Hi and welcome to this webinar on fluid therapy in calves. As many of you will know, I have a particular passion for making sure that we do the right thing where fluid therapy is concerned without making it too complicated. So an overview of this session is I'm gonna concentrate on calf diarrhoea and the silly that we see with that, because other than sepsis, that's the most likely time we're gonna use fluids in calves.
And to understand what fluids we're gonna need, gonna have a think about water absorption from the G I tract and when that can be a limitation in our hypothalamic patients, and then look at assessment of hydration status, which can be more complex in farm animals than it is in other species. And then we get to the big question enteral versus parenteral. And it's all about making the right choice rather than making the easiest choice.
So we're gonna have a look at IV fluids and the fluid types that are in vogue and those that aren't and some of the problems with those fluid types and then thinking about some new ideas regarding monitoring, which is very specific to this calf diarrhoea population. And then I'm gonna finish with enteral fluids having a think about oral fluid administration but also fluid administration, her rectum, which we perhaps haven't utilised as much in farm animals as we have in some other species, then having a think about the fluid types parenteral use and the impacts on what those fluid types are, And then, you know, really thinking about where those non parenteral fluids work really well. So let's start with causes of calf diarrhoea.
And as many of us know, there's a whole range of viruses, bacteria and parasites that can cause diarrhoea in the calf, and, depending on the age of presentation, is gonna have an impact on which of these is most likely and gonna be the cause. So we'll often see E coli in less than in calves less than seven days of age. And always remember that we're also likely to see sepsis in calves less than seven days of age and in calves.
The G I tract is their, organ of sepsis, so septic calves can often also present with diarrhoea, and the cause of that sepsis can be a whole range of things And then when we start to move to older calves, we're gonna start to see the viruses, particularly Rota and Corona, cryptosporidium. And then, you know, salmonella will will bridge that gap anywhere from sort of five days to a month. So why is this important?
Well, the reason it's important is really thinking about the impact that these bacteria, viruses and parasites are gonna have on the absorptive capacity in the G I tract. And although, calves of ruminants at this age less than 3 to 4 weeks, they are basically mono gastric. So there will be a small amount of fluid absorption from, the four stomachs.
But a lot more of it's gonna be reliant on the small and large intestine. And when we start to look at the pathology of this condition, we can see that, the principles are the same across largely across the organisms that we're gonna think of. But we're gonna start to see Vlasak atrophy and also, leaky T junctions, which then allow both bacteria and toxins to go from the G.
I tract into the systemic circulation of the calf and it we've got a two fold problem when we're thinking about, fluid balance because we're gonna get fluid. That's not gonna be absorbed because we've lost the surface area within the G I tract. But we're also going to see leakage of fluid because of those leaky type junctions into the G I tract that would normally be maintained in the body and always worth remembering.
You know, life begins in the gut, and everything is about the microbiome. And we're starting to see more and more data on ensuring that we've got healthy, good gut health early in life because that can impact on productivity and growth rates. When these animals, as these animals get older and when we're thinking about that water absorption, like I say, the large intestine, which normally doesn't feature very highly and when we're thinking about the gastrointestinal tract of farm animals is gonna play a role.
But so is the small intestine. And both of those regions are where these, where these organisms are causing problems. So now let's have a think about hypovolemia and water absorption, and we're gonna come to defining hypovolemia in in a in a short while.
But where hypovolemia is concerned we're gonna see loss of circulating volume. So within the intravascular space and the first response that the body has to hypovolemia is it tries to direct blood flow to the areas of the body that need it. So it will direct fluid away from the skin, which is a luxury to provide blood supply to the skin.
And it will keep that blood supply aiming at those essential organs. So the brain, the heart, often the kidneys, depending on what state of disease we're in. But again, it will often direct it away from the G I tract and that can have a real impact upon water absorption.
And we've already said we may well have disease that's impacting on that water absorption anyway. But if you don't have a good blood supply to the G I tract, then many of those normal functions, including motility, are gonna be impacted. And so we often have this rule when we're thinking about it that when we start to see fluid deficits more than 8 to 10% we have to think that that fluid is probably not gonna be absorbed that we put into the G.
I tract and depending upon the type of fluid it is, is going to, we're gonna think about what sekely we might see. So, for example, if we're given lots of milk, that milk is likely to start sitting around rather than being moving through the G I tract being broken down and being absorbed, which can then lead to, bacterial overgrowth, particularly with organisms like Clostridial difficile. And we can go from making a bad situation worse.
And that can also be true. When we're thinking of oral hydration solutions that have got glucose in them cos again, glucose is a great medium for bacteria to grow. So when we think about those changes that we see in calves with diarrhoea, we've got hypovolemia and we've got dehydration, and we're much more likely to see dehydration in farm animals than we probably are in other species that we deal with.
So when we're thinking about hypovolemia, we're gonna see hemoconcentration increases impact cell volume increases in total solids. Although remember those total solids might not be increased because of the loss through the G I tract, we're gonna see hyper lactate temia, which is caused by increases in L lactate, and this becomes important. As we move forwards and again, this is probably our most sensitive marker of hypovolemia in all species.
And then we'll see hypernatremia when we've got clinical dehydration. Now, just to add, complication to the to the challenges that we've already got in, calves with diarrhoea that will develop some very complex, metabolic derangements is we see AD lac, Leia now D lactates produced from bacteria. And we start to see that, within the blood of, of calves and sometimes adult, cows due to bacterial translocation.
Now, in all cases, whether it's caused by hypovolemia and increases in L lactate or D Lamia, because of, because of bacterial translocation, we can often start to see very severe metabolic acidosis. And again, try and remember that when we're thinking about the fluids that we're gonna talk about in this presentation. Now, what I would argue is we've come a long way in terms of, animal side monitoring in the last 10 years, and and this is where I think lactate metres can really be valuable to us in decision making, where fluid therapy is concerned in, sick recumbent calves.
So the lactate metres on the market will only measure L lactate. So that can be really helpful to determine whether we're dealing with a severely hypovolemic patient or whether we've got a sick, recumbent patient that does have severe metabolic acidosis but is in fact due to D Latia and I think this could be game changing in making sure that we choose the right fluids at the right time. Go ahead.
So it's always tricky where enteral fluids are concerned to do really good quality studies in clinical patients in clinical veterinary patients. And I think that's confounded even further in farm animal where we've we've got a multi multi causes of diarrhoea, but also they can be multifactorial, and the pathology that occurs in the G I tract is similar, but it's not identical between those organisms. So what do we know from other species?
Well, actually, there are very few studies comparing enteral versus parenteral fluids. There is one really good systematic review that looked at gastroenteritis caused by E. Coli Children and unsurprisingly, E Coline Children causes very similar pathologic changes to what we would see in the calves.
And what they found in this large, systematic review of, tens of thousands of patients was that enteral fluids reduced hospital stay and that there was no difference between administration of enteral and or parental fluids regarding duration of diarrhoea or weight gain. And so this, was the basis for the nice guidelines concerning what fluids we should give to Children that have got E. Coli diarrhoea.
And the conclusions were, that enteral fluids would be efficacious for in mild to moderate hypovolemic patients, but that if, more than moderate hypovolemia was present, then IV fluid should either be utilised or utilised alongside those enteral fluids. So I've been chatting away about hypovolemia and dehydration, and many of us have been brought up using the wrong term for what we see in our patients. And that's not helped by people using that very unfortunate term of percentage dehydration when actually, most of the measures that we've got are measures of hypovolemia.
So we're gonna try and put the record straight and move forward because again, this becomes quite important when we're thinking about fluid types that we might want to use. So when we think about Hypovolemia. We have great markers of hypovolemia available to us.
And this is, as I said before, loss of circulating volume from the intravascular space or the extracellular fluid and good markers for hypovolemia are increases in heart rate increases in capillary refill time increases in P CV total solids taken into account. Total solids may not be increased if we've got, protein losing enteropathy L lap tomia, urine output, urine specific gravity. And the other thing about these hypovolemic patients is we know we want to replace those deficits pretty fast, and we know that we've had both salt and water loss, which is why we don't see changes in sodium associated with hypovolemia.
But when we move on to think about dehydration, this is loss of body water, and this is water from both the intracellular space and the extracellular space. And we've got really poor markers of dehydration. We've got reduced body weight, which is all well and good.
If you knew what it weighed yesterday, which in some carbs we do, but not always. We've got sunken eyes. We've got tachy mucous membranes.
We've got increased skin tent now where we've only got a hypovolemic patient. Sorry where? We've only got a dehydrated patient.
We're gonna want to replace that fluid deficit much more slowly because we want that fluid to go from the, intravascular space. And we want it to diffuse into the interstitial, into the interstitial fluid and also to enter the cells. Now, in dehydration, we only see water loss, which is why HYPONATRAEMIA is a sort of surrogate marker for dehydration on our blood work.
And so I would argue that's why we should use the term fluid deficit rather than percentage dehydration. And the reason for this if we look through these clinical pathologic signs that are associated with it, Many of them are markers of, are markers of, hypovolemia and and or a combination of markers of hypo and dehydration because again increases in creatinine concentration that we, we call pre renal, disease or prerenal. Failure is again just a marker for hypovolemia.
So we before we get into the nuts and bolts of fluids, I want to give you the take home message, and that take home message is keep it simple. The dumbest kidney. As long as it's adequately perfused is smarter than any of us and really bear that in mind because it's very easy to do harm with fluids and more of something that's very complicated isn't necessarily better.
So keep it simple. So my rules of thumb when I'm thinking about enteral versus PARENTERAL. And I appreciate that some other factors come into this which include logistics and cost.
But my rules of thumb are Don't use oral fluids in animals that have got ileus. And we talked about the reasons for that fluid won't be a absorbed it can cause distension remembering, you know, with these young calves with, and the Rin or Groove, we often aren't gonna have fluid that's gonna be sitting in the room and we're gonna be pushing fluid, into that distal G I tract so it can cause distention discomfort and pain. And then the other thing is, as I've said, we can get bacterial overgrowth that can in fact, hasten the, the demise of those animals because of overgrowth of bacteria like C difficile, they are all they are usually cheaper, but they're not always beneficial.
But we need to judge each case individually, as we've said, because logistics and costs definitely do come into play. So let's have a think about the IV fluids that we've got available and think about their pros and cons, so we'll start with Hartman's. Hartman's is a balanced electrolyte solution, or lactated ringers, which is almost identical.
It's a balanced, isotonic crystalloid. It's got a relatively neutral PH, and it's got both electrolytes, and it's got, and it's got a buffer, and the buffer is in this case is lactate. There is absolutely no problem using lactate as a buffer, even in hypovolemic animals, because once you restore blood flow, you'll find that lactate will get metabolised.
And in fact, lactate is a very good energy source in neonates, and is often preferred as an energy source by the brain. So if in doubt Hartman's is a great choice, it's pretty difficult to do too much harm with it. My only exception would be perhaps, in those water deprivation salt toxicity cases where it might not be ideal.
We. Then you move to 0.9% sodium chloride, and this is obviously an easy fluid to make as homemade fluids.
But the key thing with it is that it is an Acidifying fluid, so it's a crystalloid, and, it's a balanced isotonic crystalloid, but it's Acidifying. And if we've got clinical signs associated with severe metabolic acidosis, 0.9% sodium chloride might not be the ideal fluid of choice.
Now this is hotly contested in human medicine, where they use a lot more 0.9% sodium chloride probably than we do in in veterinary, patients. But it's just something to bear in mind, so easy to make, not always ideal.
And when we've got, young animals that might be off suck or might not be, either consuming or absorbing as much of their diet as we would like. They're often quite reliant upon that diet to supply other electrolytes, like potassium, magnesium and, to some extent, calcium, which we're obviously not gonna be providing if we use 0.9% sodium chloride.
So if it's all that you've got in your car, it's absolutely fine. But if you have a choice, it might not be the best choice. We then moved to 5% dextros, so 5% dextrose is not a resuscitation fluid and is a really old tricky fluid to use that probably should be largely avoided in practise.
So 5% dextrose is made up of dextrose and water. So the minute that the dextrose gets taken up by the cells, we've just given water into that animal's veins. So although it starts off as isotonic, it ends up hypotonic, which can result in cell swelling, cell death and quite severe electrolyte derangements.
Also, if you work out caloric requirements for these animals 30 to 40 kilocalories per kilo per day, that's not all of them. But some of them we're gonna really struggle to provide anywhere near that without causing some very, very severe, acid base and electrolyte challenges. With, we're gonna struggle to provide those calories with 5% dextrose.
And then we move to hypertonic saline, one of my favourite products in adult animals. We use it as a resuscitation fluid. It will increase the circulating volume, particularly if we follow that up with, other isotonic fluids or fluids of some form given either IV or ally.
And it's a great way to resuscitate big animals. However, it's not such a brilliant fluid in, it's not such a brilliant fluid in calves, because NNH just don't cope with big slugs of sodium. All that well, so and normally we're not gonna be dealing with an animal that's more than 50 or 60 kg.
So we're gonna be opening bags of hypertonic and giving small amounts of it. We're probably not gonna want to give more than 4 to 5 million per kilo. And so that bag can go to waste.
So my top tip is, always make sure you check before you administer fluids that you are not giving whole bags of hypertonic saline to, to neonate because it's not gonna do them a great deal of good. And then we've got plasma, so we might wanna use plasma. If we've got very low proteins, we might wanna use plasma, usually in the form of blood.
But we might wanna use plasma if we've got, if we've got, failure of passive transfer, so plasma's a another. Another fluid in the armoury, and I'm gonna come back and talk about sodium bicarbonate on its own in a minute. So let's talk about sodium.
So let's talk about sodium bicarbonate. So This is a tricky fluid to use, and my my takeaway message is more is not better. So making sure you calculate how much you're gonna give and don't give more or double it or finish the bag would be my piece of top advice.
So we're gonna think about D lactic acidosis a little bit more. So we've got our calves, they're recumbent and they've got diarrhoea. And there's gonna be a significant number of them that their clinical signs relate to AD lactic acidosis, severe metabolic acidosis That is not due to hypovolemia and the clinical signs we're gonna see with D Lactic acidosis are gonna include ataxia obtundation impaired posture, change in behaviour and one of the I'm not gonna call it pathognomonic.
But one of the signs that might push you further towards these animals having AD lactic acidosis rather than collapse because of poor circulating volume is this impairment of the palpebra reflex. But just remember, there's gonna be some overlap here between these clinical signs and those that are gonna be seen by in in in animals that have got sepsis and or hypovolemia and severe dehydration. And I would argue again, that's where a lacto metre, which is relatively cheap and cheerful, can play a role.
However, if we're thinking about, the lactic acidosis, we are gonna want to go somewhere in the ballpark of 250 to 750 milli equivalents of bicarbonate. And most people will start somewhere around 2. 50 to 300.
And I would say exceeding 500 is usually never never necessary. And we've got bicarbonate in two formulations. We've got hypertonic, which will need following up with some, with some form of isotonic fluids.
And we've also got isotonic sodium bicarbonate. And this way we can work out how much we're gonna need And, how much we're gonna need and making sure that we give the right amount. You know, we can mix bicarbonate and so you can take your hypertonic solution, and you can add that to other fluids.
But remember, by adding hypertonic bicarbonate to 0.9% sodium chloride, you're gonna be making that fluid hypertonic. So if you've got it available, isotonic sodium bicarbonate has the least bad effects in terms of other electrolyte derangements.
Because we're not giving these calves this big slug of, sodium But if we can't do that, then using Hypertonic sodium bicarbonate and then chasing that with Hartman's ideally would be a good choice. You can see precipitation if you use bicarbonate alongside calcium containing fluids, but it is pretty unusual that you do that. So So this is the you know, the real indication for using sodium bicarbonate is the management of D lactic acidosis.
There is controversy about the value of bicarbonate when we're dealing with L, lactic acidosis or, if you like, increases in lactate that are due to hypovolemia, And my simplest analogy is that it's a bit like a ha. It's a bit like a stew where you've slipped with the salt and then you think you're gonna counteract the real saltiness by adding some sugar. Now it might improve your stew, but it's probably not the same as removing your source and starting again.
But when we look at the proponents of using bicarbonate sodium bicarbonate to treat hypovolemia, the proponents are it will improve tissue perfusion, which will help reduce the acidemia because we're in. We're making sure that those cells of have got have got oxygen and nutrients that they need, and it might help with impaired cardiac contractility, which we know can increase risks of, dysrhythmias And maybe why we see, occasional sudden death in these patients. The risks with it, particularly if we use hypertonic, are volume overload, hyponatraemia and overshoot metabolic alkalosis.
I can say I have never caused a metabolic alkalosis in a patient. You've got to really try very, very hard. But but remember, animals cope very poorly with an alkalosis, and especially when it's caused by bicarbonate because it puts a lot of pressure on the respiratory system trying to expel all of that extra CO2.
So the the other side of that argument is that the metabolic acidosis not when it's very severe but when it's M moderate, mild to moderate is it's actually protective against ischemia because it mini minimises hypoperfusion induced tissue injury. There's also some data to suggest that in the face of L Lamia hypovolemia sodium bicarbonate isn't very effective. And although the bicarbonate in the blood transiently increases, it seems to worsen that intracellular acidosis.
And this can in fact increase lactate production. Because of that increase in CO2 and bicarbonate. And remember that if we can perfuse animals.
They can make more bicarbonate because that's the job of the enzyme carbonic anhydrase, which predominantly does this role in the kidney but can also do it in the lungs. And then I come back to my take home message of the dumbest kidney as long as it's adequately perfused is smarter than any of us. So let's take our, let's take our recumbent C.
We've got a recumbent cough and it's, obtunded depressed. It's got no suck reflex. It's got a small amount of diarrhoea.
It's got cold extremities got an increased heart rate. It's got, tacky mucus membranes with an increased C RT. Well, how do we know?
Do we know and we're gonna go with? We can't decide whether it's palpebra reflex is changed or not. How are we gonna know?
Does it need harmans or does it need sodium bicarbonate? And that's where I think a lactate monitor or a measurement of lactate can really help us. So the calf that I'm thinking of that's in my head.
Is we? We measured a lactate, lactate was 18. So my view on that case is this Animal's got a severe hypovolemia.
It's also had cos it was a you know, it was a valuable calf. We'd got some blood gas measurements on it as well had a very severe metabolic Acidosis got a low bicarbonate, but it's got a lactate of 18, and normal lactates are gonna be less than 1.5 to 2.
So my view would be we're gonna bolus that 50 kg calf with a litre of Hartman's, and then we're gonna see what it looks like and the calf looks brighter. And so we give it. We redo our measurements.
Heart rates come down a little bit, Pil refill. Time has slightly improved. Extremities aren't quite so cold, so we give it another litre of Harman's.
By this point, it's quite bright and it's Studder and and then we can try and work out. You know, where do we go next? What's the cause of its diarrhoea?
Is it in fact, septic and that we need to be thinking of something other than a primary enteral pathogen? The pathogen is going to have come from the G I tract. It's just whether or not that's where it's doing most of its damage But then let's take the calf.
That is exactly the same is recumbent. You measure its lactate and it's two and it looks really sick, down and out and really sick. Probably giving that calf big bonuses of Harmans isn't gonna be what it needs.
So then thinking about well, I'm gonna give it 250 or 300 mini equivalents of sodium bicarbonate And then I'm gonna see what it looks like because by that point, we the sodium bicarbonate, will improve of its perfusion. Depending which formulation we use, how fast it will do that. And then we can then make a judgement a clinical judgement on whether that's worked.
My word of warning is just because it looks a bit better. Don't keep giving it more and more cos it is a surefire way of tipping, quite sick neonates over the edge and then resulting and and resulting in having dead calves. So when we think about the fluid combinations that we've got available, common combinations are gonna be crystalloids and sodium bicarb.
Ideally, harmans, because of that Acidifying nat nature of 0.9% sodium chloride in older animals, we've got hypertonic saline and colloids, which for most of us is gonna be in the form of of blood, usually to restore plasma or to restore oncotic pressure. And by combining hypertonic with isotonic fluids, we often get more rapid resuscitation.
But I would argue that's more relevant in adults than it is in calves, because calves just don't like that big slug of of sodium colloids. Plasma blood can be really helpful in animals that have got very low protein that can really give them, give them a boost and really give them a chance to maintain their circulating volume. And in a minute, we're gonna talk about different ways.
We give fluids it in giving IV fluids, and it's just worth remembering that we shouldn't ever give more than four mils per kilo of hypertonic and, that in the short term, Hypertonic saline has about 3 to 5 times the effect of the equivalent volume of CRYSTALLOIDS Harman's 0.9% sodium chloride. So let's have a think about fluid rates, and this is an area that has changed since a lot of us graduated.
So option one is that we assess the animal we assess the fluid deficit. We work out its fluid deficit in litres, which can often be a lot more than you were expecting it to be and that we then give half that deficit. As a bolus, we re examine the animal, and then we give the rest of the deficit, plus its maintenance requirements.
And remember, in calves, maintenance requirements are double that of adults. So around five mils per kilo per hour. And then we might add in anticipated losses.
Or we might just check the animal and then redo how much fluid we think it needs quite a tricky thing to do. If you're not there, and but you certainly can get farmers to help you with that. So if you like, that's probably a scenario that we use quite often because we can give the fluid that we want to in one or two bonuses, which can normally be done in the in the time that we're visiting.
The second option is that we give we check the animal, we estimate a fluid deficit, and then we give a fluid challenge. So fluid challenges for calves are an an adult cattle at 20 mils per kilo. If we were thinking that we were dealing with sheep and goats, they're a little bit more like cats.
They've got more sensitive lungs. We would give fluid challenges of 10 mils per kilo and then we would check them again and we would give a second fluid challenge. And then again, you can work out what your remaining fluid deficit is, how you're gonna replace it.
And it might be by that point, it's bright enough we can use enter fluids. And I suppose that's sort of the option. Option two is the one I've just gone through with that that first calf example where it's 50 kg, 20 mils per kilo is gonna be about, a litre we get.
And that's handy cos that's the size of a bag so we can give it a litre and we can look again. And then we can think about giving it another litre. But we know that if it's down, it's probably got an 8 to 10% fluid deficit.
So we're gonna be looking at a 4 to 5 litre fluid deficit before we think about maintenance requirements. And then the last option are total shock fluid doses. So this is the 60 mils per kilo for sheep and goats and 90 mils per kilo for, for farm animals, sorry for for for cattle.
And we now don't think that this is a great option. It's a very large volume of fluid for some animals. It's far too much for other animals.
It might who are very sick. It might not be enough. And this number came from This is the, amount of isotonic crystalloids that are equal to the patient's healthy blood volume.
Well, the patient hasn't got no blood volume or it will be dead, so it's not surprising that some of these animals end up having too much. So this was something probably many of us were were brought up on giving these really big volumes of fluids, and we now know it's too much. And if we give them too much, especially when they're sick, we're gonna be at risk of them developing pulmonary edoema or, tissue edoema or the tissue edoema.
And so these were just some some numbers to put in here, and these are numbers I've put in specifically for, for calves. So you know, shock fluid dosages, which I would strongly recommend you don't use for isotonic fluids. It's around 80 mils and then fluid challenges would be 20.
And if we give hypertonic saline, make sure you try to never go above four mils per kilo. And then I just wanted to put in. These are some recipes for IV fluid formulations that are adapted from a really Nice Vet Clinics article written by Jeff Smith in 2009.
So the top one is obviously the easy formulation that we can use to make 0.9% sodium chloride. Just remember, it's Acidifying easy to make, but Acidifying and then some of the others S mimic more closely.
Electrolyte solution two probably mimics Hartman's much more closely, although it obviously doesn't have a have a buffer like Hartman's would and the reason for putting this in. As many of you know, we go through periods of time, and we're in one at the moment where IV fluids are in short supply. But also IV fluids are expensive and that sometimes we want to create electrolyte solutions that match the needs of our patients better than we might be able to get from the two that we've got on the shelf apartments or 0.9% sodium chloride.
The other thing to just note with this is, it's helpful if you can use sterile water. And the best and cheapest sterile water comes from those, water bottle units that you often see in different offices and you can buy buy those from companies in bulk. Obviously, if we're dealing with small amounts, then we can boil the water.
But about 10 years ago, there was a, large fluid shortage that meant many large animals. Especially in North America, ended up receiving, homemade IV fluids, both neonates and adults. And a very nice study came out of, one of the North American universities that showed, In fact, they didn't see, significant, clinical signs that were associated with sepsis and bacteremia.
Using these fluids, they didn't see an increase in, catheter complications. So although it's a compromise, it's sometimes a compromise that we can make because these are obviously gonna be, financially and easier to do. So let's move to the second part of the talk, which is about enteral fluids.
And the key thing when we're thinking about enteral fluids is it's all about osmolarity and tonicity. So really thinking about what is the fluid that you're administering? And how does it compare to plasma?
Because if we've got an isotonic fluid and we put it in the G I tract and it's not quite as simple as this, but we're gonna go with this for now is that fluid is likely to largely stay in the G I tract, which is useful if you're trying to deal with a Luminal impaction or an impaction of other parts of the G I tract. If we give hypotonic fluids, then that fluid is gonna be absorbed from the G I tract simplistically. And if we give hypertonic fluids, we're gonna get fluid sucked into the G I tract so you can see we don't really want hypertonic solutions because if we use those in a diarrhoea case, we could worsen the diarrhoea and worsen the hypovolemia and or dehydration.
So really thinking about when fluids are being made up that we're using. Think about what it says on the label because changing how much fluid you administer them with or the type of fluid that you administer them with can really have an impact on how those fluids are gonna work. And then obviously we can provide calories via enteral fluids.
But we need to think about the impact that those calories have on tonicity as well. And then this is all confounded by this is what happens. Normally it's all confounded by we know we've got some sign significant change in that gut barrier, which is gonna have an impact on what fluids and what calories are absorbed.
Because we've got this big reliance on that, on some of those exchanges that are either likely to have been destroyed or be present, I much fuller numbers. So, I was lucky enough to do some work several years ago with Forte. And we, the, question that was brought to me was could I design the ideal enteral fluid for calf diarrhoea?
And I was like, Well, that sounds like a really cool challenge that, I'm a big, big lover of acid base, and I'm a great lover of looking at what's needed. And again, there have been some really great studies in calves looking at the needs of these calves when they've got diarrhoea. L generally, so you can.
So this table on the left sort of goes through what is ideal, what's perfect in terms of these ideal enteral fluids. So we know we need a particular amount of sodium particular amount of potassium. We need some form of sodium transporter because we know that sodium is absorbed with products such as glucose or glycine.
We know we need an amount of chloride we know we need We've got to have a particular, osmolarity. And although I said to you, we want them to be isotonic, we do know that sometimes slightly hypertonic solutions will help improve, absorption and energy levels in those animals. And then we need some alkalis ability.
So I sat there and thought, Well, this sounds like a really relatively easy challenge. We can do this on a and a few, pieces of paper. This sounds great.
So you come up with what looks like a perfect solution, but is it gonna be palatable? Cos if it's not gonna be palatable? This is not gonna be a product that's gonna be at all useful in clinical practise.
And then we've got all the products that you've chosen actually allowed to be used as ingredients in, in in products that are gonna be given to food producing animals. So you sit there and you're like, Oh, it's quite complicated. So, I can tell you, we had a few iterations, a few of the original recipes, there was no calf that was going to go anywhere near it.
And the OSMOLARITY was a really tough thing that actually the lower the osmolality often the more palatable the product. Not always, but often So So I'm just trying to explain to you about the very complex nature of what we know about enter fluids and what calves need. So in the end, hydro fasts came up with.
We did manage to get ideal sodium concentrations that were gonna be good for water absorption and rehydration. There were there was enough glucose to provide some energy, but certainly not all the energy, which is fine when we're often given this alongside milk. We had buffers that included, acetate propionate.
And then citrate was the, was the acid buffer buffer and the other cool thing about acetate and propionate is they'll act as those sodium cot transporters. So not only does the sodium help absorb them, but they help absorb the sodium we had, glycine added, which helped facilitate, sodium absorption and play some role in mucosal restitution. So that was pretty good.
I'd wanted to have glutamine in this product. Glutamine is a product used, in human medicine, often to help again, help improve, mucosal restitution and healing. Anyway, that wasn't allowed.
So we couldn't have that, And so this was how this product came about. So my I suppose my take home message with it is and I'm I'm certainly telling you about hydro Fust cos I know the most about it is not every enteral fluid is the same, and the newer products are using the the latest data that we've got available on what is the best? So in the, in the past, where we've had products that have had sodium, maybe potassium and glucose, very simple products, they're probably not, we now know that they're they're not gonna be giving the best results in terms of enteral fluid therapy.
And I shouldn't say you probably get what you pay for. But my guess would be some of these products that have got science behind them. Utilising research are gonna be, are gonna be a bit more expensive, but hopefully we'll you'll see the results that you want.
And then the last part of my talk I wanted to talk about protolysis and protolysis is utilising fluids per rectum, and this is not a new thing. And what protolysis can do is it can provide, fluids if IV access is difficult or not, possible for other reasons. And it can provide a and or either to supplement enteral or IV fluids or to be used on its own when enteral fluids aren't tolerated.
So we can give twice maintenance requirements. Per rectum safely. And its first major use was during the first World War.
And it was seen as a game changer in terms of survival rates during the, during the first World War, compared to, wars before where people had got hypovolemic shock, due to, loss of limbs. The other thing that seems pretty cool about protolysis is that fluids are absorbed better from the rectum in the face of hypovolemic shock than they're absorbed from other parts of the G I tract, and we don't know why that is. But it seems to, but certainly it is probably of benefit to us.
So the species that it's been used probably the most in are elephants, which, although they're very large, they are very difficult to gain vascular access to. And when you do gain vascular access to them, they're very good at removing their cannulas. And again, lots of studies have been done in, experimental rabbits.
I've done some work in using it in in horses in certain circumstances as well. So the other thing to note is that probably water, but not electrolytes, are absorbed from the rectum, and we don't know that's true in all species. But we certainly know it's true in some.
So in terms of practical uses, a soft, catheter that you can pass into the rectum, which is not gonna cause any damage. And then you can absorb fluids. Sorry, you can administer up to five mils per kilo.
My advice is, don't, administer it too quickly or you get a sort of reflex, rectal contraction. And, it either ends up on the floor or it ends up all over you, and we would use water for that. And if if you so wanted to put these, cannulas in, you can, then, either Chinese finger trap them to the dorsal part of the anus or find some way of attaching them to the tail.
So I think protolysis is a not a route of fluid for every scenario or every patient, but just might be worth thinking about as something additional or supplementary particularly, where IV fluids prob may be indicated, but for various reasons can't be utilised. So in summary, enteral fluids are always best. But there are a few exceptions.
And those exceptions are you've got really, really, hypovolemic, patients. IV formulations are not the same, and they've certainly got different benefits in different scenarios. And I really think you know, we we're at the point with, calci testing where if you can measure a lactate, you're really in a good position to say, Does it need Harman's?
Does it need sodium bicarbonate? And lots of these new enter formulations have tried to use data based on, optimal, management and absorption for these diarrhoea cases. And I would urge you to if you've always stuck with the same formulation, have a look at it.
Based on that table that I've just put up and have a look at some of the other products that are on the market and again, rectal fluids might have a role. And the good thing about them is, they can, as long as you give them the right type of tube can be safely administered by farmers and keepers. And with that, thank you very much for your attention if you have any questions, always happy to help via email.