Hi, welcome to this webinar looking at updates and practical approaches to equine gastric disease. My name is Gail Halliwell, I'm an internal medicine specialist, and medicine consultant at Medicine Vet Equine Referrals. So I thought I'd start by thinking about what we know and don't know about squamous and glandular disease.
And then look at the current data we've got regarding efficacy of therapy and then thinking about when treatment's non-efficacious, and I thought we could have a look at a a few cases at the end. So I think when we're talking about squamous disease, we've probably well got it pretty well nailed in in terms of management. So we know in terms of protective factors, we've got high fibre diets and turnout, small amounts of feed prior to exercise.
I think there is a bit of controversy about alfalfa and we'll perhaps revisit that as we move through the talk. And then we know the risk factors too, we know when we're using, when we're feeding large amounts of grain, more than 2 grammes per kilogramme, when horses have got intermittent access to water. And, and then if they have er intermittent access to forage.
Now I think one of the interesting things is many of the studies that have looked at squamous disease have used a fasting model, and we know that if we fast horses for a few days, we can cause the development of squamous disease. Now, I think that it's always difficult whether we do clinical studies or whether we do experimental studies, but I do think it's always worth remembering that most of the time, the squamous disease that we see in horses isn't caused by fasting and so we really need to interpret the findings of studies very, very carefully. But the one overarching factor that we do know with squamous disease is that it's an acid dependent disease.
So then we moved to gastric glandular disease and I first became involved in glandular disease research cos I wasn't truly convinced that this disease caused clinical problems, which I don't feel like that now but I certainly did 20 years ago. I think what's really frustrating with gastric glandular disease is we know a lot of the things that it's not associated with. But that we don't really have a good understanding of the pathophysiology.
And I think that the reason for that is it's likely to be a multifactorial syndrome and some of the options we've got in terms. In terms of causing that syndrome are, is it caused by acid, which seems pretty unlikely as the glandular mucosa is designed to be bathed in acid, or is it simply that glandular disease is healing of those lesions that has formed, is hindered by acid being present? Is it caused by poor mucosal blood flow, that's certainly supported by data in other species and the fact that we do see glandular disease in sick foals.
Is it an extension of inflammatory bowel disease? And I think when we come to look at the efficacy of therapeutics, it becomes pretty clear that probably one size doesn't fit all in terms of that aetiology. But what do we know?
Well, we've not identified any nutritional risk factors, and that is interesting when we have got very clear, nutritional. Benefits and risk factors for squamous disease. So, because I think some of these cases are associated with as an extension of inflammatory bowel disease, simplification of diet, removal of multiple cereal proteins and potentially alfalfa might be beneficial.
The other thing is trying to avoid any supplements that might be irritant, especially being administered on an empty stomach. And there have been multiple studies looking at risk factors, and the, a few of them have come up with similar risk factors in a and and then we've got additional ones in individual studies. So, we do seem to have identified in a few studies.
Increased number of caretakers and riders is important. An increased number of days of exercise, and that was a study I did with, Ben Sykes a long time ago, and we had that cut off of 5 days. So, horses that were exercised more than 5 days per week had an increased prevalence of glandular disease.
We then had a few studies looking at horses that have got less experience or that are competing at lower competition levels. And I think that that comes back to perhaps fitting with that increased number of caretakers coming under that that banner of stress. What does stress mean to a horse, but probably, you know, if we've got those less experienced animals, we're usually pushing them to try and get them to that next competition level.
And then we've got duration of exercise and that's been particularly identified in endurance horses. In terms of, trainer perception, glandular disease has been associated with reduced perceived performance. But the one thing that's come out in several studies is that it's not associated with non-steroidal administration, and I think that's true for squamous disease as well unless we're using, subtheray, sorry, we're using supratherapeutic doses, you know, 4 or 5 times what we would normally administer to our patients.
And then I think what's become quite interesting, I'm gonna talk a little bit more about this, is this is association with pain and that pain might be dental disease, it might be lameness, it might be back pain, it might be other conditions. And I really think if my one take home that you take from this webinar is we need to stop looking at the stomach in isolation and we need to start really reevaluating it and looking at the whole horse. So what about the latest?
So, several people involved in, in gastric disease research, including myself, went out to the, to Florida last, January, 25, the coldest week Florida's seen in a little while, unfortunately for all of us. And we had a Havermeyer work. Shop, trying to really look at where people were at in terms of their, research and where we needed to go and what questions were still left over.
And I thought I'd just present some of the highlights of that. So, I, I went through our case series of gastric disease cases. Cases from the last nearly 20 years and we had seen about, with some colleagues, about 3000 cases.
And we looked at the prevalence of glandular disease, which had certainly increased in our case population, which is predominantly sports horses in the last sort of 10 or 12 years. And we found the glandular disease prevalence in this sports horse population of around 56%, and I was really interested to look and see what were the risk factors to those lesions not healing, and we called those treatment failures that the lesions, didn't, didn't heal. And then what about the lesions that were refractory, so you know that they improved, sorry, they improved but didn't heal, whereas treatment failure was they neither improved nor healed.
And this becomes really important when we're client facing because this disease can be both very frustrating but also very expensive for for clients. And our population, we didn't actually have that many horses with squamous disease. There'd been a real drop off from about 2010, 2011.
But of the horses that did have squamous disease, 60% of them also had glandular disease as well. And then there were two other, really interesting presentations that have one has now been published and the other hasn't. And one was, from Hoyt Charamy, who works for Bowringer now but used to work for Meriel.
He'd looked at 1400 gastroc. Escopic exams and had shown association with glandular disease with bad attitude and girthiness, and again back to that whole diet factor, found no impact of turnout and this was a mixed horse population predominantly in the United States. And then Nana Luthson's work was very interesting, she's been scoping groups of Icelandic ponies, not necessarily that have got any clinical disease, she's been scoping whole groups and looking at them in different seasons and in different, in different er er environmental conditions.
So, She's looked at these horses that are largely treated like wild horses, they're turned out the weather in Iceland is obviously pretty harsh compared to what we would have here in the UK. And one of the things she's found is that actually pasture access is not protective. Horses that are stabled and warm and don't have to compete for food are much less likely to have glandular disease than those horses that are outdoors in big groups, perhaps in less ideal weather conditions.
And I think we, we need to challenge Pat that this sort of. Challenges that status quo about how we should keep horses and that perhaps one size doesn't fit all. Lots of horses love being outdoors.
They love access to grass and being with, in a group, but always remember there's always that exception, or that horse that's in a group that is, is bullied and and and probably is in a very stressful situation. So let's move on to therapeutics, and I think that, you know, a summary is treating squamous disease is easy, except for that perhaps 5% of the of the population that that don't respond appropriately to to medication. So when we look at this data, we've got oral omeprazole, this was a licenced oral omeprazole paste and you can see we've got 80% heal rates at 20.
At 28 days. We've then got a sustained release injectable omeprazole given every 7 and 5 days, and again we've got healing rates at that same time period, 21 to 28 days, between 80 and 95%. Again, healing rates with these omeprazole around just over 80%.
And then some of the non-enteric coated granules where we've got slightly less efficacy. So it's always worth if clients have been acquiring omeprazole to try and understand where they've acquired that omeprazole from and you know, not, not all omeprazoles are the same. But we've got a pretty good, we know that we can manage squamous disease, it's acid dependent.
If we can suppress acid, we are likely to see. Improvements and healing. I think the thing to remember is, we do need, it is our duty of carers, as vets managing these cases, not just to give them out drugs but to really talk about what management changes they're gonna make, because otherwise, this disease is going to come back and we're gonna be in that cycle again.
And then we move to glandular disease and you can already see we are suddenly not doing quite so well. So the one thing we do know from from many of the studies that we've got is that oral omeprazole on its own is not appropriate for treatment of glandular disease. We've got very poor healing rates, around 20% and it can't be recommended.
When we look at omeprazole and sucralfate, we see improvements of around 60%, and this is becoming a real challenge in studies because what one person regards as healing, another person regards as improvement. And at the Havermeyer that I was talking about earlier, we, we still don't really have the answers as to what that means and how we're going to come up with definitions. We then move on to look at misoprostol.
This was a small number of horses, but we've got improvement in around 95% and healing rates somewhere in that sort of 60, 60 to 70% range. And then we've got injectable omeprazole. So, sustained release injectable omeprazole, we've got 80% healing rates and 90% improvement.
And I think it's really worth bearing in mind that many of the studies that I've got displayed here are for particular groups of horses and that in fact when we look at this overall, and we're certainly when I'm talking to clients, I usually say we're probably going to expect that 28 days. A healing rate of around 60% with these three groups and possibly misoprostty and injectable omeprazole do do slightly better than omeprazole and sucralfate, but I do believe that is very dependent on the type of lesion it is and the, and the cases that we're dealing with. So in my big group of horses, I tried to tease out what those risk factors were for treatment failure.
And the things that I found that were risk factors were the raised nodular lesions versus other types of lesions, fibrinous operative versus other types of lesions, if there was more than one lesion, and if they were subjectively identified as being moderate to severe versus mild. And I just want to put a caveat in here that I have a very hard line of what healed is. So for me healed is that the mucosa is normal or nearly normal.
And that can be really tough when you've got those raised lesions that are gonna take a long time to model back to being normal if they ever do. The other risk factor that we found, and this was in a smaller group of horses, was if they had concurrent disease and specifically inflammatory bowel disease, and this has really triggered how I approach these cases as we move forwards. So let's have a think about why treatment fails.
So I think you're either using the wrong treatment for the condition being managed or the drug that you're using is not effective in that patient. So when we're thinking about glandular disease, we know it's an inflammatory, not an ulcerative condition. And so we've sort of got two arms that we can go down.
We've got the gastroprotectants that are going to allow healing of those lesions, so that's gonna include acid suppression with drugs like omeprazole or esomeprazole, and then we've got mucosal support in the form of sucralfate or misoprostol. And then we've got the disease modifying drugs such as misoprostol and the corticosteroids that may well have that that anti-inflammatory action. So I think that becomes important and I think when we're thinking about squamous disease and we've got those horses where treatment's failed, it's either because we are not able, or the client won't change the adverse management factors or that that horse is not responding to omeprazole in the way that we would like.
And we're going to talk a little bit more about that. So let's have a think about these drugs and how they work. So it's worth noting we've got these groups of drugs and they are gonna be doing different things on different receptors.
So we know that gastrin is released in response to feeding and that that gastrin will start to trigger the production of hydrochloric acid. And when we look at the drugs that we've got available. Ranitidine, which we don't use very often anymore, that is an H2 blocker, so that works on that gastric parietal cell to reduce acid production.
We have got, the misoprostol, which is a PGE analogue, which again helps to both improve mucosal blood flow, but it also seems to have an impact on acid production. We've got sucralfate, again, probably has some effects on improving mucosal blood flow as well as er potentially becoming a sort of a slime or a barrier over those lesions, perhaps to help protect them from acid. And then we've got omeprazole and esomeprazole, which are proton pump inhibitors, and we know that they're the mainstay of management, at least initial management of gastric disease in people and small animals.
So let's have a think about omeprazole, what do we know? And then we might be able to, you know, use our detective hats to look at why this might not work. So we know it's a proton pump inhibitor.
We know it has the best absorption with fasting and goes through hepatic metabolism. We know that where healing of squamous lesions is concerned in, and this was work done in a group of Australian racehorses where, there were many risk factors, they didn't always always have, ad lib access to forage and. Had a high grain diet, we know that those lesions healed as well with 1 milligramme per kilogramme of omeprazole as they did with 4, and I think that's something we could, we should consider, when we're thinking, about prescribing these medications.
We do know about variable absorption following oral dosing, that's not just true for omeprazole, it's true for lots of drugs as we know. But there's also a variable response from the proton pump, so not all horses will have the same effect of an amount of omeprazole as as others. And then we certainly know from people that there is a genetic variation in metabolism and we don't have that data for horses, but it seems reasonable that we probably will see that as well.
So then what about esomeprazole? So esomeprazole has really taken over as the as the frontline drug in in people, and you can, as many of you will know, you can buy that for yourself in the supermarket. And what we know with esomeprazole is that it has slower metabolism and a higher bioavailability.
Most of the studies suggest it has superior acid control, and we think it probably has less variable drug metabolism. From studies that we've seen, it's probably got higher healing rates and there was one study that suggested that it also was more effective, where we've got horses that have been fed a hay diet, we know hay has a, a significant impact on . The efficacy of omeprazole, and it seems that is omeprazole, perhaps that is a bit less, less true.
So then let's have a look at misoprostol. So misoprostol is quite an old and dirty drug and because of its mechanism of action, it does many things. So we know that it works with local receptor stimulation.
It will help stimulate mucus production, help stimulate bicarbonate production and secretion locally. It seems to have an impact on increasing epithelial cell turnover and tight junction integrity, which is going to be pretty important for healing. It seems to improve mucosal blood flow, and there is some data that it will suppress acid via cyclic AMP and we keep seeing more studies come out looking at its anti-inflammatory effects.
So this drug works locally in the stomach and it is acid, but it's acid labile. So there are potential synergies with sucralfate, omeprazole, and also pectin lethain. Now.
There is worsening of both, glandular and squamous disease reported with misoprostol, and that probably does happen in a higher prevalence than it does with other drugs, but certainly I have seen that with injectable and oral omeprazole as well. So then we move to sucralfate and sucralfate is, certainly when I was, was training, thought to be a pretty poor drug. And again this is another older drug that has multiple mechanisms of action.
So we know it's poorly soluble and that it polymerases in acid when the pH is less than 4. And it binds to surface proteins acting as a physical barrier, so theoretically we would want to give it prior to acid suppression in order for it to have that to have been be most efficacious as a physical barrier. It also stimulates prostaglandin and EGF production, which is not a pH dependent and it's thought that it's theoretically not valuable with injectable omeprazole, but certainly, in some cases I, I do, I do use them together.
So I think it's, you know, certainly not a drug we're gonna use on its own, but I think it's got some additional benefits, especially when we start talking about those cases we're really struggling to, to treat. So I thought we could have a little look at what my management is for some of these cases and I usually have a pretty straightforward approach to squamous disease, always try and look at these horses prior to gastroscopy. Do they have any pain on back palpation?
Do they appear to be lame? Talk to the client about diet and and and increasing or adding in pectin letsin either as a supplement or with sugar beet. And then I'm gonna treat these horses with 21 to 28 days of oral omeprazole and based on the study that Ben Sykes and I did, it will depend how severe their squamous disease is as to whether I use 12 or 4 milligrammes per kilogramme.
I then re-scope them and if they have not healed, if they've improved but not healed, then we might think about optimisation of dosing. If they have not improved at all, then I'm, I may well switch to injectable omeprazole or oral sorry, oral esomeprazole. And then I'll re-scope them again at 28 days.
So, I think it's really understanding that these horses should be fixed at 28 days, and if they're not fixed, then we really need to go and look deeper into why, why, why is it that they haven't responded. And then we move on to glandular disease, and glandular disease I've got two, I've got two of these charts which I, will depend on various factors as to where I go. Because glandular disease is not an ulcerative disease, I don't always start with oral omeprazole and we've got good data now showing that oral omeprazole monotherapy anyway is not effective.
So I'm much more likely to spend time looking at these horses, especially subsequently, but even at the time, really getting to the bottom of, you know, what is it these horses do. So if we identify glandular disease, then thinking about, I'm probably gonna treat them for 6 weeks. In our sports horse population, we see a lot of these raised fibrinous operative lesions.
If we've got flat hemorrhagic lesions, which anecdotally I do think heal quicker and better, I might scope them at 4 weeks. But use injectable omeprazole and sucralfate, and then I'll re-scope them. And if at this point.
They've improved and not healed, then I'll bring in abdominal ultrasound because of my concerns that this could be an extension of inflammatory bowel disease. Have we got any evidence of abdominal dysbiosis or thickening of the small or large intestine? If it looks like we do have an intestinal component as well, then I might, might at this point add in, equinectar, corticosteroids, and, faecal transplantation and some form of omega 3 oil, and my current favourite is, is codlavine, as a, as a fish oil base.
It might be that we try an analgesia trial and it, I'm sure many of you have experienced this concept that clients have got stiff horses but not lame horses, so sometimes, and sometimes we may not identify a source of pain on, on our physical examination either, but we might try an analgesia trial and normally my analgesia trial will at a minimum involve a traditional non-steroidal and paracetamol. And then what I do in terms of next steps for the glandular disease, I might add or switch to misoprostol, it will really depend what I've found and or consider corticosteroids. My other option that I've got is I might start with misoprostol and sucralfate, follow the the same pattern that I've got here, and then if they have not healed or not improved, then I would consider switching to either injectable omeprazole or esomeprazole and sucralfate.
So, This is a lot more fluid and there might be other things that I try to bring in, so you know, consultations with physiotherapists, trying to get saddles, make sure that saddles are fitting appropriately, etc. And then we come to what outcome do we expect? Well, we don't know, so I think that the, if you ask 10, gastric disease gurus, everyone will come up with a slightly different response.
I think the one thing we do all agree on is that probably this mottling that you can see, I know this horse does also have a lesion at 7 o'clock, but we'll ignore that for now. But this mottling that we can see on this image. Is probably either normal or iatrogenic, so caused by, it can be artifactually created depending on how you've got your light source set up for your endoscope, but also that we are inflating the stomach and that can cause this sort of blanching effect.
So if the only thing you've got is that, that's probably, you've done a great job, you it's a, we're gonna call it a variation of normal. I mean, in an ideal world we're gonna see a pylo pylaris that looks like this, where it's, beautiful, it's shiny, as you've gone, you've tipped underneath the lesser curvature, you can often see those mucosal stalactites, which I like to see, suggests that the stomach is. Producing, mucus, they may not be healed, those lesions, but sometimes that might give me a different path that I'm, that I'm going down.
And we will, at least at the first examination, always go in and examine the duodenum and see what the duodenal mucosa looks like. And then obviously we do not expect to find this lesion that we have got on the right hand side, and this is an example of a gastric metaplasia. And these lesions controversially, obviously you can see in some horses they could cause pyloric outflow obstruction, but they are not responsive to the the other medications that we've got and usually require, removal or at least attempts at removal with with laser.
OK, so I thought now we would go on and we would look at some cases. So the first case is a seven year old thoroughbred gelding, and the lesions keep returning when full dose omeprazole is stopped. And these are like a sequential set of images that each time we stop the omeprazole, we fix the lesions, but the lesions have been getting progressively worse.
They are worse along the greater curvature, although they are present along the lesser curvature, and you can see these lesions. Are extensive and really deep. So this was one of those cases where, I saw this case before injectable omeprazole was available and it's like we really need to be thinking about the management.
Is this horse truly a non-responder, which was not true because the lesions would heal. It's just that they kept coming back. And it transpired that this horse lived in a group.
He was bottom of the of the pecking order in the fields, and he was quite often bullied and he was pushed away from the feed. And that when he was on omeprazole, that seemed to be fine. So the suggestion was we moved him into a smaller group.
He was turned, still turned out in the same way. And we would see whether that was our fix and indeed it was. So he was turned out with one other horse and that seemed to solve the problem where the, we're going to call it stress, but the the stress or it in limited access to forage and and and water because they would chase him away from those was playing part of this, part of the role.
So you know the and once we we changed the his environment, he didn't actually need any more omeprazole. The next case is a 14 year old Irish sports horse gelding, which is used for low level show jumping and eventing. Initially presented with girthing pain and a marked grimace under the saddle, no obvious lameness, and when he was on treatment, he was much better, better propulsion, no grimace.
And but the minute we stopped treatment, his clinical signs returned, and he received long courses of, injectable omeprazole, oral misoprostol with or without sucralfate, steroids. And then we turned him away, and even when he was out at grass and not in work, the lesions returned. At this point we were supplementing with a pectin lettuceine supplement and corn oil.
And he's one of my failures because, you know, we looked at his saddle fit, we looked at his back pain. He did have some mild thickening of his small intestine, which was why we tried steroids. I tried simplifying his diet.
I tried an analgesia trial, and we ultimately, you know, we really did feel that this horse's clinical signs were associated with these lesions that you can see. And, eventually we ended up having to euthanize him, and I haven't had too many failures like that, but he is certainly one, and I, I don't have a, a solution, and I feel we tried all the avenues that we know about anyway, and we were not successful. The next one is an eight year old warm blood mare who was evening, presented with poor behaviour and generally just a bit of a bad attitude.
She was, you can see the lesions here on the right hand side. Normally I don't find these lesions super challenging to treat. You can see they're sort of hemorrhagic and sort of flat.
They are bleeding in places, so they were, they were severe. So she was initially treated with long acting injectable omeprazole, lesions improved but didn't heal, and the horse developed squamous disease. Now for me, if I can fix the glandular disease, I feel like I've won.
I've won my battle, especially if my clinical signs have improved, and because I know that we're gonna be able to manage and treat that squamous disease in 95% of of cases. Anyway, while she was, she was being managed, the behaviour under the saddle worsened, so she got treated with 2 weeks of oral omeprazole and sucralfate. She was re-scoped, squamous lesions healed, glandular disease, sorry, glandular lesions looked exactly the same.
She then got treated with 2 months of oral omeprazole, glandular lesions healed, squamous lesions returned. And, you know, she had got a reasonably good diet in terms of she was fed long fibre, she was turned out, she had small amounts of of grass nuts. And you know this is quite an interesting case.
She went through a bunch of different treatments, where we did ultimately fix her glandular disease and her clinical signs, but that both two lots of treatment caused the development of, of squamous ones. So. She was er she was challenging but fixed in the end, and again, not a horse that had any any evidence of lameness or pain elsewhere.
This was a 10 year old Cob Crossgelding that presented with recurrent colic. And the reason that I'm talking about him is that. When we look at the data that we've got.
We do see colic associated with feeding with very severe squamous lesions, but I'm not sure unless we've got very, very severe glandular lesions that that's something to be concerned with, and I certainly think it's always something to consider. We know glandular disease is quite prevalent. Is it, is it a bystander and are there other issues involved?
And I would strongly encourage you to always think about the rest of the abdomen as well as the stomach and not just think about the stomach on its own. So this was a horse that, these, these were its initial lesions. It then got referred to me because it continued to have recurrent colic whilst it was on.
Management for its glandular disease, and you know, these are the lesions that it's got here. They are what I would regard as significant lesions, but I wasn't convinced that they were the cause of its recurrent colic. And actually when we did, a full abdominal scan with motility studies, we actually found this horse had got reduced motility, it got thickened, small and large intestinal.
Wall, it had got fluid, within its colon and its cecum, and that when we managed its dysbiosis, we did in fact manage its colic, and in fact, these lesions, stayed pretty senescent, but quite a lot of money got spent trying to treat these for the management of its recurrent colic. Now I'm not saying that's true in every case, but I would say it's true in more cases than not. And my next case, I'm sorry, this is a slightly grainy image, but this was a 9 year old Andalusian stallion that was living on a livery yard.
He was used for dressage and he developed girthing pain. No squamous lesions, and you can see he's got this sort of raised, multiple raised hemorrhagic lesions, around the sort of top 2/3 of his pyloric antrum. And this was a really great case that I was so glad I saw on the yard and not that I'd seen in the clinic.
So, you know, he was a very well mannered stallion, and I said, oh, does he get turned out? And she said, oh yes, he gets turned out. But got turned out surrounded by mares and this stallion had been used as a breeding stallion when he was young.
So I did suggest to her, she hadn't got lots of money and I did suggest to her that perhaps he was moved somewhere else where he didn't have to be surrounded by mares and be able to smell mares all the time. So we moved to a small yard with two other geldings and without any treatment because treatment, the cost of treatment was a problem. These lesions resolved and his girthing pain went away.
So again, I think that detective work about that their management and environment's so important. And then this last case was a 12 year old warmble gelding with girthing pain. He had initially been treated by the referring vets with injectable omeprazole and then with ora misoprostol and sucralfate.
And this horse had, the, the, these lesions were as they were, so discussion was had about removal, . About removal of these lesions with the laser. And the lesions were, were removed, two of them were removed, and.
The horse then became really colicky while the procedure was being performed. I hope you can see from these, they've got a really, really wide base. And in fact, so 2 got removed and then the horse started being very colicky.
So we stopped and said, we'll bring the horse back in 2 weeks to have a try at removing the others. In 2 weeks later, the lesions had returned. And in fact, at this point, We discussed with the client, you know, these are likely gastric metaplastic lesions, .
Are they, are they the cause of this horse's clinical signs suggested that we did a more, a further workup with this, with this patient. And in fact this patient had got, a hindlim lameness. The Hindlim lameness got managed and his general demeanour, improved despite the fact that these lesions remained present and looking very similar to how they do in this image.
I'm gonna leave the foal for now. No, I'm not. So the next one is a 3 week old foal that's got broxysm and mild to moderate colic post feeding.
You can see that these lesions in the glandular region look very different to what we would see in an adult and that they are around the body, they're quite extensive, they aren't deep, but they are very extensive. And that we know that in many foals, the gastric pH is not low, this is not likely to be caused or being stopped to heal because of low pH. So this foal was managed with oral sucralfate, which I think is fairly much a, a mainstay now for.
For the management of these, of these cases in, in foals, and, he was re-scoped 4 weeks later and the lesions had resolved. And I think that the key with this, he was quite interesting, he'd been a dummy foal, he had, required plasma and some intermittent IV fluids early in life and you just wonder whether that had. Played a role or was a precipitating factor in the development of these quite severe lesions.
And then my last case, or, or at least my last foal case is, was a 3 day old Criola thoroughbred fillyfoal that presented with marked colic. This is it, radiograph, and no one's gonna be surprised if I tell you that it had got a meconium impaction and you can see that that we've got a reasonable amount of gas distension. This foal was pretty bloated.
I saw this foal quite a long time ago and at which point we didn't know any better, but the foal got treated with . So we, we, we saw this fold, it got an enema, we managed it. It wasn't particularly hypovolemic.
It got given some, carrofen as it's, as it's analgesia, and it went home. Two weeks later, the fall's been normal since discharge. It represents with mild signs of colic.
And at this point, we, on physical exam, heart rate was increased a bit, respirate was 18, temperature was top end of normal, and it got. Reduced ball break me. And the signs of colic were definitely worse after feeding.
So, it was gastroscoped, and you can see it's not got lesions quite as deep as that first one, but we've got these sort of, sort of bleeding. I always think of them as like scrapes, through that glandular body. So, because of when I saw this case, as I said a long time ago, it got treated with oral omeprazole because we didn't know any better.
So it was discharged on oral omeprazole and the clients reported that its signs had improved, not stopped, but that they were pretty happy with how it was. It then presented 3 weeks into treatment, depressed and off suck, and this was it's abdominal scan, you can see it's got quite a lot of free fluid in its abdomen and peritoneal tap recovered milk. And this foal had ruptured, had a got a gastric, we, we euthanized the foal and it had a gastric rupture.
And I've thought long and hard about this case over whatever it's been, 20 years, and I think that most meconium impactions are really straightforward, but that some, it probably does result in reduced blood flow and maybe ischemia to the bowel. The omeprazole. Remembering that hydrochloric acid has a role to stop bacteria that animals eat entering their intestines, probably didn't help with, with the, with the amount of bacteria that were both residing in the stomach and through the intestines and perhaps that gastric health.
You know, really was maybe was secondary to reduced blood flow either from that incident of the meconium impaction or before. But anyway, I definitely don't use oral omeprazole in foals, for either prophylaxis or treatment anymore. So in summary, I think to say most squamous and glandular cases are gonna heal.
Squamous more than glandular, I do try and prepare clients with glandular cases to expect that it's not gonna be a straightforward role. I really think we need to consider the whole horse and environment and not just the stomach, and we'd need recommendations for management beyond therapy because we don't need these conditions to keep recurring, where treatment, whatever treatment plan we choose is expensive. And one of my colleagues in Germany, she has a really interesting approach to the glandular cases in that.
She scopes them, she talks to them about management, and then she gets them to call 7 to 10 days into whatever treatment protocol. And if the horse's clinical signs have not improved in 10 days, then she considers changing that treatment plan before she re-scopes them, because her view is if they haven't improved in 10 days, it's either not their gastric disease or they're on the wrong treatment. And I think that's something we could consider.
As it might save our clients money if we've tried multiple treatments. I think for refractory cases, we need to think about concurrent disease and why treatment might have failed. And for glandular disease cases, definitely we always need a Plan B and a C.
And thank you very much for your attention. If you have any questions, you're always, very welcome to email. Thanks very much.
