look at this area. You can see that there is a large mass, but the adjacent. Issue is uninvolved, and that should clue you in that you are looking at episcleritis and as it says here, this is more likely to be secondary than the nodular disease which is more likely to be inherited or primary.
Scleritis, unlike episterritis, is more painful. It causes intraocular disease, OK. So you said that episterittis may be secondary to ocular disease.
Here we are looking at the flip side of the coin and it causes intraocular disease. It may cause uveitis, it may cause glaucoma. So here we have a severe case of actually Scleral rupture due to scleritis.
So, yeah, it frequently leads to blindness, to in nucleation and definitely carries a worse prognosis than episcleritis. However, if you look at these pictures and the pictures that I showed you previously, you will be forgiven for saying, hey, they all look the same and indeed you are Right, they have similar clinical appearances and actually if you look closely at the literature, there is lots of confusion and, lots of names for anti-clinical entities of very similar appearances and therefore, the diagnosis is ultimately in many cases histopathological. And yes, we do need to take histopathology in many of these cases because we need to rule out neoplasia.
Looking at this eye, it may very well be lymphoma, squamous cell carcinoma, melanotic melanoma. So, yes, you do need a diagnosis, a histopathological sample or biopsy in order to rule out . Neoplasia and confirm the diagnosis of scleritis or episcleritis.
Once you determine its scleritis or epistcleritis, do examine the patient for intraocular disease, which, as I said, in some cases may be the cause of epicleritis. And in other cases, it may be the consequence of scleritis, so you need, regardless of whether it's the chicken or whether it's the egg, secondary intraocular disease, or I should say, I shouldn't say secondary, intraocular disease may be present. Treatment.
Well, it is challenging, we are talking about an immune-mediated inflammation. So just as in case of PANUS, we'd start with steroids, and try and taper them. However, many of them do not Respond to steroids and we would have to add oral corticosteroids, subconjunctival injections, maybe switched to heavier guns such as azathioprine, cyclosporin, either topically or systemically.
Tetracycline and sinamide as an immunomodulatory treatment that we sometimes use in systemic lupus, etc. Or surgical excision of the involved nodule or nodules, and again, it should probably be combined with supportive adjunctive therapies such as cryotherapy or radiation. So this concludes a very quick review of some.
Diseases of the cornea that are non-obsertive in nature but as you saw, may be painful, may cause secondary ulcers, may lead to loss of vision. Yes, you do need to know how to recognise them and treat them, and I wish you best of luck with your next presentation of congenital diseases, corneal edoema, crystalline keratopathy, pinus, and scleritis. Thank you very much and goodbye.