Hello, my name is Louise Southwood, and I'm an emergency clinician at New Bolton centre, which is the large animal hospital for the University of Pennsylvania. I am going to talk to you about my approach to the equine patient in an emergency situation and a lot of this is is sort of back to back to basic stuff, however, sometimes I think a more basic, more logical approach to some of these. Patients can be very, very helpful with the decision making and to make the best decisions for both the client, and the animal so I always like to start you know with talking about history even though the history doesn't all need to be obtained before doing a physical examination and even in a lot of emergency situations before resuscitating the patient.

And so I start with the presenting complaint. Why did the client call you about the animal and it's important, I think as we're going through our workup not to lose sight of that, because sometimes, you know, we see some blood work, you know, we see something else and we get, you know, we get off track, so keep in mind that presenting complaint the specifics of why the owner called you. The other important information that we really need to get from the history, even prior to looking at the animal except if it's extremely emergent, is understand the character consistency and duration of the clinical signs the animal's been showing.

An owner might call you and say, My horse has colic, for example, and asking the owner specifically what that animal is doing, ask them to describe what that animal is doing to make them think that they've got colic is, is absolutely critical. Cause a lot of times, you know, the animal might be just down in the field. Maybe it's not colic.

Maybe the animal's, neurological, or maybe the Animal is, I had one horse that was bleeding, haemorrhaging, it was found, and they thought it was, colic. So being very, very specific about the signs that are shown. Another example is I've had some animals come in, for lameness, and it turns out they were actually coli.

So, so asking them to describe what the is doing is, is, is a key part of getting the history. You want to know the consistency and also the duration. Sometimes it's hard to really determine the duration because a lot of these, most of our horses don't live in our house.

They're out of pasture, and they're not observed 24/7. So finding out when the animal was last normal is when, you can kind of get some idea of the duration. Find out if there's any underlying disease, and if the animal is currently on any medication for any other disease process.

Several reasons for that. One is you wanna make sure if an animal is gonna be hospitalised that that medication. Is continued on that treatment for any underlying disease is continued.

Some of the treatments for underlying diseases can also cause other problems. So for example, your antimicrobials, and we all know about antimicrobial associated colitis. And so that should be on a differential for any animals say presenting for colic or fever that is, is already on antimicrobials.

Similarly, in non-steroid or anti-inflammatory drugs can cause problems such as right dorsal colitis, which can also cause things like colic and diarrhoea. And so knowing that history is absolutely critical. Also, if the animal is already on, say, an NSAID because they have chronic laminitis.

You don't want to go ahead and give the animal additional non-steroidal anti-inflammatory drugs because you yourself could create toxicity. So knowing what medications the animal is on is absolutely critical, not only for you differential diagnosis but continuing care, but also for preventing drug toxicity. The other thing is some owners are going to have given the animals some medications for the current problem.

For example, it's not uncommon for animals to have given a dose of clonexamagloin, prior to the vet arriving for animals with colic. And so you want to know that because that's gonna change a little bit how you, interpret your clinical findings. And once again, you don't want to give them another dose on top of that, that can create toxicity.

Understanding just any other underlying disease of this animal, or also any other animals on the farm as well, can help with your differential and work out what's going on. If it's a mare, I always want to know her reproductive history. Has she been bred?

Is she in full? What's the, at this point, where is she at in her pregnancy, the length of gestation? Where, has she recently fall?

How long ago did she fall? Has she Had problems with previous fallings because that is gonna change your differential diagnosis list substantially. Similarly for stallions, it's good to know if they're an active breeding stallion, if they've had previous history with, say, inguinal hernia, can be absolutely critical for working out what's going on with some of these animals.

I, also like to know, for me, knowing, is the animal eating, drinking, defecating, and urinating? To me, this is sort of the basics of, how an animal is doing, and I think And knowing this information can help you determine is this an emergency or is this something that you know, can wait and either come in or be evaluated on a more elective basis and both as primary care veterinarians in the field and also as veterinarians working in a hospital, we have to be able to somewhat triage and so, you know, knowing is the animal doing these basic things you know, can help us discern that as well as obviously their, their clinical signs. The other thing about this, it's good to know some of the basic management factors, for the farm.

So what are the animals fed, how are they fed, how are they watered? What's their water source, especially during, say, winter, is there, if their water source is a, is a, a creek or something, it's probably gonna be frozen depending on where you live. And also for defecating, the type, the consistency, the frequency, the volume of manure that's been produced in the last 24 hours.

And then obviously vaccination, history and andlementtic use, is important as well, specifically for see neurological diseases, for trying to work out, what should and should not be on your differential diagnosis list. As I mentioned in the beginning, the timing of taking your history, you do not have to get all of this information before you assess or even stabilise your patient, but at some point, during the workup and treatment process you should obtain this information so you can get . A better idea of what might be going on with the animal.

The other thing is I, I sort of added this a little bit at the last minute. I'm involved in quite a bit of communication labs, and I think when you're taking a history, it's really important to consider some of the key, communication skills or the core communication skills. And then things like open-ended questions, rather than saying, is your animal sick, you can say, tell me what's going on with your animal or what has been going on with your animal.

Open-ended questions, people are going to give you a lot more information, and then taking time to pause after you've asked a question and while the owner is talking to give them a chance to talk. That pause, is awkward for everybody, but it gets the owner talking even a little bit more, and they're gonna give you more information than if you keep asking questions. Reflective listening is also, important just to make sure you've got that history right and you've got all those details.

And then, your nonverbals, how to do if it's, over a computer, a doctor's visit, but they are, they are important, and Also, expressing empathy is important as well to get a relationship with that client, so they're going to trust you to treat their animal, and also share more information about their animal with you, which is gonna help you work out, you know, get closer to a diagnosis. So that was a lot on history. It is really, really important.

The other cornerstone in my mind to good veterinary medicine is a physical exam, and I like to start my physical exam by just taking a couple of seconds to look at the animal, just take a deep breath, step back and just look at the animal. Is this animal bright, alert and responsive, in good body condition, walking normally? It doesn't look like this horse which actually had about 45 ft of nonviable small intestine associated with a strangulating lipoma.

You can observe with this horse, even though he's not showing overt signs of colic, he has abrasions on his head. He's sweating profusely. He's in shock.

He has his nostril flare. So it's obviously in some degree of pain and shock. He had muscle fasciculations.

He was dull. This is a horse that at some point, even though he wasn't obviously showing avianderal at this point, at some point he had been extremely painful. Also.

Is there any signs of abdominal distention. Is the animal emaciated, suggesting, you know, maybe some more chronicity to the disease or some other underlying disease? Do they have evidence of diarrhoea, you know, down the back of the legs, like maybe they've, they've recently had diarrhoea.

Are they, are they painful? So, this horse obviously has laminitis, how are they standing? Are they shifting the weight on the legs?

Are they obviously lame in one leg, or are they showing obvious signs of colic? Like these horses, and I mentioned on history, I had a horse, not so long ago, present to me that, had it presented for lameness, and you can see the way this horse here, on the bottom right is standing, it's sort of lifting its leg, it's acting like it wants to go down, but observing that horse. Even just a couple of seconds helped me discern that no, this horse is actually colicing and that horse was a geriatric horse that in fact had a strangulating lipoma.

It took a while for me to convince the owner of that, but eventually we were able to take it to surgery and we ended up resecting a small intestine. I've also had animals, present like this that they, they've come in as neurological, and they've actually been colicing. So just taking that time, to look at your patient is, is really, really, critical.

And just remember, the signs of colic are fairly specific. You know, if the animal's looking at the flank, if they're kicking at their abdomen, if they're going down and actually rolling. That's generally an indication that there is some degree of abdominal pain.

Now it's not diagnostic for the cause of colic, but at least can tell you that it, that it is colic. Then I like next, once I've taken a few minutes just to look at my patient, then I go ahead and I want to assess the cardiovascular system, right? That's probably the most urgent system, at least on an emergency basis in courses.

So I want to get a heart rate, and I usually don't listen to the first say 30. Seconds when I'm taking my heart rate, because if I've just approached the animal, you know, they might be a little bit, nervous, and you'll hear a lot of times the heart rate will come down after those 1st 30 seconds. And then I look at their mucous membranes, to determine the colour.

Are they pink and moist? And so what do I do with that information? So, heart rate, and I'm just gonna go through this sort of sequentially.

I can tell you, once you get to a heart rate that's over 60 in the 70s, 80s, 90s, or above, that animal isn't just painful, there's some degree of shock. And so that animal is going to really require emergency resuscitation. So when I mentioned, I look at my mucous membranes, so then putting this together, I've got a horse with a normal heart rate, so 28 to 44, and if the mucous membranes are pink moist and a capillary refill times less than 2 seconds, I've got a very stable patient.

If, the mucous membranes are tacky, the capillary refill time a little bit prolonged. I've got a fairly stable patient, but maybe they're a little dehydrated, maybe a little bit hypovolemic. Moving on, moving on to a heart rate that's, you know, kind of in the 40s, 50s, so I call that mildly increased, and, you know, maybe the mucous membranes are a little, getting a little bright, maybe they're a little tacky.

They, they're probably painful, and then they've probably got some mild, dehydration, hypovolemic. Bullimia and endotoxemia, and then as the heart rate goes up, as the mucous membranes get more either brighter or more toxic looking, you're moving into the more severe pain, more moderate dehydration, hypovolemia. If I've got a horse with a really high heart rate, red, purple, mucous membranes dry, they're that bright pink, we're usually talking urs or endotoxemia, and I'll go into some of these definitions, in the next few slides as well.

If they're pale white, if I've got an animal with a heart rate of 90 and it's mucous membranes are really pale, I'm gonna be thinking, hemorrhagic shock. And occasionally keep in mind, even though most of the time when an animal's severely tachycardic, mucous membranes, are discoloured, you know, dry, prolonged pillary refill time, that that animal's gonna have pain and some degree of shock. However, occasionally we can see an animal that's tachycardic, and maybe the rest of the physical exam is unremarkable.

Occasionally these animals can have some sort of cardiac so an arrhythmia, and so keep that in the back of your mind if nothing is really. Fitting, that there may be an an arrhythmia that's causing that tachycardia. So this is just sort of an overview of how I, look at things and how I approach my cardiovascular assessment for my emergencies.

Another key thing, I always look at the jugular refill, that can be really helpful. That's gonna tell you how full your, your vascular system is, how full your venous, system is, give you some idea of your venous return to your heart, your preload, etc. And then I always feel the pulses and I also feel the extremity temperature.

And this is a paper that I just included here, it's an older paper out of the human literature, and they actually found that the patient's big toe temperature was just as accurate or maybe even more accurate at assessing perfusion as were all these invasive measurements. So you've got to get in, touch your patient, feel your patient, and that cools inappropriately cool extremities is a really important finding for me. So what are we talking about?

We're sort of talking about, you know, we're assessing perfusion, we're assessing the blood supply to the tissues. So if you think of it at a cellular level, Basically we're looking at the balance between oxygen delivery and oxygen consumption. And oxygen consumption in horses in equine emergency is usually not that much of an issue, like an increase in oxygen consumption.

That's more for your small animal patients that are having A seizure and maybe a fall that's having a seizure will have increased oxygen consumption. But most of the time we're focusing on inadequate delivery. If the cells don't get enough oxygen, we'll talk a little bit about lactate in a bit.

They don't have enough oxygen to make adequate ATP, and ultimately you get cell death. So what about oxygen delivery? I said, that's kind of, you know, what we're gonna focus on.

So oxygen delivery is basically just your, cardiac output. And your oxygen content. So how much blood is being pumped to the tissues and how much oxygen is actually in that blood.

If we break it down a little bit, the oxygen content is dependent on your haemoglobin. On the main time we get low haemoglobin is, or the two main reasons, probably the most common one is haemorrhage. And the other one can be hemolysis as well, anaemia from hemolysis.

So that's essentially having enough haemoglobin to carry the oxygen to the cells and then the other aspect is. Your oxygen saturation. And in adult horses, you know, in animals like small ruminants and falls, you know, with underlying respiratory disease, they can have inadequate, oxygen saturation.

Adult horses, occasionally we see it. We had one horse, in the hospital recently that, that, had severe pneumonia, and had inadequate oxygen saturation. However, it's less common in, in adult horses, but that's what, the main determinants of your oxygen content, even though the oxygen saturation over here is important, because of the oxygen haemoglobin dissociation curve, it really contributes relatively little, to your overall oxygen content.

So, so then you've got your cardiac output, which is your heart rate, times your stroke volume, and if you focus on, you know, stroke volume, that's kind of how full, your, how full your vascular system is. So then you've got your, yeah, like I mentioned, oxygen consumption is not that critical, in, you know, adult horses, unless they're having, some sort of a seizure. So the stages of shock, they go through compensated, early decompensated, late decompensated and death, and we have to get these animals early on in the compensated phase and the early decompensated phase.

Once they kind of move through the stages of shock, you're gonna get into situations like multiple organ dysfunction, and that's when the prognosis is, it becomes grave. So what are some of these, what are some of these compensations that happen, they're listed here, you've got your sympathetic nervous system, you're in an angiotensin abdosterin system, any diuretic hormone, adrenal corticotropic hormone, or act, and what they do, they increase the heart rate, they increase the cardiac contractility, they cause vasoconstriction. And they increase the water content, they, they, you know, anti-diuretic hormone or vasopressin causes vasoconstriction and, has the kidneys retain water and all this is to increase your cardiac output to maintain perfusion to the brain, kidneys, and, and heart so that that animal can survive.

And then obviously with all those compensations, that's what we end up seeing, we see tachycardia, prolonged capillary renal capillary refill time, maybe some oliguria, some azotemia and and blood lactate. So that's a cardiovascular system. I also pay a lot of attention to the respiratory system, sometimes these animals presenting on emergency can have underlying or primary respiratory tract disease.

When I'm evaluating the respiratory system, I look at the effort, obviously the rate, and the other thing is especially For some stoic animals, I look at their nostril flare and we'll talk a little bit more about this when we're talking assessing the colic patient. But for me, if they've got really dilated there, and they're, they're crinkling, their nose, that suggests to me, even though they might not be overtly showing pain that they're quite painful and potentially showing signs of shock. Always take the rectal temperature.

We'll talk a little bit more about antimicrobials very briefly at the end of this lecture. You know, basically take the rectal temperature to determine, do they have some underlying infectious process or is it something else that's going on? And then I always evaluate the gastrointestinal tract, listen forbiggy, and that can help you because colic and gastrointestinal disease is, is a very common reason for animals to present on emergency.

And even though there's some signs that are fairly specific for colic, occasionally these animals can, you know, it cannot be so obvious and ruling in or out the gastroent. Tract by listening for bulburigny can be helpful. The other thing is, some animals have, you know, for example, an animal with a fracture, or a severe laceration, they can develop secondary gastrointestinal tract problems and so assessing the gastrointestinal tract and monitoring it, is also important and obviously if you think the gastrointestinal tract might be.

Involved and palpation proactum, and transabdominal ultrasound as well, is another way to assess them. And I'm, I'm pretty, you know, try and be fairly simple when I'm assessing the gastrointestinal tract. I kind of determine are the gastrointestinal sounds present or absent.

If they're absent, that's usually pretty serious. And if they're present, are they normal, reduced, or even increased? And then I look at the quadrants to see which quadrants, you know, maybe they're absent in the left quadrant, present in the right, that's gonna make me think, maybe left-sided, gastrointestinal tract disease.

And then you finish your physical examination based on, you know, we've already mentioned the presenting complaint, but you're gonna ask more specific questions and get more focused, depending on what body system is involved or what body system you think is involved. So we're gonna, we've got another lecture on last. We'll talk about that and controlling haemorrhage, we'll talk about that.

We've already talked about respiratory tract, how to evaluate that. We're gonna talk a little bit about colic, and then obviously fractures, you know, evaluating radiographically and then, you know, determining, you know, if it can be repaired and what's involved, in the repair. So laboratory data, I tend to be pretty conservative, at least initially on an emergency basis, with measuring my laboratory data.

A lot of times what we do now, like I mentioned, at least on emergency is just point of care, we do not call in the lab. What's shown here on the screen. This is actually a horse that we had come in, recently, and this is our point of care chemistry analyzer that we use and the results of this, you know, there's always a bit of controversy, are they accurate or not?

Based on my experience, yes, I do. I think they're, they're fairly accurate, but you've got Assess your own, you know, if you do get one of these machines, assess your own, point of care, analyzer. We used to do point of care, blood lactate concentration and blood glucose concentration and just had those metres separately, which are obviously less expensive and a little bit easier to maintain.

However, since getting, this more comprehensive chemistry analyzer, it is, it is more helpful. So just going through some of these things, what are we looking at? This was a very, very sick animal and then unfortunately, the animal did not make it and they did not do a.

Mortem and so we don't actually know what was going on with this animal unfortunately, it did present for colic. So just going through it gives you the pH this animal is obviously acedemic, which is pretty uncommon in an adult horse. So that's our first clue that this, this animal is very sick.

And then it does give you blood gas, but this is a venous sample, so a little bit more difficult to interpret. It gives you the electrolytes and the thing that you'll notice about this animal, the sodium is a little bit low, not too bad for our analysis. That often makes us think colitis, although I'm not sure if that's what this animal has.

This potassium is OK. The chloride is quite low, and probably the most common reason we see for hypochloremia in horses and other species as well is sequestration of the chloride, in the gastrointestinal tract, so some sort of gastrointestinal tract obstruction, which is what we thought this animal had. Calcium was a little bit low, although this animal was very sick and endotoxin, can drive calcium into the cells, so whether it was, whole body calcium or just blood ionised calcium, but we probably would have supplemented with calcium.

So TCO2 is essentially a bicarbonate. It's a little bit low, on this animal, as well. The thing of note, and I use often use glucose and lactate as sort of, screening, especially for colic patients, normal lactate for normal, completely normal animals should be less than one.

Often animals that maybe have been trailered, you know, maybe they're a little bit dehydrated, often they're less than 2, and, and generally speaking, we usually consider less than 2, as normal. Once you're approaching 10, that's, not a good prognosis. This animals like 17.

So this animal severe shock and that fit with this animal had a heart rate of 80 to 90 beats per minute. So this is poor prognostic indicator severe shock. So obviously we started fluids with this animal.

The other thing is, blood glucose, in milligrammes per deciliter, normal is less than about 120. These animals, a sick animal will often have it, for example, a sick colic will often have it, definitely over 150, but often in the 200s. This animal had 557.

This suggests severe glucose dysregulation, and glucose is usually very, very tightly regulated by the body, so except when you've got stress, you know, shock, endotoxemia, all those things lead to dysregulation, and that's, that's obviously a poor prognostic indicator as well. So I often use glucose and lactate, sort of a screening to determine how sick the animal is, you know, usually when I see a glucose this high, I'm thinking some sort of strangulating obstruction. Moving down, you can get your, creatinine, concentration.

Obviously this animal and, and what we're looking for, primarily they're on emergency, a lot of times we're looking for pre-renal azotemia, as I mentioned, as an indication of poor perfusion. Once you're getting above, say, 3, I do worry about, and this is obviously milligrammes per deciliter. I do begin to worry about, actual renal acute kidney injury and renal damage, and I would be concerned about this in this horse.

OK, so now we've got an animal presenting the colic that has a lactator 17. And a blood glucose of over 500, and we got the hematocrit, and you can also see up here, we measured this point of, point of care as well, PCV and total solids or total plasma protein, and this is, this is from the the centrifuge and the microhematocrit tubes, 36 and 6.5.

And this is a really important thing to note if you've got an animal in that degree of shock. And the PCV is only 36% and the total solids is only 6.5 grammes per deciliter.

You've probably got an animal that's haemorrhaging, and this is a really critical point, even though they're perfectly within normal limits. It doesn't match with that presentation of the animal that's severely dehydrated in severe shock. Should have marked splenic contraction.

This doesn't fit. And so, you know, when, we found these values that made us think that maybe this animal is actually haemorrhaging somewhere, and at this point they started to fluid resuscitate this animal and they rechecked the PCB and total solids and it was down to 23 and I think it was down to 5. So this animal, whenever you see this, it's, it's relatively, it doesn't make sense and so it's obviously a lot lower than this, and and the animals haemorrhaging, so keep that in mind.

I think it's a pretty common mistake to see that PCV in total solids and think, oh, it's not that bad, when really it is. So just moving through, we also have bicarbonate and then some of these other measures of acid base as well. So this can be really important to help for for prognosis, to help kind of try and discern help with your differential diagnosis and also to guide your fluid therapy and your electrolyte, any sort of electrolyte correction.

So, other things I do measure, not always on emergency but I measure white cell count, blood white cell count, and we use fibrinogen or serum amyloid A as just a measure of inflammation. And it's not uncommon that I will measure them the next day. And what I'm mostly on an emergency basis, what I'm mostly looking for with my white cell count.

Is leukopenia, as opposed to necessarily a leukocytosis because that's gonna change my differentials if I think, if I see an animal that's fairly leukopenic, I'm gonna think some sort of gastrointestinal, problem, versus a leukocytosis. If it's a severe leukocytosis, so, 20,000, 30,000, I am going to be thinking more, some sort of severe infection. So I mentioned, I've already mentioned some of these, I'm just very briefly gonna go through some of the definitions.

Just remember endotoxinia we throw that term around a lot. It is just endotoxin or lipopolysaccharide circulating in the blood. And the thing that we're really referring to when we talk about endotoximia in horses is urs.

So when they absorb that endotoxin from the gastrointestinal tract usually or from any other a source of infection. The lipopolysaccharide or the, the gram-negative bacterial, cell wall component causes, causes a big inflammatory response. And so SERS or systemic inflammatory response syndrome is simply clinical signs with two or more of the following.

So you've got fever or hypothermia, tachycardia, tachypnia or hypocapnia, and then your alterations in your Your white blood cells. So that's what we're referring to with that. Seism and shock can lead to multiple organ dysfunction syndrome, and I did mention that already, and that's when you start to get, you, you, your animals in shock and you start to get dysfunction of some of your organ systems and we saw in the The animal that I just described, that animal was in, had probably had some degree of acute kidney injury, so it had renal failure.

It, that animal likely had a coagulopathy. So, and probably had a gastrointestinal issue. And so, you can see that that animal had some degree of multiple organ dysfunction.

There's some other definitions, just people use these all the time and just so you know what people are referring to as sepsis is just SERS, so that's systemic inflammatory response with an infection. Severe sepsis is sepsis plus your multiple organ dysfunction, hypo perfusion or hypertension, and then septic shock is sepsis, so you've got an infection, and it induces a hypotension that persists despite adequate, fluid therapy. Shock, there's, there's the two phases of shock, that have been described as hyperdynamic shock.

That's when you're tachycardia, tachynic. You've actually got the capillary, the nucleus membranes are really hyperremic, and your capillary refill time is really, really short. So this is when the animal is compensating, and then that can progress if it's not treated to.

Hypodynamic shock. And that's when the, the body starts to shut down and you, move into multiple organ dysfunction syndrome. And so that's when, this is when we want to see our patients.

We want to start, treating our patients when they're in that hyperdynamic compensated, phase of shock. And the DIC or disseminated intravascular coagulopathy, you know, 3 out of 5, of any of your, you know, measures of coagulation, and, what we noticed first in these patients is obviously clinically, you know, you'd be concerned of some sort of coagulopathy whenever you've got any animal in, you know, shock or, you know, Surs or or septic shock. We often notice first with these animals, they are hypofibro.

Gemic, so I mentioned we measure fibrinogen, often not on emergency, often the next day, but their fibrinogen is actually low, and the other thing we can notice fairly early on that we measure just in our our blood work is thrombocytopenia, so a low platelet count. So that's sort of the assessment component. The next, one of the really, really important things that people underestimate is intravenous the importance of intravenous catheterization.

So that's actually gaining venous access for your patient, that's sick. And the most commonplace that we place a catheter is the jugular vein. You can also.

To use the cephalic or the lateral thoracic. I can't imagine trying to get a cephalic catheter in here, on an emergency basis, especially with a colic or a neurological case and even the lateral thoracic, most of the time you can, you know, if animals are sick, you can actually see the, the vessel filling. However, sometimes it needs to be ultrasound guided, so we're kind of stuck with the jugular vein.

I wanna say a couple of things. If you are gonna place an IV catheter in primary care, I think that's a good thing. I think it's always much easier to sedate an animal through a catheter.

It can ultimately be less traumatic, but just really make sure that it's aseptically placed, a traumatically placed, and then it's secured in place, really well. Because, you know, a badly placed catheter can lead to, problems with, the jugular vein down the road. Usually, we are most often use a 14 gauge catheter, it's a good size.

Occasionally people will use a larger ball catheter, if they want to get, fluids in faster, and these 16 gauge catheters, we'll use this if we're not administering fluids, if we're just doing a microbials or in, holes, for example. So most often and most easily placed is a Teflon catheter. The issue is these catheters can kink, they can break, and this kinking where I think, oh, it's kinked, it's not too bad.

I mean, that can be very traumatic for the brain and it can also, tear a little bit and so that any medication you're administering through a kinked catheter, that can actually end up in the subcutaneous space which depending on the medication. Can actually be disastrous. Thrombophlebitis, septic thrombophlebitis, there's nothing worse in my mind if you successfully treat an animal, and then you'll end up with problems with the catheter and these, polytetrafluoroethylene or Teflon catheters, are, are more thrombogenic, compared to some other materials such as, say, elastic or polyurethane.

So this, this is just an example from Mila, however, there are other products, they can be, given over the needle with a stele or over the wire, which is the technique described here, . And this is called the Seldinger procedure. It's a little bit more effort to put in, but if your patient is stable, it's gonna have a catheter for a while, I've been using these catheters a lot more in my, in my, patients, than the Teflon catheters just cause I've re especially recently I've had some problems with them and once.

Again, there's nothing worse than you get your animal, you know, you do this great job treating the animal, and they have a catheter associated infection or thrombophlebitis that you're sending them, sending them home with. So essentially you place your needle, and this is just an example of a 14 gauge needle, and these actually come in a kit, so it's not like you have to grab all the pieces. So you put the needle, in the vein, and then you feed this wire, you feed this wire through the needle.

And then you remove your needle, from over the wire. Absolutely, absolutely critical that you do not let go of that wire because with the flow of blood, in the jugular vein, if you let it go, it can get, sucked into the jugular vein and you can lose it. So never ever let go of your wire.

A lot of times we, then dilate the skin, and so there's a dilator that you feed over the wire, dilate the skin, take the dilator off, and then you feed, the catheter, over the wire and into, and into the vein. And then you go ahead and secure it in place, with the, with the holes and the notch. And like I said, these catheters tend to be a lot less thrombogenic, they're designed for more long-term use.ifficult to place if you've got an animal that's thrashing around, obviously, however, for more long-term use, they can be good.

So catheters, like I mentioned, they can be problematic, and you have to look out, you have to place them appropriately and you have to, look after them appropriately. They should be checked and flushed regularly. They should never be left in longer than needed.

If I'm finished with antimicrobials and fluids, I get the catheter out. I do not leave a catheter in. There's a phrase, and never let the sun go down on an unused catheter.

You've got to monitor them for kinking. If they kink at all, get them out and replace them if needed. Occasionally I've had an animal, that develops a fever.

I've removed the catheter, the fever has gone away. So they can definitely be a source of, infection. They've got to be monitored closely for any heat, pain, swelling, or drainage, anything, get the catheter removed.

And we actually usually put some, topical diclofenac or surpass, on top of, just treat it, locally with that if there is even a slightest amount, of swelling. Look for clotted blood and then obviously look for any sort of loosening between the catheter and the extension set or injection cap, because if that becomes dislodge, most of the time the animal just bleeds through the catheter, which is not ideal in itself. However, if they suck a large amount of air, that can be, that can be fatal.

So you've got to be very, very careful with that. So, fluid therapy, if you're in primary care, You know, if you're in primary care and you have a referral that's say within 30 minutes, an hour of your practise, I probably, you know, a referral is an option. I wouldn't necessarily go for this, especially if it's a colleaguelic and you think it needs surgery.

I would never give fluid therapy on the farm that might delay surgery. However, if you've got a sick animal that has a long trailer ride, some fluid therapy may be beneficial, or if you need to manage them on the farm. There's, there's several charts, some are different to this, different people have slightly different, value, values, and these are just as a guideline.

The way I look at it though, I tend to simplify this, 5, 56% dehydrated is minimally detectable. OK, so that's minimally detectable, and then I jump up to here, 12, they're about to die. And so that's kind of the two numbers, 5, 6% minimally detectable, 12%, they're about to die, and so, you can just assess your animal as being in between, say, 6% and 12%.

So if it's moderate, they're probably maybe 8% dehydrated. The really important reason that I put this up. I remember, even so for a horse, 500 kilogramme horse that's even 5% dehydrated, their water deficit is 25 litres.

And so one of the important take home here is that horses, if they're dehydrated, they need these huge volumes of fluids, giving them a litre or 2 litres is not really going to help an adult horse. So what fluids do we, so they need large volumes of fluids and typically, what we do say you estimate, you know, 25 litre fluid deficit, we'll maybe replace half of that, so we maybe will give this animal a 10 litre fluid bolus, and then we follow that up and replace the rest just with maintenance fluids at a at a maintenance or double maintenance rate. So these are tight usually in large animal medicine because we use the 5 litre bags, these are the basic fluids.

Remember, these are replacement fluids, they are not maintenance fluids, the sodium. And chloride are quite high, for maintenance fluid and the potassium is low. So usually, you know, if we're going to use these for resuscitation, they're great because the, the composition, the electrolyte composition is similar to that in plasma.

However, we usually use them for maintenance fluids as well, and so we need to add Potassium for maintenance, as well. So, often you give a 2020 mL per kilogramme bolus and then you reassess the patient. And so that works out very nicely at 10 litres for a 5 kilogramme horse or 1 litre for a 50 kilogramme neon neonatal full.

You can give it fast, you can give up to 60 mL per kilo in that first hour, however, that's a lot of fluids. Couple of things, just remember, if you've got a hypokalemic animal and you're trying to correct the potassium, you have to do that very, very carefully and do it slowly. And it has to be less than 0.5 million equivalents per kilogramme per hour.

And so you need to calculate that in, when you're supplementing potassium, most, mostly for resuscitation, but also if you're adding it to the maintenance fluid, so you do have to be careful. And then, hyponatrium hyponatrim if it's chronic, and by chronic, that's probably if it's been going on longer than 48, 72 hours, you wanna make sure that you correct that slowly and ideally at 1, less than, less than 20 milli equivalents, . Per day.

And, and so the only way to measure that, the only way to monitor that is truly by measuring sodium in the blood, so measuring their electrolytes. And it is, it is not that easy. You can do all the calculations you want, and it doesn't always work out, the way you think because of ongoing losses and other, mechanisms.

So, and then a maintenance fluid rate, we usually use 2 mL per kilo per hour and remember for maintenance, we need to add in potassium and usually we add 20 million equivalents per litre of fluids. So what happens to these fluids, you're trying to resuscitate these animals and so I just want to take a couple of minutes to, think about where do these fluids go, when we put them in. So if you think about the total body water, your estimate 500 kilogrammes or 60% is about 300 litres.

And remember that's divided into your extracellular fluid, which is both vascular and intravascular, and then your intracellular fluid. And remember across this is your cell membrane here. Water can move freely across that cell membrane back and forth, and so can small uncharged solutes as well.

And remember there's, there's a, there's an electrolyte gradient that even though they have a similar osmolarity or number of osmotic active molecules, intracellular and extracellular, and they're slightly different. And this is maintained by several pumps because these electrolytes cannot just cross between the cells. And then there's channels, pores, carrier proteins that regulate this, and regulate other proteins, and molecules going in and out of the cell.

And keep in mind too, osmosis is just the movement of water, from low solute concentration to high solute concentration, and, and something to keep in mind the way I think about it as well is water follows sodium. So that's, that's what drives a lot of the osmosis, and this is where you can get into trouble if you're trying to correct either hyponatremia or hypernatremia. What happens is, is your cells in your brain have adjusted to that alteration, in, in osmosis.

They've, they've adjusted by creating these idio. Gen ic osmos or getting the idiogenic osmos out of the cells. So they've adjusted so that there's no swelling, intracellular swelling, or dehydration of your brain, and you go correct that really quickly, that's where you get pontine demyelination and you can have neurological signs if you correct your sodium, hyponatremia or hyponatremia, too quickly.

So let's talk about the extracellular volume, because that's where most of the fluids are gonna go. So vascular is about a quarter, so 25% and extra vascular institial, about 75% and this penetrated line here represents your capillary membrane and water and electrolytes can go freely across that and then you've got. Your primarily, your proteins, but primarily your albumin that are responsible for oncotic pressure, and then you've got your water that's responsible for your hydrostatic pressure.

So, so the, the blood, comes into the capillaries, your oncotic pressure, draws it in, and then your hydrostatic pressure pushes water out of the vessel. And there's a slight, there's The hydrostatic pressure that's forcing it out is slightly higher than the oncotic pressure that's maintaining it, and then your lymph drainage picks up the extra, extra vested water and returns it to the circulation. And this is just described by Sterling's equation, you know, which might seem overwhelming, but it's it's actually fairly straightforward.

This J is your net movement of fluid in or out, mostly out of the bloodstream. The K is your capillary fluid filtration coefficient, which is kind of the surface area of the capillaries. In your, in your body over which the fluid is moving.

You've got, the pressure inside your capillaries, the pressure in your, in your, inner sicium, and then you've got your reflection coefficient, which is how easily or not, protein can move in and out of the the capillary, and then you've got your plasma oncardic pressure and your institial oncardic pressure. So it's basically the, the, hydrostatic pressure and your oncardic pressure that distribute fluid across the capillary membrane from the vascular to the extravascular space. And so then you go ahead and you give, say 25 litres of replacement IV fluids, they go nicely, you getting it into the vascular space, but it's important to keep in mind if you're trying to increase cardiac output and you're trying to get fluids into that vascular space, that 75% of those fluids are gonna go into the skinnaticium, just because of the distribution of fluids across throughout the entire extracellular space.

And that's fine because if it's the animals dehydrated, that's important too. So that you're not going to increase that intravascular space. So what's another option, you can give hypertonic saline, and this is the dose here, it's 4 mL per kilogramme, and what hypertonic saline does, because it's hypertonic, so it's usually about 7% sodium chloride.

It draws water out of the cells, the endothelium, the cells in circulation, as well as the institium, to increase your water content in your intravascular space and increase your venous return to your heart and your, and your pre-load and cardiac output. It's really important to, make sure you follow up with 10 litres of isotonic fluids for every 1 litre of hypertonic saline. You just saw that it draws all the fluid, out of the cells, out of the inner stitch, and that's how it works.

There's probably some other. Mechanisms as well for why it's so effective, but you want to replace, you've got, you've got to replace that volume. So just as a guideline, you know, probably within about an hour in followed up with isotonic fluids.

So what happens, another thing that can happen is we can use, lose albumin. We see this with protein losing enteropathy and also anytime there's sews or shock, that, that capillary membrane can become leaky, and we so we lose albumin just from the vascular space into the into the intestinal lumen, and we get hyperproteinemic, so we, that decreases our osmotic pressure, our hydrostatic pressure may also be decreased if the animal's in shock, but, our osmotic pressures decreased. And so what can happen even if we do, even if we go ahead and give the fluids intravascularally because we haven't got the.

Osmotic pressure to keep it there, we can, you know, you can develop edoema, and so that's why we can often give colloids to support these animals. And the most common, you can give plasma. The disadvantage with plasma, it's very expensive.

You need to give very large volumes, and as I just described before, albumin is primarily responsible for most of your oncotic pressure, and so, you're and you're losing albumin, you're losing it into the gastrointestinal tract, you're losing it across your capillar membrane and it's the smallest molecule, which is why it's lost so easily and primarily the primary the primarily, primary component oncoic pressure component in plasma is albumin and so you could potentially just lose it. Like I mentioned, it's expensive. It can cause an immune, A mediator response, an allergic response.

However, plasma does have some other factors. It has clotting factors, and it has other factors in it, that may actually be beneficial to the patient. The one that I use most commonly is, is head of starch, and the dose is here at 10 mL per kilogramme per day, is the maximum.

It's in humans, there's been some issues, there's obviously issues with coagulopathy, or can be. I have not observed that in my patients, not that I measure it, but I haven't observed clinically on that to be a problem. And in human patients, there are some issues with renal failure, and I personally have not Deserve that, and I use quite a bit of head of starch.

It's not inexpensive, but it's quite a bit less expensive than plasma. The oncotic pressure of the hydroxy eelstarch is higher than that of plasma, so theoretically it should have more benefit and, and the molecules are larger. So theoretically they should stay in the, the albummen.

So theoretically they should stay in the vascular space a little bit better. But you're limited to, I would not go over the dose rate of 10 mL per kilogramme per day with this, and there's a variety of products with variety of molecular sizes, variety of substitution, as well, substitution ratios as well. And then you've got Dexgens, we do not use these in our hospital.

I'm not totally sure of their availability, but they are another less expensive option but they potentially have more complications both with coagulopathy and with renal issues. So what do they do, you put your colloids in your vascular space, hopefully, theoretically, you improve your osmotic pressure and your hydrostatic pressure. And I wish the edoema went away just like that, but it, can actually take some time for it to resolve.

So, colis can be beneficial. Like I said, mostly on emergency, I, I tend to use hydroxyethyl starch, and the product we have at the moment is bed starch. And so, but, you know, plasma definitely also has a role.

It also has to be defrosted, which can take time, as well. So just to finish up, I just want to briefly touch on how I use antimicrobial drugs and non-steroidal anti-inflammatory drugs on emergency. I've, and there's a whole different lecture on antimicrocrobial drug use in equine medicine.

I have gotten a lot more conservative with my use of antimicrobials. I only use them if I think they're absolutely necessary, especially on an emergency basis. A lot of times I'll take things in overnight.

I'll be transferring them to our internal medicine service the next day, and so I tend to not, start them antimicrobials. I usually do my best if I am going to start animicrobials, I usually do my best. To identify where I think the infection is and try and get a sample for culture and sensitivity testing if it's at all possible.

And then we talk about duration of antimicrobial drug use in in a different lecture. So got my horse, I've got a fever, OK, or an increase in rectal temperature, most of the time in especially large animal medicine. Especially with adult animals, if you have a high real temperature, most of the time it is going to be a fever, it's not gonna be hyperthermia, except if the animals just raced or something, .

So I identify a fever. What do I do next? One thing is I assess my patient.

Is this patient really sick? Is it gonna be absolutely critical that I, that I start antimicrobials right away, or is it OK to wait and see if I can work out what's going on? So I look at the, I look at the nuclear.

Cell count and like I mentioned before, most of the time I'm looking for a leukopenia and a neutropenia, and if I see that I'm gonna think, OK, I think it's probably the gastrointestinal tract because any time you've got release of endotoxin into the circulation of. One of the first responses we see is a neutropenia, leukopenia with a neutropenia, and so, I, I primarily look for that and I'll be honest with you, if I have a leukopenic animal, I am probably going to be thinking that I'm not going to start them on any microbials, at least not initially. The other thing I look for is I mentioned fibrinogen.

A lot of times I do not. We don't have that available point of care. We do have serum amyloid A available point of care, and so that's another thing you can you can measure to decide am I, do I need to stop this animal on any microbials or is it not an infection.

And then like I mentioned, if I've got an animal with a fever, I go through and I try and work out which body systems involved. I sculpt the chest, and we had a lecture on this, I always use a rebreathing bag in a very quiet room. You know, if I'm concerned about something with the abdomen, I'll get an abdominocentesis.

Maybe the animal has a history of an inaptence and maybe some low grade colic. I'll look for the peritoneal cavity and like I said, I'll look for signs, any sort of evidence of diarrhoea, and ultrasound can be helpful to look for diarrhoea as well. You can look for.

The peritoneal cavity, you know, to determine if there's an increase in peritoneal fluid, potentially associated with peritonitis. The other thing is you can look at the colon, because if the colon is full of liquid, that animal is potentially going to get get diarrhoea in the near future. So, like I said, antimicrobials, I'm very cautious.

I really, really think before I use them and I think that the animal really need it? Does it need it on an emergency basis? Have I done everything that I can to determine which body system is involved and .

And get a sample. Non-steroid or anti-inflammatory drugs, OK, these are analgesics. Analgesia is obviously always important.

Like I mentioned in the history, I always make sure the animal hasn't previously been given them by the owner or in my case by a referring veterinarian. So nextamgalin is great, it's a good analgesic, . It's can also be given at a lower dose that's reportedly anti-endotoxic.

I will tell you for a colic patient that has low grade colic, even this anti endotoxic dose, can make the animal feel a lot more comfortable and and you've got to be careful if you've got a horse with colic and you're worried about potentially needing surgery or having a surgical lesion, it's not going to mask the strangulation, but other types of . Other types of obstruction it can it can decrease the signs of pain. So I don't think it's not an analgesic even at a low doses.

Penut we use that a lot more for musculoskeletal disease. I don't think I don't think, I think they can be used interchangeably. I think you can use clinic and megain for musculoskeletal and you could probably use phenylbutazone.

I know people do, for a colic, for example. You've got to be careful using these non-steroidal anti-inflammatory drugs, . Because remember, your Flenex and meglobin and your phenylbutazone, they, they inhibit both cyclooxygenase 1 and cyclooxygenase 2.

We have the newer products, ferrocoxib and meloxicam. Ferrocoxib is used in the in the US. Meloxicam can is licenced for use in the UK.

It is not licenced for using horses in the US and these are CO2 selective or preferential or I believe the preferred term is COX one sparing incense and so what. What, what do we care about that, and this is not black and white, there's a spectrum, but, cyclooxygen is one is what maintains the viability of your your organs. It maintains perfusion to the the, the mucosa, the intestinal mucosa, it maintains mucus production.

It just maintains intestinal mucosal health and it also maintains renal blood flow. So versus cyclooxygenase 2 or the inducible form is associated with inflammation. OK, so what we really wanna do is we really wanna more specifically inhibit cyclooxygenase too, which is what your products like feroxi and meloxicam and meloxicam do and obviously the side effects, the complications that we see with .

Meenobuzone and clonic and meloman are associated with non-discriminate inhibition of cyclooxygenase too, so they constitutively express cyclooxygenase which maintains intestinal mucosa health and your renal blood flow. So just briefly referral of emergency cases, what information are they looking for at the referrals and obviously they want to know the signalling. if the animal is pregnant, if it's a mare, they wanna know, everything basically that we went through the presenting complaint, how long the signs have been going on, specifically what the animal's doing, the physical exam findings, any current medication and any medication administered for the current disease, as well as times they were adminidicted and dose.

That we use. I think in addition to that information it's really important to share with the referral hospital whether or not the owner has any financial constraints because there's nothing worse than the owner making a, you know, 2.5 hour trip with a sick animal and they realise just by walking in the dorm and being admitted to the emergency room that they've spent all their money.

So having those, financial constraints, laid out is important. The other thing is owners have expectations of treatment. I want my animal to my animal needs to be able to race, or my animal needs to be able to have another fall.

She's not really worth anything and she's not a brood mare, so knowing those expectations and communicating them very clearly with the referral hospital. Can also help that referral process, and so, you know, I think communication between primary care veterinarians and veterinarians at the referral hospital is actually absolutely critical, for, you know, a successful, whether that is the animal alive or whether the animal ends up being mutanized for a successful emergency referral process for both the client and the animal. So thank you for taking time to listen, and my email address is on the notes, so please feel free to email me if you have any questions.

Thank you.