Hello, everyone, and welcome to this talk about the 5 most important ophthalmic emergencies. I have just 1 hour to cover 5 emergencies, which works out to 1112 minutes, per emergency, not much time, so I apologise in advance if I'm talking too fast, but that's really one of the advantages of, watching. And recorded lectures, you can always pause, rewind, listen again, maybe play it at a slower speed.

So hopefully, you will be able to take notes and follow everything. So the five emergencies we are going to cover today are acute glaucoma, acute blindness, traumatic protosis of the globe, anterior lens laxation, and a melting ulcer. Starting things off with acute glaucoma, so you may remember that aqueous humour is produced in the ciliary body here and it passes through the pupil into the interior chamber and where it provides metabolic support to the cornea and the lens, eventually draining through the iridocorneal angle.

Normal intraocular pressure, which is really the equilibrium between the production here and the drainage here is 15 to 25 millimetres of mercury in most species and While theoretically elevation of intraocular pressure may be due to increased production or reduced drainage, in fact, glaucoma is always due to disruption of aqueous drainage, as you can see here, the angle is significantly narrowed compared to this one. We don't have glaucoma due to increased production. So what would cause glaucoma?

What would, Oops, sorry. Glaucoma might be secondary to uveitis. The aqueous flare, the inflammatory material that leaks into the aqueous humour in the course of uveitis is rich in platelets and protein and white blood cells and all of that can Actually obstruct the drainage angle and reduce outflow from the eye, a fibrine clots such as the one you're seeing here or a large hypopion, in the anterior chamber would also disrupt aqueumer.

Dynamics if there is posterior adhesions, posterior sinicia between the iris and the lens that would also disrupt aqueous dynamics cause aquez couldn't outflow from this posterior chamber to the interior chamber. Glaucoma may also be Secondary to lens laxation. It's an upcoming topic, so you'll, we'll discuss it very soon.

But a very, very important point, if now you don't see signs of UVI or you don't see signs of lens laxation, making you suspect that glaucoma is secondary to one of these diseases, then you should suspect hereditary glaucoma even though The patient may have presented with unilateral glaucoma, very important point, hereditary glaucoma usually presents with a unilateral disease with the second eye affected about 8 months later. So the fact that it's unilateral certainly doesn't rule out the possibility that it's hereditary and we'll come back to this point in a few slides. The signs of glaucoma, of acute glaucoma include acute blindness, acute pain and lethargy.

And when I say acute, I mean the owners went to work in the morning, everything was fine. They came back home in the evening, the dog is in pain, the The dog is lethargic, the dog is blind, the dog has a red eye due to episcleral congestion cause the aqueous draining through the iridocorneal angle eventually makes its way to epicleral vessels that you're seeing here and here. So we have a red eye.

The patient will also have a blue eye, that's due to corneal edoema because the elevated pressure actually manually presses on the corneal endothelium, the innermost layer of the cornea. The corneal endothelium has pumps that are responsible for keeping the cornea in a dehydrated state and disruption of the functioning of these pumps would cause edoema. As you know, red eye and blue eye are also common signs of UVITs, and sometimes we have difficulties in distinguishing between the two, but one way to distinguish between the two is looking at the pupil.

In UVIs, the pupil will be meiotic, in acute glaucoma, it is fixed and dilated. So these are the signs that should make you suspect glaucoma, but obviously you need to confirm your diagnosis by measuring IOP, what we call tonometry. Pressure must be measured in both eyes cause significant differences between eyes are suspicious.

I did say earlier. That normal pressure is 15 to 25. But suppose we measure pressure of 12 in one eye and 24 in the other eye, pressure is normal or virtually normal in both eyes, but there is a 100% difference in pressure between the eyes, so that's certainly a reason for concern.

As I've said, aqueous drains through, the episcleral veins and eventually, makes its way to the jugular veins. So make sure your assistance is not pressing on the jugular veins when measuring IOP, in people, in fact, neck ties are a risk factor for glaucoma. So if you're looking for an excuse not to wear a necktie, you can always say you are being cautious about developing glaucoma.

And finally, please use an instrument to measure IOP, not your fingers. I've been doing it for 35 years. I still can't put my fingers on and I tell you what's the pressure.

You do need an instrument. Each and every clinic should be able to afford a shields indentation tonometer that you're seeing here. It's not a very user-friendly instrument, but with practise, you can get it to provide a good estimate of intraocular.

Press. However, your life will change dramatically if you are able to afford one of the newer electronic tonometers such as the tonalenclination tonometer or the tonove or toovve plus rebound tonometer. Once we've confirmed our diagnosis, we need to treat our patient and before I discuss the actual drugs, a couple of words about the principles, glaucoma is a painful disease.

I'll come back to that in a few slides. So the aims of our treatment are both to reduce the pain and preventing further retinal damage, and I stress the word further cause retinal damage. That has occurred prior to the lowering of IOP is mostly irreversible.

There is no regeneration of these cells in the retina and therefore sometimes we may be successful in lowering IOP but vision will not return because the retina does not regenerate. However, nonetheless, even if the patient remains blind, we do have to treat it cause it is still painful. Another important point to remember is that glaucoma may resolve if it's secondary to UVITs or interior lens taxation such as what you're seeing here.

So, If we take this patient to surgery and remove the luxated lens, we can definitely, the disease may resolve. Likewise, if we treat UVI successfully, it may resolve. However, hereditary glaucoma does require lifelong treatment.

And as I've said earlier, when talking about hereditary glaucoma, it may frequently present as a unilateral disease and therefore, when presented with such a Lateral case, you should consider referring the patient to a specialist who can perform tests on this unaffected eye to see whether it is at risk for glaucoma, and a specialist may also be able to perform surgery on this eye. However, if you're not able to refer then. Please consider providing prophylactic treatment to the other eye.

And I always try to tell my students this is the most important slide of my talk and I'd say it here, if you're going to remember just one slide from everything I'm going to be talking about in this hour, please remember this. When in doubt, Treat the other eye. What do I mean?

This patient came in with unilateral glaucoma. We start treating it with this drug and that drug and another drug, but looking at this eye, it's pretty much doomed, and I think that, in a few weeks or a month or two, you'll be taking it out. And then 8 months down the road, the owner comes back and this eye is blind with glaucoma, and the owner looks at you and asks you, doctor, could this have been prevented?

And that would be a very, very bad day in your life. Because what happened is you treated this eye, but you forgot the possibility that it's hereditary glaucoma and that this eye is going to develop glaucoma 8 months from now. So, When this dog presents prior to treating this eye or while treating this eye, you try to determine whether this glaucoma is secondary to another disease.

For example, if there is UVitis in this eye, great, treat the UVIis and More importantly, you don't have to worry about glaucoma in this eye. If there is neoplasia in this eye, this is wonderful news. It's funny to say wonderful news about neoplasia, but it's great news, you know, we can take out the right eye and not have to worry about glaucoma in the left eye.

But if you're unable to refer and if you're not seeing any signs that this is secondary glaucoma, please provide prophylactic treatment to this eye. Mind you, it's hereditary glaucoma, so this treatment is not going to prevent the development of the disease, but studies show us that it can delay by an average of 2 years. So you are buying an extra 2 years of vision in the left eye.

And just as importantly, when the owner comes back 32 months from now, rather than 8 months from now and says, doctor, can this be avoided? Could this have been avoided? You can say with a clear conscience, we did everything we could.

Moving on to treatment, acute glaucoma, as I said, the patient may present with acute loss of vision, lethargy, pain. We need to immediately lower intraocular pressure and we do that usually by Administering hyper osmotic agents, most commonly intravenous magnol, which reduces the volume of the fluid in the eye, thereby lowering intraocular pressure. The dose is 1 to 2 grammes, not milligrammes, grammes.

Per kilogrammes administered slowly every over 30 minutes and then you put the animal in a cage and withhold water for 3 or 4 hours cause you don't want the animal rehydrating itself by drinking water. Another way to reduce pressure quickly is with para synthesis. Take a 25 gauge needle and go into the eye at the limbus.

Note that the syringe here is, the needle here is not connected to a syringe. I do not aspirate. I just put the needle in the interior chamber and let two or three.

Or 4 drops of aqueous dribble out, that would be enough. Obviously, if you have no experience with parasynthesis, I recommend that you first practise it on a couple of cadavers before trying it on a patient, but that is really a very effective way of quickly lowering intraocular pressure. But then, after we have hopefully, managed to lower the intraocular pressure, we have to send the patient home, with long, with treatment and the drug of choice in canine glaucoma is proglandin analogues.

I think latanoprost is the most common drug, but there are other drugs available out there and they increase the Outflow from the eye, increase aqueous drainage, administered twice daily. As it says here, I also give them every 15 or 30 minutes as an emergency treatment. So, If the patient comes to me with acute glaucoma, we can give a few drops of metanoprost.

Every 15 minutes or so, and only if pressure doesn't go down, do we go in with the needle and perform para synthesis. Note that prostaglandin analogues are very effective in dogs, but they shouldn't be given cases where the glaucoma is secondary to uveitis cause when there is uveitis in the eye, there is already enough pro glandins in the eye and no need. To pour oil on fire by administering more prostaglandins, and we don't want to treat with prostaglandin analogues in cases of lens laxation.

We'll discuss lens laxation in a few minutes and you'll understand why. Also note that these drugs are not effective as long-term treatment in cats and therefore in cats, we use topical carbonic and drug inhibitors, which are also our second line of defence, in canine glaucoma. Again, different drugs in different countries, different preparations out there.

These are typically administered 3 times a day and there are also other preparations where the topical carbonic and ras inhibitors. Are combined with a beta blocker. A beta blocker reduces the blood flow to the ciliary body.

The blood flowing in the ciliary body is actually the substrate from which aqueous is produced. Carbonic anhydras is the enzyme producing aqueous from the blood, so we are inhibiting of aqueous both by reducing the amount of substrate and by inhibiting the enzyme responsible for production and as you can gather, really prostaglandin analogues and topical carbon contours inhibitors work in different pathways. This one increases drainage, this one reduces production, so they too can definitely be combined.

However, in hereditary glaucoma, which really requires lifelong treatment, medical treatment often fails, not just in veterinary medicine, in humans too, and patients should be referred to surgery, to specialists. As I said, specialists may, number one, examine the unaffected eye to see whether it is. Liable to develop in a glaucoma due to inherited glaucoma and we can also perform surgery to decrease IOP either by lowering production.

Here in this cartoon, we are using laser to partially. Destroy the ciliary body and reduce production that way or implanting shunts as you can see here in the eye, in the interior chamber. This one has a one-way valve here so aqueous can flow out but not back in.

Unfortunately, even surgery doesn't always succeed and again both in humans and in our animal patients, patient becomes blind and we are left with a patient that has a blind but painful eye, in which case, nucleation is the recommended treatment. Owners will frequently resist the idea of nucleation cause it It's very important for them to have, for the pet to have two eyes, even one of them is blind. You really have to insist on nucleation, even if they maintain that the eye is not painful, and here you can see.

A study showing that when they do go into nucleation comparing the behaviour of dogs before and after nucleation due to glaucoma, 96% of the owners were happy with their decisions. None of them regretted opting for nucleation and When you do a nucleate and they'll come back for suture removal, they'll always tell you how much more active and energetic and lively the dog has become. So don't listen to their arguments about the dog is not painful, convince them that it is, and they will notice a great improvement in the dog's quality of life.

Second disease I want to talk about is acute blindness and actually I want to talk about a subset of acute blindness. This is the patients that present with acute blindness and fixed dilated pupils. I'm not going to talk about brain diseases, causing acute blindness.

And when thinking about differentials for patients presenting with acute blindness and fixed dilated pupils, we have to consider four diseases, glaucoma, which we've discussed already, retinal detachment, SARS, and optic neuritis, which we shall be discussing next. So starting with retinal detachment, retinal detachment is separation of the retina from the underlying choroid. So here we have a histological picture of the three posterior codes of the eye, the sclera, the choroid, and the retina.

You can see that. To this point, the retina is attached to the choroid, so everything is nice and normal. And at this point here, there is a separation between the two, and now we have a detached retina.

When the retina is fully detached. As you can see here, it usually remains attached to the globe just or at the optic nerve head and at the very periphery of the retina, what we call or a serata, and you can also see it here, the detached retina in this histological picture. Why would the retina detach?

Well, it may be due to fluid leaking out of the choroid and this fluid may be exudate or transudate in cases of choriorotinitis or posterior uveitis, or it may be blood in cases of systemic hypertension, immune thrombocytopenia, etc. Etc. Anything that would cause bleeding.

But some kind of fluid leaks out of the choroid and pushes the retina away. In fact, here you can see the fluid that has leaked out and pushed the retina off of the choroid. However, like many ocular diseases, it may be inherited.

We already mentioned that glaucoma may be inherited, retinal detachment may also be inherited, very common in shih-tzus and in a number of terrier breeds as listed here. How do we diagnose retinal detachment? Well, basically, if we try to look at the retina with an ophthalmoscope, we won't be able to focus on it and that's because it has moved away from its natural position and now it is floating in the eye behind the lens.

And in fact, if we look at the eye carefully. Through the pupil, we can see a grey white curtain with blood vessels, as you can see here and here, floating through the pupil, OK? And notice that in all three of these pictures, I'm actually looking through the pupil.

These are not funduscopic pictures. I didn't use a special fundus camera to take them. I'm looking through the pupil and I see this grey curtain with blood vessels.

Floating in the back of the eye, it can only be the detached retina. Sometimes we'll see blood on the curtain on the retina. If it's hemorrhagic detachment, sometimes we may see granulomas such as you are seeing here, if it detached due to choreo retinitis.

The pupil is fixed and dilated, and if I shine a light into this eye, the unaffected eye will, the pupil of the unaffected eye will not constrict, but if I stimulate the unaffected eye, this pupil will constrict. However, frequently we are unable to see the pupil cause maybe they detached retina, the retinal detachment is accompanied by high femur, maybe it's accompanied by severe corneal edoema because of uveitis and therefore we can't see the floating curtain, we can't even see the PLR and in that such a case, you should reach for your ultra. Sound and if you've got a 1012 megahertz ultrasound probe, then you should be able to image the detached retina, not the similarity between the histological picture and the ultrasound image.

Again, the retina is attached only in the optic nerve head and in the peripheral aura errata, we call this. Ultrasound sign, the seagull sign cause it looks like the wings of a seagull. Here are the tips of the wings in the aura errata and here is the body of the seagull.

How do we treat the re detachment? Well, if it's due to Exudate or transodate or hemorrhagic, it's due to another primary disease, then we need to diagnose this primary disease and treat it. So if we see that it's blood causing retinal detachment, we obviously get complete blood count.

If it's an elderly patient, we measure blood pressure, check. Clotting, look for the cause of haemorrhage. If it seems to be more inflammatory such as what you are seeing here, then we do a workup for infectious diseases, again the blood counts, serology, X-rays, even maybe tapping the vitreous for a pathological sample.

We do everything we can to try and diagnose the primary cause. And if successful in diagnosing and treating it, vision may very well return. For example, if retinal detachment is due to systemic hypertension, we treat the patient with amlodipine and in the cases of CATs, studies show us that more 50% of them regained vision, OK?

So it's not a hopeless cause. Yes, it can be treated and in any case, you have a duty to try and diagnose diseases that cause inflammation or haemorrhage in that patient. If it's hereditary, then the only option is referral to surgery, and here you've got a website listing some surgeons who perform retinal reattachment surgery.

It is not performed by every veterinary ophthalmologist. This one is mostly surgeons in the USA, but we do have a couple of Europe and hopefully you can refer your patient to one of them. And here is the surgery being performed in these patients.

So we spoke about glaucoma and we spoke about retinal detachment as causes of Acute blindness with fixed dilated pupil. The third differential you have to consider is SARS, sudden acquired reckon degeneration syndrome. Once again, we are talking about acute blindness, but you're The phthalmic exam will be completely normal and the fundus will be completely normal looking unlike glaucoma and unlike creatinine detachment, which are in which a patient presents with lots of ophthalmic abnormalities.

Pupils are non-responsive to white light. Again, we're talking about differentials for acute blindness with fixed dilated pupils. However, we do have another diagnostic modality called the chromatic PLR testing whereby we stimulate the retina with both blue and red light and patient.

With SARS will not respond to red light, but their pupils will constrict in response to blue light. So this may suggest that the patient has SARS and this is really an affordable unit, can be purchased by a non-specialty clinics. But if you want the gold standard confirmation that the patient has SARS, then you need to refer the patient for an ERG recording, recording of electrophysiological activity of the retina just like ECG records electrophysiological of the heart.

ERG records the activity in the retina and in retinal degeneration, it is completely flat. Here is your typical SARS patient. It is often a middle-aged small breed female dog with a history of polyuria, polydipsia, polyphagia, weight and lethargy in the last few months.

And you look at this patient, a middle-aged, overweight female, and you hear the history, and it screamsushing. And when you do blood work, you will find many parameters that resemble Cushing or make you suspect Cushing. Unfortunately, it is not due to Cushing, and I say unfortunately, cause if it were, we would be able to treat SARS.

So I have to admit that currently we are unsure of what causes SARS, as I've just hinted, some people suspect that it's due to hormonal imbalance, be it progesterone and other sex hormones or due to Cushing's. Other would suggest that it is an autoimmune inflammation of the retina and based. On these theories, some people would advocate hormonal therapy if they suspect the hormonal imbalance.

Those who suspect autoimmune inflammation of the retina would propose immunosuppressive treatment with intravenous immunoglobulins, cyclosporin, mycophenolate, etc. Etc. However, there are no peer-reviewed publications showing the efficacy of either.

And I stress this because, you know, nowadays, the age of the internet, you tag them SARS, the owners would immediately consult Dr. Google. They may come across proponents of one or theory or the other, and they'll come back to you saying, why aren't you treating my dog with hormones or with cyclosporin?

And the answer is that Really, there are, there is no evidence that these treatments are effective. In fact, when you look at the actual treatment protocols proposed by the proponents of these theories, you'll see that we're talking about rather dangerous treatments, so please stay away from them. The 4th and final differential for.

Acute blindness with fixed dilated pupils is optic neuritis. Again, patient will present with acute blindness and fixed dilated pupils and as with other diseases we've been discussing, even though it may be secondary to another disease, they may present with blindness. They will present with an ophthalmic complaint even though they are affected by a systemic disease.

Because this is a disease of the optic nerve, and not the retina, the ERG that I mentioned previously will be normal, but we really don't need an ERG here. We can confirm the diagnosis by looking at the fundus and seeing signs of inflammation of the optic nervevehead in most cases. So we see edoema of the optic nerve.

You see how blurred it is. The blood vessels are congested. There is some haemorrhage here.

There is peripapillary detachment. Here are a few more pictures. So this is a healthy optic nerve.

You can see how sharp the borders are. You can see how clearly you can see the blood vessels on the surface of the optic nerve compared to these three cases of. Optic neuritis.

What causes optic neuritis? Well, here is the biggest study published to date on optic neuritis, published 96 cases of optic neuritis published by North Carolina State University. You can see that more than a third of the patients are affected with meningoencephalitis, 35 cases, 10% had Poplasia, some of them had microbial infection, orbital cellulitis, but the vast majority of them were idiopathic cases, OK.

Despite extensive workup in one of the leading schools in North America, they could not find a cause in 42 of 96 patients. So once again, You really have to try and do a systemic workup when presented with optic neuritis because you want to know if the patient has meningoencephalitis. You want to know if it has infection orbital cellulitis, but, warn the owner that you're going to do lots of expensive workup and maybe you'll come up empty-handed cause a significant number of these cases are idiopathic.

So, just to repeat myself, you do a systemic workup, you do a neurological workup, your neurologist will definitely consider CSF tapping and advanced imaging. If you're lucky enough to find an underlying cause such as MUE then you treat it. And if you don't, well, you could still give steroids and antibiotics and as I tell my students, also offer a couple of prayers and I say offer a couple of prayers because really the prognosis is rather guarded of the 96.

Dogs are presented at the North Carolina State University study. They had follow-up for 72 dogs. 50 of the 72 dogs with follow-up remained blind.

That's 70% of patients remaining blind, so the prognosis for this is rather poor. Moving on to our third emergency, traumatic proptosis. Owners presenting with proptosis will always ask me, Doctor, what is the prognosis for my patient?

And I try to divide this into two questions really. What is the prognosis for saving the eye and vision? Or alternatively, even if we are unable to save vision, can we cosmetically save the globe and not nucleate it?

Because as I said earlier, when talking about glaucoma, owners attach great importance to their pet having two eyes, even if one of them is blind. So here is some of the prognostic indicators that I consider when presented with this patient. Number one, what's the species and what is the breed.

The prognosis is best in brachicephalic dogs, and that's because these dogs have a very shallow orbit. The eyelids barely protect the eyes, the eyes, the eye is half out to begin with, as I sometimes say. All the dog has to do is sneeze and the eye comes out.

Therefore, it takes minimal trauma to cause proptosis in a brachycephalic dog and because the trauma is often minimal, the prognosis is very good. On the other hand, in cats with a very deep orbit and eyelids firmly surrounding the eye, and breeds like Doberman Pinscher or collies. With similar orbital conformation, it takes significant trauma to cause the protosis and therefore, the prognosis is much worse.

Obviously, we need to perform a thorough neurological exam cause trauma to the head may also involve trauma to the brain, have to perform a comprehensive physical exam cause other organs may also be affected by the trauma and a thorough ophthalmic exam, we have to consider the possibility that the Trauma caused a corneal perforation or maybe a scleral rupture. Maybe it caused bleeding in the interior or posterior parts of the eye, lens laxation, which we'll be talking about rectal detachment which we've discussed optic nerve revulsion, so lots of intraocular damage that may occur. One of the things you want to check before telling the owners the prognosis for vision is the PLR.

Obviously, we can't test menace in this patient because it is unable to blink due to the fact that the globe has now moved in front of the eyelids. You can still test the PLR. Hopefully you can see the pupil in this eye, see whether or not it's constricting.

If you can't visualise the pupil in this eye due to severe corneal edoema or due to high femur, then test the consensual PLR. Consider further workup with radiography or CT if you suspect, fractures in the orbital bones when you're palpating the orbit when if you're seeing signs of pain or facial asymmetry and sometimes you may diagnose orbital fractures and definitely you should consider perform an ultrasound if you can't do an intraocular examination due to high femur. Or due to severe keratiti, you need to do an ultrasound to rule out lens lax laxation or retinal detachment.

We've already discussed ultrasound as a tool to diagnose retinal detachment. And then once we have completed the workup and we know whether or not the globe can be salvaged, it is time to treat the patient. And I can summarise my philosophy and my approach with this sentence, you can always nucleate later.

What do you mean, what do I mean by that? Sometimes I'm 100% convinced that the globe is lost because there is cleral perforation or because there is glaucoma or because all of the extraocular muscles have been torn and the eyes hanging just by the optic nerve, in such cases, you really have to nucleate. However, if you think that there is a chance that the globe may be salvaged, even cosmetically, you can tell the owners, you know what, I know that it's important for you to, cosmetically salvage the globe.

I'm willing to go along with you. I'm willing to replace the globe, but aware that we may run into complications 1 or 2 months from now and we may be forced to perform another surgery. The dog will have to undergo another anaesthesia.

You'll have to pay for a second surgery, of course, we'll have to nucleate the eye for one reason or another. And if You present it this way, telling them, yeah, I'll play along and replace the globe, but beware there may be a risk of a second surgery, then you'll find that most owners will go along with this suggestion cause, as I've said, they really, really want the dog to have two eyes, even if one of them is blind. And then to replace the globe, we have to anaesthetize the patient, clean the globe.

It hasn't been blinking for a while, so there may be debris on the cornea and then comes the tough part of pulling the eyelids that are right now behind the globe to their natural position in front of the globe. We may use Sutures, as you're seeing here, muscle hooks, and we may facilitate it by performing a lateral thotomy, a 23 centimetre incision in the lateral canvas to increase the opening of the eyelids and then you pop the globe back into the orbit and you perform a. Temporary torsoy using simple interrupted horizontal mattress sutures for or nylon with tension relieving stents as shown here, very careful placement of the.

Sutures on the eyelid margin, as I'll show you in a minute. Some people advocate, leaving a small hole for topical treatment. I don't do that.

It's often, you know, a small breed, but it's aphalic dog, it's painful, it's just undergone a major trauma. Leave a small hole there and telling the owners, listen, try and get a drop of some drug or rather fall into that hole. It's really not realistic.

I just apply a drop of topical atropine and some antibiotic prior to closure and treat them with systemic drugs, as I'll describe in a minute, but first, as promised, here is How I place the sutures, go through your stent, go through the skin, come out through the eyelid margin. Obviously, you have to make sure you're not going through thickness because then the suture will irritate the cornea and you want to make sure that you're not coming out in the skin here because then this last bit of eyelid would probably invert and irritate the cornea. So make sure you're coming out through the eyelid margin.

Through the lead margin of the opposite eyelid, you can even use the myboingla openings as shown here as a landmark, and then out through the skin and the stent, replace a couple of sutures as shown here. Here are the two horizontal mattress, sutures replaced with their stents and then You pull on the sutures while pressing down on the globe with the tongue depressor or the handle of a scalpel and it will pop in and then you tie your sutures. Send the patient home with an Elizabethan collar, tell the owners to apply cold compresses and when I say cold compresses, I usually send them to a supermarket, .

And instruct them to buy a couple of bags of frozen peas or frozen corn kernels, and that's a bag that you can easily place against the eye and it moulds itself, it shapes itself in the shape of the eye in the conformation of the orbit. As I said, I treat them systemically with antibiotics, steroids, and or systemic analgesia. It all depends on the patient's systemic condition.

And very important point, when they come for recheck two weeks from now, I open just one suture. I don't remove all the sutures cause there is probably still some retrovulbar edoema or haemorrhage. The extraocular muscles have Been stretched.

If I remove all the sutures, the eye may pop out again. So I removed just one suture, take a look at the cornea. Now we can prescribe topical treatments, steroids, antibiotics, artificial tears, depending on what you are seeing, send them home for another 2 or 3 weeks and only then remove the final sutures.

Remember not to We remove them all at once. And if the owners ask you about the prognosis, again, you perform all of the tests I've said, but here are the numbers study by Brian Giler looking at 66 dogs with ocular protosis. As you can see, 18 had to be nucleated and 4 had to be euthanized due to trauma to other organs.

So that's 22 out of 66 dogs, lost the globe or were euthanized, but 2/3 of the dogs. Either had a visual or a visual or a non-visual globe. So the prognosis is rather good in dogs, as I said, especially in the brachycephalic dogs.

In cats, as you can see, the prognosis is much worse. 2/3 of them had to be nucleated, another 4 had to be euthanized. Only 2 of 18 globes were salvaged.

All of them were blind. So this is the prognosis. Moving on to our 4th emergency and anterior lens laxation, which is what you are seeing here.

Whenever you see a round structure floating in the interior chamber, and I know this is the interior chamber cause you can see it here in front of the iris, in front of the pupil, this round tissue can only be the lens. Why would the lens laxate? Well, it laxates because of Tearing of the zonules that suspended in the middle of the pupilonules originating in the ciliary body.

When the zonules start tearing, then we'll have subluxation. The lens starts moving, but it's not fully luxated. It's fully luxated when all of the souls are torn, and then we have two possible scenarios.

One, The eye can fall to the bottom of the lens, sorry, can fall into the posterior part of the eye, settle down here, which is what you're seeing here, posterior lens luxation. You can see that the lens is behind the eye. Picking out here, we have a large part of the pupil without a lens.

We call it an afaic crescent. Ahahaco is the lens haic without a lens. So this is the fake crescent due to a posterior lens luxation.

This is something we can live with. The worst scenario is if the loose lens goes through the pupil and into the interior chamber, here is interior lens taxation, clearly seen cause lens is also cataractors, so in fact it's obscuring our view of the iris. Why would we have lens laxation?

Well, once again, you always have to consider the possibility of inherited eye diseases. We talked about inherited glaucoma, we talked about inherited retinal detachment, inherited lens taxation, especially in terrier breeds. We may get anation due to a blunt trauma.

I'm not talking about a trauma caused by the claw of a cat, but a blunt trauma, that would generate, energy waves inside the eye, so being hit by a car or by a closing door or kicked by someone. The soules may weaken with age, they'll weaken with, uveitis because of changes in the composition of the aqueous humour, may weaken the sons, and in glaucoma, when we have bufalmus, the zonules will stretch and eventually tear. So, if we are unfortunate and the lens moved into the anterior chamber, the patient will usually present with acute pain and the acute pain is due to two reasons.

Number one, the dog is very likely to have secondary glaucoma cause obviously a lens sitting in the interior chamber will disrupt the dynamics of aqueous, . And prevent outflow through the angle. This also explains the point I made earlier.

We don't treat these patients with prostaglandin analogues cause prostaglandin analogues cause meiosis. This will constrict the pupil here behind the lens and trap the lens in the interior chamber. Another source for pain or another reason for pain in these cases is trauma to the corneal endothelium and the cornea.

The lens is sitting here in the interior chamber. Every time the dog shakes its head, the lens strikes a cornea, strikes a corneal endothelium. It is very painful.

Obviously, it also causes trauma to the corneal end. And these patients will often resolve present with corneal edoema and as I've said, you will be able to actually visualise the lens in the interior chamber. Here it is transparent, here it is semi-active, but in both cases you sit in front of the iris, in front of the pupil.

This is the lens. Because the lens moved forward into the interior chamber, you can see that the interior chamber is actually deep. The iris has been pushed forward, backwards, sorry, instead of being convex, which is its usual angle, it is now concave.

However, often you'll not be able to see it maybe because of severe corneal edoema or pain and therefore, to confirm the diagnosis, once again, we can reach out for our ultrasound. So when, if you have a patient presenting with unilateral acute pains corneal edoema or secondary glaucoma, you should definitely suspect lens laxation and ultrasound the eye. Here is the ultrasound of a normal eye.

Here is the iris on one side, here is the iris on another side. Here is the lens filling up the pupil in normal position. Here is a lens that underwent posterior lens luxation and here is a lens that underwent anterior lens luxation.

Again, as I've said in the previous slide, you can see how much deeper the interior chamber is and you can appreciate the fact that the iris has been pushed backwards. We consider anterior lensation an ophthalmic emergency because, as I've said, it is very painful and because it is likely to develop secondary glaucoma and irreversible, trauma to the endothelium. So you should refer it for immediate surgical removal.

If surgery is not feasible, if you don't have a specialist nearby, if the dog cannot be anaesthetized, then you may consider, or try to actually push the lens from the interior chamber into the posterior segment. What we do in such cases is administer manitol again with holding water for 3 or 4 hours, we want to shrink the amount or minimise the amount of fluid in the eye. Dilate the pupil with tropeamide.

We want a white pupil so the lens can be pushed through it, but not with atropine because it is long lasting. Sedate the dog, and #1, cause it's an unpleasant, procedure, and number 2, you want all the extraocular muscles relaxed, and then you simply push on the cornea, applying pressure on the lens. So admittedly with my hand or maybe with, with my finger or maybe with a Q-tip or a swab, we push on the lens through the cornea and sometimes we're lucky it falls back to the posterior segment.

Give it protagonian analogues immediately to cause meiosis, continue this treatment for life and hope that it stays there. And here is a study published showing that vision is retained in 55% of eyes that undergo this procedure one year out. 4 down, one to go, melting ulcers.

So sometimes we have patients presenting with superficial stromal ulcer. These are usually caused by mechanical abrasion, maybe eyelid or eyelash problems, dysthychia, or entropion, it may be too dry eye, it may be too scare, the proper name for the so-called boxer ulcers. You can look at these ulcers and even though it's a two-dimensional picture, you can see that they are Superficial, they are not deep, they are often uncontaminated and without and here without blood supply.

We call them simple ulcers cause they are simply to treat. However, you have to remember that the cornea is only 0.5 millimetre thick, OK, not 0.5 centimetre, 0.5 millimetre.

So even when it's superficial also, we're talking about the superficial defect in tissue that's only 0.5 millimetre thick to begin with and unfortunately, these ulcers can sometimes become contaminated. And they can become contaminated with fungal agents, most commonly aspargillosis, bacterial agents, sorry, such as Pseudomonas, and the problem is that these agents contain proteolytic enzymes, they contain collaginases, enzymes that actually degrade the collagen, they degrade the corneal stroma and you can see that what was previously a superficial ulcer very quickly becomes a deep ulcer.

You also look at the surrounding cornea and you can see that it's infected. You can see that it's undergoing the path. Process.

OK, again, in the uncontaminated ulcers, here is the ulcer, but you can see that the rest of the cornea is healthy looking. Here too, the rest of the cornea is healthy looking, just an ulcer and some edoema around it. Here you can see that the ulcer here but is here, but really the entire cornea has this sponge like.

Appearance, mashed potatoes like appearance, it is actually infected. It is being degraded and sometimes very, very quickly. Again, remember, we have only 0.5 millimetre of safety margin.

When you're seeing such a cornea, you definitely have to consider cytology and culture. Cytology is taken because you don't have time to wait for culture. For example, you may see, fungal hyphae and know that you need to prescribe, .

Antifungal treatment, so we usually take both cytology and culture. If you're as old as I am, you were probably taught that first we do the culture and then the cytology cause cyt to take cytology, we need to Put topical anaesthesia and we were taught that topical anaesthesia has preservatives that may affect culture, but now there are a number of studies showing us it's not true, so you may do them in any order. And if you are afraid of taking the culture swab and Rubbing against a very deep ulcer, you can also culture the conjuncti phonics instead of the ulcer as shown here, and that would also yield a diagnostic culture, so no need to touch the actual ulcer.

Submit both fungal and bacterial cultures. As I said, you, contamination with fungal agents is a definite possibility in these patients. And then while waiting for the results, obviously, we need to treat the patient.

So first and foremost, we treat the infection, we look for a primary cause of the ulcer. Maybe there's entropion that needs to be fixed. If you don't fix it, the ulcer would never heal.

Maybe there is dry eye and you need to supplement the treatment with artificial drops until the cyclosporin kicks in. Look and for primary cause and treat it. And Provide antimicrobial treatment, different drugs in different countries, but, wherever you are, I'm sure you have a wide spectrum antibiotic that would hand a mixture that would handle both gramme positives and gramme negative.

In such cases where the cornea is really contaminated, I would also add some sort of fluoroquinolone, ciprofloxetine, or fluoxetine, or moxifloxetine. People automatically add gentamicin sometimes, because they are terrified of Soudomonas, and you have every right to be terrified of Sodomonas cause it's really terrible bacteria with very high proteolytic activity. However, gentamicin is epielotoxic and it has a detrimental effect on corneal ulcers and therefore I don't use it unless I have culture confirmation that there is actually pseudomonas in the ulcer.

Consider adding systemic antibiotics, especially if the cornea is vascularized, because actually, if there are no blood vessels in the cornea, the antibiotics are unlikely to reach the cornea. The doxycycline, tetracycline family is the one exception, this is a class. Antibiotics that's secreted in the tears.

So even if you give them orally, they'll reach the eye through the tear film. Other antibiotics will reach the eye in efficacious doses only if the cornea is vascularized. So we have to treat the infection, but another very, very important component of the treatment is to stop the melting, to stop the activity of the degrading enzyme, and the most efficacious way to do it is by treating the patient with serum or plasma that contain alpha 2 microglobulins that bind.

These enzymes and inhibit their activity. Serine plasma are wonderful substances cause they are extracted from the blood, so no contraindication, no toxicity. It's impossible to overdose.

If we have a case of a melting ulcer, we'd sometimes apply the drug, . 30 minutes every 1 hour until the melting stops. It is cheap and available.

It's extracted from blood and it doesn't have to be extracted from the patient's blood. May be extracted from the blood of another dog or another species even. Because the beneficial properties of the serum are cross species.

So in a teaching hospital like ours, we take blood from horses and dispense it to dogs. If you're in a small annual practise, maybe a large dog comes into the clinic and you ask the owners to take some blood, much easier to have it stored in the freezer instead of fighting a small painful. Pekinese to extract some blood and after a long vicious fight, you're extracting maybe 3 CCs of blood which will yield 1 cc of serum.

It is much easier to have it stored in your freezer, reach out for a bottle, dispense it to the owners, but as it says here, instruct them to throw it away after 8 days because it is easily contaminated. Additional components of treatment, these patients will have secondary UVITs which must be treated with atropine. Two reasons we give atropine, one for analgesia cause the secondary UVIis is accompanied by spasms of the ciliary body which are very painful.

You paralyse the ciliary body and that brings great relief to the patient and also they atropine dilates the pupil, reduces the contact between the iris and the lens and reduces the risk of posterior synechia and secondary glaucoma. Because of the UVI, you should also consider non-steroidal drug, especially if there is severe secondary UVIT. So this is a patient with severe secondary UVIis we can see the hypopion here, even though the ulcer looks rather superficial, there is significant secondary uveitis, so this patient will definitely receive systemic.

NSAs, topical NSAs should be used with caution. We are learning and we are finding out that they may be harmful to an ulcerated cornea just like corticosteroids, which everyone knows should be avoided. As I grow older, I administer less and less topical NSAs to these patients.

Consider tetracyclines because as I said, they are secreted through the tear fins, and another reason to give them is that they also have immunomodulatory properties and may help the healing and please don't let the owners walk out of the clinic without beating caller. I know we all have a owners who say that, ah, there's no need for a collar. My dog doesn't rub.

Remember, you had half millimetre to begin with. Now you're down to maybe 0.1 millimetre.

This patient must have an Elizabethan collar. . I know that some people out there when presented with a corneal ulcer may try to quote unquote treat it with third eyelid or flap or temporary torsoy.

These procedures are great for protecting the eye, but they are not a treatment for corneal ulcers because they do not feel the defect in the cornea. They don't promote healing cause they don't promote vascularization. And just as importantly, you have covered the eye.

You can't see what's happening. You don't know if the ulcer is improving or deteriorating, and you can't apply topical drugs. You certainly can't apply them in the case of temporary torsoy.

In the case of a third eyelid, maybe you could apply them, but most of it would get absorbed by conjunctival vessels. Little will reach the eye, so. If you think the eye needs surgery, if it's a deep or contaminated ulcer or maybe amatocele reaching all the way down to the Smith's membrane, then it's time to refer to a specialist who would perform a conjunctival flap.

We harvest conjunctiva from the globe, suture it directly onto the ulcer that fills the defect. Now we have much more than 0.1.

Millimetres of tissue, the conjunctiva is incorporated into the cornea. As you can see, it brings its blood vessels, its lymph vessels. The eye remains open so the owners can apply topical drugs and you can monitor the status of the eye, but obviously this is done only by a specialist because it requires special equipment and training.

So this was a very quick review of 5. Oophthalmic emergencies in our patients and I wish you best of luck next time that the patient with acute glaucoma, acute blindness, protosis, anterior lungsation or a melting ulcer walks into your clinic. Thank you very much for your attention and I'll see you in December in a discussion of an interactive live discussion of cases in ophthalmology.

Thank you and goodbye.