Thank you very much, Sophie, pleasure to be with you guys again. So, as you said, the topic of tonight's lecture is CAAC and what can I do about it. I definitely do not intend to turn you guys into cataract surgeons.
That requires a three-year residency. However, a referring veterinarian has a very, very important role to play in cataracts, the referral, the pre-op evaluation, the post-op evaluation, client education, etc. Etc.
Timely referral, and this is the message I want to get across, cause without your help, cataract surgery will fail. By the way, this is a picture of cataract surgery in Germany in the 16th century, I believe. This guy here is a patient.
This guy here is the anesthesiologist. As you can see, the anesthesiologist's job is holding the patient's head. That's restrained for you and this guy here is a surgeon and the surgeon is holding a spoon and what he's doing is really pressing on the cornea with a spoon, applying pressure, pushing against the lens.
Eventually ripping all of these zones and causing a posterior lens laxation, causing the cataract lens to fall into the back of the eye, thereby removing this opaque obstacle and restoring vision. We've come a bit since then. We've improved our techniques since then and we will be discussing it in today's lecture.
As always, I must to reveal any financial or commercial relationships. I really have none except one which I call a disclosure or shameless advertising as I've co-authored a book together with David Max from the University of California, Davis and Paul Miller from University of Wisconsin Madison, Fundamentals of Veterin almology, and many of the pictures I'll be showing here are from this book. So what is cataract?
Cataract is basically an opacity of the lens or its capsule due to disruption of the arrangement of the lens fibres. So just like the cornea, the fibres of the lens are arranged in a very parallel and orderly manner, as you can see here, and as long as they maintain their parallel arrangement, waves of light can pass between these fibres without being scattered and disrupted. However, if this arrangement is disrupted, then the waves of light will be scattered as they pass through the lens fibres, and this really will cause an opacity.
So what causes a cataract? Well, we have numerous causes of cataract. Cataracts can be caused by developmental diseases, for example, persistent pupillary membranes.
Here we can see the embryonic blood supply of lens during embryonic development originating in the yelloid artery, branching off to a rich vascular bed covering the lens, it's supposed to regress and absorb after birth, but sometimes some of it remains, and that may cause an opacity. Sometimes the posterior yoid artery may remain and cause an opacity on the posterior aspect of the lens, which is what we're seeing here. We may have cataracts due to nutrition causes, mostly in puppies and kittens, orphan puppies and kittens that they get replacement formulas, and if these replacement formulas are deficient in arginine, then they will cause cataracts.
However, I should point out that this is the only type of cataract that is reversible and once nutritional balance is restored and the puppies or kittens are fed with arginine, then the cataracts are reversed. We can have cataracts due to metabolic disease. This is a picture of a cataract caused by hypocalcemia.
Senile cataracts, huge controversy. We see lots of cataracts in elderly patients and often we ask ourselves, are these due to age and senile changes or are these late onset hereditary cataracts, which is why we have the question mark here. I won't get into this controversy.
Suffice to say that yes, we do see lots of cataracts in sin patients. We see cataracts due to trauma. Here is a cataract caused by a lens A cat claw injury to the lens, and obviously a cat claw is not very conducive to the parallel arrangement of lens fibres, so that causes an opacity of lens fibres.
We can get cataract due to ocular disease. Here is a picture in horse, and you can see lots of inflammatory debris covering the ventral 80 or 90% of the lens capsule, lots of Green and white blood cells and platelets adhered onto the interior lens capsule. So that obviously reduces the clarity of the lens capsule, causing secondary UVI cataract secondary to UVI.
Persistent retinal atrophy gets 3 question marks. I'll get back to it. But basically, if the, we have lots of dogs that present with both cataracts and retinal atrophy, and sometimes it's a question of which is the egg and which is the chicken, we can say that.
Excuse me, maybe retinal atrophy preceded the cataract and as the retina was degenerating, it releases . Free radicals and other toxins into the eye and that causes secondary cataract or maybe the cataract induces uveitis that causes the retinal atrophy, or maybe we're talking about two independent diseases. I'll get back to it later, but anyhow, we can see both diseases together.
Toxicity, lots and lots of drugs have been proved in experimental studies to cause secondary cataracts. The only one of relevance really is catconazole, which may cause secondary cataracts. However, as you can see in the title of this slide, in the preceding slide, I am talking about miscellaneous causes of cataracts.
Really, there are two major causes of cataract. The first one is diabetes. Cataracts develop in 50% of all diabetic dogs within 6 months of the onset of diabetes.
Within 1 year, 80 to 90% of diabetic dogs will have cataracts, and this is because diabetes causes hyper osmolarity of lens. Here we have the major pathways of glucose metabolism in the lens. And as you can see, due to all those reducta activity reducing glucose into sorbital inside the lens, we have hypersimilarity of the lens.
This causes water to ingress into the lens, and this induces vacuoar changes in the lens. You can see them here in the periphery of this lens. We had to dilate it to see these vacuoles in the lens.
And one typical aspect of diabetic cataracts is that they are progressing very, very fast. Within a few weeks, the dog can go from a totally clear lens to a totally opaque cataractive lens. So if you get a history of a dog with very rapid onset of cataracts, please suspect diabetes and do the appropriate workup.
So this is one very important and leading cause of cataracts, diabetes. The second one is inheritance and genetics. These are tables from a paper published in the University of Florida by my teacher, Kirk Glat studying 730,000 dogs, almost 3/4 of women dogs, over a period of 40 years.
As you can see in mixed breed dogs, which were half a million dogs out of the 730, the overall prevalence of cataracts was 1.6%, which would be all these secondary cataracts and diabetic cataracts that I told you about earlier. Any dog breed that has prevalence higher than this baseline of 1.6 should be suspected of having inherited cataracts.
Definitely when you get to these breeds up here like the Michon Frise, Boston terrier, miniature poodle. Toy poodle, etc. With prevalence of over 10%, American cocker spaniel 8.7%.
So breeds with a prevalence of 678 times higher than the baseline should definitely be suspected of having an inherited cataract and indeed here is a list of dog breeds predisposed to cataracts or where inheritance is suspected. I don't expect you to remember all of these breeds. In fact, I challenge you to find a breed that is not on this list.
Many, many dog breeds are suspected of having inherited cataracts. And in fact, In some breeds, it has been proven to be inherited. So previous table was dog breeds suspected of having inherited cataracts.
Here we are looking at dog breeds that are proven to have inherited cataracts, and these differ in mo mode of inheritance, as you can see, most of them have autosomal recessive. This includes the Afghan hound and the Boston terrier. And the miniature schnauzer and the staff bull terrier and the standard poodle, etc.
Etc. But others may have dominant cataracts such as the Australian shepherd or incomplete dominant such as the Chesapeake Bay retriever. They also differ in the age of onset.
Some of them are congenital. Mitro Schnauzer, for example, may be born with an inherited cataract, as well as the Welsh springer spaniel and the Westie. Other dogs get it when they are a few months old or when they are elderly, so differences in age of onset.
And differences in the mode of inheritance in here, in the age of inheritance in here are probably due to the mutation that causes inherited cataracts. For example, we know that a mutation in the HSF4 gene causes. Cataracts in these four dog breeds, but not in others.
So some breeds are predisposed to mutation here. In other breeds we have yet to identify the mutation, but this is what accounts for differences in mode of inheritance and the age of onset. Breeds may also differ in the location of the initial lesion.
So this is the previous table that you saw, but now we have another column here showing the initial location of lesion which may be in the cortex, interior cortex, in posterior cortex, in the nucleus, etc. Etc. They differ according to different breeds and this is very important forgnosis.
What do I mean? For example, here is a triangular, cataract, which is typical for the retriever breeds, as you can see here, the golden retriever, the Labrador retriever are characterised with inherited cataracts that are posterior subcapsular, triangular in shape. So if I see this type of cataract in the golden or Labrador retriever, I know it's an inherited cataract, and I can discuss with the owners the prognosis as far as progression, inheritance, and implications for offsprings, etc.
Etc. However, if I see a different type of cataracts in a golden or Labrador retriever, then I know it's not an inherited cataract, and then my talk with the owner takes on a different perspective as far as inheritance and prognosis go. But definitely many, many cataracts are either diabetic or inherited and Dogs with cataracts that are suspected of being inherited should not be bred.
This is a very, very important point, demonstrated by this paper published by my German colleagues a couple of years ago. What they did was study, was examine. Cataracts in German dachshunds and Using the results of these examinations to make recommendations for breeders as far as should you breed this dog or shouldn't you breed this dog.
And based on the recommendations over a 113 year period, they managed to reduce the prevalence of cataracts by about 70%. So definitely recommendations to breeders play a very, very important role in preventing cataracts. So, as I said, cataracts may differ by the age of onset, they may differ by the cause, they may differ by the initial location, they may differ by the inheritance mode, but really clinically, the most important distinction is the degree of maturation which impacts the questions of visual deficits on the one hand and when do we go into surgery on the other hand.
And based on the degree of maturation, we divide cataracts into 4 categories. The first one is we call incipient cataract, which is early focal changes. Here is an example of one, you can see an opacity here in the centre of the lens, but as you can see, more than 90% of the lens is purely transparent and clear.
So yeah, we do have Small opacity here that I can have some dirt on my glasses on my car windshield. That doesn't really cause significant visual deficits. So really an insipting cataract.
There is another example, one which we saw earlier. Peripheral vacuolar changes due to diabetic cataract, seen only following dilation. However, neither one of these have significant effects on vision cause they affect only a small part of the lens.
Unfortunately, most cataracts are progressive and these small opacities will progress and affect greater portions of the lens, which is what we're seeing here when we're talking about immature cataracts, when most of the lens is involved, you can see here capacity really involving most of the lens maybe a transparent area here and here. And again, another diabetic cataract here involving all of the lens nucleus and the periphery here, maybe a small band of clear lens here. So basically, most or all of the lens involved is involved, but as you can see, It is not yet opaque.
It is still transparent. Transparency has been reduced, but you can see green typical reflection here, orange reflection here. So we can see the reflection.
And vision is present. I compare these cataracts to having fog on your car windshield or on your glasses. You can see, yeah, it's foggy, vision is reduced, but it's present.
However, as I said, these are progressive, and this opacity, small or loss of transparency I should say, will progress into total opacity, mature cataracts, where the lens is completely opaque. You can see here there is no fundus reflection. I can't see any details of the fundus, the funders cannot see me.
This eye is totally blind. Some more examples. This is a bush baby, a primate.
You can see by the typical reflection that this eye has a totally transparent lens. This eye has a totally opaque and a lens due to a cataract. Here was a puppy, remember I told you that cataract may be Congenital or may begin or present at a very early age.
You can see that this eye is totally opaque, no fundus reflection on this eye. Here there is loss of opacity here, some peripheral reflection, green reflection of the epitium here in the periphery. So mature cataract in this eye, immature cataract in this eye, but As I said, counteracts are progressive.
It won't be long before this eye looks just like this eye. Unfortunately, things do not stop here. They do not stop at the mature stage, they progress into a hyper mature stage.
In the hyper mature stage. What happens is that the lens protein is digested and breaks down and eventually leaks out of the lens capsule and you can see it here. Look at this iris here.
Here is a pupil and you can see, literally see lens protein leaking out of the capsule. So this is a hypermature cataract. Here, the process has progressed into a stage whereby The cataract has resolved or been digested from all of the lens periphery.
So really the cortex of the lens is clear now. You can see a cataract remaining in the lens nucleus and at the bottom of the lens here due to sinking of some proteins. Very important to point out that at this stage we get lens induced CVI and this is because the Lns protein is antigenic.
It triggers an inflammation in the eye, . In dogs, what happens is that the immune system develops after the lens capsule and therefore, first we get development of the lens capsule which wraps up the lens protein, later. The immune system develops, so the immune system never gets a chance to recognise the lens protein in dogs, and when they eventually leak in hypermature cataracts, such as you see here, the immune system regards it as a foreign body triggering an inflammation lens indubiitis.
Fortunately, we people, humans do not get this because in humans, the Development is reversed in order. First, the immune system develops, then lens capsule develops, so our immune system in people gets to recognise lens protein. Lens protein is not a foreign body in humans and therefore we don't have so much lens induced uvialities in people making the prognosis of cataract surgery or cataracts.
As a whole, in people much better than in dogs. Fortunately for people, unfortunately for dogs. In young dogs, this.
Resorption process may be significant enough to actually restore vision. You can see here that this dog actually regained vision in the periphery, and if it's a young dog, maybe the cataract in the nucleus will also resolve and become transparent. So actually, vision may be regained if you want, you could say that the dog performed cataract surgery on itself.
Again, it triggered severe lens-induced CVIS which has to be monitored and treated, but vision has been regained in this talk. Couple of more examples. Here are a few more, a couple of more, cases of lens in, sorry, upper mature cataract.
You can see here the resorption at this point, maybe some leakage here and in this picture here you see. Crystals and that's another sign of hypermaturity and you see this shrinkling of the lens capsule, which is another very important sign of hypermaturity in cataracts. I always compare it to a raisin, so a cataract may or a lens, I'm sorry, would be compared to a whole grape and then as it resorbs.
And leaks out of the capsule and shrinks, becomes like a raisin, and the capsule becomes wrinkled like a raisin, and that's why you see this wrinkling that you are seeing here. When talking about maturity of cataracts, I should mention one other entity which is not really a cataract, it's nuclear sclerosis, which is what we're seeing here. But I mentioned because it's frequently confused with cataracts.
So what is nuclear sclerosis? The lens may be compared to the rings of an onion or a tree, sorry, in that. The lens capsule determines the volume of the lens, and this is something that does not change through life.
So we have a lens capsule determining the volume of lens through life and Therefore, as fibres are formed in the periphery of the lens throughout life, they push younger fibres towards the centre of the lens so that new lens fibres are constantly formed here in the periphery, constantly pushing lens fibres towards the centre of the lens. So that if you form a transverse section through the lens, this would be the embryonic nucleus containing embryonic lens fibres, foetal nucleus, then fibres in young puppies, young adults, adults, elderly dogs, etc. Etc.
And this would be the most recent fibres that constantly keep pushing fibres towards the centre of the lens. And so that if you cut the lens, then as I said, like, Onion ring onion rings or tree rings, you'll have the oldest fibres here in the centre, the youngest fibres here in the periphery. And if the dog is old enough, Then the nucleus fibres will become so condensed that they will become visible.
They are visible as a nuclear sclerosis and opacity of the nucleus. It looks like a cataract. Look at this.
It looks like a cataract. However, that fibres have still maintained their nice original parallel orientation and therefore it's not a true cataract, it is just a senile change. It is frequently confused with cataract unless we dilated the pupil.
So here are a couple of pictures illustrating this. Here are two opacities in the lens nucleus. One here and one here.
Yes, they both cataracts, but if you dilate the pupil, you will see that this one is indeed an opacity, this one is indeed cataract. This one is transparent. Stand far away from the patient, use a good source of light with your trans illuminator, and even though it looked opaque initially, you will be able to see through this lens nucleus which I am depicting here.
So this is nuclear sclerosis, not to be confused with cataract. So now that we know what cataracts are, obviously, the next question is how do we treat them? So, as I said earlier, cataracts may resolve in young dogs, with high premature cataracts.
They may resolve to the point where vision will be restored, but as I said, it will trigger an inflammation, lens induc Citis, and therefore, the patient must be monitored and treated for lens induced CBI. In cases of a nuclear cataracts such as you're seeing here, if we provide mide or atropine and die to pupil, then patients may be able to see through the periphery of the lens, and this will allow vision through peripheral vision in cases of nuclear cataracts. There are studies that, indicate that some drugs may slow the progression of diabetic cataracts, which I mentioned earlier by inhibiting the aldose reductase enzymes that I mentioned, that's responsible for the, Genesis of sorbitol and the hypersimilarity of the lens, and in fact, one of these drugs may soon receive FDA approval from the US Federal Drug Administration and maybe we'll have some drugs to delay the onset of that cataracts, but I want to stress that there are no drugs that dissolve or prevent formation of cataracts.
And those of you who've been to my previous talks know that I always have a slide where I say, this is the most important slide of my talk. Please forget everything else, just remember this slide. As far as I'm concerned, this is really the most important slide of my talk.
There are no drugs that dissolve cataracts or prevent the formation. And I say this because Today, this day of age of Google and internet, etc. Etc.
People can advertise anything they want without offering any proof. Here is an example. Can see eye drops, I love the name, can see.
Can see eye drops safely reverse cataracts in dogs? Wow, this is amazing. Put in a couple of drops and you reverse the cataract in your dog.
Clients often find this drug or similar drugs on the internet and they come to me asking, hey, why do I need surgery? Can I give this to my dog? The answer is no.
I'm very sorry. I wish it were true, but no. I should point, what I tell my my clients is that cataract surgery is the most common surgery in humans.
Not just the most common ophthalmic surgery in humans, it's the most common surgery in humans, period. Cataract is a problem. Affecting millions and billions of people, costing millions and billions of pounds in surgery and insurance costs.
If anyone were to discover a drug that dissolves cataracts, they wouldn't be selling it on the internet for $100. They'd sell the patent to authorities for a billion dollars and then they'd sit home waiting for a phone call from the Nobel Prize committee, OK. No no drugs have yet been proven to dissolve cataract.
You can claim it on the internet, but unfortunately, these claims have yet to be validated. I wish it were true, but right now, at this point in time, cataract is a surgical case. So, let's talk about surgery, which is where you as a general practitioner and as a referring practitioner come in.
And when we're talking about Cataract surgery. There are really 4 very important questions which I, the surgeon, and you, the referring vet, have to ask. These are how mature is the cataract, retina functioning, is your secondary ocular disease and patient and owner selection.
And I'll go through these points one by one. First point is when should we operate at what maturity stage should we operate? Again, I remind you, cataracts may be incipient, incipient, immature, mature or hyper.
So, In cases of incipient cataracts such as this small triangle, obviously, it's much too early to operate. Maybe the cataract will not progress. And in any case, it is still visual.
I mean, it's got a small opacity here, but 99% of the lens is transparent. This patient doesn't have any significant visual deficits that justify surgery. So at this stage, we just monitor the patient for progression, we monitor it for lens-induced CVI and You should consider referring the client to and for an exam by a specialist because at this stage the funds can still be visualised and I'll explain the importance of this in a minute.
But definitely much too early to operate at this stage. On the other hand, when it's a high premature cataract, such as this one, and again, you can see the crystals here and the wrinkling of the capsule. This is far too late for surgery.
This is a hypermature cataract with significant lens induced CVI which will lower the prognosis and therefore this is far too late for surgery in this patient. A mature cataracts such as these two is a little too late. I say a little too late cause surgery is more difficult at this stage.
The lens is tougher, so it's more difficult to extract it. There is some lens in DCVIs even at this stage of mature cataract. Indeed, you can see the pigment on the lens capsule here and the leakage here.
So there is some lens in DCVITs. So for these two reasons, I don't want to operate on this at this stage. It's a bit too late.
However, the advantage of operating at this stage is that the animal is already blind and this is a very important consideration cause cataract surgery, just like every other surgery, is not 100% guaranteed success. Some of them may fail, and if surgery has failed in an animal that's already blind, well, You can tell your patient, I'm sorry, the client, I'm sorry, but you know, at least we didn't make things worse. It was blind to begin with, we didn't make things worse.
And back in the days when I was training in Florida in the 1990s, we used to say, let's wait for this stage because animal is already blind, we have nothing to lose. However, As I've aged and as cataract surgery technique has improved and the instrumentation has improved and the pre-op assessment has improved, etc. Etc.
We have come to recognise that we prefer operating on cataracts that are immature, such as these two. You can see that the entire lens is involved, but you still get some green reflection. Yellowish orange reflection here from the tepium.
So immature cataracts, these are ideal because at this stage the lens is soft, so the surgery. I There is no lens induced UBI. However, you have to consider each case and judge its merits, judge the visual, visual deficits, and the progression is cataract, surgery justified at this stage.
Let's look at a couple of examples. So this puppy that you saw earlier, this eye has a totally opaque lens. This one is Half opaque, I would say so mature here, immature here, but cataracts are progressive.
We know that very soon this lens will be as bad as this one. So yeah, it's time to cut both of these lenses. This one is a diabetic cataract due to the vacuoles.
I know that within a few weeks it will be totally opaque. Let's cut this one even though the eye is still visual. This one, however, yeah, a lot of lenses involved, but the dog is still visual.
I'm not sure about the rate of progression of these opacities. Maybe I'll invite this talk for check in a few in a few months and decide what to do. So this is the first consideration, what is the stage of maturity?
The second question I'm asking myself is whether the right now is functioning. What I tell my clients is obviously there is no point in Doing cataract surgery on the dog, if the retina is not functioning, I always give the analogy of camera without a film in case when cameras had filming them. If there is no film in the camera, then changing the lens will not enable you to take a picture.
If there is no functioning retina in the eye, then taking out the cataractus lens will not restore vision. And this comes back to what I mentioned earlier that there is significant linkage between PRA between retin atrophy cataract, maybe lens-induced uitis induced retinal degeneration, maybe the atrophying retina, . Cause cataracts because of free radicals that were released by the degenerating retina and maybe we're talking about two separate diseases, inherited diseases, cataract and rectal atrophy in the same dog.
I don't know. I really don't care at this stage. The problem is Is there retinal degeneration in this dog, and the problem is that the question is whether there is retinal degeneration in this dog, and the problem is that when we have a cataract, I cannot examine the retina and I cannot determine whether the retina is healthy or degenerate.
So how can I find out whether it's Healthy or not if I cannot examine it. Well, sometimes you can look for clues in the signalment in history, like if the dog is from a breed that's predisposed to retinal atrophy, and if the owner is complaining about loss of nighttime vision, you may suspect retinal atrophy, however, this is just a clue. I should mention that pupilary light reflex and dazzle reflex, such as you are seeing here are largely preserved even in advanced cataract because you need minimal afferent input to trigger PLR or or a dazzle reflex.
So neither of these is considered a reliable test to rule in or rule out degeneration. What we should ideally do is examine the patient in early stage. Such as this one, which takes me back to a very important role you play in the time your referral when you first see the initial lesion such as you're seeing here.
Early stage cataract, please refer the patient to the surgeon who will eventually operate. I imagine each one of you has a, a, an oralmic surgeon you're working with, so refer them at this early stage when the fundus can be examined for signs of rein degeneration or What we do In advance of every cataract surgery is ERG electroretinography, recording of electrophysiological function of the retina. If the retina is healthy, then we record normal function.
If the retina is degenerate, then we can pick it up in our ERG recording. We also would like to do an ultrasound exam before the cataract surgery to diagnose possible retinal detachment or decreased detachment of degeneration such as you are seeing here. The third question you want to ask yourself is whether there is secondary ocular disease and again the most important one that we're concerned with is lens induced CVI.
Here is a picture of a Normal I quote unquote normal, it has a cataract but no UVIT. Here is significant UVIis due to rupture of the lens capsule. So we're looking at health status of the eye, such as lensitis, health status of the patient, diabetes, urinary tract infection.
We want control for all of these conditions before operating on the patient. And finally, very, very important point that should not be underestimated patient and owner selection, especially the ability of the owner to provide post-op care. Number one, can the owner afford surgery which costs in England, I believe something like 5000 pounds.
And just as importantly, can the owner provide postoperative care? As I mentioned time and again, cataracts and cataract surgery will trigger significant inflammation. The owner must be able to provide post-operative care.
The owner must commit to frequent trade checks. In order to treat and monitor the lens indu CVI. So it's a, if it's a very aggressive dog that can be treated or it's, if it's an invalid owner that cannot provide treatment, it's a waste of time, it's a waste of money, it's And really surgery that has a very, very poor prognosis.
Willingness to pay costs is not enough. The owner must be able to commit both to treatment and to the rechecks. The treatment, I won't go into it.
I would say that, the number of veterinary ophthalmologists equals the number of protocols for pre-operative and post-operative, treatment protocols, basically we're talking about significant massive anti-inflammatory, midriatic, and antibiotic treatment, sometimes prophylactic glaucoma, etc. Etc. As I said, you are probably working with one.
Veterinary ophthalmologist and you will get to know his or her protocol for pre and post-operative care. State of the art technique for removing cataractive lens is fake commodification, using ultrasound energy to shatter the lens. And now, most people, most clients are under the illusion that we use laser to remove cataractus lens.
No, we do not use laser to remove cataracts. Lens not in humans, not in animals. We use ultrasound, fake modification.
The energy of the ultrasound is used to shatter the lens, and the probe then irrigates the lens capsule and aspirates all the particles of the lens to reduce the lens in to the IS. Following surgery, as we removed the lens, we removed a refractive organ in the eye. The dog is now.
Hyperopic or far-sighted because it lost a refractive organ. This can be corrected with an intraocular lens implanting an intraocular lens in the eye will restore focused vision. And this is shown here.
You can see that with an IOL inoperative lens, the focus is much better than in an eye that has not been implanted with an IOL. However, it is very important to explain to the owner, that vision is possible even if we did not implant an IOL, because Really, the most important aspect of cataract surgery is removing the opaque obstacle that impeded light and did not allow light to reach the retina. The lens is really not essential for vision.
Most of the refraction in the eye is done by the cornea. The lens provides only about 1/3 of our accommodative power, not our, the dog's accommodative power and therefore vision is possible in dogs, even if IL has not been implanted, though it will be very poor. Lots of, sorry, lots of intraoperative complications, lots of post-operative complications, virtually every ophthalmic disease.
Surgery, I would say that immediately after surgery, more than 90, more than 95% of dogs regained vision. However, with time, this percentage of success decreases due to UVI and due to declining owner compliance, the compliance in treatment and the compliance in rechecks. So basically, the questions you should discuss with the veterinarian, or sorry, the veterinary ophthalmologist you're working with is what is the long-term success rate of surgery.
Not 2 weeks down the road, but 2 months or 2 years or 5 years down the road, and whether you should perform unilateral or bilateral surgery, should we keep the other eye in reserve, quote unquote, when the first eye fails. So basically the points I want you to remember is that in non-diabetic patients, please consider inheritance as a primary cause of cataracts and discuss neuturing with the owners. In early stages of cataracts, please discuss with the owners the progression possibility and referring to the operating surgeon for early fundus examinations.
As the cataract progresses, please treat for lens-induced UVITs. Please explain to the owner that there is no medical treatment for cataracts and that if they won't go into surgery, they must commit to very, very rigorous post-op rechecks and treatment, plans. I thank you very much for your attention and cause I can't see you or hear you.
I brought my own applause here. Thank you very much. I'll be glad to take your questions.
Thank you very much, Ron. That was absolutely brilliant webinar. So we do have some time for questions.
If you do have any, just hover over the question answer box at the bottom of your screen and pop them through to me so I can read them out to run. So we do have a comment from Ian. It's not so much a question, more of an observation.
Having viewed the world through bilateral cataracts and 16 diopters of myopia for well over 30 years, I'm really pleased to hear that we humans do not suffer from lens induced uveitis and tend to do much better than dogs. I actually drove home without glasses, a total life changing and life enhancing operation. I totally agree with you, Ian and I'm very happy for you.
And then we do have one question, how long does post-operative care go on for? Well, in many ways, I would say months to years to life. It really depends on lens-induced, definitely months, some patients for years and sometimes for life because there would always be low grade inflammation and that is what causes the eventual.
Loss of vision, secondary glaucoma, etc. Etc. In our patients.
So really there are lots of studies showing 95% success rates immediately after surgery. We're probably down to 70% 2 years after surgery and less and less as time goes by. So in some cases, I would say for life.
Lovely, thank you very much. We don't seem to have any more questions at the moment. Ah, there was one.
Yeah. . So this is not the same as people, is that correct?
When you say this, what do you mean by this? I think the point that you've just been talking about. Yeah, no, 000 yeah, definitely, humans, when they undergo cataract surgery, they get Topical medication for 2 or 3 days, maybe 7 days, and that's it.
Whenever I talk to MD ophthalmologists, they are shocked by how much medication I give cause of the lens-induc CVIS. They simply do not comprehend this and really some of the worst disasters I see is when MD ophthalmologists. Undertake cataract surgery in dogs.
I'm sure they're brilliant surgeons and they do an absolutely wonderful surgery, but they're totally unaware of the lens in UVIs because we don't, they don't have it in their human patients. They discharge them with drops for a few days and I think that's it. They don't realise the massive UVIS.
So yeah, in dogs we treat for months and years. In humans, they treat for a few days and that's that. Lucky for us as patients and fortunate for us as surgeons.
Lovely, thank you very much. And the next one is what drops do we use for LIU? OK, thank you very much for this question.
Basically, we're talking about, OK, so, anti-inflammatory treatment, or LIU treatment has two components. We're talking about metriatics and anti-inflammatory. Metriatics probably will not be used in most LIU cases.
We reserve atropine for cases of UVI is due to Systemic diseases, etc. In LIU usually the UVI is not severe enough to warrant atrophy. So we're looking at Anti-inflammatory treatment, usually topical treatment would be enough.
We don't need systemic treatment, and the choice of steroids or non-steroidals would really depend on the dog weight, size. And systemic conditions. So if it's a healthy, large sized dogs, I would probably go with steroids and prednisolone would be my drug of choice because it penetrates the eye better than dexamethasone.
If it's a small dog where I would be worried by possibility of iatrogenic cushion due to long-term steroid treatment, then I would probably go with non-steroidals such as diclofenac, etc. Thank you very much. And the next one, there's two parts to this question.
So what would your treatment of choice be for lens induced uitis in a diabetic patient? And could the topical steroids cause destabilisation or trouble stabilising? Wow, that's OK, I always divide questions into very good questions and interesting questions.
Very good questions is when I know the answer. Interesting questions is when I'm not sure of the answer. So this was a very interesting question.
I'm not sure of the answer. I have the luxury of working in a teaching hospital and I usually consult with internal medicine people. Sometimes they would let me use steroids, sometimes they wouldn't.
It's really, there, there is no one rule for all of them, case by case, . Judgement according to how severe is the UVI versus how severe is the diabetes, which scares you more. Sometimes I win the argument and we go on topical steroids, sometimes internal medicine wins the argument and we just go with non-steroids.
Lovely. And can nucleosclerosis progress to a cataract? No, totally unrelated diseases.
Nuclear sclerosis is an ageing change in the lens. It does not cause significant visual deficits as opposed to cataract, which is a consequence of diabetes of inheritance and is an opacity of the lens, so totally unrelated. Lovely, thank you very much.
And other than a couple of comments just saying how useful and interesting this this topic has been, seems to be the end of our questions. So I'd like to say a massive thank you to our attendees for listening tonight, and please do fill in the feedback form that will have popped up in your browser, and a massive thank you to you, Ron, for taking your time out to deliver such a wonderful webinar.