Hi everyone, and thank you for joining me on my presentation which will try to give you a taste of sheep dairy production. My name is Y Avalon Gilboa, and I'm a farm vet. I work in the southwest of the UK in the county of Dorset.

It's a farm practise that's called Fris Livestock Health. Myself and a few of my colleagues have a special interest in small ruminant, dairying, and we've set up the dairy, sheep and goat Consultancy Service, so we do see quite a lot of these farms and try to learn as much as we can about them. What I'll try to do today is give you an overview of the industry, talk a little bit about the breeds, the yields, and the products that we see, discuss, fertility and young stock management, touch a bit on milking parlour settings, other health, and data analysis.

And finish off with the treatment options and the drug usage that we can, or the drugs that we can or cannot use, dealing with, diseases, especially a few of the specific production limiting diseases that I will mention later on. I'm sure quite a few of you have dealt or are dealing with commercial sheep, and all I can say about dairy sheep is that they are the same animal, but only slightly different. The main breeds we see globally are the East Friesland and the Lacoon, which originally comes from France.

These are the main breeds we see here in the UK, definitely. And I know it's the same in New Zealand and the US. Having said that, there are a lot of, milk breeds in the world.

In the Mediterranean, you can have the Italian sada, the Greek chios. The Man Manchega sheep in Spain, the Israeli Assaf, which is basically a cross between the traditional Aasi fat tail sheep and the Friesland, that gives a very hardy sheep but with a very high milk production, and the Netherlands and the UK, so. All have their own sort of sheep breeds or compositions.

What we do see a lot in our, flocks is Dorset crosses, and that's for two reasons, basically. A, it gives the lambs that you want to market a better confirmation. They're more meaty.

And also because the Dorsets are easy to breed. All year round, so you can have a lot of out of season breeding without having to resort to hormonal, nutrients and the likes. And recently, we've had the chance of working with a few sort of peculiar breeds, which are not really milk breeds such as the Welsh clin sheep.

And, here and there we see dotted all sorts of flocks where people will milk the local breed. And that gives some sort of a specific special link with the terroir and the flora and fauna of the area and gives it in what the French would call an apeacionorein controlle which is basically a unique selling point. Having said that, it's not very easy to milk, wild reeds, if you like, because these animals have to be handled daily, even when they're not housed in no pasture.

They have to be brought in to be milked twice a day. So they are handled very often and see people, and it's best if when they see you, they don't start jumping off the walls. I'm not going to talk a lot about housing sheep, but just a couple of slides.

If you have a look at the slide in front of you, you can see a group of sheep that are actually struggling to eat. They have to extend their necks, they're on their knees, and it's not the best way for you to eat. You can see that that bar is not really located well.

It should be either lifted or pushed out to allow them better access to feed. And you can see that on the other side, Where I can tell you, you won't see it yourself, that the, bars are arranged in a different kind of way. It's a lot easier to feed, and hence you see a lot more, sheep, basically bunching up that site, which causes a queue, which is not optimal as well.

So making sure that your animals have got the adequate trough space and it's easier for them to feed is very, very important. And when you're dealing with milking animals or commercials, water is really, really important. So water has to be freshly supplied and readily available, not so much like what you see here.

So, water supply, clean, fresh, and changed readily, is really, really important when you're housing cheap. So in the UK when we talk about sheep milk production on the commercial commercial side, we usually link that straight away to lamb growth rates. But in the world, sheep milk is the 4th species of milk consumed globally, as you can see in that picture.

It is the main source of protein in third world and developing countries. There is a long tradition of milking in the Mediterranean basin in European countries with a lot of fantastic products produced, and there is a growing, sorry, there's a growing market worldwide estimated nowadays at about $8 billion US dollars, and that is continuously growing. Here you can see an advert with a very famous Chinese athlete, so I'm told, that is trying to convince the Chinese to drink milk.

That was done back in the 80s and the 90s, so the Chinese market is demanding milk. However, there are some issues with lactose intolerance in Chinese children, so sheep milk is a lot more adapted to it. Some of our colleagues in New Zealand have tapped onto that, and there are a few quite large and very, very efficient dairies in New Zealand that have been set up in recent years to produce milk powder.

In order to go for milk infant formula, and that is an ever-growing market and it's doing really really well. In the UK Sheep, milk, and milk products are a high-end sort of artisan product. It has perceived health benefits, again, easily digested, possibly better for lactose intolerant people, and there is a growing demand there as well.

You can see it mainly in farmers' market, but you can also see it nowadays on the shelves of all the supermarkets. There are about 80 or so members of the British Sheep Dairy Association milking between 20 to 30,000 ewes. The numbers are a bit difficult to come by.

The flocks vary in sizes. You have people milking two animals in the backyard, up to people milking 2000 milking flocks of 2500 animals. And in the north of the country, there is a cooperative milking about 8000 ewes between them, but they're separated and they're milked on a few farms.

But overall, there's a flock, they are 8000 animals strong. Sheep lactation is not very long. This isn't a cow and definitely not the goat that you can carry on milking for 2 years.

Sheep lactation usually lasts only 7 or 8 months. Some tapered breeds like the AAF can do 9 months or 10 at the most, but that's at the push, and the yields would be up to 700 or maybe 900 litres, but usually if you're making 2000 to 400 litres per sheep plantation, you're quite happy, especially if you're doing that on grass. If you look at milk composition, that's the sheep milk, and the striking thing is that Solids are really, really high, which really lend itself to sheep production or milk powder production.

If we have mentioned lactose, it's not as if sheep sheep milk does not have lactose. It actually has more lactose than goat and cow's milk, but it's in a different is on there in a different way that can be digested potentially more easily. What products are being made?

Well, in the UK and I believe globally, between 75 to 90% of the milk is turned into cheese, and fantastic cheeses indeed. The French hot for, the pecorino, which is made in Sardinia. So pecorin asada or, in Italy, Manchego cheese in Spain and the famous Greek feta.

But a lot of other products are made as well, yoghurt and milk, and as we mentioned, milk powder is an ever growing, Sort of baseline product that can be used. Energy drinks as well, cosmetics, you can do a lot with sheep milk. If you're a farmer producing milk for human consumption, and you're working with the dairy, you'll probably get anywhere between 115 to 135p per litre, and your cost of production, depending on your efficiency and your intensiveness or extensiveness would be between 80 to 50 PBO cost of production.

In New Zealand, I believe you will get $60 New Zealand dollars for a kilo of, you know, solids, which would translate to about 5 litres, which would mean 168 pence per litre. So farmers can smile about the return they get from sheep milk. If you're at the farm gate, if you're selling your products yourself, you can sell a bottle of milk, 500 millilitres for 1 pound 99.

You can charge £5 for 0.5 kg of, a tub of ice cream, and you can produce 22 yoghurt pots 1 litre and produce. And, and sell each for 1 pound 33.

The same pot of yoghurt will be sold for almost double that in the supermarkets. And cheeses can be, have a starting point of 25 pounds per kilo, and it can go ad infinitum, depending on your, The level of expertise, your marketing, you can charge quite a lot or you can get a really, really good return on cheat sheets. So, in order to make the cheese, you have to milk the animals, and in order to milk them, you need to manage them for fertility, so, they give you milk.

There are many production systems practised. Some people would only milk their sheep once a year, or they'll have one milking group, which will be quite seasonal, and other farms would have 6 different groups lambing at different times of the year, producing milk all year round. Well, it's no surprise that the processors are quite keen on all year round milk production, and they would sometimes give an out of season milk bonus, which some people are very keen to go for, but it means that you have to potentially Make the animals breed at least annually, and sheep can be bred while they milk to lamb annually, but it's not uncommon definitely in Israel for animals to lamb 3 times in 2 years.

In Canada, you have farms that would milk, or sorry, with lamb to milk 5 times in 4 years, so animals can milk, not just, or can lamb more than once. Once a year. So out of season breeding is very common and so is synchronisation in order to get a compact lambing season, which would make your workload and production management a lot slicker.

So, how do we synchronise them and cause them to breed out of season. The two main things that people use, especially if they're organic, are the ram effect and teaser RAMs. The Ram effect means that basically you hide the boys away from sight, sound, and smell for about 4 weeks minimum before you introduce them, and then you introduce them together and Everybody's really happy to see each other, and most of the news with ovulate within 6 days.

Some of that would be silent heats, but then within a short period after, most of them will be mated. And if you put rattles on the rams, you can see how well they've worked and all the sheep are coloured very quickly. The other thing you can do is you can use teaser RAMs, so you can keep the, rams away from sight sound and smell, and you could introduce some teaser rams who've had the operation to remove the plumbing.

So basically, they can do the deed, but they would not deliver semen. You use 2 to 3 teasers for 100 years, and you keep them with the animals for 2 weeks. And then you replace them with the intact rams at a ratio of 1 to 20, and most of the animals will be served by about 18 to 25 days after the teaser introduction.

We have organic farms who are breeding groups of ewes out of season, and they regularly will send. 450 used to be teasered and then tapped, and they would get 350 lamb, 350 animals in in lamb, which means 77% success rate, and that's out of season. So that's pretty good without using any hormones, any hormones.

So you can use all sorts of hormones to help you, melatonin implants. Plus or minus light manipulation, you want to introduce those about 35 days prior to the mating season, mating date, and just bear in mind that the rams have to be done a week earlier and they have to be given 2 or 3 implants to increase their libido and semen production. Recently in the UK, we had some availability problems, something to do with the minimum residue level of the product, and I'm hoping that would be resolved fairly soon.

Progesterone implants, either chronic sponges or cedar ovis that you can see here, can be used. They are introduced into the vagina in a clean and careful and safe way and are left there for 12 to 14 days. If you're out of season, then when you remove the implant, you give them an ECG or a PMSG injection between 200 to 500 international units, and that makes sure that they're all be ready.

Very soon afterwards to be mated. You introduce the RAMs, and you want to make sure that you're using RAMs which can make, which can mate, annually. So all year round, like the Dorsets, and you would do that at the low round to U ratio, something between 1 to 5 or 1 to 20, because it will be quite a batched season.

The other thing you wanna do is you want to give the RAs a fitness examination and MOT to make sure they are ready for the task. And this is perceived to be the best way to do artificial examination and out of season. So, on to deal with the lambs.

The lambs, because we're interested in the milk for human consumption, the lambs are reared artificially, and they need to be separated from the dams fairly early. Many different practises, again, the, I think the beauty of sheep production is that there's no one way of doing things, and there's a lot of different miraculous, wonderful ways, and you learn a lot when you deal with sheep, with milking sheep and the farms. So the lambs can be either snatched at birth and being fed colostrum, as you can see this lady doing here, or they can be left with the ewe for up to 60 days, as they commonly do in the rockfall region.

And, the cheese is produced alongside the lamb's actually sucking. There is an issue with, dairy breed of lambs because they're quite sinly and quite dly little things, and the confirmation is not very good, and they're not really well looked or well sought after by the local butchers. So what we recommend to our, breeders would be to, to breed the top 25 or 30% that they use to dairy breed rams.

And then breed the rest of them to meat breeds to have a better lamb confirmation so they can sell more easily. But that means you require data and you need to know which of the uses are doing well and which are not. When you're rearing lambs, care, cleanliness, and consistency has to be practised.

Everything has to be clean and, consistent. And you can do a bit of praying as well. Or, what we're actually doing here is making sure that the air at the lab level is suitable for breathing, and it is here because you can see how nice and clean and freshly bedded this pen is.

But that is an exercise we do with our farmers quite often, not because we're mean, but because we want them to understand that standing above the lambs in the pen doesn't really give you an idea of what they're actually breathing and the risk of pneumonia that can be, . As a result of that. These are a series of pictures I took in a recent visit to the Netherlands where I was quite impressed by the lamb rearing unit.

First of all, because you can see it, there's a physical barrier which you're only crossing if you've got shoe covers. The owner is snatching all the lambs at birth, and he's reaming them for a few days in individual clean, fresh cardboard boxes. He's doing that because he's trying to get rid of Yoni's disease, which we'll deal with a bit later, and After a week or so, he batches the lambs together.

You can see how nice and clean and how happy the lambs are. He allows them initially 4, but then 2 teats for 10 animals, and he protects the teats with a a wooden bar with some holes in it. He says that it makes sure that there's no teeth biting and the animals are not fighting each other when they're about to, when they're going to drink.

You can see that there's still a bit of a, an accumulation of lambs, and usually when one lamb goes to drink, the others will follow, but he says it makes them calmer and it's easier for him to maintain the tes. And of course, from day one, he produces both forage and some lamb nuts because those would help with ruin. On to talk about milky parlours.

Again, we see a lot of weird and wonderful homemade operations like this one here, in the Flinn Peninsula, and these are the famous, clean milking sheep, but you can also get, A top end partner available with all the bells and whistles, and you can see me here wondering which button I should press to do what because these can be quite sophisticated, or maybe I'm just too simple for those. The parlour settings, the pulsation rate is 120 to 180 BPM, which is 2 to 3 times quicker than any cow dairy pulsation rate. And these are one of this, that's one of the things that you notice straight away when you go into a sheep milking parlour.

The pulsation is, is very, very rapid. The background. Usually, we would say use 120 if you're using rubber liners and a pneumatic pulsator, and you can move up to 180 if you're using silicone liners and automatic electronic pulsators, and the pulsation ratio is 50/50.

The vacuum at the claw piece is 28 to 39, so slightly lower than cows because the teat structure is slightly different. And again, you have here the vacuum for low and high lines as well. Milking up times for sheep is between 1 to 2 minutes.

So much quicker than a cow, but sheep can hide about 20% of their milk as residual milk, and hence farmers would resort to bumping the other in order to release to have that second release. Or you have to, if you're using ACR, automatic cluster removals, you have to set them appropriately to accommodate for that 20% residual milk. And if you're doing it, .

By hand, then you need to avoid over milking, and you have to shut the vacuum as this person is doing, pressing that clip here before you manually remove, otherwise you'll make some teat and damage. As with every parlour of every species, you have to, milk hygienically. We recommend our farmers wear gloves, which are easy to disinfect and wash in between lines, but clean hands are.

Perhaps not as OK, but our second best. You can see this person here having a glove on one hand and a bare hand on the other, not sure why, but that was part of the reason I took that photo and for the fact that he was sort of pressing on the . Sort of valve here to shut the vacuum.

These again, a series of photos I took in Canada. This is Chris Bushbank, who is actually a vet herself and she milks a group of recent ewes at home. The youths have just come.

Back from the pasture, and you can see the pasture is well drained and dry because the animals are nice and clean, they're not mucky at all. She dry wipes them with an alcohol wipe, then she checks the milk for any clots to make sure that they haven't got mastitis. Then they go on to be milked and at the end, she does a post dip.

With povertyidine to prevent any of the chronic contagious bugs migrating into the other. If we're talking about levels of mastitis, then we see low levels of clinical mastitis. Which is great.

Nutrition is key for both yield and for immunity. And the good thing about milking sheep is that there's no two hungry lambs biting on the teeth and causing damage. But the other has to contend with milk milk.

Hands, hence they have to be nice and clean. And the milking machine, which again has to be maintained well, the liners have to be changed, and the vacuum has to be looked after and the ACR, sort of adjusted, so we're not causing any teeth and damage. What we do see a lot is the subclinical mastitis, which is basically only detected if you're looking for it, but we do see cases of clinical, sorry, subclinical chronic cases, which brings upon low yields and low solids, and solids is what we're looking for.

And because in masittic milk you'll have all sorts of inflammatory mediators, it brings on what we call low cheeseability, so the cheese doesn't form very well. Most of the bugs we see are contagious stuffs and streps, and how you find these things is when you look for them, usually by using somatic cell counts, because the count on these subclinical ones, which, as the name implies, do not show you any signs, is, that you, you can spot them because they all have high somatic cell counts. This is a group of 30 Us we were looking at during an lactation.

In blue, you can see the level of solids for each individual U. And in red, I'm not sure why we have a line here, but the dots, look at the dots in red is the level of somatic cell count, and you can see that the majority of the ewes with a high cell count are producing less solids, which is, is fairly understandable, but this is a nice visual we think. What are those somatic cell counts, just to recap.

The cells found in milk, 5% of them are lining cells, but the rest are the white blood cells of the immune system, and they're the first line of defence of the immune system. And when you have an inflammation, then you have a rise in these cells and a neutrophil surge. So the polymorphic nuclei are are represented much in much higher numbers.

So if you have a subclinical. Mastitis, you will have a higher level of cell cancer. Now, just a reminder that the milk production in sheep is by apocrine milk production, not neocrine like cattle.

So meocrine is when just the milk globules are leaving the milk producing cells, but in sheep, actually the, the end of the cell is being pinched, and then what it gives you, it gives you a higher somatic cell count reading. Having said that, Cell counts are still an excellent indicator of mastitis. We believe that fro level should be below 500,000 cells per millilitre, and if you see an individual with over 400,000, then there is another health issue there with that individual, and we have quite a few flocks who are milking well below 2000, 200,000 of these.

Again, it depends on the stage of lactation and parity of age, so the older the U is and if she's well into her lactation, usually the cell can creep up a bit. This is another, table that can show you. That's the somatic cell counts, and in sheep here on the left, goats on the right.

Healthy other up until 200, 300, and from 400 onwards, we are looking at some level of mastitis, usually subclinical. If we talk quickly about milk quality, then some countries present a legal limit on certain milk parameters, and we'll give you a price incentive for things like somatic cell counts. In the UK, for instance, we don't have any legal limits, but the processes have their own guidelines.

If you look, for example, on the BSDA guidelines. These are one of the advantages of Zoom that you can get close to the screen. You can see these are the BSDA targets for bugs and, butter fat and protein, and also for somatic cell counts, which we're looking at less than 500,000.

Surprisingly, the European Community and the specialised cheese Association are not looking to limit the level of somatic cell counts, but BSDA targets are definitely looking at under 500,000. This is a table taken from the somatic cell count milk scheme, sheep milk scheme in the Israeli board, and you can see starting in 2016 and tightening till 2018, they are given a Price difference for the level of cell counts that you have. So your target price will be given to you if you're producing milk with only 500 to 600, cell counts per mL.

And, if you go under. That you get a bonus, and if you go over 600,000, you get a penalty which is paid into a levy. And if your quarterly average is above 1,500,000, then your milk is rejected and not taken away, which is quite a blow.

This is the age of technology. Each and every one of us probably has an iPhone or another, sorry, another, mobile phone, which, has a processor in it which is stronger than the one that landed Apollo 11 on the moon. So technology is there for us to use, and the UK has actually announced a new initiative for precision livestock farming, so to base quite a lot of the farming practises on advanced technology.

We are looking for sustainable production. But in a way, simple milk metres on some of the parlours would see would be a good start, but other parlours can have a really well integrated farm managing system that would allow you to get where you need to go in a sustainable way and cut your losses and be more efficient. As you know, these are readily available, fairly cheap to have, .

Electronic identification devices which would identify individual use and collect quite a lot of information. You can now scan your use using a portable Bluetooth scanner. All the information, as we said, is onto your mobile phone nowadays and linked together to a computer.

And this is Sarah, one of our, shepherdesses in one of the flocks. You can see above her head is 6 different groups because that is the, Flock that is landing 6 different groups in a year, and they have cameras in the parlour to make sure that everything works well. You can see the VAT, the vet's van, so I'm quiet that my van is well looked after, but a lot of technology, cameras and a lot of data recording is happening to make sure that production is efficient.

Farm management system, as we said, they collect individual and group data, and they are looking at parlour performance for identification of all the animals and the milking parameters, and they give you a fantastic tool, as I said, for performance monitoring and making decisions for breeding, who's going to be bred, who's gonna be culled, if she's bred, is she going to be bred to a, a milk breed lamb because she's doing really well, or can we breed her to a dorset for lamb confirmation? And we believe that the dairy sheep and goat Consultancy group that adoption of technology is key for sustainability, even in smaller flocks. This is part of what Dela Val Delpro sheep and goat software is recording, and you can see quite a lot of parameters are being gathered from feeding records and cunning decisions can be made, drug records and daily milk recordings, what the parlour is doing, all these things are recorded and integrated to allow you to make good decisions.

This is what the parlour has been doing on that day, that's morning milking in blue. Afternoon milking in green, you can see the milk yield in either of these groups, you can see how many milk was produced in an hour, how many sheep. Were milked in an hour, the average yield for you and the total milk, a lot of information is gathered.

This is a view of an animal that's about to get some medication, so that's an individual file. That's the animal, that's her number. She's 2 years and 8 months of age, had two lactations.

Her average yield is 0.75. She's already bred and she's still milking.

You can see all her history, any treatments that she had, groups that she's changed, and here, the drug that she's about to get, including the meat with whole days and the milk with whole days. And how frequent that drug can be given and the application method is subcut in this incident, so a lot of information is gathered to allow you to make the right decisions. Speaking of drugs, Drugs and treatment options.

Basically, it's quite limited. There's limited availability of drugs and vaccines for milking sheep. Some of the drugs are not at all licenced for sheep in the UK.

Unfortunately, Metaam, which is a very, very important non-steroidal anti-inflammatory, is one of them, and some of them. Are not authorised for sheep producing milk for human consumption, like betamox and all the other amoxicinins, which I, I've chosen beamox which is that's quite a common drug to be used in commercial sheep production. Metaan, however, is licenced for sheep in the in Australia, New Zealand, and Canada, but you're not allowed to use it during lactation or 11 days before lactation starts, so quite restricting.

Vets should observe the cascade when prescribing, which would allow us to use drugs that are potentially not licenced, and unless they're forbidden, you can use them but apply a 7 day milk withhold. But farms should try and do their best to rely on good management and disease prevention for a sustainable future. So try to avoid or try to make your farmers and help your farmers avoid buying in diseases when they do buy in animals.

You want them to be quarantined for a set period of time and observed, and you want to vaccinate them if you can. The housing is to be clean and dry and well ventilated. Pasture tracks and gateways have to be managed properly so they're not full of mud and muck.

Stocking rates both inside the sheds and on pasture has to be managed carefully. And as I've mentioned in my one of my first slides, feed and water trough space and availability are quite important. These are two drugs that are commonly used against commercial sheep production.

I'm happy to say that haptava Plus, which is the vaccination we use for clostridial diseases, is very, is allowed to be used with no milk withhold in dairy sheep. It doesn't really matter because we usually give it in a dry period, 4 to 6 weeks before they land to boost the immunity. So, but it's nice to have something that you can give to, milking sheep.

And enamycin, and most of the oxytetracycline injectables will set you back 7 days in milk with, which is something to consider. I'm moving on to talk about production limiting diseases. So the diseases we see more commonly, which have a huge impact on production.

The first one is lameness, and it's no surprise because sheep farmers would tell you love to go lame. Internal and external parasites, and then all the classic iceberg diseases, those hidden diseases that we see, and of which we won't have time to speak about all of them, but we'll talk predominantly about Jones disease. So lameness, lameness is one of the main disease conditions of many dairy sheep farms and commercial farms.

They have wet conditions on pasture, high stocking density when housed. And you get name sheet. In the UK we have a 5 point plan to allow farms to tackle lameness, so let's try and see what's applicable to dairy sheep.

Can't repeat cases in order for them not to be a focus for reinfection and you can definitely do that. You can quarantine incoming stock to make sure you don't buy in any virulent footro, any CODD contagious ovar digital dermatitis. So that's definitely what we recommend.

And you want to avoid infection and spread again through gateways and tracks, sheds, facilities, and if you have lane uses, you want to gather them together in the dump group and make sure they don't just roam the rest of the, sheds or the pastures. Vaccinate is one of the key components of the five-point plan, and foot vax is available when we're dealing with footrot. Having said that, foot vax is not allowed to be used in lactating dairy, dairy sheep.

It can be used during the dry period, because they're not lactating at that time, but then the dry period falls a lot of the times, at the wrong time. So, Not easy to utilise foot facts when you really need it because we see foot rot in times where the animals are in peak production in spring and summer, so. Treating cases early or treating case properly and early is the 5 pillar, the 5th pillar, and Again, non-steroidal anti-inflammatories are indicated.

They're not licenced in sheep in the UK, but actually we can use MetaCam, and we need to apply a 7 day milk withhold. In a way, our condition and situation is better than New Zealand and Canada because in the UK we can use it under the cascade, only we need to apply 7 day milk withhold, whereas over there they're not allowed to be used during plantation. Antibiotics, or the oxy tetracycline, which are indicated predominantly for foot rot, can be used, but have a 7 day milk withhold.

And oxy tetracycline spray has got a zero milk withhold. So if you catch the animals early when they're only at the scold stage of the disease, that would, not set you back at all. So, early detection of lameness and prompt treatment would pay dividends here.

Parasites, we're worried about all of them basically. Nematodes, so strongiles and Aunchus, which we see quite a lot, trematodes, liver fluke, lice. Flies for fly strike and the dreaded scab mite, all of them causing huge production and welfare concerns.

For instance, this is a liver of an animal that had died of liver fluke. You can see it doesn't really look like liver. We've lost two foetuses.

You can see one of them here. So tremendous effect or negative effect on production and that animal's welfare, for sure. And again, the other thing is, is that treating those animals, there are well established resistant issues, resistance issues in quite a few of those nasties.

What can we use in milking sheep? If you look at the white drenches, which we use for worms, or the trilobendazole, which we use for the young forms of Fluke, then panicure we can use with a 7 day milk with hold, and the rest are not to be used for sheep producing milk for human consumption. Try clobendazole, don't use it for use producing milk, including the dry period and 1 year prior to first time.

So basically, put a sticker on the bottle and say, don't even think about it. Now, all these parasites, when you use them, you have to use them on the whole group, not so much the individual animals, which means that if you give them panicure. You need to observe a 7 day milk withhold for all of them, which is no milkshake.

If you are looking at the yellow drenches, again, not to be used for sheep using, producing milk for human consumption, same for fluivar, the Levicul, closamectin, Trodax again, don't even think about it. The only drug we can use here in the UK for fluke, although it's not effective for immature fluke, is Xanil, which again will carry a seven day milk. If we're looking at the clear drenches, against the again, the majority of them apart from yin drench are not to be used for dairy sheep at any stage of their life, or definitely not when you're, when you're milk producing.

Sydectin drench can be used 5 day milk withhold. When you're looking at sheep scab, which sidedectin 12% is one of the better treatments for, and another one is an organophosphate dip, both of these are not allowed to be used in sheep producing milk. So again, treatment for sheep scab are not, readily available.

There is one product called Eronix Multi, which is a poon, which has 0 days, no milk withal, which is wonderful, and it is licenced for sheep and goats here in the UK and in other places in the world. The issue is that porn is not really optimal for internal parasites and not really optimal for scam. Having said that, it is licenced and I've spoken to quite a few colleagues in Spain and Greece who have been using it quite successfully, so I'm definitely not knocking it.

But when you use it, you don't just put it on the fleece like you would some of the fly treatments, but you have to apply it with a specific nozzle onto the skin. Epreys 2% is an injectable for cattle with 00 megal in cattle, and I believe the company is hoping to licence that, for use of milking sheep and milking goats. At the moment, if you do want to use it, you have to use it under the cascade, although that's difficult to justify because you have got a licenced product for it.

The 4th and 5th generation of wormers, the Zorviks and the Startected, are not to be used in sheep producing milk for human consumption, which creates a bit of a problem with our quarantine trenches, so it's something to consider. If we're looking at the spot-ons for lice, for instance, the deltamethrine spot on Spotti or are not, is not allowed to use, but deltonil is with 0 days, so a bit of an oddity. And if you're looking to prevent flies with insect growth regulators such as click, you won't be able to milk the sheep, or you can milk them, but you're not allowed to market the milk for 7 days.

So, You can see it's a bit of a minefield. You have to know your drugs, and you have to look for the right drugs at the right times, but basically, if you can, try to avoid disease. Which brings me to talk about the last of the diseases I want to mention, which is Yoni's disease.

Yoni's is perceived as the highest risk for the national flock productivity and sustainability in the UK. In a recent survey, about 64% of faecal samples from commercial lowland flocks were PCR positives, and observing those flocks over three years, we've seen a much reduced life expectancy of use, with only 17% of them versus 40% remaining in the herd over 3 years, so quite a substantial early exit. This is some government data about all the diagnosis of iceberg diseases, and you can see that in pink, or orange, Yonni's disease is the highest.

In, most years. Just a reminder Jone's disease or tuberculosis, identified in 1895 by Heinrich Johanne, who is a German physician caused by mycobacterium IV para tuberculosis, and as we're such good friends, we call it ma. It's present worldwide and affects ruminants, and the main route of transmission is faecal aura.

Most infections would happen in very young animals between 0 to 6 months of age, and what comes after that is a slow progressive thickening of the ileum until it looks like that, very thick, very corrugated, so. You get malabsorption and protein losing and neuropathy. The animals will eat at the initial stages, or even at later stages before they crumble, but they won't absorb much.

So you get wasting disease and immune suppression. This is how the disease will look at later stages in cattle. They will always scour profusely.

The problem with sheep is that they might look thin, but they don't always scour, so a bit more difficult to detect. Sheep are unlucky enough to be infected by both the sheep and the cattle strain, and when they get the disease, they can either, some of them might miraculously clear it and be asymptomatic, and the rest would go on to develop one of two forms of the disease, the multibacillary or the foci bacillary, which are different in the way the, the immune, system is going, and the oy bacillary will have a lot less antibody production. You have late intermittent bacterial shedding, you have some breeds who are more susceptible to the disease than other, and there are quite a lot of issues with test specificity and sensitivity, which makes it very difficult to control the disease.

Animals would be 2+ years and they start wasting away. We see production losses even before that, due to lameness, mastitis, and fertility because of low immunity and, of course, lower milk production, which is something we're interested in. You have increased culling rate, as we've said before, but it's often Attributed to other conditions and not necessarily to yonis because they grow lame or they don't conceive or they get mastitis, and they exit for various reasons, which is for poor body weight.

On average, if you look at studies, they're looking at gross margin loss of 8.5%, which is quite a high loss. And the The thing that we all need to consider is that MA is linked to Crohn's disease, and in a university of Hiros Hiroshima, if I'm not mistaken, they found that even mA particles or muck antigens can induce gut pathology.

So not only viable bugs, but also bug particles. So when we're feeding clients with natural sheep yoghurt, or now that we're all MasterChef winners and we all sort of dish our lamb pink. It's not something we need to think about.

Also, some studies have shown that map was found in powdered infant formula. Quite a few of the samples were PCR positive. There's a bit of a debate whether you could actually culture any viable bugs from it, but definitely you could culture bugs from retail milk in the UK and in other countries.

So milk that was bought on the shelf and cultured, viable bugs were there, so pasteurisation is not 100% effective. That brought the dairy cows, dairy cattle people, to come up with a national Yoni's management plan. The plan was started, started in 2016, and farmers had to declare their herd status by a minimum of 30 cows screen.

And if any animals were found positive, the whole herd was tested between 2 to 4 times a year ever since. They had to liaise with the Action Yoni's delivery vet. And they had to decide and sign a plan of action by October 31st, 2016, and annually since then, and we as vets with our farms have to show annual improvement.

And at the moment, some of the Supermarkets and milk buyers would insist that any positive cow would exit the herd, the cow herd within 60 days. So, is yonies a concern to milking flus? We believe it is, it is quite a big concern.

First of all, you have production losses, and in this day and age, we're all talking about sustainability and better, more efficient production. It is a huge animal welfare concern because the animals are sick, and we have the issue of product safety. So public perception and consumer trust can be dented quite badly if they sort of start thinking or if they're aware of yonis in sheep milk.

And just bear in mind that we are, people are choosing to use sheep products as a healthier option. So if we don't make it a healthier product, more so than the cows, we're basically committing, some sort of a sin. This is a clip that was taken from Waitrose Facebook page, a member of the public, Lisa George, asking if the cows are from Yoni's free herds.

So it's here to show you that basically the public knows about the disease, some more than others, and we definitely have to take notice of it and make sure that the product is safe to use. The good news is that we have a vaccine. We have a vaccine for sheep and goats.

It's an activated map strain, it's a 1 mil single injection dose at early stages of life between 4 to 16 weeks, and it's been found to reduce shedding and clinical disease by up to 90%, which is pretty good. It costs about in the UK about 3 pounds excluding VAT per dose. So I'm not saying you should vaccinate 600 uses.

All in one go, but you can definitely, vaccinate your replacements annually, and within 3 to 4 to 5 years, the herd will be, protected. It is cost benefit if you have a mortality rate over 1%. That was found in a New Zealand study in 2018.

So if you have more than 1% mortality due to Jo Jones' disease or Yoni, then making that investment is, is a good thing to do. One thing to bear in mind is that it's potentially interfering with Yoni's serology testing and the skin test, if you're unlucky enough that your sheep have to go through one of these. The not so good news is that the diagnostic tests, or the serologies and the PCRs which you can do pool samples.

Have got issues with a cost, intermittent and late shedding inhibitors for PCR and the oy bacillary stage, which again have got very little antibody production. And if you vaccinate the animals, then, results have to be interpreted with caution. Postmortem examination is quite an important one, especially if you open the animal and immediately see this sort of corrugated, thickened yellowy, piece of gut.

You know, you've got yoni in front of you, but you should definitely send for histology. Faecal culture is basically the . Gold standard, but it is gold standard because it's quite expensive and it does take about take about 16 weeks to get results.

There are a few new tests that are being checked and I think that during the webinar vets, conference that we are part of. There is a presentation that I'm really keen to hear about a new QPCR test forgers disease in milk. So there are new tests coming that would hopefully increase the sens sensitivity, specificity, and we look for the bugs and not necessarily the immune response, which would allow us to vaccinate our flocks and still test for gurneys.

Do we need a control strategy? Yes, I think we do, and my colleagues at the consultancy service think we do. We need to ask our farmers to cull any suspect or any tested animals quite aggressively.

You want to vaccinate your replacement new lambs, and you want to group your suspect and then use the lambs separately and not retain any of these lambs for breeding. Abattoir and falling stock surveillance would be good, and perhaps we need a national monitoring and control scheme like the cows do. I always believe that if the sector itself, farmers and vets and the BSDA would come up with a plan, it would be better than any plan that would be forced upon us by the supermarkets, which have a slightly different agenda to the producers.

So, coming up with a robust scientific plan. Vet led would be quite a good thing before one is forced upon us. Because the cattle National Joies .

Management plan will impact milking sheep, as will consumer perception and consumer trust issues. So just my final slide is to say that the sheep milking sector. Is enjoying a continual global growth with some fantastic products.

This is a fantastic Rockfield cheese produced by my friends at Velvet Cloud in Northern Ireland. Continuous global growth. As vets, we're dealing with open-minded producers who have got a thirst for knowledge and are thinking outside the box, which is great to be around these people.

And the production systems are a lot more suited than cows for soil health and sustainability, so the future is basically quite bright. I want to thank you for listening to this, to this presentation, and I'd like to welcome you to our webpage, the DairySheep and goat.com, where you can find information about us and the Dairy sheep and goat conference, which is an annual event till the pandemic hit.

So there's no, conference running this year, but hopefully the next. And please feel free to note down my, email address and I'll be very happy to share all the information that I have with, anyone that's interested. Thank you very much.

Hello, Anthony Chadwick from the webinar vet here. Welcoming you to our third lecture, live lecture on association Day. Amazing how many associations we've got involved, this time, at this conference, WVA WSAVA, BCVA, NZVA, BVA, AVS, BVDA, IVSA, RWAF, Abravec, ABCR, TTVA, SBS, ICVA, CVSS, Avazu, A L V E FAS, BVRA.

HKVA. Acom V and MC VMA. So, so pleased to have all of those associations working with us today, and I do hope that everybody's enjoying the session so far.

Do go and have a little look in the vet exhibition. We're really proud of what we've put together there to make it a more interactive experience for you. We do have some stands and and various goody bag.

Competitions that you can go into. I, I noticed there were some really nice prizes like Lipman stethoscopes. So do go in and have a little look at that.

And then at 4 o'clock when this finishes today, we will be inviting you to come to the networking, the vet or the nurse networking room, you can go into whichever room you want to. And we've got some really cool. Video software so you can actually video chat with each other as well.

So if you've got some friends you want to see, you can invite them in, and of course the rest of the conference continues tomorrow. We've recorded a lot of pre-record hours, so if you do want to have the whole experience of the conference and you haven't bought a ticket yet, there's still opportunities to do that via the website, so do go in and have a nose around the websites as well. So that is that.

We're very fortunate today to have Kieran Borgia, who's gonna be speaking about a rational approach to using cardiac therapeutics. Kieran has worked in first opinion and emergency. And then he decides to undertake a residency in cardiology.

He's an American and European diplomat. He's got a particular interest in interventional surgery and feline cardiomyopathy, of which he's already spoken about at the conference. He's spoken internationally on feline cardiology, but he still finds tabletting his own geriatric cat a challenge, and don't we all?

So Kieran, it's over to you. Thanks very much, Anthony, and thank you to all the associations and all the sponsors who've been involved in in getting today to go ahead and and the whole congress. It's it's a real honour to be a part of things.

So we're gonna talk about a rational approach to. Prescribing cardiac therapeutics, when to treat, why we're treating, what we're treating, we're gonna cover a lot of basics, and I don't mean to come across in a sort of patronising manner here. Many of you are gonna be familiar with or at least have come across the things we're talking about before, but what my aim is, is to try and update you on what we consider the best practise to be, and, how to kind of prioritise some of your decisions that you'll need to make along the way.

Cardiology and treating heart failure is not just an exercise in polypharmacy in that we just don't prescribe everything in one poly pill, if you like, and there are times when we give things and times when we don't. So, things that we're gonna cover today, we're gonna consider pathophysiology of heart failure, and we're gonna focus on mitral valve disease. And the reason we're gonna focus on that is it makes up 85% of all the heart disease that you're gonna see in primary care practise, wherever you are in the world.

It seems to be the commonest disease. If you're located in Asia, especially Southeast Asia, there is a huge amount of mitral valve disease, because many of the dogs that are owned in that area of the world are smaller breed dogs, and smaller breed dogs are predisposed. .

We're gonna identify at which point treatment benefits dogs with mitral valve disease. I'm gonna just mention DCM. I don't even think I've put it in the slides, but we're gonna talk a little bit about it as a comparator cos it's very different and actually it's much more challenging to identify disease early.

And then we're gonna take the mitral valve disease situation and we're gonna contrast that with cats, and then how to treat cardiomyopathy in cats because they are very different and our approach is very different, and we're gonna think a little bit about why that might be the case. Things we will not cover. I, I'm hoping I don't see numbers of participants drop massively on this slide, because anyone who's here to to talk about refractory heart failure cases, I'm happy to take some questions on it, either here or via social media is absolutely fine.

But I, I haven't put it in the lecture because we, we've got 45, 50 minutes, and if we want to cover a fracturey heart failure, we're gonna have to have another 30 minutes on top of that. If we want to cover antiarrhythmics, give me your afternoon, and I can help you with that. Pulmonary hyper.

Attention will take us up to tea time tonight. And if we want to talk about congenital heart disease as well, that's a whole another thing. And actually, we have got a pre-recorded session, as part of the congress on congenital heart disease, and interventional cardiac surgery.

So any of you who are interested in congenital heart disease, how we might make decisions about that and what surgeries we can do, there is a separate webinar for that, that, I would encourage you to watch, because, not that I'm especially brilliant presenting it, but just that there's some really pretty pictures to look at along the way. So a lot of this stuff is witchcraft, especially antiarrhythmics, and refractory heart failure cases. There's a bit of science, but there's not much science, OK.

So it's quite important with with these more advanced cases, if you're not confident with them or not very experienced with them, or the dog's just doing something that. It doesn't normally do when you manage these cases. Speak to a cardiologist.

Most cardiologists are happy to give telephone or email advice about cases. And this witchcraft, you know, is where really the science drops away, and we have experience and, and, and, people's own, opinions coming into the matter. So we're gonna think initially about congestive heart failure.

I'm highlighting the word congestive here. I will say heart failure as a term throughout, but what I mean is congestive heart failure. So what are clinical signs of congestive heart failure?

Well, it's fluid accumulation. That's how we define heart failure in docs. If you are a human, and I am a human, then we would define CHF as chronic heart failure.

And the problem with this is it's not always fluid accumulation that's present when a human is diagnosed with CHF. So chronic heart failure is a sign of exertion or fatigue. So if, humans with, say, a cardiomyopathy, develop a little bit of, a little bit of tightening in the chest when they exercise, and when they go upstairs, they feel a bit short of breath, they'll be called CHF, chronic heart failure.

They may not have pulmonary edoema or ascites or pleural fluid or whatever but these, these are the typical signs that we see in our patients when they've got fluid accumulation. So pulmonary edoema is caused by left-sided heart failure where predominantly we have left-sided heart disease. That's the vast majority of our patients, mitral bowel disease, DCM HCM and other feline cardiomyopathies.

We see tachynia, we see dyspnea, so difficulty breathing, fast breathing in, patients with pulmonary edoema. These are the cardinal signs. Coughing is still a little controversial.

Luca Ferrisson is a cardiologist who's done a lot of discussion and sort of publicity around cough, and he really has, has taught us, by, you know, some research that he's undertaken, but also by teaching us about human literature, Luca has has shown us that cough is not a cardinal sign of pulmon edoema. There are the occasional dog that we see where on radiographs they have pulmonary edoema and they're coughing, and we say, oh well, they must have respiratory disease causing a cough and pulmonary edoema caused by heart failure. And we treat the pulmonary edoema and the cough improves or goes away.

So sometimes we see coughing in patients where we may not expect it, where they, the, the cardiac problem may be the only issue and. Certainly cardiomegaly can compress airways and trigger cough receptors, and certainly increases in in atrial pressure and pulmonary venous pressure may also trigger cough receptors. So some patients we see coughing.

The point of this really is for me to say, don't increase diuretics in a patient who is coughing, but has a normal respiratory rate. OK? So, cough is not the cardinal sign, respirate should trump that every time.

On physical examination, we might find loud adventitious sounds or pulmonary crackles suggestive of pulmonary edoema. It's worth mentioning hand in hand with pulmonary edoema that most cats who develop left sided heart failure will also have some degree of pleural effusion. Now in cats we've got a slightly different anatomic situation.

We've also got the the fact that cats will often develop bilateral heart failure right. And left-sided heart failure, because of the way their pulmonary vessels react to having increased pressure in them. So dogs will often do left-sided heart failure, and then some months or, or, or years later may even go into right-sided heart failure because of changes to the pulmonary blood vessels.

Cats will do it after hours or days. So cats will often present with, with pulmonary edoema and pleural fluid. And if you have a pleural diffusion, we'll have du dull lung sounds ventrally and also there may be dullness on percussion of the thorax as well.

Of course, the true, the same is true in dogs with pleurofusion, but the pleural effusion won't be caused by left cellular heart disease in a dog. Ascites is the cardinal sign of right-sided failure, so here we've got abdominal distension and a fluid thrill, on abdominal belotment of the abdomen. That often will again go hand in hand with pleural effusion in the worst cases.

Now, another thing to look out for in patients with right-sided heart failure who have ascites is something called the the the positive hepatojugular reflux or jugular distention. And this is something that I used to forget all the time and I, I would kick myself out, you know, my, my supervisors during my residency would say, have you looked at the jugulars like oh. I've forgotten to look at the jugulars again, I'll look now.

So try and get yourself into the habit of looking at the jugular veins. It's super useful because if we have got ascites caused by the heart, so we've got right sided heart failure causing peritoneal effusion, what happens is you may have distension of the jugular veins because the pressure in the right atrium which is driving that ascites will also cause pressure waves or or pressure distension of the jugular veins. It's not always the case that they're distended at rest, if you like, but have a look at them, and they should be, they should not be easily visible in a dog who's standing up.

If they're lying on their side, you will see them because they'll be the same height as the heart, but if they're standing up, you shouldn't see them much beyond the thoracic inlet. So I tend to try and raise them, let them down to see them, and you may be able to do that without clipping, but obviously in some dogs you may need to clip the hair to identify that. So I raise the vein, drop the vein so I can see where it is, and then I, I let it be, and I see if it looks distended, and if there's any pressure waves, any pulsation in that jugular vein, when you're not raising it.

Now, if the jugular looks normal, you need to then get an assistant. So here I have a lot of students around who can help me, but also, another clinician who can help or a nurse. If they can just put some pressure on the abdomen.

So by that, what we're doing is we're lifting up the abdomen and causing an increased pressure in the liver, which increases pressure in the coral in the cava. The pressure wave then in a normal heart would go into the atrium and the heart has got such good compliance it can just take that increase in pressure by squeezing the liver and get rid of it. You won't see that pressure wave come from the caudal vena cava into the cranial vena cava and jugular veins.

If someone palpates the abdomen, pushes on the liver, and you see the jugular vein distend, that is patinnemonic for right-sided heart failure. It's true also in pericardial effusions, so I think they can be quite difficult to diagnose. I sometimes see dogs who've been diagnosed with heart failure after an ex lap, or diagnosed with pericardial effusion, during the middle of an abdominal ultrasound scan.

And actually if you do a good physical exam with a jugular inclusion there, you can differentiate whether the ascites is caused by heart disease or non-cardiac causes, such as, hepatic disorders or pre-hepatic disorders. So how do we define congestive heart failure? Well, I've said it's clinical signs caused by fluid accumulation, pulmonary edoema, and pleural effusion, ascites.

You know, we've all seen cavaliers with pulmonary edoema. We've all seen cats with pleural fluid, and, and pulmonary edoema. We know what these patients look like when they come into the clinic.

How do we confirm our diagnosis, that we've had on clinical exam and history? Well, radiography is the best way of looking at the lung fields. An echo is OK.

It's pretty good in cats for looking at the lungs, but ultrasound is not that accurate in dogs to detect cardiogenic pulmonary edoema. So radiographs are an incredibly useful tool for us. So we can look for the sort of holy trinity, if you like, the key three things on a radiograph to diagnose left sided heart failure, which is cardiomegaly, particularly left atrial dilation, pulmonary venous distention, particularly the cranial and caudal lobar vessels, and also interstitial or alveolar infiltrates.

Bronchial patterns may cause respiratory signs, but they show airway disease. Bronchial patterns do not indicate pulmonary edoema. But sometimes we get this kind of zebra that walks along, not the common horses we see every day, but the zebra, which is the peribronchial alveola infiltrates, and I've been fooled by those before, where you see the alveoli infiltrates around really obvious bronchi in the middle.

And I thought, hm, looks a bit like respiratory disease to me, but it's a Doberman with tachypnia, dyspnea, a little bit of cough and a big heart. So we treat what's most likely based on the clinical picture and those infiltrates go away. So we can get perironchial patterns, and they can be quite hard to know if they're respiratory or cardiac.

So in that scenario, put it into context with the rest of your patients, your physical exam, your history, your other imaging findings. Let's look at some radiographs. This is a normal dog.

This is a Labrador, I think. The reason I say that is the breed is quite important because that tells you a bit about thoracic conformation. And we all know that dogs who've got a short, wide chest, like, the bulldog breeds, they have a heart that looks big.

They have a large vertebra heart scale, and they are dogs weighed. Very easy to diagnose cardiomegaly. Spaniels are similar actually.

Cocker spaniels are similar. If we have a a a tall, thin chest like a Weimaraner or a Dalmatian or a Doberman, their heart should measure quite small on things like vertebral heart scale. So Labrador is somewhere in the middle.

This is kind of an average dog, and the upper limit of normal, for the vertebral heart scale should be somewhere around about 10.5 or 11. Here we can see, I'm just gonna put my laser pointer on, so you should be able to see that clearly.

We've got the cardiac silt in the centre here, we've got the coralvena cava there, we've got the aorta coming arching up out of the heart. We've got the trachea here bifurcating into mainstone bronchi, and here we've got cranial lobar vessels. So we've got the artery and the vein, in the middle we've got the bronchus.

And we can see in the lung fields, we can see nice clear thready vessels, we can clearly see the crawa of the diaphragm separated, that means this is the left lateral, if they're overlying it's the right lateral. And we can see also around the bony structures here, we've got a little bit of change to the bone, which suggests this is an aged dog. This is not a young dog.

So this is a normal looking Labrador. This is not a normal dog. This is a Doberman, actually, who has pulmonary edoema.

So, can we see Cardiomegaly? Well, if we were to measure this heart, which we're gonna do in just a moment, this is a big heart for a Doberman. If you look at the DV, that's a really useful view for identifying cardiogaly in a quick and easy way.

So the He should be no wider than 2/3 the thoracic width at its widest point, at the widest point of the cardiac celerate. And here we can see it's maybe 3/4 of the thoracic width at this point. So we can clearly see this is a big heart.

In this view here in the lateral view, we can see in the position of the left atrium, which is the sort of cordo dorsal aspect of the cardiac silhouette. We can see a bump here. So this drug has a big left atrium.

If you draw a line between the carina, so the bifurcation of the trachea, and the margin of the, the, the dorsal margin of the corral vena cava where it touches the heart, so from here. To here, there should be none of the cardiac silhouette above that line. And we can see there is.

So this dog has a big atrium, the only structure that will be is the left atrium. I think we can see that the lungs look fluffy, don't they? They look sort of like there's an alveolar pattern here.

There are some broncho grounds. And amongst you may spot that we've got the artery, the bronchus, the vein, and the vein here is wider than the artery, and also the caudal lobar vessels over here, the vein is wider than the arteries. So that tells us we've got cardiomegaly, increased venous pressures which link the left atriumum to the lungs, and in the lungs we have got some alveolar edoema.

So this is typical for congestive heart failure. This is a normal cat. So cats have a different thoracic shape.

You can see it's like a funnel, isn't it? And we've got these longer vertebrae in the spine which tell us it's a cat, and the bone density is a little bit different as well. Here we can see the cardiac so that in the middle, we can see the cordal vena cava, coming in a bit, bit longer than in dogs coming back up to the diaphragm, a bit more of a gap between the heart and the diaphragmatic cora.

We can see the aorta arching out and up along the spine here in the cat. We can see this nice pattern. Blood vessels over the lungs in the cao dorsal area of the lung fields.

I often think this looks like a leaf, sort of the veins on a leaf going back up here. And I want to see though, that leaf nice and clearly. If I can't see it clearly, or if I can't see the coral vena cava clearly, it suggests there's some pulmonary infiltrates, so there's some fluid in the lungs.

If we want to look for the cranial lobar vessels, we can see them here. We've got artery, bronchus in the middle, and the vein. And in cats, they're smaller than the ribs.

They're very thready looking in normal cats. This is not a normal cat. This is a cat with heart failure.

So here we can see in the lateral and the dorsoventral projections we've got cardiomegaly. Again, that 2/3 width of the thorax rule applies. You can see that the margins of the cardiac cell here are quite challenging to identify on the right side because we've got a very dense lung pattern, which is much denser looking than maybe in the lateral we we might appreciate.

Although cordo dorsal in the lateral, that's quite dense lung pattern here, and this is a mix of interstitial and alveolar pattern. How do I know it's alveola? Well, I can't see the blood vessels.

I can't see the leaf, I can't see the cordal vena cava. So it has to be fluid in the alveoli, facing the blood vessels, by which I mean the fluid in the alveoli, makes the the normal contrast you see between the wall of a blood vessel which contains fluid and the alveoli, which contain air, there's normally a big contrast boundary. So you very clearly see a vessel here we've got fluid that effaces that border.

So if you lose the vessels, that's an alveolar pattern. Here we can see the cardiac cell and I think we can probably reliably trace it around here in the DV. So this heart looks quite rounded looking, but also it occupies more than 2/3 the thoracic width, which is typical for cardiogaly.

Look at the, the stomach, there's air in the stomach because this cat's definitely dyspneic. This is a radiograph that I didn't take, and there's a couple of things that tell you that. First of all, I wouldn't take a radiograph of a cat who's this dyspneic.

I would always use ultrasound to make that assessment in cats. The second thing is this cat is anesto and intubated, so you can see there's a tube here, an endotracheal tube. I, I think we can make this diagnosis without having to anaesthetize these patients.

I, I'm, I'm not wishing to appear critical. The decisions are made, they may. The diagnosis, they treated the cat cat did very well.

But it's not how I would approach it. And I'm just clarifying that, because if any of you have seen me speak before, you will know that I, I really am not very keen on taking lateral radiographs of dyspneic patients, if it can possibly be avoided. I, I can't remember the specifics of this case, but maybe this cat was, was just too stressed and too aggressive, or they were just too worried, and they said, you know, we just have to intubate it and ventilate the cat while we're doing that, we'll get some radiographs.

So that's possibly why we have these images here. So we've got radiographic diagnoses of left-sided heart failure. Ultrasonographic diagnoses are important, and I think in the acute patient, more useful in cats than radiographs are.

So if we do a thoracic ultrasound in a in a tachy called dyspneic patient, we may see pleural fluid, that will give us a diagnosis of of why there's respiratory compromise and allow us to proceed by draining some of that, either for diagnostic purposes or most commonly for therapeutic purposes to stabilise the patient. If we've got beelines on lung ultrasound, and I'm not going to go down the road of talking much about thoracic ultrasound, there's lots of good resources out there. Look for review articles by Greg Leandro, and also, some research by Jess Ward, because that, they're the group at North Carolina State who have done a lot of this, this work in lung ultrasound in dogs and in cats, and they're producing a very beautiful body of work on lung ultrasound to identify heart failure in dogs and cats, and ident Fight other diseases as well.

And if you have bilateral beelines, on lung ultrasound, in cats with dyspnea, that's got a very high level of accuracy for suggesting cardiogenic edoema. In dogs, it's probably about 50/50, maybe 60% of them have, cardiogenic edoema. In cats, it's more like 95% have cardiogenic edoema, so it's a very strong test in a cat and can be used in lieu of radiographs in an unstable patient.

So, we're here to talk about treatments, not diagnosis, and I wanted to clarify a few things just so we're all on the same page and also just to get our head into gear thinking about heart failure. So. Why do we get heart failure?

This is a very fundamental thing to understand why we bother with treatment and where the treatment is acting. Well, the trigger for congestive heart failure in all cases of heart failure is a reduction in cardiac output. OK, there's very rare.

Things that cause a situation called high output heart failure, and we might see that with a PDA or some sort of AV malfunction, but that's very, very rare. And, in most cases in practise, we've got a reduction in cardiac output triggering various processes which lead to the end result of heart failure. So, I've put the three common pathophysiologies here.

We've got to the left mitral regurgitation. This is mitral valve disease. You know, if you're into cardiology particularly, you might think about congenital disease like mitral dysplasia.

It's the same pathophysiology as mitral valve disease. Reduced contractility is in the centre there. This is what we see in dogs with dilated cardiomyopathy.

It's also what we see in dogs with tachycardia induced cardiomyopathy. So again with arrhythmias that are chronic, we can get changes to the heart which reduce contractility. We may see the same thing in patients with infarction, we may see the same thing in particular inflammatory diseases or toxicities.

OK, so I'm not just talking about mitral bial disease and DCM and HCM here, I'm talking about. Pretty much everything we see can come down to these three pathophysiologies. So reduced contractility is the second, reduced filling is the 3rd.

If you imagine we reduce how much the heart can fill. Well of course, what goes in is what comes out. So if we reduce the filling, we reduce the output, and that has a reduction in output in the same way as reduced contractility might, but the cause of it is different.

So that would be typical for a cat with hypertrophic cardiomyopathy, or potentially it may contribute to the situation in, a dog with subbiotic stenosis that's bad enough to cause severe hypertrophy. These 3 pathophysiologies are crucial because they all reduce forward flow. That is the starting point for heart failure.

So actually, secret. Cardiology is really easy. Because actually cardiology boils down to what happens when you get a reduction in cardiac output, and then you work backwards from that reduction to work out what's going on with the different diseases.

So we would get a reduced forward flow. How does the body sense that? What does the body do?

Why, why do we end up in a situation with heart failure? Well, there are various systems that are in place to help you live long enough to reproduce and pass on your genes. So evolution has created some systems that will keep you alive if you bleed or if you get so dehydrated that you've got a reduction in circulating volume.

So. We are not evolved to deal with acquired heart diseases that occur in middle age to old age. That's not why there's been evolutionary pressure to cause these things.

And I know this sounds like I'm going off on a tangent. But when I first came across these, I used to think, well, why, if these are are such good mechanisms, why do they end up causing heart failure? And the answer is they're supposed to be switched off once your circulating volume is restored.

So after you've replaced your blood volume that you've bled out after your fight with a bear, or once you've replaced your. Fluid volume and your blood volume has normalised after your severe dehydration and gastroenteritis has resolved, these mechanisms will be switched off. In heart failure, the inciting cause is never switched off unless you undergo something like mitral valve repair or a heart transplant.

Those are the only ways to turn these things off completely. So we get a reduction in cardiac output within microseconds, the barrow reflex is triggered. The barrow receptors are located in the aortic bodies, the carotid bodies, and they sense a reduction in the stretch of the vessels, so a reduction in blood volume or or blood pressure.

The response is to increase heart rate, increase contractility and vasoconstrict, because that's a vasovagal loop that occurs. It happens in microseconds. This is what happens when you're standing up from tying your shoes.

If you did not have this, you would fall over, perhaps die after tying your shoes, because you're a biped, and as a biped gravity is our enemy. So, this reflex is used all the time in humans, so it's not meant for long term activation. The secondary reflex, in the sort of medium term in hours to days, is activation of the renin angiotensin aldosterone system, the RAS, and the RAS is something that again is meant to replace your blood volume, replace your circulating volume, and be switched off, in, in, you know, days, if not a couple of weeks.

The problem is that with longer term activation of the RAS, weeks, months, years, as happens in heart disease, we get significant changes to the heart, to the blood vessels, which contribute to a downward spiral of function in the heart, and this is called maladaptive neurohormonal remodelling, if you like, or or changes to the rash. Let's walk it through. So we're thinking about the second by second basis here.

This is the barrow reflex. We've got a reduction in cardiac output. You get an unloading of the barrow receptors.

These are stretch receptors, so they are stretched less and they fire less frequently. So then this reduces the vagal tone that's going back up into your medulla oblong arter, and your medulla says, oh, bad news, chaps, there must be something dropping blood pressure. We've got to maintain the fusion of the brain.

So what do we do? OK, we'll increase the sympathetic drive. And what that does is increases heart rate, increases contractility and vasoconstricts.

This is solely meant to preserve cerebral blood flow so that you don't faint and fall over an inconvenient time. So vasoconstriction tachycardia and positive inotropy occurs. This maintains normal blood pressure, which keeps you alive, which is fantastic, and we're all a big fan of the barrier reflex.

But it does increase myocardial work. So even that push to increase heart rate and increased contractility and work against the, the, the increase in resistance to the blood vessels when they vasoconstrict, that increases myocardial work. In the short term, that is probably coped with OK.

But in the long term, increasing myocardial work is not good if you have heart disease. So now we're thinking about over the hours to weeks, so this is the, the RAS activation. This is a little more complicated, the renal angiotensin aldosterone system.

So it's sensed, we have a drop in blood flow to the kidney. And this is sensed by the kidney actually via a slightly circuitous route, and the kidney monitors the sodium concentration of the distal convoluted tubule. So the macular denser is is monitoring the composition of that filtrate which eventually becomes urine all the time.

And it says, ho ho, we've got a drop in sodium concentration. Well, of course, the reason for that would be that we've got a drop in GFR which of course means we have a drop in blood pressure. So here the kidneys are saying, right, the brain's being perfused, but we're not being perfused, great.

We need to help ourselves. So the kidneys. Trigger the beginning of the renin angiotensin aldosterone system.

So the renin is a hormone that's secreted by the juxttoglomerular cells, so next to the macular densa, and that converts angiotensinogen, which is an inert compound to angiotensin one. Angiotensin one, it does a little bit via some secondary receptors, but not very much of import. Angiotensin 2, however, which is created by the conversion of Angiotensin 1 to Angiotensin 2 by angiotensin converting enzyme, or ACE, Angiotensin 2 is one of the bad guys.

If this was a cowboy film, this would be one of the black hat wearing bad dudes who's holding the the the bank to ransom, because Angie-attensin 2 causes a lot of negative consequences. So, what do we do? We want to preserve renal perfusion, so of course one of the first things that happens is vasoconstriction.

So we get vasoconstriction, and particularly constriction of particular vessels within the region of the nephron to increase filtration pressure, at the glomerulus. But also generalised body wide vasoconstriction. That will increase myocardial work, as we said a moment ago.

We get sympathetic nervous system activation, so we get an increase in noradrenaline, norepinephrine, if you like, and this will increase contractility, increase heart rate, and remember, just like the barrow reflex, but being sustained more long term. It also causes release of ADH or vasopressin. And ADH antidiuretic hormone, if you're British, will increase free water reabsorption in the collecting ducts, by the insertion of aquapore into two channels.

All these. Words probably, you know, if you're not familiar with them day to day, they ring bells from vet school, don't they? We always talk to our funnier students about this, and they're like, wow, I remember the words, from sometime in the past.

And ADH is an important thing that increases free water reabsorption. Angiotensin 2 does something else, it causes aldosterone release. And aldosterone will increase sodium and water reabsorption.

And longer term will cause cardiac remodelling and fibrosis of blood vessels. So aldosterin is supposed to be a short term thing and by increasing sodium and water reabsorption, it will increase circulating volume, which maintains renal perfusion, and cerebral perfusion. But also by causing fibrosis of blood vessels, it helps to maintain blood pressure without this sort of active vasoconstriction.

So you can see how these things may be detrimental. So on the one hand, we increase our circulating volume, and therefore we maintain normal blood pressure, but on the other hand we increase cardiac work because we've got more blood to handle and more pressure in the blood vessels to act against. And more chronically, this RAS activation is very detrimental.

So the increases in angiotensin 2 and aldosterone cause ventricular fibrosis, a cardiac fibrosis and rigidity. He doesn't feel as well, heart doesn't pump as well. We get an increase in cardiac chamber size.

The barrow receptors are actually reset so that instead of working at a normal set point to maintain a normal blood pressure, what they do is they're reset higher, which is more efficient for the body long term, but it's not good because it means your blood pressure baseline rises. And alongside ventricular and cardiac fibrosis, we get vascular fibrosis which can cause changes to the pulmonary and the systemic blood vessel. So again, it maintains normal blood pressure.

It's OK, minute to minute, day to day, but long term it is detrimental to cardiac patients. So the RAS is not evolved for this, it's not meant for long term activation, nor the bar receptors. So they, they deal with it as best they can, but they don't deal with it very well.

So, where do the drugs fit in to all this pathophysiology? So let's think about the mechanism of action of the common cardiac drugs and see how we can slot them in to this diagram, this, this RAS diagram especially. So here's the rash diagram again, I've taken the colours off to make it a little bit less confusing and imposing.

So furosemide is the cardiac drug we all know and love the best and you love it if you're like me, because furosemide is the thing that improves your patient's welfare today. So I have a patient comes in with new onset heart failure, they feel breathless, they feel a bit like they're drowning, you know, it's not very nice, and potentially they require hospitalisation for that. We give frozamide.

That patient can be looking much better within 1 hour to 2 hours, you know, of the first dose of frozamide, so we can see a significant improvement in those cases. So rozamide will reduce your circulating volume. So it counteracts the sodium water reabsorption of aldosterone and of angiotensin 2, of ADH by increasing your sodium excretion, or sorry, reducing your sodium reabsorption in the loop of.

Henley. So this causes the urine to become less concentrated because wherever sodium goes, if you put more sodium into urine, more water will follow. So we dilute the urine and pee out the circulating volume.

Frizamide also has some beneficial effects on pulmonary fluid uptake. It also can help reduce any inequalities in ventilation perfusion in the lungs. So it does some other stuff as well that helps.

If you give it intravenously, it's quite a big veno dilator. So that can help to reduce atrial pressure in the acute patient. So if you give risemide IV you can get a vena dilation in about 20 minutes, and that will help stabilise the patient quite early on before it even has a diuretic effect.

So rosemide IV is really good for the acute patients. Orally you don't get that same vena dilation, but it's less important because you're giving it orally, they're by definition more stable patients. Pimerendin is another drug we use frequently in cardiac patients, especially dogs, and pierendin helps to just increase cardiac output.

It's a positive inotrope, it's also an arterio dilator, so it reduces some of the vasoconstriction over here, which angiotensin 2 may be inducing, but it will help to increase cardiac output without increasing myocardial work. That's important because the heart's already failing, the last thing we want to do is make it work harder. We've got the ACE inhibitors, it's pretty obvious where they act.

They act on ACE angiotensin converting enzyme which lives in the pulmonary endothelium, and the ACE inhibitors will reduce the activity of ACE and therefore lead to more angiotensin 1, which doesn't do so much and less angiotensin 2, because the angiotensin 1 is not converted to angiotensin 2, and that's the big vasoactive compound. And finally we've got Spronolactone, which is a competitive antagonist at the receptor site to aldosterone. So Spronolactone inhibits the effects of aldosterone, it does have a mild diuretic effect because it reduces that water reabsorption, but longer term it seems to be very beneficial in reducing cardiac remodelling, and potentially fibrosis.

So again, just to, to reiterate, in the chronic rash activation, we can see Pimabendin helps reduce chronic rash activation. ACE inhibitors fit in here, as do spronolactone, or as does spronolactone. So when do we treat?

What's the rationale behind the decision making in terms of timing? This is where we're gonna specify about mitral valve disease, because this is the best studied disease in dogs. It's the most common heart disease.

There's a huge amount of data out there in numerous studies, and there's also consensus amongst experts on how to treat it. You probably know as well as I do, if you get two specialists into the same room, you often don't get a straight answer. But here we've got a panel of experts who have come to a consensus on recommendations.

So this is a real rarity and something that I think should be, paid attention to. The other thing with natural bowel disease is easy to identify because all these dogs have heart murmurs. So this is an echo of a dog with mitral valve disease, we can see we have the left atrium here, mitral valve in the middle, left ventricle, and the mitral valve looks sort of thickened and gnarled.

If we put the colour flow on, we see the green mosaic of turbulent flow. This is the jet of mitral regurgitation. And this is the left atrium.

Compared to the aorta. Many of you will know that the left atrium should not be more than 1.5 times the aortic size in dogs, and here we have a huge left atrium compared to the aorta.

It's probably 3, 3.5 times the aortic root size. So this is definitely a big left atrium, and we see the big left atrium occur before the onset of heart failure signs.

Cavalier King Charles spaniels are really affected by this disease. We see other breeds too, but Cavalier King Charles spaniels, just to give you an idea, have a 47 times increased risk of mitral valve disease compared to a non-pedigree dog. That's a shocker, isn't it?

Other breeds that are at risk. The most at risk of the breed in the UK is the Chihuahua, which has got 6 times, risk compared to non-pedigree, and a whippet, which is almost 5 times the risk of non-pedigree. So mitral valve disease in cavaliers really, you know, is a big deal.

It's got a prevalence of 100% on pathology studies in dogs over 10. So not all dogs over 10 have a murmur, I acknowledge that, but the prevalence on path studies is about 100%. That's, that's madness.

It can be diagnosed in 1 or 2 year old dogs. I sometimes see it in in dogs who are who are 18 months or 2 years old. And the males get the disease younger or potentially more aggressively.

It seems more rapidly progressive in cavaliers and other breeds, and it's certainly much more prevalent. And we know that in cavaliers, but also other breeds, sudden death is relatively common. In one study by Melanie Hazell, one of my colleagues, about half of dogs with microbial disease drop dead, .

And that's something that may not be appreciated by most vets, because maybe they never hear the outcome of these individual cases. And probably this is caused by a full thickness endocardial tear, actually a rupture of the atrium caused by the severity of the mitral valve disease, or a ruptured cai tendon causing a huge worsening in mitral regurgitation. Broader categories to define which drugs are at risk, 7 years old or greater, less than 20 kg in body weight, and they have an audible left apical systolic murmur.

This is based on large epidemiologic data. This is the consensus statement I talked about. It's from the end of 2019, and it's available freely online through the Journal of Veterinary Internal Medicine.

And this is a panel of experts on mitral valve disease. Between them there is little they don't know, that anyone else does. And they stage mitral valve disease on a four stage system, A, B, C, D.

OK, so A is at risk, B is where we have mitral valve disease and a mitral murmur, but no clinical signs. C is where we have overt clinical signs of congestive heart failure. And D is where we have refractory congestive heart failure defined by increasing diuretic dose.

Importantly, stage B is split up into the low risk and the high risk stage. So stage B1 and B2, and stage B2 is defined by particular parameters of cardiomegaly. It's the consensus recommendation, Stage A is monitor.

Stage A is just a cavalier that's been born and is walking down the street. You monitor for a murmur, you don't start imaging all those dogs unless they're for breeding purposes. Stage B1, if we find we've got a dog with a mitral murmur and a normal heart size, we can just image them annually.

We don't need to worry about anything more intensive. Stage B2, we know these dogs benefit from pre-clinical treatment. Stage C, we've got clinical signs of heart failure and therefore diuretic treatment plus more is indicated to control these clinical signs and improve welfare.

And in stage D we intensify diuresis, we do slightly more complicated voodoo, to, to improve the quality of life in these patients that often involves intensifying the medication regime. What's the evidence behind the pre-clinical treatment? You probably have all heard of this.

There was a large multi-center trial called the EPIC trial, and my kids refer to everything as EPI. So I find it funny that, this is the EPIC trial. It was published back in 2016 now, so it's positively geriatric.

There were 360 dogs enrolled over 10 centres on three continents, that's a pretty good for a veterinary trial. And this is the largest study of pre-clinical disease ever. Including in humans.

So that's quite a big statement to make. It changed how we view mitral valve disease. So the epic study, which this is the reference for here again, 2016 by.

The in the Journal of Internal Medicine, it's own access to read if you haven't read it, and they followed dogs to the onset of congestive heart failure. So this graph here looks at the two groups of dogs given Pimmoendin or placebo, and remember these dogs are all asymptomatic, but they do have cardiomegaly. You can see that over time there's steps down on this graph, and each step down is a dog either dying or going into heart failure, mostly was going into heart failure.

So you can see here that if you're in the blue group, you go into heart failure over less time than if you're in the green group. And that diverges pretty early on, and that difference between the groups lasts long term. Such that if these dogs were given immobendin, they lived on average 15 months longer than if they were given placebo.

That's quite difficult because average is, you know, half of dogs. About half of dogs do worse. So one way to think about it is that if a dog in stage B2 microbial disease is given Pimabendin, their risk of going into heart failure is 30% that of a dog who's not given Pimmoendin.

OK, so it's 1/3 of the risk, so that's quite an important statistic. The Epic trial is such a big trial that they've published 3 papers, so I, I call this the epic series, not that kind of epic series, nor that kind of epic series. But the 3 papers that came out of Epic, are quite important.

They're published every 2 years, and you know, it's almost like the authors have thought about this and plan. In advance. The first study was the one that we've talked about showing longer survival before the onset of heart failure, with Pimabundan.

The second was actually a validated quality of life score, was proven to be better in dogs on immo. So not only did they lived for longer before showing signs, they had a better quality of life and their hearts got smaller. And the third one wasn't really looking at emo versus placebo, it was looking at what predicted going into heart failure best, and they found the best predictor was something the owner can do for free at home, which is just wonderful, and that's monitor respiratory rate.

So we know from this series of papers that actually treating the pimabendin in stage B2 benefits quality of life and outcome. So identifying stage B2 is very important. We know that this improves survival, it improves quality of life, and it improves owner awareness, so they can monitor early and start diuretics earlier when they can when they need to.

So how do we identify stage B2? Well, radiographs. They are insensitive to early changes, but they're pretty good.

Vertebra heart score, greater than 11.5, is likely to indicate B2. And a vertebral left atrial size, a Vlas greater than or equal to 3 is likely to indicate B2.

So what do those things mean? Well, let's take this dog, this dog has got heart failure. Let's look at the vertebral heart size, we measure the long axis and the short axis of the heart like this, and we hear we're getting a vertebral heart size of 11.5.

So that is indicative, or suggestive, strongly suggestive this dog is in B2, it's got a left atrial dilation. The problem with vertebra heart size is there's some compound error, taking two measurements, adding them together, if you get them both a bit wrong, you can end up being quite a big difference. But you can measure one measurement of vertebral left atrial size, which is measured from the bifurcation of the trachea here from the carina, to the dorsal margin of the corral vena cava where it intersects the heart.

I said anything above that line is the left atrium, there should be nothing above it, but if you measure the width, that quantifies it. And 3. Here we've got 2.8, cos I'm very honest, I'm telling you what I genuinely measured, but 3 suggests stage B2, so you know what, I'm, I'm gonna go with this dog being in B2 based on both the vertebral heart size and the VLAS.

So if we're using echo, we need left atrial dilation and left ventricular dilation. So the left atrium to aortic ratio should be 1.6 or greater, and the left ventricular internal diameter in diastole normalised for body weight cos obviously a big dog is different to a small dog, that should be greater than 1.7.

Looking at another study, this is a really useful thing. This is looking at murmur grade and which dogs with different grades of murmur would benefit from treatment. And actually if you look at the graph here, dogs with a low grade murmur grade 1 to 2, only 10% or less would benefit from treatment, so 10% or less were in stage B2 or C.

Grade 3 murmurs, it's more than half. Grade 4 is about 80%, and grade 5 or 6 murmurs is 95% would benefit from treatment. Now I'm not saying you just treat them based on the murmur, what I'm saying is if you've got a grade 3 murmur, that's very different to a grade 2 murmur.

So that means we're going to be much more likely to help a dog with a grade 3 murmur. So if you've got an asymptomatic murmur, if it's an older small breed dog, it's probably mitral valve disease, grade the murmur. If it's grade 3 or louder, recommend imaging.

If it is cardiomegaly, treat the pyabendant based on results of those epic trials or the epic series of papers. If there's no cardiogaly we just. Monitor and monitor the imaging and if you do have a radiograph that can act as a baseline.

In stage C we treat with frozen mind. We can treat controlled dyspnea. So in the acute patient we can give it IV or IM.

IV has that advantage of renal dilation. And once they're chronic or or they're stable, if they come in and they're stable, we can just treat with oral stabilisation at home. And there's some nice data out there suggesting that a dose of 1 mg per gig twice a day in dogs has good diuretic effect.

We start somewhere between 1 and 2, and often we'll titrate that to the lowest effective dose based on owner monitored respiratory rate. What else do we do in stage C? Well, if they're not already on Pimendin, they should receive it.

We know that it causes big benefits in stage C mitral valve disease. We know from some invasive studies that actually reduces left atrial pressure. And we can use RAS inhibition.

So ACE inhibitors, papers from back in the 1990s show a benefit of an ACE inhibitor in canine heart failure, in addition to furosemide. And a paper from 2010 suggests that spronolactone may have a survival benefit. It's not an amazing paper, which is why I've not gone into detail.

On it, but it suggests that there is some benefit there from using spronolactone. So the consensus recommendation is that immobendin, ACE inhibitors, spronolactone, and frozamide should be first line therapy for dogs with stage C mitral valve disease. The same is true for DCM with overt clinical signs, and in DCM we also know that dogs benefit from pre-clinical pimaendin treatment.

It's just harder to identify the disease in those patients early on because less than half of them have a heart murmur. So they're much more challenging and therefore they're much, less comprehensively studied than dogs with mitral valve disease. But the same general rules are true if you identify the disease.

So just to summarise, this is where our drugs are working in heart failure. So when do we treat nitro biopsies? Well, in stage B2 we give himendin.

In stage C we give frozamide and immobendin. And if they can afford it or they tolerate the tabs, the tablets, spranolactone and an ACE inhibitor. We're going to quickly talk about kitty cats, cats versus dogs.

They are different. This guy that I saw just yesterday does not want you to consider him along with dogs. He is a separate species, and he will remind you of that as often as possible.

And for that reason, Virginia Luis Fuentes and a bunch of other amazing feline cardiologists published a consensus statement at the beginning of 2020, looking at, classifying, diagnosing and managing cardiomyopathy in cats. Very similar to the mitral biel disease progression, we have an ABCD system and we have stage B divided into B1 and B2. So B2 is where we have left atrial dilation, therefore these are at risk.

The other main difference is that they can have clinical signs of heart failure or arterial thromboembolism to be classified as stage C. So what are the differences? Well, in cats, HCM is the most common myocardial disease and that's a disease of filling, we know that.

Mitral valve disease or DCM in dogs is a disease of volume overload or output. So the end result is the same, but the pathophysiology is a little bit different. And cats also have a greater risk of thrombobolic complications than .

Dogs do. I, I think I've once seen a dog with an intra-attrial thrombus, and that dog didn't have mitral valve disease. It did have DCM and atrial fibrillation, and it was a huge dog to Bordeaux.

So I have seen those before in, in, in dogs, but they are super rare compared to cats, where we believe that probably 10% of cats with heart failure caused by HCM develop a thrombus. So in terms of response to drugs, there's some interesting data out there, maybe 3 years ago I would have said to you there's a bit of an evidence vacuum in cats, but that's not the case anymore. We know that most cats do not benefit from ACE inhibitors when they're in heart failure.

We also know that Spranolactone can be helpful, but there's not a strong proof of benefit. We know it's safe, but there's not a strong proof of survival benefit. And Pima Bendon, based on a paper published just last week or the week before, is not useful for most cats with HCM.

These are really important, research studies. So, this is a paper from a couple of years back now looking at Benazepril in cats with heart disease, and this is a prospective randomised, blinded, placebo controlled trial. Wow, why wasn't there more made of this, I heard you say, because this is a rarity in veterinary medicine.

Well, the answer is it's not a great trial. The inclusion criteria were slightly loose, so not all these cats were in heart failure. It was a bit of a difficult paper to interpret.

What we can say. This curve on the right here is slightly different to that survival curve. Before in the previous curve, they dropped down when they died or or or or went into heart failure.

Here, it steps up. This is like a mortality curve, if you like. And you can see here that actually the two lines, the Benazapril and the placebo group, are very similar to one another.

OK, so there's no significant difference in i.e. Intensifying treatment, going into heart failure, dying.

There may be a subpopulation of cats with cardiomyopathy who benefit from ACE inhibitors, but we don't know who those are based on this data, and what we can say is that most cats don't benefit. The size of cat study was looking at spronolactone in cats with heart failure. Again, there were some problems here, the groups were not evenly matched, and it turned out the cats who were in the placebo group actually had much worse heart disease than the cats who were in spronolactone.

So the study said, oh well, spronolactone actually improves survival. You can't say that because the spronolactone group had less bad heart disease and therefore they might have just lived longer anyway. So there's some problems here, but it appears to be safe and well tolerated, and we don't know if it helps survival or not.

Per Bend in this paper, as I say, is very recent, and we can see from the study curve here, there's no difference in the time to endpoint, in these cats. It's much smaller than the Pyendan studies in dogs, but we can see there's no difference in time to endpoint, and that suggests that pimerendin is not useful for the average cat with cardiomyopathy, with HCM, I should say. However, look at this curve, the Pimerin is the red line, and they seem to live longer and do better.

This is a subpopulation of cats who don't have outflow tract obstruction. So probably there are a number of cats who do benefit from Pinabundan, but we need to echo them and make an assessment of their function before we know if that's gonna be a valuable treatment option or not. Is the drug safe?

It appears to be safe, yes. This is looking at clopidogrel. Now we talked about thromboembolic embolic consequation consequences, excuse me, and clopidogrel is an antiplatelet drug which reduces the risk of thrombus formation in cats with cardiomyopathy.

And here, again from the survival curve, we see one curve, the red curve, live longer before dying or getting another thrombus than cats who are on the blue curve, and the blue curve is aspirin and the red curve is clopidogrel. So we know clopidogrel is effective and it's better than aspirin in preventing ATE. How does this come back to our cats?

Well, we know that cats with a big atrium are at risk of thrombus formation, even without having had an ATE before and without having clinical signs of heart failure. So this is the B2 group, this is the pre-clinical group. So we don't treat them the same as dogs with mitral valve disease, but we do treat them, we treat them with clopidogrel.

Once they display clinical signs of heart failure, or ATE, we treat them with frozamide and clopidogrel. Frozamide only if it's heart failure, OK? Now we may choose to treat the pumabendin, we may choose to treat the spronolactone depending on various factors, and that's where I think the expertise of someone with experience in feline cardiology comes in.

We don't treat with ACE inhibitors, they're not beneficial to this group of cats. So, wrapping up key points, well, first of all, frozamide should only be prescribed in heart failure, it's not gonna help your asymptomatic patients, it might actually worsen the situation. So it's important to be able to identify heart failure confidently using different imaging modalities.

Staging mitral valve disease and feline cardiomyopathy is absolutely vital because you have to stage it to make a decision about what to do to help your patient. And that's reliant on combining our clinical findings, history, physical exam with cardiac imaging findings. And the treatment for stage B2 and stage C is underpinned by good evidence now in both cats and dogs.

Heendin is useful in stage B2 mitral valve disease and in stage C. It's not beneficial to all feline cardiomyopathy, maybe a subset. ACE inhibitors are beneficial in stage C mitral valve disease, they're clinical signs of heart failure, and they don't seem to have the same benefit in cats, so they're a waste of a pill in a patient who may not be very compliant.

Spronolactone is beneficial in dogs with stage C heart disease, and the consensus panel recommends using it as part of first line treatment. We don't tend to use it first line in cats, again to minimise the number of pills that they are receiving. And finally, clopidogrel is useful in cats with stage B2, cardiomyopathy and stage C, but there's no requirement for using clopidogrel therapy in dogs just because of species differences and differences in pathophysiology of disease.

So thanks very much. I ran slightly longer than I intended, which may cut our time for questions a bit, and I apologise for that. But I'm more than happy to take some questions now if we do have time or via social media, I'm available to to take questions on my Instagram account, which is at vet_cardo.

There's no conflict of interest there because I don't make any money out of that at all. It's purely to share some fun pictures and some education. So thank you very much for tuning in.

And a great picture of John Lennon at the end as well, so yeah, I thought you'd like that. All good, all good. Yeah, no, that's fine.

So we've also got the Hoover app, Kieran, which I don't know if you have downloaded. But, people can go there. But obviously Vett cardio is also, it's well worth following, so do, do follow that as well.

I've, I've just been, found my one of my editions of In practise, which was a whole addition on cardiology, in practise focus, sponsored by Siva. And of course, first article. By somebody that we we all know quite well.

Doctor Doctor Borge, yes. If anybody er doesn't get in practise and would like this copy, just message me on LinkedIn with an address and I'll get it over to you so you can enjoy it as well. I think we are tight on, on time, but if somebody's got one question, let's do one question, then we'll have to take that offline because we have, you'll have coming up just after, just on 12 o'clock to talk about dairy sheep, which I'm looking forward to as well.

I'll be tuning in for that one. It's a, yeah, I think it's, it's very interesting, it's a, it's a growth industry, so it'll be interesting to see what he has to say. Richard is saying, what about blood test for enlarged heart pro BMP?

Yeah, that's a super good question. So NT pro BMP is a molecule which is released to counteract the RAS. So we talked about the RAS, and there's a natural braking system like there is often in biology, which is the pro BMP system.

The problem with pro BMP is he's not very good at stopping the rash, so we use it as a biomarker rather than as, say, a treatment. We can't give it to, to reduce RAS activation. And it is elevated in dogs and cats with heart failure, and also it's elevated more in dogs and cats with worse heart disease compared to early heart disease.

So theoretically, it sounds like it's going to be a really good discriminatory tool. The, the problem with it is there's a huge overlap between groups. So between, say B1 and B2, there's a massive overlap on the box plots there of of the pro BMP.

So it's not a very good, decision maker in terms of when to start treatment. It may be useful in those patients who are asymptomatic with a murmur, where an owner says, ah, I'm not really sure what to do, and we check on antiro BMP and it's very high, we say, OK, you know what, actually it would be worthwhile imaging, but we would never recommend treatment based on a Pro BMP. That's great.

Kieran, that's fantastic. Do, do ask questions on the Hoover app or but do also follow Kieran on at Vett Cardio. I will check in with the Hoover app this afternoon and over the weekend.

Yeah, that's brilliant. Thank you so much, Kieran. Just, people were asking, it, it was, it was a focus edition, so it was, I think it was part of June 2020, so I, I think there was probably a, a full in practise magazine, but this was just looking at cardiology, congestive heart failure in dogs and cats.

So if you want more reading, this might be a nice little magazine to follow. So June 2020, but I'm happy to send this off to somebody of you. Go onto my LinkedIn profile and send me your address.

I'll post it out to you. Kieran, thank you so much, thank you so much for supporting the conference. Always great to listen to you and I hope you have a great weekend.

Take care, bye bye. Welcome to my presentation for on my live one anyway, for VC 2021. As Anthony said, we're gonna talk about improving your ovulation prediction skills.

As if any of you have been to a presentation that I've done, you know, I like to try and keep these things as interactive as possible, so. It's obviously a little bit of a challenge in the environment we've got, but we've got some poll questions which I'm, I'm hoping will work, and they'll give you a chance to make a little bit of input and keep it as interactive as possible. So, why pick this as a, as a topic?

Well, yes, everybody perhaps often thinks about pregnancy detection, and dealing with problem mares in equine reproduction, but after practising it for more years than I care to remember, really predicting ovulation is the. Is, is the core of of what we do, that really forms the bulk of, you know, a typical day if I'm looking at a large number of mayors, the majority of them, I'm going to be looking at with an aim of trying to predict ovulation. So what I'd like to share with you over the next 45 minutes, an hour or so, is what I've found useful over the years to try and help me improve my ability to predict ovulation.

I, I'll try and avoid a didactic presentation of just talking to you and I'll try and put in some sort of. Anecdotes and little tips that I've found useful which are are either you don't find them in textbooks or you, or, or they don't, they, they don't come across very well in text. It's better in this speaking format where where I can engage with you via that way.

As Anthony said at the beginning, I set up equine reproductive. I, I, I worked for a fair time at the vet school in, in, in the Royal Vet College in London, and did a PhD there on problem mares. I then went into private practise, and 20 odd years ago, we set up equine reproductive services, which now, after me starting on my own, is now, a, a, a core of 6 vets, if you count me still as a consultant.

And then of course, during the breeding season, we get more people to help us. So that's a little bit of my background. I, I have written a number of or or edited a number of textbooks, which will contain more information than we're going to be able to get through in this session today, .

Many of those are available, and if not all of them. I mean, current therapy and equine reproduction is several years old now, but I still think that's a great book for practitioners and, some of the techniques we'll talk about and tips we'll share today, you'll find in that. In that book.

Our bigger textbooks are McKinnon's and Squires, Wendy Vahl and Dickon Varner's equine reproduction book, which, I've done a few chapters in, that that's a massive, cover all type book. And then a neat little book which perhaps isn't quite so well known, an Atlas of equine ultrasonography, which is equine work in general, where ultrasound is applicable, and I did a chapter in that on the problem. So, when we're doing a gynaecological examination, first and foremost, we want to be safe.

We want to be safe for everybody. Preferably, we want stocks. Stocks are just the term we use in case it's not translating well, stocks for, you know, Restraining the mayor, they can be.

These, these are moderately fancy ones, but you can have a much simpler type, some kind of restraining device for the mayor. Not only does it mean you're safer because the mayor's restrained, it means you can have your ultrasound machine nearby, and very importantly, of course, in these days where we're focused in on. Disease, precautions to avoid it, and so on.

It's much easier to do everything in a clean environment. If we're bringing the mare into the one place where we're working, we can have gloves in there, we can sanitise that area, and so on and so forth. So, I think, even if you're not doing large numbers of mares, you should encourage any client who wants you to examine a mare, to, to provide you with a safe environment and I, I think doing it round the corner of a, of, of, of a box, not only is it, is it not particularly safe, I don't think you relax very well and it's much easier to make mistakes.

So, try and get a a a set of stocks to examine them there in a safe. Clean environment. Work methodically, as you can imagine, is important in many aspects of veterinary medicine.

The same applies to follicle evaluation. Work methodically, have an organised system of palpating. For me, I, I go and, and palpate the left ovary first, then the left uterine horn down to the uterine body, up to the right uterine horn, and onto the right ovary.

And then I repeat the whole examination. For a second time and check the uterine body on the way out of the mare. Of course, if you want to start with the right ovary, that's absolutely fine.

But whatever, I think, develop a methodical system. And I'm sure you all know that, just be careful and gentle with mares when you're examining them. If you're not able to palpate a structure or the mare's straining quite a lot, well.

Come back another day or another time. Graphically, you can have a look at that. Here's a sort of basic palpation technique.

I actually generally palpate mares with my thumb folded inwards. So, I just think there's then less of a risk of doing some iatrogenic damage to the rectal wall of the mare. And I run my, four fingers, for me, my left hand, I palpate and scan measure my left hand, You can palpate the relevant structures.

Very, very, very important, to always palpate the me thoroughly before going in and doing your ultrasound exam. Several reasons for that. Probably the two most important ones are, although you can see in this graphic we've got or image we've got here, it looks like the uterus and, and, and left and right ovary are all laid out neatly.

In, in, in, in the real. Time situation, of course, they may all be intertwined and you know, displaced by a full bladder or full intestines. And so doing a basic palpation first allows you to organise a structure such that when you go in and perform your ultrasound exam, everything is going to be in a neat, laid out system for you.

The other reason is, you should make an accurate assessment about how the structures palpate. Ultrasound gives you a massive amount of information, but of course it doesn't give you a direct assessment about the texture of structures. So how soft the follicle is or how firm the uterus feels, for example.

That's a palpation skin. So, after our palpation, we're gonna go on then to do an ultrasound examination, and as you can see, I have my thumb folded over the bottom of, of the cable of the transducer, and I think that's better than having your thumb sort of stuck out when I guess there's a, an increased risk of causing some rectal damage, which we don't want to do. And then similar to the palpation we've just performed, we have this methodical approach, so for me, it's onto the left ovary, then I do the left uterine horn, down into the uterine body, up the right uterine horn, onto the right ovary.

Then I. Repeat the whole process coming back down the right ine horn this time, try and body, back up the left Uri and horn, and onto the left ovary. And by doing everything twice, I think we minimise the risk of any structures being missed.

Now, part of being methodical is we've got to record that information somewhere. Now, we don't want to record it on the back of your hand, the back of the rectal glove box, whatever. You need some kind of system.

We actually use a loose leaf and individual sheets of A4 paper in a ring binder file for the, for the largest stud farms. You could use a smaller book or something for, for, if you, if you've only 2 or 3 mares to look at at a premise. But on the large stud.

Farms we go to, we tend to have each mayor with this mere gynaecological record. We, we would have the name of the mare, obviously, to identify it, age, breed, which stallion she's going to, which stud farm she's at, how she's being bred, so natural for the thoroughbred mares, then with various types of semen for the sports horse mares, maybe even embryo transfer mare. The owner's name and address, which helps us back at the practise for billing purposes.

Contact details probably would be email address now, of course. History, is she a maidenma, just for those of you who, who, who may be listening from overseas, maiden just means being bred for the first time. Barren means not pregnant.

Generally it means, perhaps left empty last year, no one tried to go in foal last year, or people tried and failed. Or she's an info, may that fo this season, and then we give the foaling date. And then we record any endometrial cysts, the presence of them, .

And This system works well for us. I'm not putting it down as the approach that you have to use. You use whatever works for you.

But this kind of recording system has worked well for us. I'm not showing you it's on this, this image slide here, but we would have 6 of these boxes, 123, laid out. And then we have a silhouette diagram, as you can see highlighted by the big arrow, LO and right are just obviously left ovary right ovary.

The date of our examination, how the cervix feels, cervix such an important structure in the mare. Underrated by veterinary surgeons. Too many colleagues don't make an accurate assessment of the cervix.

We'll come on to that a little bit later, but. You know, nail that one down as well. Checking the cervix, if you don't already do it as a, as a, as a a important part of every exam you do, then, I, I would suggest you did.

Uterrus, edoema pattern in the uterus, we'll talk about edoema, may even be some free fluid within the lumen of that uterus. Any treatment we're giving to the mare, if it's a post-breeding check, if we're gonna do a lavage or if we're gonna give oxytocin. If it's a pregnancy check, preg scan, well, we'll give the details of the pregnancy, how large it is, whether we can see the embryo, whether the heartbeat looks good, and so on and so forth.

Now, on the ovaries, we actually have a silhouette diagram there of the ovaries, so we can actually record, draw in on those ovaries. Schematic representations, what we actually feel, and that's really what I've put by that arrow there. What do we record in the ovaries?

Well, we record the presence of the corpus luteum. That's another thing I think has served me so well over the years, and an area where I find some colleagues don't quite see the significance of doing that, but every time you examine a mare, be it for follicle evaluation, be it for pregnancy testing, always record the presence of a corpus luteum in the left or right ovary. And then of course, the title of the talk is follicle evaluation.

So we're going to have to record the presence of any follicle. Now I've put in there a question mark. Any follicle over what size?

Any follicle over what size in millimetres do you think you could record? Now, we're going to try one of the poll questions here. You can see I've put above what size should follicle data first be recorded.

So have a think. In your practise, you first record the follicle, 15 millimetres, 20 millimetres, 25, 30, 35, or 40 millimetres. Now, I can see quite a few of you there not voting.

Try to remember it's all anonymous, so, we can't see what you, and you've got to be quite quick with these, a little bit of a snappy thing. We're not gonna have it lingering too long. I think you get 25 seconds, half an hour.

We want them to be bold, don't we? Yeah, I've gotta be bold here guys. Nobody can, nobody can see you.

So this was a little starter for 10 for you. We've got, we've got a few more coming, so you'll be able to see those then. Do you want me to share those numbers or can you see them yourself, Jonathan?

I can see them, Anthony. Can everyone see those? I don't think so, so it's worth going through them.

OK. OK, what we found was we've got 15 millimetres, we had a number said that, 20, a number said that, 25. The majority of us went for 25, some for 30 and some for 35.

Now, I should perhaps say here, I was talking about a typical thoroughbred or warm-blood mare, so obviously if you've got different sorts of mares, you may. You know, there could be a difference, heavy draught mare, they may be over 40 millimetres, smaller pony type mare, they may be younger, so, you know, this is how these things, are. And I, I should also say there probably isn't really a right or wrong answer, .

So, as it happens, . I would be with the people who, I think that I can share results, so can I, yeah, yeah, we've talked about those, you don't have to linger those, but I've shown you those results there. Most of you went for 25 millimetres now.

I'll just close that down and go on to the next. Ignore these, these are, but this is quite interesting actually, because this was a poll, back when, back in the day when we could do live presentations in front of people, and here are pretty similar stats actually, which I think's good, that, that's quite an interesting thing to talk about. The majority of you have gone for 25 millimetres.

Almost half of you in this case, and I think that was a similar figure in in what we had. And I think that's, that, that, I'll nail my colour to the mast, if I put it there. That's what I do.

Any follicle over 25 millimetres. Now I'm not saying those of you who went for 15 millimetres or 20 millimetres are wrong, I think you will, you're just making quite a bit of extra work for yourself because whilst a follicle can ovulate. Under 30 millimetres.

It's very, very rare. Most times, that follicle will be 30 millimetre plus. So, I don't begin to recall the follicle until it's over 25 millimetres.

Now, I did see one or two of you have gone for 35 millimetres. You guys will be a little bit bold. I think if you're doing that, because I think there is a risk if you don't begin recording the presence of that follicle till it's achieved a diameter of 35 millimetres, you are at risk for missing some of those ovulating.

So, all in all, for your typical thoroughbred warm blood mare, I'd go with a follicle over 25 millimetres. So, whilst we're on follicle diameter, I want to make this point which doesn't always get picked up. I, I'll have, I realised over many years colleagues would ring me up and say, John, the follicle's gone from 37 millimetres to 39 millimetres.

Do you think I should be inseminating that mayor, or do you think I should be ordering chilled semen, sending her for covering? They were putting a lot of emphasis on the fact the follicle had increased in diameter by 2 millimetres. Now, I, I don't, clearly that follicle gone from 37 to 39 millimetres was close to ovulation, and when a follicle's close to ovulation.

Well, I don't think follicle diameter. Is particularly useful because when the follicle is close to ovulation, it's become soft and it's changes its shape. It is no longer spherical.

So a follicle diameter is a very useful tool early on through to the middle of the follicular phase. But as the follicle is in the last 24, 36, 48 hours before ovulation, I think we've got to look at other things because the follicle is so soft, it doesn't have a spherical shape. So, let me have another look, if that isn't quite clear what I'm meaning.

Follicle diameter is a useful tool, whilst the follicle retains its spherical shape. Look, this structure is pretty spherical. It's a roughly 3 centimetre follicle.

Just shows you, you only really need to measure 1 diameter, which is all we tend to do in practise, because they're so similar. So, 28 millimetres that way, 29 that way. This is a follicle, perhaps on day 234 of the follicular face.

It is spherical, so we can accurately measure that diameter. Have a look at this follicle here. This is a follicle probably within 24 hours of ovulating.

What do we think of that follicle? What if I said to you, let's measure its diameter? Well, yeah, if I put the calliper from there to there.

It's gonna be different than if I put it there to there because it's elongated, it's softening at the bottom. So my point being, when we're in this phase of 24 to 36 hours before ovulation, I don't think follicle diameter is a particularly important parameter to measure. I think we want to look at these other ultrasound changes.

We want to look at an increased egogenicity of the follicle wall. We want to look at these small ecogenic particles that appear in the follicular fluid. They become better indicators of closeness to ovulation when we're in this last 24 to 36 hours, because, Diametter itself isn't isn't the important characteristic, and I don't think that comes across very well in a lot of, a lot of books.

So I just wanted to make that point for you. Now, mayors always break the rules, as, as many things in nature do. So this next series of slides is, is to try and make that point to you, because not all mayors read the textbook.

So let's have a look at what's going on here. This is an ultrasound image of the left ovary of a mare. What can we see?

Well, I, I've obviously put a set of callipers top and bottom, and I've come up with 2.68 centimetres, 27 millimetres. What are we thinking of that?

Oh, pretty small, we wouldn't ordinarily think that was close to ovulation. Because, you know, crikey, I said, well, we only begin recording them at around 25 millimetres plus, so I would be expecting us to, examine this over the next, +23, maybe even 4 days before it gets up to 35, 38, 40 millimetres, and then going on to ovulate. But not so.

We've got a 27 millimetre follicle, but what do you think of its shape? What do you think of ecogenic particles in it down there? So we've got a mixed message here and and that's that's life.

Welcome to the world of mares. We've got a mare here with a relatively small diameter follicle, 27 millimetres. But other signs are giving me the impression she's closer to ovulation.

Oh, ain't that a shame? Well, yeah, maybe, but there's nothing we can do about it. We've got to make as clinicians a judgement what we're gonna do here.

So the overarching question for us in this situation, and we've got another poll question here, so I think the clever folks at VBC will be able to put up a poll for you, assuming this mayor has an edoema pattern and an open cervix, so I'm setting the scene. She, she's not, it's not a luteal follicle. It's a, it's an edoema pattern and an open cervix.

When do you think she'll ovulate? Within 12 hours, 12 to 24, 24 to 36, 36 to 48, or above 48. Now you've gotta, you, you've got to begin to sharpen yourselves up a bit.

We want to try and get up to, to most, we've got quite a lot of you lurking out there. I mean, it's, it's, you know, forgive me if it, English isn't the first language for some of you, and that's fair enough, but. Shall I, oh, he's in, in my, my hands is Anony to end the polling.

Well, I think we've, we've probably had long enough there, yeah, so good, that's perfect, that's perfect, and you can see those. Yeah, within 12 to 24 hours. That's good.

That's, that's what I think. So if it's any consolation to you that the the the the biggest percentage of went within 12 to 24 hours, that's what I think. But you could well be wrong with this man.

It, it could conceivably, it could certainly be within 12 hours, could be within 36 to 48. So, I think everybody who voted here is, is, is right. But sometimes we have to, we use an expression nail your colour to the mast, or, you know, we make a.

We make a judgement, and I think within 24 to 36, it's possible within 12 to 24 it's possible. So, I don't know, wherever I was last time. Yes, they were a little bit braver.

They were thinking this mayor, the biggest group were 36 to 48, wherever I did it last. I think that's a little bit, risky. I, I certainly would be either 12 to 24 or 24 to 36.

I, I, I wouldn't be going into 36 to 48 hours, but hey ho, what, what do I necessarily know? The point is, nobody knows for sure with that. But we've got to make a judgement.

So, I, this looks like a poll question, but guys, it isn't, it's, it's just an ordinary slide. I did poll it at somewhere, but it would have been made for the session too long. I didn't want to go over time.

So, I took, I, I, I'm all having a theme on this same slide. We've got a man, which is presenting to us with a smallish follicle, so we've got a smallish diameter follicle in terms of thinking she's close to ovulation. But we've got other signs saying.

She could be close to ovulation because we've got a follicle change in shape, and we've got ecogenic particles towards the bottom. So, that's why in the polling question, I got you all to have a think about when you think that may may ovulate, and a number of you went for 12 to 24, some for 24 to 36, 1 or two of you above 36 hours, some for under 12. So, who would breed this mare with fresh semen or natural cover if she had edoema and an open cervix?

Now, this was . 2/3 of people, wherever I asked, or 60%, let's put it that way, not quite 2/3, said yes, they would breed her. A good 40%, almost half, said no.

Now, I would, with fresh semen on natural cover, I would be firmly of the opinion to breed this man. Why? Because the semen's gonna live with natural cover or fresh AI minimum 345 days.

So even if this follicle is gonna take a little bit longer to ovulate, then it's softness and ecogenic particles would think. Well, the semen's still gonna be alive, so I would argue, why take the risk? Let's get this mare covered.

Or inseminated with fresh semen, so I'm making that decision to go ahead and breed this mare, because of the breeding system we we we we we we we we we're selecting. We're using fresh semen on natural cover in this example. I, and I think all these, these, talks are going to be available on a, on a demand basis.

So if, if any of you are wanting to go back and feel so inclined to look at them again, I'm, I'm pretty sure you get the opportunity to do that. Anthony will confirm that at the end, I think, but I'm pretty sure you can. Because it's quite a conceptual set of slides, is it, but I think it's a good way to illustrate the often problem we get or or situation we get of a mare and, and the follicle diameter not quite correlating with softness and other other things in there.

So, remember I said I would breed that mare with fresh semen or or natural cover. Who would breed this mare with chilled semen if she had edoema and an open cervix? Now.

When I polled that, yes, more skewed towards not doing it, because, and I think that's probably right because. I, I, certainly the system in the UK, and I, I don't know whether the majority in the UK or wherever you are, semen come that we order chilled comes overnight. You can make arrangements to pick it up directly, but by and large, it comes overnight.

So, the point being here really, look, you know, if, if that mare's ovulated by the time we get the semen, well, the whole thing's a little bit wasted. It seems to me it's going to be very difficult to predict what that follicle's going to do. So, there could be a, you could back yourself and think, oh well, I'll be able to order that semen and and get it here tomorrow, and she still won't have ovulated.

So it's a more difficult decision was the point I was making, to decide to breed this mare with chilled semen. Easier decision for fresh because go get it covered, we know the semen will last. With chilled semen, we've got the problem of ordering it in a day's time, and then once we've inseminated the mare, she really has to ovulate within 18 to 24 hours of that semen going in.

Now finally, in this little scenario, who would breed this mare with frozen semen if she had edoema and an open cervix? What I was looking for here, which was quite good, was no, because with frozen semen. You've got that semen sitting in the tank.

You don't need to pull it out. Don't need to inseminate that mare until she's ovulated. So if you see a mare like this, which has got, a little bit of of differing signals, it's giving you a relatively small diameter, but other changes such as shape and follicular particles are giving you the clue she's close to ovulation.

Then what you have to do with these mares is just examine them every 6 to 8 hours. There's no way around that. And don't inseminate them, until you detect an ovulation, because you're examining them regularly with the, you know, she can only have ovulated at most, 456 hours ago, so the ocy should still be viable, so you can quickly take your frozen semen out of the tank, thaw it and put it into the mire.

So that's, that's trying to illustrate how, not only can we sometimes find mas with different parameters indicating, some, one or two indicating a little bit off ovulation, others indicating close. But our decision as to what to do may depend. On your breeding system.

So, there's a lot to think about really with these things. Now, we said follicular particles within the follicle. Is a sign of that mare being close to ovulation, and that is true.

But what do you think here? What can we see here? We've got a 6.05, so I've measured this follicle at 6 centimetres, 60 millimetres.

Now, yes, mares get large follicles, often ovulating around 40 millimetre to 45 millimetre. 60 millimetres is a big follicle for a, for, for a thoroughbred mare, and it's ringing a bit of an alarm bell for me. I, I don't, I was gonna say I don't like to see a follicle that big.

I'm not sure like is kind of the thing. It's, it's not to do with a preference. It's, it's, I, I'm, I'm a little bit, I find a follicle of that size hard to decide what it's going to do.

And I find this harder still in this situation because there is a widespread number of follicular particles. Not only they aren't just in the ventral margin, look, they're kind of spreading almost throughout this whole follicular structure. I don't like to see that neither.

I would sooner we just had these ecogenic particles in this lower margin of the follicle. I don't like to see them widespread throughout all the follicle. So I'm maybe giving you a little bit of a clue.

I think we've got this as a, a polling question, a little bit of an easy one, so let's try and get nearly all of you voting here. After all, it's only a binary choice, so you can take a, take a guess. Will this mare ovulate normally?

We've got a 6 centimetre follicle and quite widespread follicular particles. Now, we've got 11 out of 40, we want to get up better than that. Come on, some of you are lurking out there or.

Not voting, so, yeah, come on, let's try and get at least above 20. Tempt any of you out? Nearly, nearly, it's just like waiting for the last.

I've got it to 18, OK, we'll call her. We'll end it there for you. 84%, good.

I, I say good, I don't know, you could, the yes camp could be right, . My feeling is that that mare won't ovulate normally because I think 6 centimetres is too big, and I think the follicular particles are too widespread. So I don't know for sure, .

I don't know for sure, but I think. I would be in the no camp, and wherever I was, then, yeah, not quite so much. I, I think I'd be quite firmly in the no camp, but could be wrong.

You could go back to this mayor tomorrow and. There there are whites you could even be ovulated, but I don't think so, and the two reasons I don't think so are the size. I think it's in inverted commas too big, 6 centimetres, and.

Too many ecogenic particles, so. Yeah, I'd be in the, I'd be in the know. I don't think she will ovulate normally.

But I'll just make a note, in my, in that mere gynaecological record, I would put query hemorrhagic follicle. We're not going to talk about abnormal follicles today, but that's what I'm thinking. And those of you who do a reasonable number of mares will know what what we mean by hemorrhagic or anovulatory follicles.

That's, that's what I will be tending to think that follicle is gonna do. It's gonna become an anovulatory hemorrhagic follicle, not ovulate normally. But I could be wrong.

Not very often, but I can be. I'm just gonna try and show you it graphically here, similar sort of thing. I'm gonna block this in a minute, and look, try and stir up those.

I'll just show you that again, maybe we'll, we'll try and go to that, look, just having a look at this video. Lot of particles there in some sort of almost like clumping things that could be a bit of an artefact. And it was quite large.

Look at this one, Stranger still, huh? I mean, you know, it's always hard when you look at structures which look quite bizarre. That, that, that structure looks quite bizarre.

But in fact, this was just a hemorrhagic follicle. It was referred into us at the practise as as a granulosa cell tumour and arian neoplasia, and I, I can fully understand that. It's very hard, .

If you don't perhaps examine large numbers of mares to think, oh goodness me, what on earth is this on this mayor's over, it's got to be something. You know, it's something large, it's 6, 60 odd millimetres. It's got all these bands in it.

Oh, I, I, I, I remember about granulosa cell tumours. It'll be a granulosa cell tumour. Well, it isn't this may, and again, we can't go into a talk on, on the ovarian abnormalities.

You would notice I did a little bit of that blotting with the, with the transducer. As a, as a rough rule, a helpful guide you might find, if those strands move around when you beot them. That always steers me away from being a granulosis cell tumour, and much more likely to be a hemorrhagic, and ovulatory follicle.

Of, of course you, you look at the other ovary in a granule cell tumour, is it very small, and of course we can do blood samples for . In, in, in Hibbing and all kinds of things. So, you know, we can diagnose granulosa cell tumours, relatively straightforwardly, but you get a quick clinical impression, and if you can blot it and those strange looking strands wave around, then it's unlikely.

In, in, in my experience to be a granulosis cell tumour, it's much more likely to be. An anovulatory follicle. OK, we're moving quite nicely through for time.

Now, endometrial edoema. I said we would talk about edoema at the beginning. And great friend of mine, Juan Samper, some of you may know, may have been lucky enough to hear him.

Juan did two papers. He is actually two presentations at the American Association of Equine Practitioners, the AEP. So in 1997, quite a few years ago now, when first documented, or was one of the first to document that there's an edoema pattern.

As the mare progresses through the follicular phase, I'm gonna come on in a minute to what we mean by edoema, I'm sure most of you know, Then W 10 years later, did another presentation at the AEP. Also an endomeral edoema, but with a different angle to it, and I'm gonna talk about both of those papers over the next 3 or 4 slides. First off the bat, we've got to establish our grading system.

what I would say is it doesn't matter how you grade endometrial edoema. But you must develop a system that works for you. It's a, it's a relative thing, so it doesn't matter whether you pick scores from uterus E1 to E5, E1 to E3, whether you give it names, slight, moderate, or marked.

It does not matter because in essence it's a relative thing, it's what you need to understand, is it more or less than what you saw the day before. So I'm, I'm, I'm going through my system which we grade edoema, . 0 to 4, or 0 to 3 plus some, some, I think some colleagues in, in the practise do.

But whatever, the point being, it does not matter as long as you develop a grading system which works for you, so when you look at the mere record, you know what you meant. So I, I'd call this a grade one uterus a D. One I'd call this a grade 2, a nice 35 millimetre follicle plus, it'll just be starting to lose its spherical shape.

There we've got a grade 3, and, and this would be your grade 4 or 3 plus, whatever you want to call it. Very, very intense edoema pan, edoema being, it's a it's a bit of a mouthful to say, but it's alternating and intertwining areas of hyper. And hypoecogenicity.

So these would be the hyper ecogenic areas. The black areas would be the hypo ecogenic, and that's, are you trying to deem a score of 4. There's even some free, you know, edoema being fluid within a tissue.

We, we, we know about intraluminal fluid in mares. That's a big problem for those of us in equine reproduction, free fluid within the actual uterine luminum. This mare would appear to have some to meet, you know, a, a small depth of free luminal fluid in, in, in, in, in the uterus.

So, this is what we would grade in our practise, a score of 4. But you know, you use whatever system you like, just use a system. And grading endometrial edoema is really useful because when we think we've got an edoema at its maximal level, Benny mas don't reach a grade 4, that their maximal edoema pattern is a, is, is an E3.

And at that point, that point. That's when I think I'll be reaching for my ovulatory induction agent, be that HCG Coriollo, or be it a GNRH implant or or a a a a Desloelin injection. Whatever you're gonna use, whatever ovulation induction agent you use, I use maximal edoema pattern, along with other parameters such as size of follicle, .

Softness, open cervix and so on, but using that marked, the, the, the endometrial edoema pattern to say right, this is when I think my ovulation induction agent will have most likely to have the best effects. Now, I think we've got another, polling question here. What percentage of mares have no edoema pattern in the uterus at any stage of the follicular phase?

I, I prefer the term follicular phase to estru, but many of you may know it as ester. The same thing. I'm talking about a mare with a growing follicle, open cervix.

Does not develop an edoema pattern. What percentage do you think it is? And again, folks, there isn't a right or wrong necessarily answer here, .

I'm just curious what what you guys think. And yeah, I know it's a little bit quick, but we we we. I like polling questions, but they are quite time consuming, so I've deliberately cut down the number we're using, so I'm not gonna give you too long to think .

And yeah, it's working, there you are, the ones who who are coming up with the answer are getting it it pretty quickly. 10%. That's absolutely fair enough.

I would, I, I, I'd be in 5%. I think it's, it's, it's, it's, it's, it's 5%, possibly even 3 or 4%, but, you know, that's just an observation I have, so, . I certainly would go, go with the, go with the 10%'s perfectly reasonable.

I don't know what, out of interest, let's see. Yeah, that's similar to you there, probably more to 5. A good number of you went for 10%.

I, I just personally think it's less than 10%. I think it's quite unusual to be monitoring a mare through the follicular phase, and she doesn't develop an edoema path. I'm gonna use that word like again.

I don't like to see that. I get nervous, well, I don't know whether nervous is a slight exaggeration. I don't get nervous about much, but it it it's, it's.

The follicle's growing, the cervix is open. That's all looking good, but no edoema patterns developing in this me. Oh dear, I don't like that.

Do you know what I do with those myths? It's an interesting little tip for you. You won't, you won't read this anyway.

Do you know what I do with those myths? Do you know what I think might be happening in them? And I didn't used to believe it was possible.

I think there may be a little remnant. Of luteal tissue. I don't want to get too much into endocrinology, but if you will, an endocrinologist will think this is incredible oversimplification.

But of the two steroid hormones, oestrogen and progesterone. Progesterone is the dominant follicle. You can have, sorry, is the dominant hormone.

You can have a. Three follicles, but if you've got 1 CL that mare will not be in the follicular phase. She won't have an edoema pattern, and she won't show estres if you were able to tease her, and her cervix won't be open.

So if I have a mare which is, is, is the follicle is growing, I, I, I'm, I'll obviously be looking at the, the two ovaries, and I'm not seeing an obvious corpus lute, and that's the point. We, we get, when we first observed this phenomenon of not producing an edoema pattern in the practise, we sat down with her, well what's going on? And we thought, well, I, I don't know, maybe somehow.

The oestrogen for the follicle is being suppressed, well, that can only be via progesterone. Well, I can't see CLs in any of these ovaries. Maybe there's just a kind of remnant of luteal tissue.

I took some time to buy into that idea. Well, I, I think that you either have a CL or you don't. But now I think you can have mares where you cannot see an obvious corpus luteum.

But there must be a remnant of luteal tissue. Of course, you could take blood samples, but I'm, I, I see such large numbers. I haven't really often got time and I want to try and work out an answer for myself as a clinician straight away.

So I tell you what we do with those mas. I asked you that beginning, I'm now going to tell you what we do. We give them a very, very, very low dose of prostaglandin.

And it's amazing in how many of those mares with a 30, 35 millimetre follicle. No edoema pattern. You give the the prostaglandin to them the next day.

Marked edoema score and maybe a 38 millimetre, and I feel much more comfortable about going on and breeding those mares. So, I think it's, it's, it's personally nearer 5% of mares only have no edoema pattern. And when I'm discovering that happening, monitoring the follicle, I'll always give those mares a little touch of prostaglandin.

So, here's our, our final poll question I think. Is it normal? Normal's an interesting word, is it normal for a mare in the follicular phase, estrus to have no edoema pattern in the uterus?

Now this I'd like to see. Moses, what do you think? It's a little bit of a, a kind of play on normal, I think, really.

You probably could put is it, is it, well, that was really the point of this slide. It's, we know it's not usual for a mayor in the follicular phase to have no edoema, we've just answered that in the previous slide, so it's not usual. I've kind of moved on to this.

Is it normal? Is it normal for a mayor in the follicular phase to have no edoema pattern? Well, I'm in the no camp, I, I, I I don't think it is normal and.

We, we thought that, and I think, yeah, I don't know where I was, we did a lot of work for this in the Netherlands, and maybe I was in the . I was in the Netherlands when we saw that, . Because 100%, everybody in that audience said no, it's not normal.

And I don't think it is. And we, so I thought, well, we'll do a little bit of work on that. So I'll tell you what we did.

That's what I think, more than 95%. So that's why I said most of you are in the 10%, don't have edoema. I said it's, it's, it's less than 10%.

I said it's 5%. So that's, hence it's my bullet point. More than 95% of mares have detectable endometrial edoema when in estrus.

Meres that do not display edoema when progesterone levels are based on an oestrogen is high, should be considered abnormal. Back, whoa, crikey, possibly some of you weren't born then, but years ago, look, we did this study while I worked at the university in Utrecht for a couple of years, and we had a wonderful endocrinology lab, and we found hormone levels were just all wrong. Our y quality was poor, they didn't ovulate normally.

So I think if you don't see an edoema pattern when you have truly got a basal progesterone level, there's something abnormal in that man. Most times, when we see it in practise, most mayors, even if we go with your 10% of, of, of mayors not producing an edoema pan while the follicle's growing. If you give those meds, .

Prostaglandin, which will take their progesterone levels to basal values. Like I said, oftentimes, 90% of times, they will develop an edoema pattern. So, they, they're, I'm only, I'm saying they're abnormal only when we have got progesterone levels of basal values.

So giving those mares prostaglandin isn't gonna do anything because there clearly isn't any luteal tissue to eliminate. Now, What I want to just draw things to a conclusion with is To talk about mares which have this intense edoema pattern, grade 3 or grade 4. And Normally edoema begins to decrease immediately prior to ovulation.

We know that, that most of you know that, and probably all of you, but there are some mares which will ovulate. While still having a marked edoema score. And this was the gist of Juan Sampa's subsequent second presentation back in early 2000s, I think.

And Wa suggested, and I agree with him, that mares which ovulate with a marked edoema score, either that edoema score not reducing, must be considered suspicious of being wind suckers, challenging pneumovagina, challenging air into the uterus, pooling some urine, I irritating the endometrial lining, because irritation will cause edoema. It edoema doesn't only have an endocrinological, endocrinological basis. If you have a challenge to the uterus, be it wind sucking, setting up a bit of inflammation, or urine pooling, again, those mares, don't wait for the edoema score to go to 1s and 2s in those mares, before breeding them, because they, they, they'll catch you out.

They'll ovulate with, with a grade 3 or grade 4 edoema pack. And also mares which are susceptible to fluid accumulation. We know about those, the mares which we need to lavage, oxytocin after breeding.

We've talked, you know, any of you'll know, I've talked about that for, for many years now. These mares susceptible to fluid accumulation. And, and I think that's right.

I totally agree with what Juan Samper. You can go online and, and, and, and, and, and get a hold of that AEP proceedings relatively easily, I think. He doesn't quite flag up, but, but I always like to point this out, and I think there are two exceptions to that.

There are two examples where I think mares will ovulate with a marked edoema score that aren't wind suckers, aren't urine poolers, or aren't susceptible to fluid accumulation. And they are mares which have been given of your plant. I think Deslorein will drive the follicle to ovulate.

So don't, once you've injected a mare with Desloelin or put a, a desserelin implant in a mare. Then I think you are playing a risky game if you wait for the edoema pattern to decrease before breeding the mare. Desiwein will, will drive that follic to ovulate, even with a marked 3, grade 3, grade 4 edoema score.

And the other exception is if you're breeding a mare at Foley, that's the whole talk in itself, whether or not you should breed a mare at Foley, but if you breed a mare at the foalley, the first postpartum ovulation. They will quite often ovulate with a marked endometrial edoema score. If you wait for that endometrial edoema score to drop down.

Then, then I think you're gonna be at risk for missing those mares, not getting them bred before they ovulate, because all this grade 3 edoema, this mare isn't going to ovulate for 24, 36 hours. Oh, bang, go back the next day. Still got your grade 3 edoema score.

The mare's ovulated. You'll see that at Foley's, I promise you. We did a published a couple of papers on that now.

So, this, if you will, would be Wan's first paper on endometrial edoema. SH you're just standing heat. So look, 34567 days of Easter, as he calls it.

I, I prefer follicular phase, but it doesn't matter. Endometrial edoema score peaks here, they got to somewhere between 3, 3.5.

36 hours or so before OVD ovulating, so we kind of know that bell-shaped curve, and that's for the normal, the normal mare. These abnormal mares, mares that may urine pool, that may take in air to challenge the endometrium, or may be susceptible to fluid accumulation post-breeding. They ovulate still with a marked endometrial edoema score, and that's something very important to remember.

And, if you will remember the two exceptions. There are two normal categories of normal mares which will have this endometrial edoema pattern of ovulation. They're mares which you've put in a, Desslarein implant and the mares which you've bred at foal heat.

So, how do we actually know the mare's ovulated? Well, in most cases, relatively straightforward, a 38, 40 millimetre plus anechoic, non-ecogenic, black, whatever you want to describe it, follicle is replaced by, in the 1st 24 to 36 hours, is, is an intensely ecogenic, quite grey, white almost structure, the early corpus luteum. Let's have a look on.

As it happens, this is a left ovary there with two follicles, 240 millimetre follicles. Common enough to see multiple ovulations. Here they're gonna be slightly asynchronous because this was the next day, when I looked the next day, Pingo, one of the follicles had ovulated, one hasn't.

Now, I, I like this slide because it makes a point to. Detecting ovulation is easy if you went the day before. So, yes, we, we know, if, if we examine this mare on, on Thursday, yesterday, and we look again Friday, oh well, that, that 40 millimetre black follicle's gone.

So yes, I can see a fresh ovulation. But a very fresh ovulation can be difficult to detect. Imagine if you just examined the mare for the first time.

On this occasion, you would think, oh, yeah, here we've got a nice 38, 40 millimetre follicle growing. You may well miss not detect that fresh ovulation. So that can be problematical for you.

Of course, the one day on again from that image, oh, it's, oh, yeah, wow. Actually this multiple ovulates. She's got two follicles, because we've got 2 CLs, 2 corppo lutea.

So that's gonna have an impact, of course, when you do your pregnancy detection. Because you're going to look very carefully for twins here. So yes, notionally it's very easy to detect ovulation with ultrasound, but a fresh ovulation can be quite difficult to detect.

So getting used to, I, I said at the very beginning, very important to record the number of corporal lute. So, here, look, not actually it's this slide shows you not only how it's important to count numbers, it shows you the the the num the massive number of appearances. There's no set appearance for the early corpus luteum.

So look, here we've got one CL, quite a degree of central lacuna, some hypoechoic areas there. This may have had a double ovulation, one CL there, one CL there. This may actually had a triple ovulation, 1 CL there, 1 CL there, and then a third CL in the middle.

So try and develop your skill. Excuse me, try and develop your skill for detecting the number of ovulations. But Also, remember the point that the first time you examine the mirror, it can be quite difficult to see an ovulation.

You may have to make your mind up the next day. So, say you examine this mirror, cervix may well still be open, and you think, oh yeah, well, we've got a 25 millimetre follicle growing here, early days. Mm, OK.

What, what can be difficult to see is this. Fresh ovulation here. I've, I've just outlined it there for you.

It can be quite difficult to detect that. But of course, if you go back the next, so I would often write in my book, you know, oh, query, fresh CL. I can't be sure, none of us can be sure.

I'm gonna see this mayor again tomorrow. When you go back tomorrow, you'll see a much more obvious, you know, white ecogenic corpus luteum there. And just making the point, look at all these different types of CL, some with a lacuna, some more solid.

Some with the, you know, there, that's a normal corpus luteum just has a thinnish border of luteal tissue, that can be difficult to detect. You know, some people can say, oh, that follicle's still there, no, that is ovulated. Just a thinnish border of luteal tissue.

And like I say, we'll just finish, we can't get into an ovulatory follicles because it's, it's a topic for another day, but just as we're talking about ovulation, I just want to make the point, . When you get these abnormal ovulations, they're quite difficult to tell. You can't always be certain.

I showed you, you remember I show you that example of a 60 millimetre follicle with, with those ecogenic particles, and we asked, will that ovulate normally, will it not? You to just factor in well, it's a little bit large, there's a lot of part. There, it's not going to be, I don't think it's going to ovulate properly.

Easier with this structure because it's gone straight from a 35 millimetre follicle to this structure. The odds are that is not gonna be a normal, you know, you, you haven't had the collapse stage in the refill. That's gone straight to an anovulatory hemorrhagic follicle.

But, you know. It's difficult to tell and and anovulatory follicles are are are really important structures for us to recognise, but they'd be a. They'd be a topic for another day.

That's, you've done well to hang on there for that hour folks. I'll, do you want me to stop sharing the screen now, Anthony? No, that's fine, you can keep the screen OK.

OK, Jonathan, and if people do have any questions, I'm sure we can. We can get one or two in, before we finish, then we've got a gap for an hour and we've got Stefanos Clodais gonna be talking about perineal hernias in dogs next, just so everyone knows. You get a varied topics there are very very very fabulous you guys.

I would just say I, I saw you if any of you, if anybody comes up with a question later, . I, I, I'm sure Anthony or his team are very welcome. If I don't pick it up on your various apps and things, you're always welcome to forward, the, the, the team will forward them on to me and I'll answer them for you.

So that's great. I, I know some of you maybe don't think of, of, of it at the time, so you, you can forward it on and and Anton and his colleagues will send it to me and I'll, I can get back to you that way, . Which because sometimes you think you, you, they are available to rerun through these, are they, if somebody hasn't.

Yes, they're available for 12 months, so there's plenty of time, and I must say, Jonathan, I, I, I am taken by your COVID curls there. Yeah, yes, you're letting the hair go a bit long. Yeah, yes, yes, I thought that.

It's always hard. I, I love anyone who've been to my talks on the live. I, I, I, I tell quite a few jokes.

It's a little bit harder to tell jokes when you've, in, in a virtual environment, but I would have made a good joke. My hair, I thought it looked marginally better than Boris Johnson's I must say. Well, it, it definitely does.

But I think if it grows a little bit longer, you could get an electric guitar and auction for audition for some of the heavy metal groups. You're always very kind, very kind. Let me see if anybody's come up with any questions just so we'll give.

Well, I often find they want to think of them afterwards, so if somebody does digest it, as I say, they're welcome, but if anyone's got anything burning now, I can. Christopher has just said the small dose of prostaglandinomeral edoema, have you got a dose for that? Yes, yes, let, let's talk a little bit about that.

Let's just set the scene. It's those mares where we're monitoring them during the follicular phase and we, we, we're seeing a follicle grow, and we're, we're doing a speculum exam, we think the cervix is opening but we can't be quite sure. And, and it's so great for us that.

The majority of those mayors will be developing edoema patterns, so once we see edoema, we're home and hosed, we know that that mare is under oestrogen dominance, and she's gonna be ready to be covered or inseminated. Now, the scenario is, we've got this follicle growing. We think the cervix might be open, but we're not quite sure for whatever reason.

But we're not seeing an edoema pack. And what I think happens in the majority of cases, or or is happening in the majority of cases, is there is a remnant of luteal tissue, not such an obvious corpus luteum that you can detect it in the left or right ovary, but there's, there there there is, is some residual luteal tissue. Luteolysis, the start of the follicular phase.

We, we didn't get complete luteolysis. So we've got a remnant of luteal tissue. And we want to give prostaglandin.

Now, what, what has been shown is that the the dose we've been using of prostaglandin, which in the UK or our practise, there are two main types in the UK I think possibly 3 now, but we, we tend to use estromate, which is cloprostinol. And the dose in the UK, Is 1 ml, but, but under normal circumstances, we only use half a mL. When I'm using it for this low dose, we call it, you know, our stud managers get very, they know what we're doing.

They'll put low dose PG when they know what we're gonna do. We mean for that literally 0.1 or 0.2 of a mL, so a very low dose of prostaglandin.

I, I actually inject it just we get those 1 CC syringes because well, at most the two Cs. Cringe. So it's a very low dose of, it would be the same, I don't know, I think, I think loutilize is a bigger dose, as I say, I don't use it, so I can't remember offhand, but it's, it's certainly, it would be about 50% of what the recommended dose is.

So something like that, Richard, so, yeah, a low dose. I mean, I, it probably doesn't matter. I'm just the difficulty if you give two bigger doses, what, what a lot of people don't remember is that.

Prostaglandin actually has a slight luteolytic, yes, has a slight ability to indu LH like activity as well. So if you give too big a dose, I think that the big follicle that you've got there may go on and ovulate before your prostaglandin has had time to drop the progesterone levels down, the cervix opened better, and your edoema score develop. So that's why I'd caution you to use a low dose.

Whether it's 0.1 of the 0.2 of a mil doesn't really matter.

Don't use the full 1 mL recommended by the manufacturers. I hope that makes sense. That's great, thanks, Jonathan.

It looks at a fabulous picture there and of course, not a lot of social distancing going on, but quite a while ago this photograph. That was quite a while ago, yes, that's quite a while ago. That's out in Switzerland, a lovely part of the world.

It looks beautiful. Let's hope we can start getting out before too long and we will, I might come down to Shropshire and see you again. I'm sure we will and thank you very much for putting this on, Antony, it's great you and your colleagues put .

I mean, you know, this fantastic source of . Of educational content, and as a speaker I found it It's a great way that we can still, you know, we all enjoy teaching and most of us who, who do these do and and without organisations like yours, we'd be, we'd be stuck. So I think it's been a tremendous service and I hope everyone has enjoyed it and well, we'll get something out of it.

So thanks to you and your team, Anthony. As, as I've been saying to people recently, I, I've spent the last 11 years preparing for the pandemic. You were ahead of the game I just didn't realise.

I just didn't realise. But anyway, it's great to see you. Fabulous.

Thank you so much for the other lectures that you've given, which people can go and view if they've got an interest in this topic. If you haven't got a full ticket, then do get in touch with us and we can sort you out with one of those. But it's been great to have you on, Jonathan.

I'm going for a little lie down and I think, and then 3 o'clock it's back on with Stefanos on perineal hernias, but thanks once again Jonathan. Thanks everybody, and thanks Anthony and the rest of your team. Bye bye.