So we're gonna start really, considering the adult horse, and we will look a bit at weanings, but we're not gonna venture into fos cause they could have their own 45 minute session in this area. And we're gonna consider a, a logical approach to start with. So we'll try and, and help you make a logical approach when you're looking at these cases to consider possible differential diagnoses, and we'll look at acute and we'll look at chronic diarrhoea.
We're gonna then cover the main underlying causes of diarrhoea in the adult horse. And from that, we'll look at what tests you need to take to help determine that cause, and then what tests you need to take to determine the severity of systemic illness. We'll look at what treatment can be offered in the field, bearing in mind that only some horses can be treated in the field, and we'll consider very briefly what can be offered in a hospital situation.
What do we know about diarrhoea? 100 litres of fluid in 24 hours enters the GI tract in your bog standard sized adult horse. And it's reabsorbed in the large intestine in a moderately pointless cycle, potentially.
Diarrhoea in the adult horse is large intestinal, and that means that you can produce up to 100 litres of diarrhoea for 24 hours, in a, in a bog standard sized adult horse, and that's gonna make a very, very sick and very dehydrated horse. But of course, there are huge variations. So there's variations of norm.
So, you've got the horse that just has a bit of the squits when you put its travel boots on, all the way up to horses with disease. But if you're considering the diseased horses, you've got acute or chronic, and then massive variation in severity to something that's really very livable with, maybe abnormal, but very livable with up to something that's severely life-threatening. The mechanism, well, it's through inflammation.
Inflammation of the colon is called colitis. And how does inflammation result in the diarrhoea? So through malabsorption, you can see on that top slide that it's losing the, the, the absorptive surface of the gut, increased secretion because of the inflammation, and then decreased transit time, which is, it's not just that things go through faster.
They, they travel through in an abnormal, fashion. So what's gonna be our diagnostic approach to these cases? So obviously you always ask your usual history, but the things that we need to focus on the key areas are, how old is the horse?
Is it acute or chronic in onset? Is there recent dietary change? What's the deworming history?
Are others affected, and has there been any recent nonsteroidal or antibiotic use or abuse if they've been perhaps, you know, giving out themselves and, not perhaps using an appropriate dose. And and those questions need to be asked sometimes quite sensitively, but it is important to try and find those answers and we'll explain why next. So how do I make a differential list as part of my diagnostic approach?
Now, I don't use this mnemonic for every type of medical condition, but it is really, really useful to help us build a framework to hang our potential diagnoses on when we're looking at diarrhoea cases. So, it's the gin and tonic differential. And I've just put the, little things that stands for there as a reminder, but we'll look at them applied to diarrhoea next.
So for chronic diarrhoea. There isn't a lot for genetic. Move on.
We're gonna move on straight into, infections. So we've got bacterial, and then we, we can drum that down, chronic salmonellosis, Lawsonia, which is more likely to be in yearlings and we'll cover that. Parasites, so strongylosis, hostoysis, inflammatory, sand, autoimmune, so inflammatory and, and granulomas is bowel diseases.
Neoplasia or chemical and toxic or iatrogenic, so non-steroidal use or abuse. So can you. It's actually, although when you see these cases, you sort of, it's quite easy to kind of panic and think, oh, there's so many things that could be causing it.
If you use this mnemonic and then you can hang your knowledge onto it, there's actually not that many things. And I quite like to use this to explain to the client what could be causing it. You know, especially when they Come up with their own ideas, of varying levels of sanity as to what could be, what could be causing it.
If you bring them back to this pneumonic, then you, you got it all covered. And I find that quite helpful. So we can do the same for acute, but it's actually a bit tighter still.
So very, very similar. So bacterial, for infections, so salmonella, clostridia, but toxin producing will cover that. Microbiome dysbiosis, is that cause, is that effect, it's important, it's unclear, we don't really know yet.
Parasitic, probably predominantly systemiasis, viral, coronavirus, they get everywhere. But we don't know very much about that yet. Nutritional sudden diet change, but they shouldn't be sick.
That's quite an easy one to rule out if they're sick. Idiopathic, at least 50% of acute colitis is, they do have a cause. We don't know what they are.
I think that's probably because we actually underdiagnose, viral causes. We don't really test for many of them. Because we don't know much about about them.
So, so a lot of times you don't find the answer. I do you think it's important to explain that to the client because you're gonna run a bunch of tests to find out the cause of the diarrhoea. But half the time, you're not gonna find out what that cause is.
It's still important to run these tests because it can change the way you treat things. But, it's before the client then whinges about the bill, it's good that you, you tell them beforehand, I, I may not find anything. And I'm, and that, that, that, that's what I expect in half of cases.
And then chemical and toxic or arogenic, non-steroidal use abuse and antibiotic induced, so there's actually not that many things that can be going on. And I, and that's quite helpful because it helps direct how we manage diagnosis of these cases. So that's my differential list.
So I think at this stage, it's quite useful to look in a bit more detail at those differentials, which is sort of slightly not quite the way you would manage the case in practise, because you'd go and see the horse, and then you'd get, get a bunch of tests and then you'd go from there. But it means that we understand why we're taking the tests we're gonna take and what we're looking for. So if we consider our bacterial causes, salmonella, not terribly common in the UK, I would say, partly maybe because it's not very easy to test for.
But it is quite common in other parts of the world. So, it can't just be that we don't test for it very well. For clinical syndromes, which, are as, as below, so inapparent infections with latent or active carrier states, depression, fever, anorexia, neutropenia without colic or diarrhoea.
Acute enterocolitis with diarrhoea and sepsis with or without diarrhoea. So it's fecal-oral transmission, and it can persist in the environment. And if you want to hear any horror stories about persistence in the environment, talk to any, anyone who's worked at the universities of Pennsylvania or Oslo, who really struggled to get it out of their hospitals.
And if your immune defences are compromised, for example, stress or illness, which is, you know, these are the horses we're seeing, carriers can get diseased and it's easier to get infected. Both carriers and infected risk, nosocomial infection and zoonosis. Fecalal transmission, this is one of my favourite pictures.
I just walked through the hospital and asked one of the interns if I could photograph their hands. I wouldn't, I didn't choose a particular intern, it was just the first one that walked towards me. And this is what they were like, just walking through the hospital.
So, hopefully, with the current pandemic, we're more aware of hand washing. But, really, really important, don't, even ambulatory practise, you can still at least sanitise your hands, try and wash them. And it, it's really basic, basic hygiene, but makes a really big difference.
And I, I guess, taking home salmonella infection, which a couple of my colleagues have done and ended up in hospital, is important to avoid. So if we're considering acute enterocolitis, which is sort of the one that most applicable really for this lecture, you get severe inflammation, ulceration, even infarction. And the first clinical signs are usually of fever and anorexia.
So you've got a horse that's a bit hot and a bit sad and a bit off its food, and then things get quite exciting quite quickly. They can become severely endotoxic, so the, with the inflammation bacteria, LPS can cross to the bloodstream, resulting in endotoxic shock, your signs of that, fever, tachycardia, congested mucous membranes, weakness, organ failure, resulting in a risk of laminitis and a risk of thrombophlebiti. About 24 to 48 hours after the onset of pyrexia is when the diarrhoea starts.
It's the, the, these are the 100, 100 litres in 24 hours ones. It's really severe, they become very dehydrated. They often have mild or moderate colic and a protein losing enteropathy.
And they're neutropenic early on. So you might miss it, but it is a blood test to take. Are they neutropenic?
Because then you, you, you would increase your suspicion of salmonella. And as a little reminder, most hospital policies are any two of pyrexia, depression, diarrhoea or leukopenia should result in isolation, and always err on the side of, of caution and if you're not sure, isolate. So how would you're gonna diagnose salmonella, and I've already alluded to the fact that it can be quite challenging.
So clinical suspicion, and then faecal samples. So, 3 to 5 serial samples, that will depend on your hospital policy, but, usually 12 to 24 hours in between each sample. For culture, but also really PCR, is more helpful.
Certainly, if you get a positive, the vast majority of places would say you need 5, serial negative samples before you can say you're happily negative of salmon Lear and can go out into the community. Sometimes if you're really sure the horse has got Sal Leonard, it's coming back as negative, you could take a, a rectal biopsy for culture. I think it's only something I've done once or twice, and probably not so useful now we have PCR.
So how do these guys get on? Well, you need lots of aggressive treatment, so these are not ones to try and treat at home. There's a high risk of complications.
There's a risk of them becoming carriers. They can develop chronic salmonellosis. And certainly, if they do develop chronic salmonellosis and they still have it 4 or 5 weeks on, they do seem to, they seem to carry a poor prognosis.
Now, some of that may be that they just They carry on, if you want to shifted in 4 to 5 weeks, you stay a carrier, or is it, when you look a little more at the data, is it just that after 4 or 5 weeks, everyone's a bit sick of it, and they run out of money, and they didn't give them any longer, so perhaps a little bit difficult to untangle there. So moving on from salmonella, another bacterial cause, would be Clostridia. Now, if you just take, a faecal sample and ask for clostridial testing, it'll come back with lots of Clostridia.
And that is because poo has lots of Clostridia in it. What we're looking for is enterotoxin producing Clostridium. So these are the ones that are not part of normal gut flora, but they can be triggered, for example, by antibiotic administration.
And that, and that's the classic. Antibiotic induced diarrhoea is, is clostridial often. So what do you do?
You take a faecal culture for testing and you'll find high numbers of Clostridia, but also the toxin, and the toxin is what, is important to explore. And they're gonna look like other causes of colitis, they'll vary in severity depending, on the individual, but you'll often have then this, this history of antibiotic administration, certainly not always. Material ones.
I thought it was important to talk about Laania, even though it's not really an adult horse thing. I have had it in a couple of adult horses, but those were in a kind of rescue horse population. So, be compromised to, to, to some degree by their, their previous management.
So, increasing incidents, we're certainly more aware of it. So there's, there's always that confusion of do we just know more about it. Or is it really increasing in incident?
I think it probably is actually increasing in incidents as well. Potentially faecal oral transmission, and therefore, if one is affected, I'd always think, check its, it's friends out. And often its friends may look OK, but actually, have a low albumin, or, or other such challenges.
What is Laania, it's an obligate intracellular pathogen and it induces proliferative enteropathy in the small intestine. And this proliferative response of the intestinal mucosa, as we've mentioned before, with, with, with colitis, alters absorption of fluid or absorption of nutrients, sorry, alters fluid, secretion, and it does this by disrupting the architecture of the vili and altering maturation of epithelial cells into absorptive cells. It's really just changing your gut lining quite dramatically.
This inflammatory response and malabsorption is what gives you the diarrhoea. But these cases because small intestines affected as well, severe weight loss, and not just because it's the small intestine, but they get protein losing enteropathy, and the protein loss or albumin loss can be really quite remarkable. So your clinical signs, you're looking at weaning folds, 4 to 6 months old.
So that's the vast majority of cases, but it, it can stretch a bit further than that. And they'll present with varying, levels of, of acute and chronicness, but i'll thrift, weight loss, peripheral edoema, diarrhoea, colic, and sometimes they look OK until you start doing some tests and realising that their albumin is very low, and you do the test because their friend is unwell. So moderate to often severe hyalinemia, so as I said that the albumin can be really quite shockingly low, high fibrinogen and they can be anaemic as well.
And on ultrasound, this is what you see, these great big fat thick edematous intestinal walls. How do you then go on to diagnose it? You need to, again, it's not that easy.
So to increase sensitivity and specificity, you're gonna do a serology and a PCR. And for a definitive diagnosis, actually, you need a, a, a biopsy. So hopefully, you don't need to do that.
But certainly, if you had to put one to sleep, then that, is something that you may wish to do for, a herd medicine point of view. So how are you gonna treat them? So supportive, and that may well include plasma transfusion for these guys because their albumin is so low and they may well need more than one.
Doxycycline. And how long do you keep them on doxycycline for until their clinical signs, hyperproteinemia, and ultrasonographic evidence of intestinal thickening resolve? How do they do?
Well, it's a lot of them do very, very well. And it's one of these things. It's it's a bit like Rhodococcus, because a lot of them do very well.
People often expect them to do very, very well. But there are still horses that do not do very well with Rhodococcus, for sure. And it's a, it's a similar situation with Loseno.
You'll get studs that have had it lots of years and they can get a bit blase about it, and a bit surprised when some of them don't make it. Prognosis depends on duration of disease, degree of fibrosis, and destruction of the intestinal architecture. So it's still in, the world of infection, but moving on from bacteria, we are gonna look at parasites.
So, scyathostemiasis is, is the one. And, actually, it really is the one at the moment. It's supposed, it's supposed to all get exciting with the syathostes, perhaps slightly later in the year, but, but certainly in the, in the Southwest, they've had a bit of a party early this year.
So the thy life cycle, the important part of it, is the migration of the 4th stage larvae through the mucosa of the large intestine, and they can insist. So that's called hyperbiosis, and they can insist in the wall of the large intestine, which I'm sure you are well aware of. And they emerge in response to an unknown stimulus, in early spring, late winter, it's, now is the 2nd week of January, and all the horses in the Southwest have decided to emerge some cy of stones, it seems, and get colitis.
It's actually now got colder, so maybe things will settle down again. What happens with this emergence? So, you get massive, massive inflammation of the colon.
And as we've talked about, what does inflammation of the colon do? It'll give you diarrhoea, protein losing enteropathy. Young horses tend to have a higher burden of syho stones, and, and you will know that those are the ones that are, are at risk.
How do they present usually acute diarrhoea? And, it can then become chronic. Weight loss, ventral edoema because of low protein, intermittent pyrexia, intermittent colic, and variable really degrees of, of severity.
So sometimes the worming history can be adequate. What do we want most of the times it isn't, what do we want it to be, for the insisted stage they should have in the winter. Really, they should have moxidectin.
5 dayenbanazole does appear to be significantly less efficacious at the moment. Sometimes you will have a history of a recent deworming which triggers colitis because of an inflammatory response to lots of, of dead parasites that may also be there in, in, in the worming history. Diagnose it.
So you're gonna diagnose it on history. You might find larvae in the faeces, such as this, and I lovely picture here. You may find larvae in a faecal sample, potentially a rectal biopsy.
I mean, ideally, you do a large intestinal biopsy because that's where they've existed from. But of course, you're not actually going to do that, because it Really wouldn't be ideal for this horse's recovery. And, no surgeon wants lots of diarrhoea, all over their operating theatre.
So I'd put that in tiny, tiny writing. The rectal biopsy, sometimes you do find evidence of, of insisted cystone, but you're taking a rectal biopsy to tell you about something that's going on in the colon. So, Not that useful, really.
And, and sometimes you will only diagnose them on, on postmortem. Most of the time they are a bit easier to diagnose. We've now got the ability to do an Eliza, which will at least tell us whether we're likely, to, to, to have had a high burden recently.
And I think that doing that is, is useful, to add to our armoury. So how are you gonna treat these guys? So, as for colitis, and we're gonna cover that, towards the end.
But you do need to deworm them as well. But when you do deworm, then you're gonna get massive inflammation when you kill the parasites. So that's gonna make the colitis worse, but you don't have a choice.
You've got to do this. So, how, how are we gonna treat them? Amoxidectin, rather than fenbendazole, because there's less than.
And it's often more effective, but if you're looking at all the textbooks, they have it the other way round. So, just as a, as a reminder there, and although the evidence isn't really there, the logic is to give them corticosteroids concurrently to reduce that inflammation. So moving on from those causes of diarrhoea.
We're going to look at toxic iatrogenic, causes. So we'll start with non-steroidal induced. So, usually, there's inappropriately high doses, so you'll get the owner that has some left from treating another horse and thinks it's a tremendously good idea to give Fluffy 3 sachets of be twice a day for 3 days, after he has a sore foot or something.
Or they've had it for a long, long time. So, you know, perhaps it's a riding school horse that's managed for a, a long time on a sachet of be twice a day. Or they've got, sort of other underlying problems, but, but, but not always.
You can get an idiosyncratic reaction to a non-steroidal resulting, in right dorsal colitis. And I certainly have, fond, I don't know if that's the right word, memories of an Icelandic stallion who had, reacted to a single dose of flinnexen for a, you know, that was given for a cut in the field. And it was a, you know, normal.
1.1 meg per dose of intravenous flinexin. And, and he ended up having, thousands, thousands of pounds, of money spent on him.
Or thousands of Swedish cra, cause that's where I was working at the time. But he, he rank plasma. It was incredible to try and keep his, his album and it's something that, that, that could keep him going.
So, he was very, very unlucky. So what happens with this non-steroidal induced? So right dorsal colitis, we get inflammation and ulceration of the right dorsal colon.
We don't quite know why, it is the right dorsal colon predominantly, but it has a slightly different blood supply and neural supply. So I assume that that is somehow involved. How do these guys present?
Well, the first thing that happens is quite often they get off their food and they're a bit sad. One of the problems with that is that they only goes, Oh, he needs some more painkillers, and gives them a bit more. They then will move on to develop colic and diarrhoea, varying in severity can be acute or more chronic, and they do usually get protein losing enteropathy and, secondary ventral edoema.
Not always. So diagnosis, obviously the history I think will, will send you hunting this direction. You may see a thick colon wall on ultrasound.
It does have poor sensitivity and specificity, but I think it's still quite a useful test because it helps you know whether things are getting better. Treatment, say standard colitis treatment, and stop non-steroidals and advise against non-steroidal use in the future, which can cause difficulties because there was a reason the horse was on a non-steroidal in the first place, and that may not be, that condition may not be manageable without non-steroidals, for that individual. Difficult.
Now, right now, how are you gonna, provide analgesia for the colics, so opioids, buscopan, potentially paracetamol. And very rarely these horses need surgical resection. Sometimes they do.
So, it depends how bad they are, whether you can manage these guys at home or not. This little chap, is, is a tape here, and I, I, I've momentarily forgotten his name. Which is a shame.
He's a very nice man. And he is a Bristol Zoo taro. He's actually now moved to a different zoo, but, he presented with colitis.
And tapi, are just small horses, who knew? And he had been treated for sore feet, which is a tapir thing, or a captive tapir thing. They like to get sore feet in captivity, even though he has these lovely rubber mats.
And he was given what was assumed to be an appropriate dose of Mesoam. But of course, no one really knows yet, do they, with zoo creatures. And he developed quite severe non, nonsteroidal associated colitis.
But, we managed to sort out what was going on. I did attempt a rectal biopsy successfully, but I hadn't quite realised quite how small the rectum would be. Which did help us because the, the history was a bit confusing, but we, we got there in the end and, he made a very happy, very happy recovery.
So what about antibiotic induced, and we have mentioned this a little bit when talking about Clostridia. So I think probably all antibiotics can cause colitis. If you look at the literature's most commonly penicillin that causes it, but, that's the most commonly used antibiotic, largely.
And there's a possibly a higher, a higher risk for tetracyclines, but again, perhaps a little bit unclear. There are papers from Sweden showing that that there's a sort of high risk to the dam, if, if they ingest the falls erythromycin or, the, when the fall's being treated for Rotococcus. And that is a, is a real concern when I worked there, but we don't tend to see it so much elsewhere, but I think we need to be very careful of not allowing the dam to get any of the fals erythromycin.
And by that, I mean, Any that gets smeared around the face, and clearing up any of the foal's faeces, you know, not the ones in the stable, but the ones that dripple down its legs and she gives it a good clean. And certainly broad spectrum and oral antibiotics cause more problems. How do they do this by disrupting bacterial flora and most commonly resulting in a clostridial overgrowth.
So tell me, you're gonna treat your antibiotic induced colitis, so you're gonna treat them as for colitis, but you have to do something with the antibiotics now. If it's mild, just stop the antibiotics. Although, again, there was a reason they needed the antibiotics in the first place.
So don't forget that. But, but if they are very severe, I, I, I will, rightly or wrongly, treat them with penicillin, gentamicin, and metronidazole, to try and sort of almost start again with the gut flora. But it is an area we are, are, are learning in, a lot, and we can debate antibiotic use in, in diarrhoea for.
For a long time with not being sure of the answer. So the next thing on our, differential list was the inflammatory bowel diseases. They often present as, as a chronic diarrhoea, but you can have an acute exacerbation.
There's a number of different diseases. Are, are they, are they more common? Are we just more aware of them?
And they can affect the small and or large intestine. They'll present with weight loss, if the small intestines involved, and diarrhoea, if the large intestines involved, and if you're really unlucky, both will be involved and you'll get both. And I think it's not wrong to think of the inflammatory bowel diseases as being on a spectrum.
So it's normal for some horses to get a bit of diarrhoea when they're excited, etc. Some will get diarrhoea if they eat haled. They don't seem to cope with that so well.
And then you'll, you'll get some that are really quite unwell with, diarrhoea, colic, and bloating. On diagnosis, on ultrasound, some will have a thickened cut wool, but as you said, that is perhaps useful for monitoring but poor sensitivity and specificity. On a peritoneal fluid sample, sometimes you'll see an increase in inflammatory cells, but we are unsure of that, .
Sort of relevance for management and diagnosis, I suppose we don't know how sensitive and specific that is. Biopsy is gonna be the thing that tells you what's going on. A rectal biopsy, I, I do like to do them because they're so non-invasive, but I think we can be very, very cautious of our interpretation because you're taking a sample of rectum to tell you about the large intestine.
So it could tell you something completely different. They take a lot of care with interpretation, and it may be that we end up doing small or large intestinal, biopsies doing that either standing laparoscopy or or laparotomy depending on, on the case and which bit of bowel you need. Treatment, I mean, this is medicine, isn't it?
So, steroids, rarely resection. And sometimes I have used a short fibre diet, so I've had some horses that just cannot cope. The large intestine cannot cope with, breaking down lots of long fibres.
So they are moved to a short fibre diet. So grass and then on on the last chough, ready, ready grass, that kind of thing, but quite, quite labour intensive. So I try and avoid that.
But I will have, I have had the odd individual who can only manage that way. And then YSA, there is, some evidence there that that helps with, reducing inflammation, through, I think increasing pH so in the, in the large intestine. It's certainly not going to hurt.
So the prognosis, I, I would say varies much more with the individual than with the severity or the type of inflammatory bowel disease you get. So, sometimes you'll, have an extremely sort of sick looking horse and has, you have one shot of steroids and it just turns around. And others won't look too bad, but you can't ever quite get on top of them.
And the same goes with the pathology. So you'll, you'll, you'll get your biopsy and it'll be, you know, an extremely severe. Inflammatory bowel and, and it'll be osinophilic or it'll be, liver lymphhoplasmactic, and it'll look dreadful and actually do extremely well.
And you'll get others who don't look too bad and don't do very well. So I think it, it, it really varies, much more in the individual. Some need one course of steroids and never look back.
Some need repeated courses, some stay on steroids forever, and you can't get them off and some just don't get better. And maybe we're, we're missing something in the diagnosis of these ones, but we don't know what that is yet. So to take you to a case, this was sort of one of my More interesting, inflammatory bowel cases.
I think this was a, a 16 year old Swedish form of gelding. And the only reported is have very sensitive guts. It's very quick to get a bit of diarrhoea and what have you, but nothing, and a bit of colic, but nothing that they couldn't manage.
But this winter increased in severity, had recurrent colic, bloating and diarrhoea, and he was under the weather. And this is him actually looking, pretty sad. He's, he was a very smart, a very smart horse actually, but he does not look, smart in that picture.
That is him looking. A little bit sadder than you should in Sweden in the end of October, November when you haven't got any snow yet. On ultrasound, I had thick and large intestinal wall.
I don't know the cause for that. I did a periconeal fluid sample and had lots of eosinophils. And what of course we, that's abnormal, but we don't quite know where that, where that fits on or, I think it, in this case, it did suggest we had an eosinophilic inflammatory bowel, but what we don't know is if you don't find them, is, is that still an eosinophilic inflammatory bowel?
On a rectal biopsy, we had a neosinophilic proctitis, and we made the assumption that this horse was likely to have osinophilic colitis and tried, treatment, with steroid, but we didn't, you know, with a view to if that didn't respond, that we would go in and do, exploratory laparoscopy or laparotomy. So we treated him with prednisolone and he had a fantastic response. I have a 3-year follow-up on this guy, and he needed a low dose of prednisolone to get through the winter when there's sort of not really access to any short fibre at all because of the snake.
And he didn't need any treatment at all in the summer when he was out on the grass. So this is him, and actually, you can see how quickly he's recovered. So, the top right pictures him looking.
Very sad. And then he's only been on prednisolone, really just a few weeks. So we now have some snow on the ground.
So we're a little bit further on in, in the winter, but you can still see where I shaved him for his abdominal scan, his big triangle, and you can see this guy's already, you know, put on weight and, and looks full of beans, and then that's one of him the the following summer. So, a pretty remarkable effect. Do, do you like steroids.
Marvellous. So idiopathic, don't find a cause for most acute colitis. You treat symptomatically, and do remember the rules for isolation.
As I say, I like, I do like to warn owners that with acute colitis, this is, is maybe where we're gonna end up, even if we take lots of tests, because I want them to know that there's a reason for me taking the tests, but that, if I don't find the cause, that's not because I've done something wrong. So what tests can we take? So, we're gonna need to consider how sick is the horse, and then what's the cause.
So we now know lots about the different causes. We know how histories to take, and now we need to kind of nail in, is this a horse I can manage in the field? How sick is it and what could be going on.
So, to assess the effect on the individual, consider dehydration. Obviously, just acute cases, the chronic cases should tick along. Heart rate is the most important, I think.
The one that you can do easily in the field. If you remember, cardiac output is, heart rate times stroke volume. Then if your, straight volume goes down, your heart rate goes up to maintain cardiac output.
So if you're drying out, your heart rate goes up. PCV and TP, can help with that. Certainly, PCV TP is all gonna be a bit confused by protein using enteropathy, slash, lots of globulins if you've got, salsone.
Endotoxemia is also gonna push up your heart rate, and you won't be able to tell with a high heart rate how much of it is dehydration and how much of it is endotoxemia, really. So clinical exam, look at those lovely mucous membranes, heart rate. And then, Are they inflamed too, are they pyrexic?
Routine loss, so don't forget to take, not just total protein, but an albumin as well. The albumin is, is gonna be the thing that's gonna give them ventral edoema. But if they're really, really dry, I mean, they don't have enough fluid to make ventral edoema, so don't, don't be conned into, a normal take or protein and, and, and a ventral edoema thinking that you don't have hypoalbuminemia, you may well do.
And actually, that, that horse may well be quite a lot thicker because it is so dehydrated, it can't make ventral edoema even. Electrolytes, I would take in acute cases and acid base, but I would do that in a hospital. So, you know, if I've got a horse that I think, hm, this horse is really dehydrated, a bit toxic, I'm not gonna try and manage that one, in the field.
And then the tests to find the cause. So faecal samples, for bacteriology, so the serial samples for salmonella PCR Clostridial toxins, egg count, and then you can do this viral, PCR as well on your faeces. Biopsies you may wish to do, for inflammatory bowel disease if you suspect neoplasia, possibly for, for culture PCR for salmonella, possibly for insisted sciatic stones.
The rectal biopsy we've talked about as being easy, low risk and cheap, but often not useful. I think you've got to be very careful with them. And therefore, you can, you can do laparoscopy or laparotomy.
But obviously, it's, it's case-based, whether you do them at all, and whether you do them standing or GA. And it, it depends whether, on, on, on the individual, whether it's acute or chronic, how healthy the horse is, what you're gonna benefit from, from getting the, the. It's gonna change your case management having your biopsy results, so it will vary very much on a case by case basis.
Belly taps, how useful are those? So, if you're considering neoplasia, about 25% of lymphoma cases and 3/4 of squamous cell carcinoma cases shed cells, but that was when, from a study that took 2 samples a day or so apart. So, if you're just doing one sample, obviously, you're gonna halve your chances of finding those cells.
So if you don't find Neoplastic cells on your belly tap, then We do further forward, but if you do find them, then that's very relevant. And the inflammatory cells and IBD are possibly a thing, but we're not quite sure how that fits in yet. Abdominal ultrasound, so look for a thickened intestinal wall.
You might see that in some cases of IBD right dorsal colitis, neoplasia, but poor specificity and sensitivity, but I said, it can help with monitoring response to treatment. Are you gonna treat these guys? Chronic diarrhoea, usually the horse is relatively stable, even if the underlying cause is serious and therefore your priority is to reach a diagnosis and then treat the cause.
With acute diarrhoea, some treatment will be specific to the cause, but in general treatment is very similar and depends on severity. Remember the rules for isolation. They are only suitable to treat in the field if they're not significantly dehydrated and toxic, sick.
And I think heart rate is your best in the field way of assessing this and just how sad they look. If they're sick with acute colitis, so the prognosis is 35% die with intensive care, and you cannot provide intensive care in the field. And it's unfair of an owner to expect you to.
If you did try to do intensive care in the field and you charged a privilege for your time, you could well be more expensive than a hospital and you'd be more likely to have a non-survivor. So don't feel guilty about explaining this. You shouldn't have to try and treat these horses in the field if it's not possible.
You are better to, euthanize them if a hospital referral is not possible than spend some money and have a dead horse anyway. And a lot of stress for you. So what's suitable and possible for suitable cases, they feed them.
You need to feed a horse with diarrhoea. It's the best way they're gonna sort out, electrolytes and things like that. Clean them, make them feel better, buy a sponge, probiotics, possibly, faecal microbiome transplantation.
And if you reach a diagnosis then targeted treatment for the underlying cause. Close monitoring, and if they start to get sick, they need a hospital and obviously all of these treatments are gonna be used in hospitalised cases too. It's a little bit more on those.
So bio sponge is, a type of mud, titrioctahedrals spectite, and there is in vivo and in vitro evidence that it binds toxins. It should lead to a decrease in secretion. For a useful dose, you need to stomach tube, it in twice a day.
And then I think you need to do a cost-benefit analysis on those you're dosing twice a day for several days. You know, if you're just giving a little bit by mouth and a little syringe, you're not gonna do anything useful. It's a lot to give by stomach even.
You need to decide whether that's the right thing for that individual, cause obviously you would have to sedate it and stomach to it. So cost benefit analysis on a case by case basis. What about probiotics?
So we know that you get sequel microbiome dysbiosis with colitis, and we can't, as yet untangle what's cause and effect. It's likely a mix of both. And in theory, therefore, probiotics should help.
But all that's been done experimentally with probiotics so far, what, what we've managed to do is actually induce diarrhoea. So I think watch this space, probably not useful at the moment, but they will be. So, something to watch for the future.
What about faecal microbiome transplantation, i.e., u see?
The idea is to repopulate the gut with a healthy diversity of bacteria, and it can have amazing results in people. Most work done on cases of C. Diff.
But in horses, there actually is a bit of work and there's fair evidence. Even though it's difficult to administer, there's acid in the stomach that can kill small, and, and the small intestine that can kill the bacteria. But there is still evidence it's useful.
You can potentially reduce the acid risk, by pre-treating with omeprazole for 48 hours, but then you delay starting your faecal microbiome transformation. And the same with antibiotics. So if you're giving them antibiotics, do you bother with giving them poo?
Well, I tend to do the poos while they're on antibiotics, and then when they come off antibiotics, do them again. What's the right way of doing it? You need handfuls of faeces, ideally from the rectum, if not freshly produced, of a healthy horse from the home yard for the right mix for your horse.
And you sieve it through gauze swabs and you administer it by stomach you in 5 litres of water for a 500 kg horse for 3 days, and I will certainly do that again. Dehydration, so make a fluid plan. Current dehydration, ongoing losses and maintenance, treating with IV crystalloids, and I think that's extremely difficult to do in the, in the field.
Electrolyte imbalance, so feeding them is the most useful, and spiking fluid bags as required, and acid base there's there's other things you can do, but hydrating them is the best. And again, we're we're talking hospital care. For low albumin and plasma transfusions, you often need to repeat them and they can be very expensive.
Endotoxemia, Flinnexin, so but but good study cos you can give colitis from Flinnixin in itself, polymexin B for binding L yes, and icing feet for laminitis. Colicolonexin, you may need opioids, spasmolytics. Do you put them on antibiotics?
I think that's really difficult, and I could literally talk to you for, for just as long again on, on how to decide. I guess the, the crux of it is in the hospital case, if they're sick, I will put them on penicillin, gentamicin, and metronidazole. After I've taken my faecal and blood cultures.
But it is very challenging to decide. You know, it has to be on a case by case basis. There's certainly no good evidence, actually, to use antibiotics in sick colitis unless they've got Clostridia.
And then there's some evidence that you shouldn't maybe use it in Clostridia, although I do. So, yeah, I could talk to you, in another session on that, but, you might not wish me to do that. What other treatment can you do?
Encourage blood flow to the colon wall for healing of inflamed colon, and including colonic ulceration. So how do you do that? Oral sucralfate and oral mesoprostol, they'd be very careful with that drug.
Both are prostaglandin agonists. How do you manage inflammation? You, you judicious use of steroid, case by case, day by day judgement, and the inflammation can cause the the colitis, the diarrhoea, but steroid is immunosuppressive and the sick cause may be back to remix.
So, you can make the wrong decision, without being negligent, but you need to have evidence that you've thought about whether you're going to give this drug or not, not, not, not just put them on a course of it. And to finish up with a case, you've got a 2 year old thoroughbred, across Philly. It's the spring.
And the owner reports an acute onset of severe watery diarrhoea two days ago, and now the horse is weak, but the diarrhoea has stopped. And, the classic, of course, is the only think the horse is a little bit better. But, however, your clinical exam, she's, she's weak, she has a heart rate of 100, a respiratory rate of 34, and ventral edoema.
So, you know, she's not better. She is really dehydrated, isn't she? PCV of 58%, total protein, 89 grammes per litre, but she's hyper-albuminemic, markedly so at 15 grammes per litre.
She is asidedemic and has a low potassium, which is kind of what these guys do when they have a lot of, diarrhoea and don't eat. So you do a rectal exam on this horse, and here are, was what you're expecting. Lots of, little worms.
This is a terrible video I know, but I was quite excited at the time, . I've got them here as well, just on my finger, which is quite gross and thank goodness I had gloves on. So that's what you find on rectal.
So you suspect this horse has sappotomiosis, and when you do your deworming history on this horse, it has not had oxidectin. Bacterial is, is another differential for this horse, but no one else is affected if that matters. There's no history of antibiotic or non-steroidal administration.
And of course, it could be idiopathic. But with those, worms, I think you can quite happily diagnose this horse with systemisis. How is she going to be treated?
She needs to go to hospital with an estimate of 3000 to 5000 pounds and quite a poor prognosis. What will they do in hospital? Correct the dehydration?
Correct the hyperbo anaemia, correct the acid bain electrolytes, feed her, look after her, and do all the other bits and bobs that we've talked about. So, buy a sponge, possibly probiotics, probably not at this moment, but certainly some poo soup, judicious use of steroids, deworm with moxidectin. Non-steroidals but careful, but she's end toxic so she might well want them, she might want some polymix in B.
Do you do antibiotics? Go steady, maybe, maybe not, depends how sick she is, and watch her for laminitis and thrombophlebitis. This is actually not her, but, but, this is one that was diagnosed at postmortem, and you can see how severe the sciatosomiasis, You know, that the inflammation that you get in this large intestine, you can see really why this horse didn't survive despite treatment.
So it can be an extremely severe, severe problem. So in summary, take a, a clear approach to the differentials for acute and chronic diarrhoea, and that means you have a clear approach to testing and to explaining what you do to the client. Take tests to establish the severity of systemic illness, test to establish the underlying cause.
Remember the rules of isolation. Don't try ICU in the field. It's not your fault you can't, and you can always ring for advice.
