Hi, thanks for joining. Today we're gonna talk about the raging rapids. So we're mainly going to concentrate on the nursing considerations for acute hemorrhagic diarrhoea syndrome.

So, AHDS as it's shortened to, is what used to be known as HG, or that hemorrhagic gastroenteritis. The definition of that has changed slightly, and that's because of studies and because of the suspected pathophysiology that's come about for this acute hemorrhagic thyroid syndrome. So it says it in the name, it's often an acute onset.

It's bloody in nature, and they obviously have that diarrhoea. I've not put that many pictures of, hemorrhagic gas like hemorrhagic diarrhoea into the, lecture. So I don't really want to like traumatise you or if you just had dinner or about to have dinner, you don't want to be seeing that.

We all know what it looks like. So hemorrhagic gastroenteritis, or like I said, it's now renamed this acute hemorrhagic diarrhoea syndrome. It's a disease that's often without a particularly known cause.

So we're gonna talk about the overview of the potential underlying pathophysiology, and how it most commonly comes about, but with the caveat that it is still kind of unknown really. We have to find it more prevalent in smaller young breed dogs, at young small breed dogs, but it can strike any dog at any age. I'm I'm from any breed as well.

I'm, I don't know about anybody else. But we currently at least have 1 or 2, acute hemorrhagic hemorrhagic diarrhoea syndrome patients within the hospital each week. And so whether that's because of the prevalence of lotrogen, which we'll talk about in the next slide.

But again, we have varying ages for these patients. Sometimes we have much older patients with that that we're seeing. And these are obviously have their own set of subset of risks.

I'm being older, I'm and and therefore thinking about fluid, I'm overload and things like that, and I'm, you know, risk of sepsis. So it's thought to possibly be caused by an exposure of a novel food item, so it's kind of like an IBD reaction, or an atypical immune response to bacteria, which is most commonly reported. So we'll talk about recognising these patients, and how to do it when we use our triaging of these patients.

We'll also talk about, and, and think about the aggressive treatment that's required in these patients, thinking about the amount of volume of fluid that's lost in these patients and how that can be detrimental quite quickly for them as well. So I'm dogs that are suffering from this acute hemorrhalodi syndrome are often previously healthy. And before that, and they, as I said, acute, I'm acutely developed, I'm potentially hematochezia or vomiting in addition to that as well.

So by quick recognition of that problem and aggressive treatment by the veterinary team. The prognosis for these patients is actually quite good. So it's just managing these patients and the nursing care of these patients is quite large.

We're gonna be the ones that like kind of at the forefront. I'm unfortunately, mopping up the poop. So on top of those nursing considerations, we're gonna have a little brief look at infection control.

And how that ties in with this one, with these patients, obviously these patients having high volumes of diarrhoea, potentially caused by bacteria, so can potentially be transmitted to other patients. So we need to really be on top of our infection control. There's a little bristle stool chart here on this slide.

What we do with our patients, we will, use a stool chart for every single time they go out. It doesn't matter whether they've got acute hemorrhagic diarrhoea syndrome or not, but we will score them. And then this thing, we can see whether our patients progressing through their treatment, whether that's, BC is starting to firm up with the treatment that we're giving, for these patients.

So as I said, I'm that unfortunately, I'm aetiology of acute hemorrhagic diarrhoea syndrome isn't like 100% known. Though, abundant Clostridium, perfins, are often shown to be present in the duodenum of affected dogs. So they did studies, and they found that these Clostridium profusions, in the duodenum were the most commonly found in these patients.

So, this, Clostridium is a gram-negative bacteria, and it's found in soil, in insects, in decaying vegetation. It's found in the intestines of, humans, as well, and other vertebrates. So in some respects, It's just a natural part of life as bacteria, but what we see is this, inappropriate immune response to this.

So almost in the same way that sepsis is a dysregulated host response to bacteria. It's very similar, but on a much smaller scale, whereas sepsis, we get these cytokine storms. I'm, and I'm, and, you know, an abundance of I'm anti and pro-inflammatory measures.

This is like on a smaller scale that just kind of in the guts that we're seeing these patients are being affected. Other hypothesis about where this pathophysiology of acute hemorrhagic diarrhoea syndrome comes from. Or HGE, is, as I said, dietary indiscretions.

So potentially think about your patients that are prone to pancreatitis. They eat something they shouldn't have eaten, and that severe dietary indiscretion causes, the guts basically to, to panic and, and causes, hematitudesia. So, other things as well, to be micro microbial toxins.

So with prevalence of things like our, heterogic micro toxins, and because of things like global warming and climate change, and we're seeing a lot more incidences of these, and they're also starting to change slightly, in their path physiology and proliferation. So. Potentially this is why we're seeing now, more and more patients that have incidences of this acute hemorrhagic diarrhoea.

I'm so. I'm It's sort of unclear about whether the, Clostridial proliferation is is the cause or whether it's a consequence of a disease process. So this is something that they're still kind of looking into.

The Clostridial, difficile, and toxins slightly differ from this. And they don't often be. They're not often shown to be involved in the pathogenesis.

But there is a new, like newly founded, cytotoxic toxin, caused by Type A Clostridium hogens. And they're, they've been co-localized with severe necrotic intestinal lesions infected dogs. So often what we see, and kind of think about with these acute hemorrhagid diarrhoea and, like I said, I've not put many pictures in here, but I'm sure you'll have seen the ones that have, you know, this awful bloody liquid essentially.

It's just liquid, but often they'll have like little clumps in there. And sometimes that's kind of associated with like that, that necrotic intestinal lesions that are kind of sloughing a little bit. And potentially that then firms up and becomes colitisy, but that's what we're talking about that sometimes these patients have severe nephrotic intestinal lesions, maybe that, again, whether that's the origin of pathophysiology or whether it's a result of this new cytotoxic toxin from this Clostridium.

So this acute, enteritis strongly impacts, intestinal micro microbiome, and that, is in particular with like the species diversity. And can cause this acute dysbiosis causing this acute hemorrhagic diarrhoea, and when these patients get really sick, they're losing lots of volumes, losing lots of plasma proteins and and potentially, you know, red blood cells as well, which can be detrimental to these patients. So Clostridium like I say is a spore forming pathogenic bacteria.

And it, it's in that soil. So when we think about these patients, often the owners have brought them in, they've recognised that these patients already have this, hemorrhagic diarrhoea. It's not often that, that we're triaging these patients and then discovering that they have hemorrhagic diarrhoea, unless, for example, we are doing a, a temperature check and we pull out the thermometer and there's how much cheese you're on there.

But this disease often will just start with dogs exhibiting maybe depressmentation, and the dog might start vomiting potentially. But the signs basically are that explosive and volumous, hematgesia, which is really malodorous as well for these, for anyone really dealing with it. You know, the, the feeling when you walk in and, and you can the smell hits you straight away, .

So, as I said, what we have is this potentially large numbers of clotted red blood cells in the diarrhoea. It often has this appearance and apologies if this puts you off strawberry jam forever, and it's often described as strawberry jam, in appearance. So owners might know anorexia, potentially for the diarrhoea, but often what we find is is patients have been healthy and all of a sudden they start having explosive diarrhoea.

So we'll talk a little bit about, in a minute about getting a complete history of these patients, thinking about, what medications they're on, whether they are up to date with prosthetic, prevention care, or whether they have any, known diseases. So similarly as well, acute hemorrhagic diarrhoea syndrome, is a syndrome essentially of a disease, but we, when we think about our diagnostics, and we should take the steps to kind of rule out diseases that have similar clinical presentations. So hemorrhagic diarrhoea and vomiting.

And that might come on, the dogs, signalment, so like their clinical signs, the environment that they've been in or been exposed to, and as I said, good history and physical exam. So, lots of diseases will often present with similar clinical signs. So we think about recy toxicity.

If they have no clotting factors, they are going to start to get, hematochezia, hematosis. And potentially anorexic, depressed. Again, septic patients will often have, some sort of hemorrhagic diarrhoea or vomiting.

And again, this, I shouldn't be confused with acute hemorrhagic diarrhoea syndrome. Bacterial infections, thinking about those patients are salmonella, Pylobacter, . Giardia, E.

Coli. Any of these patients, so for example, is that patient rawford, is that gonna be a concern that we now start to think about testing for salmonella, or E. Coli and Pylobacter, again, thinking about patients, young patients that have been, The new pups that have come to you with this, hemorrhagic diarrhoea?

Have they, been around, you know, been in an environment with lots of the dogs? Have they potentially been exposed to Parva virus, or, Giardia? Are we going to start to think about doing 4DX tests, to try and rule in or rule out things?

Mushroom toxicity sometimes can cause hemorrhagic diarrhoea and vomiting as well. So again, thinking about, whether this patient is prone to picking up things or whether they've been on a walk somewhere new and the dog was gone somewhere. Just getting a really good comprehensive history as part of our triage.

And again, this is something that, as nurses, we can be valuable to picking up things from this owner that, might be, present. Again, parasitic preventative care. So does, does this patient have regular lung worm, preventative care?

And if they're not, we're thinking about, again, lung worm often will cause, bleeding into cavities or hemorrhagic diarrhoea. And this good history is gonna go hand in hand with our physical exam, because this is potentially again, this physical exam is gonna I like any slightly, different clinical symptoms. So for example, tication, we might start to see this in the late stages of this acute hemorrhagic diarrhoea syndrome if they've left this patient or this patients have been having very large volumes because we think about, that.

Consumptive process. We've lost lots of red blood cells, we've lost lots of plasma proteins and, and therefore lost clotting factors. Eventually, these patients might be at risk of, coagulation problems.

But initially, if we're thinking, that we're putting this together with our good history. Is that, for example, vitamin K, antagonist denticides that are causing, a depletion of the coagulation factors, we are gonna see that particularation quite early on. We are gonna see potentially increased respiratory rate or increased respiratory noises, as a sign of kind of wet lung.

We might see beelines, if we're using a point of care ultrasound scanner as are, . As our like triage tool along with our physical exam, or we might see, you know, fluid in cavities, so things like pleural effusion or abdominal effusion when we're sticking a probe on there. Thinking about again, pancreatic patients that acute necrotizing pancreatitis.

These patients are gonna have extreme, abdominal pain. They're gonna be really nauseous, and very depressed, depressed in mentation. Things like intestinal.

Volubus, can cause, again, hemorrhagic diarrhoea, but these patients are going to be in excruciating amounts of pain. Not to say that our patients with acute hemorrhagic diarrhoea syndrome aren't in pain. They often will be uncomfortable in their abdomen.

But when we think about the difference in between, pain scoring. These patients with acute hemorrhagic diarrhoea syndrome versus, interception, intestinal vouss, or acute necrotizing pancreatitis, these are gonna be much more painful on that scale. Acute liver disease, again, we might see that abdominal pain, but we may also see that jaundice in that patient and again, petiation because the liver is responsible for the production of coagulation factors.

I'm thinking about other patients as well. So hyperadrenal corticism patients. So again, this will not be part of your good history taking that you, ascertain whether that patient's been on any medication for that, and whether this might be potentially more like an Adisonian crisis or whether You know, whether that patient might be going through an Addisonian crisis or whether they just have acute hemorrhagic diarrhoea syndrome.

I immune mediated thrombocytopenia, again, that's gonna I. Consume our thrombo thrombocytes, . Our platelets, and that's gonna cause petiation, bleeding into cavities and and that hemorrhagic diarrhoea.

So we're trying to differentiate between other similar causes of this hemorrhagic diarrhoea. So again, good history taking there is an acute onset. The patient was healthy and fine beforehand, and it's been a very short, duration, whereas some of these other ones might, happen over a period of time.

And that depressmentation might be more visible with those patients, for example. So you can see on the right, that's that appearance of kind of those blood clots within there, that kind of strawberry jam appearance, and, and again on the left, . I, like the raging rapids, right?

That's explosive. There's lots of it. They, they, there's kind of no warning either.

It's not like they, you know, other patients that maybe cry to go out. It's just these patients will do it anywhere and everywhere. So we'll talk about infection control point of view, especially with like, where we're walking these patients and how we're keeping them and, and where we're, how we're cleaning up this, especially if we're outside.

So clinical presentation, as I said, these are typically presented with an acute onset of bloody diarrhoea. And possibly with things like vomiting or hematosis, so blood in the vomit and often these patients are anorexic, potentially some element of kind of nausea, especially if they're vomiting. That's causing that, anorexia.

Percentage of these patients, are lethargic, and this might be a result of either the dehydration. So thinking about, dehydration happens over a period of time. We get a loss, from those, extracellular fluid that I'm.

Extravascular space. Or shock, where we have that in from that intravascular space, we have loss from that and often that's, as a result of severe dehydration. In these patients.

Abdominal pain again is sometimes common, but I'm not to the extreme that we're just talking about those are the diseases. I'm, if your patient's in shock, you're gonna have tachycardia, peripheral vasoconstriction, so things like pale mucous membranes, delayed refill times, cool distal extremities, or that hypothermia. Depressed mentation, because of that shock, because shock is, causes hypoxia, and potentially muscle weakness as well.

With our dogs with dehydration, we think about, The signs. So when we think about a shock, that's the signs of the intravascular loss. So when you don't have enough blood or volume in your veins, the, the body compensates by increasing the cardiac output and the systemic vascular resistance to increase that cardiac output.

So the cardiac output is, The heart rate and the stroke volume. And so the veins all constrict to get all the blood back to the heart as quickly as possible. The heart is beating as fast as possible to get the blood around the body, and so that patient isn't losing oxygen.

So think about that in the way that then when we start to get to decompensatory phase of shock, that now the blood's being diverted to the main organs. The kidneys, the, the heart, the lungs and the brain. And therefore, that's why you start to get those cold extremities, delayed capillary refill times, hypothermia from that rectal temperature, because the blood is being diverted elsewhere to where it's needed.

When we think about our dehydration parameters, there's gonna be weight loss in that patient, we're gonna have skin tur so again we've lost water from the cells in the body, so we start to see this the, I'm Sunken eyes, because there's no water in the cells around the eye sockets, dry mucous membranes again, there's no water in the cells. And there's no water in the cells to create elasticity. So that's why we get that skin tur as well.

And so thinking about the difference between the hydration and shocking these patients, that's gonna be really important when we come to our our treatment. I'm So as well as this, I'm just as a side note, the dogs with acute hemorrhagic diarrhoea syndrome, I often get things like a severe mucosal necrosis. So this, I talked about those intestines kind of almost like dye and slough.

And then what they get is this minor neutral infiltrate in the small and large intestines. And that causes secretary and malabsorb if and malabsorptive diarrhoea. So translation of water, electrolytes, protein, .

And disrupted transport mechanisms are going to lead to a massive significant fluid loss, as well as electrolyte loss as well. So what are we gonna do? And, and as part of our triage, this is the thing that we're mainly gonna be thinking about.

I'm and we're gonna be thinking about throughout the treatment of this patient. So when these patients arrive at the hospital, they should be immediately triaged, and their perfusion status is the thing that we're really gonna know. So we're gonna think about our heart rate.

Ms membrane colour, capillary refill time, pulse quality and blood pressure, and that's gonna assess our perfusion. As I said, there's large volumes of liquid diarrhoea can quickly lead to hypovolemia, and often these patients will already be exhibiting clinical signs of shock. So the cause of shock in small animal patients is the result of a deficit of oxygen supply.

And to the tissues and, and oxygen demand from those tissues. So the barrow receptors within the body. They notice when there's a decreased blood flow, and they will warn the body, to try and avoid cell death, necrosis, and those are in the aorta and the kidneys.

So, your, juxtaloma cells and hold those stretched cells in the kidneys. And when we have hypovolemia, what happens is they, they send the signal back to the body that blood flow is lacking. So this is where this rein angiotensinol detro system and is kicked off, so in the kidneys.

So. Like when we have hypertension and hypovolemia in the kidneys, renin is released from those jux glomerullar cells. This renin acts on circulating angiotensin, angiotensinin, and it changes to angiotensin one.

So angiotensin 1 is then changed to angiotensin 2, and that is, that occurs in the lungs. So what happens is that there's an angiotensin converting enzyme, ACE. So if you've ever heard of ACE inhibitors, this is what they do.

They block that change from angiotensin 1 to angiotensin 2 in the, in the lungs. Because Angiotensin 2 is great for a very short time, but what what happens is this kind of vicious circle where this keeps getting released, especially if you're losing volumes and not replacing it. So angiotensin 2, what it does is it causes vassal constriction, and it also causes increased sodium retention.

By the kidneys in that loop of Henley. So this increase in sodium is going to cause, an increase in circulating volume, because what happens is the sodium that's circulating in the blood, in the veins changes the osmotic radiant. And so when you have a change in your osmotic gradient, the body tries to regulate that by water will move wherever sodium is to balance that out.

So what happens is that water moves out of, the cells of the body into that intravascular fluid to, to make that sodium. Balance the same as the The ones in the cells. But obviously these patients that are already dehydrated, there's not going to be much more water.

So now I've just got increase in sodium levels in our patient. But initially, what that will do is, is going to cause this this water movement to create an increase in your intravascular volume. So it's gonna increase the circulating volume, increase your blood pressure because you've got that .

That vaso constriction and what also happens is that angiotensin 2 will signal to the adrenal glands to create aldeerum. Aldosterone also signals to the kidneys to retain sodium and excrete potassium, and this will further contribute to increased circulating volume and increased blood pressure for the patient. So this makes sure that there's the cells are potentially well oxygenated and that blood pressure's maintained.

But this compensatory effort, basically, You only see as very subtle clinical signs, and this is what we call early compensation phase of shock, where either the heart rate and the blood pressure kind of normal, may be a little bit higher than they usually would be. But then what we start to see is this decline in shock. So we start to see things like compensatory shock, where we have this decompensatory shock, where we have a low blood pressure.

High heart rate, nothing is, nothing is going right for this patient. So in the only compensatory phase when these RAS system is doing its job, it's kind of almost seems like business as usual. But what happens is they get overwhelmed and they can no longer keep up that kind of business as usual.

And so vaso constriction begins to preferentially decrease blood flow to make major organ systems, you know, to maintain perfusion as much as possible to the heart, the lungs and the brain. So that decompensatory, where you may see pale mucous membranes, poor pulse quality, decreased blood pressure, and depressmentation. So if we're ignoring these signs, and we're not administering treatment immediately when we see these signs, we are, our patients are gonna have organ failure, they're gonna have lack of oxygen, that hypoxia, they're eventually going to get hypoxemia, and the patient's gonna die, unfortunately.

So shock is the one that we need to immediately treat. Shock happens acutely, we treat it acutely. With dehydration, it's lost over a slightly longer period of time, so we replace it over a longer period of time, but it's not necessary to say that we should just completely ignore that.

So when we think about our perfusion status, we think about mainly our shock parameters that we've just gone through. And then this line is put through to the, the other ones that are going to be our dehydration parameters are things like our weight, skin turgia with our weakest membranes are tacky. Whether we have the sunken eyes as well.

And so these aren't gonna potentially kill our patients unless we have like severe dehydration. But often when we get severe dehydration, that tips us into shock. So these patients need treating very quickly.

But when we think about our treatment in a minute, we'll talk about dehydration. So the initial stabilisation of these patients, and we've just talked about the importance of making sure that those patients no longer are shocky and that we're replacing those fluids so that our RAS system doesn't have to overwork itself and going into decompensatory shock. So we've recognised that our patients have hypovolemia.

We're going to start to think about IV access in these patients. So getting set up for IV access, thinking about where are we going to put those IVs. So we don't want to be putting IVs in the back legs, they're gonna get skanky, they're gonna get diarrhoea all over them.

They're gonna be really hard to maintain, . Avoid all costs. So we're potentially gonna go for cephalic.

So making sure that we have a really clean site. So thinking about infection control, and we are doing a tree trunk clip, so we clip all the way around, especially if you've got feathers. We are doing a good scrub with our good contact time with our Or scrub solutions of lorroxidine, so not just doing a quick wipe, like these are IV sites, they are indwelling devices, .

And they need to be super clean. Think about like the bacteria potentially this patient has bacteria, but I don't of clostridium. There's gonna be diarrhoea, you know, often these patients will twist.

You know, they get, they get really upset for themselves when they're having diary in the kennel, which sometimes isn't avoidable. And, so we want this to be a secure, clean IV line. We want it to stay in as long as possible.

So remembering again that we only have two cephalic veins. We might put them in other places, but the cephalic veins are going to be precious gold. We may think about, central lines in these patients.

If they're going to be in a very long time, they're gonna be on various solutions, like, for example, if they're anorexic, they might be on glucose supplementation, if they're small patients, and this is often best, best done in a central venous catheter because of the risk of phlebitis, if we go any, any higher than a 5% solution. Again, we can take multiple blood samples. So if you're thinking about with these patients have electrolyte imbalances, and we're gonna be thinking about, that we're gonna be taking multiple samples from these patients, patient comfort, not just the fact that it's easy to get the sample.

The jugular vein, is gonna be much further away from the bum than anywhere else. And you can, and it's a larger ball. And so we can give fluids quite quickly in this as well, potentially we give them lots of different fluids and medications.

And so this might be our preferential one if our patient doesn't have any, clotting factor problems. So, potentially when we're doing our initial admit, we might think about this long term. These patients are often in for more than 48 hours, because we're waiting for that, hemorrhagic diar to resolve, or to thicken up, .

And so I, I doubt I've ever seen a patient say less than 24 hours for acute hemorrhagic diarrhoea syndrome. So thinking about your IV access it's really important getting everything that you need ready, like I say, doing doing your contact time, doing a swab, I'm, you know, sterile, I'm alcohol swab. And taping it in securely, thinking about these patients, if they, if you have seen dehydration parameters in these patients, or these patients are in shock and potentially have had fluid loss over a couple of days if you've had diarrhoea.

That patient's gonna be dehydrated. They don't have water in their cells right now. So when you tape, and you tape kind of tightly, when that patient rehydrates, that's immediately gonna swell because the cells are swelling back up with water.

Your tape is now gonna be even tighter, and that's how they get big fat huts. And so again, thinking about this kind of stuff. We have in our hospital, that we break down the site twice a day, but we also have, like tegaderm type clear plastic things over the actual insertion sites.

You can see the insertion site because, again, these patients, though they're not septic, are at high risk of sepsis. I'm thinking what's going on. They're having that dysregulated response.

They've got necrotic tissue potentially in their intestines. These patients are prime candidates for sepsis. And we all know that hospital acquired infections are very common.

And so again, think about your infection control. And in terms of that, your, IV lines are going to be a big one for that. The minute that patient gets phlebitis, there are increased risk of hospital acquired infections and potentially sepsis.

So we're thinking about initial stabilisation and potentially this sometimes it's done before we do more diagnostics. We might have done a point of care ultrasound as part of our triage. And we potentially, when we put our IVs in, we might take bloods from our IV catheters.

Or, separately depending on how sick our patient is. But when we're thinking about replacement of fluids, so again, as nurses, as a nurse consideration, we're not necessarily prescribing this because that's what the vets are doing. But maybe we think about what fluids we can prepare for this patient, and work together with the vet kind of work on a fluid replacement plan, and work on what kind of fluid replacement is going to be best for patients.

So, these patients often have a loss, an acute loss of salt through and water through that vomit and diarrhoea. So crystalloid fluids, isotonic balanced crystalloid fluids, potentially gonna be our number one, and that's because they've got water in there as well as those electrolytes. And within that we might need to give additional electrolyte supplementation.

So lactated ringing solution, Hartman's plasma light A are all going to be really good solutions for replacement losses. And maintenance losses as well. And sodium, I'm not.

9% sodium chloride, we can use because we've had obviously that loss of salt and water, but that's not a balanced solution and it's an acidifying solution. So often these patients, if they've not had vomiting, they've just got diarrhoea, they will often have a metabolic acidosis. So consider again if you've done blood gas analysis, thinking about a balanced solution.

And again, if we restore, let's say we have a deficit in sodium because we've had so much salt loss, if we start restoring with 0.9% sodium chloride, quickly, we can potentially cause problems for our patients. So it will raise the sodium too quickly.

And we can get these idiogenic osmools in the brain, and that can cause brain swelling and seizures and death. So think about our fluid choices very carefully. So again, shock, we're replacing quickly, so we're gonna administer quickly to restore that circulating volume.

And, . Thinking about like. How that fluid sits there.

So with our crystalloids, that will, that fluid remains in the intravascular space for about 45 minutes. So within that 45 minutes, you can improve perfusion, oxygen delivery, and then that will shift into other areas of the body, so into those extra vascular spaces. So other areas, obviously, and it might include intestinal and testitial space, but that might include GI tract, lungs.

So thinking about, fluid overload, as a concept. So, I think previously in the last sort of 10 years, we were very gung ho with fluids, like really replace, like go as quickly as possible, like put pressure bags on the bags and push the fluid in. But that's not necessarily the case anymore.

And so we're a lot more conservative, and so a lot of research in veterinary, veterinary medicine. Now I've started to look at the possibility of doing a pre-challenge, fluid bolus before doing fluids like a 1 to 3 mL per kilo, fluid bolus over 10 minutes, to see if that patient responds to whether the heart rate improves, the blood pressure improves, whether that patient's mentation looks slightly better. And with the pulse quality is slightly better and then going for our shock replacement.

So shock replacement 160 mL per kg per cat, or 90 mL per kg per dog, but we don't give that all at once. We usually give that in Aquats. And that way, that way we can measure the response to that fluid challenge, and see whether it's an appropriate response.

So, what we often start with is like a 10 mL per kilo bolus over 15 to 20 minutes. You might go more rapid than that if you've got very, you know, very severe clinical signs, like, I, I think back on that other page. The blood pressure there is 45/15.

We're gonna be panicking a little bit about that, and starting to think about getting that blood pressure up as soon as possible. So we're gonna be doing that with our intramuscular fluids. Potentially might start to think about visa presses to kind of assist us in that as well, while we get that volume restored.

And especially if they're not fluid responsive, I'm thinking about our visa presses. So we've monitor the vitals closely for improvement whilst on that fluid bolus, but then again, we also do those vital signs. We reassess them once we've done that.

So we'll talk about that on the next slide. So the Ebola amount might be repeated until those vital signs are like what we consider to be normal and that patient looks a bit better. So it's really important as veterinary nurses that we closely monitor those patients, that's often our job, the vet sets the, the fluid.

Maybe decides on the fluid bolus rate, and we'll maybe go off to other consults, look at the patients, we're the ones monitoring those patients. And just as a tip as well, if you're using a bolus on a fluid pump, what we have now is like little laminated, Cards that we stick on the front so that nobody comes along and goes, the fluid pump's beeping. I'm just gonna start that again because that patient is then potentially going to be at risk of overload if we keep pressing that again, or leaving it on for, you know, 30 minutes longer than we should have, which I've definitely seen in the past, hence why we have those now.

We're gonna look again. We're gonna look at heart rate, memory and colour, play full time, blood pressure. All the signs of losses, but we're also gonna look at things like urine production, how much diarrhoea is now being produced, we might have more, vomiting, think about respiratory status, so looking for increasing respiratory signs, listening to our chest for crackles, potentially using our point of care ultra.

To see if we have anything. If you are familiar with point of care ultrasound, you can start to think about doing like a caudal vena cava, diameter and potentially collapsibility index. I'm not gonna go into that otherwise it's going to be too long.

But go look it up if you're interested in it. But that stabilisation period is gonna be lengthy, because it might take them hours to kind of normalise their heart rate and the blood pressure. So again, really looking closely for fluid overload, as well as monitoring that temperature, so you should see that that temperature now increases as you start to give fluid therapy.

So sometimes when we normalise those perfusion parameters, we see ECG changes, things like reperfusion injury and ischemia can cause, ventricular permaal complexes, VPCs, and so we should listen out for arrhythmias as well. And also pain causes, arrhythmias like BPCs. And so again, pain relief is gonna be important for these patients as our initial stabilisation.

So as I said, that main treatment of acute hemorrhagic diarrhoea syndrome is maintaining perfusion. So looking at these, using these monitoring tools, so blood pressure, ECG, point of care ultrasound. And what we're now going to start to be thinking about, especially when we think about our dehydration plans, is, weighing the.

Ins and outs. So incontinence pads down, in the kennel, to weigh out if they're having frequent diarrhoea in there or we'll talk about it in a minute, but faecal catheters are really useful for these patients, especially when they're so liquid, we can really accurately measure the ins and outs, as well as weighing the patient and thinking about the dehydration game. So body weight should be measured every sort of 8 to 12 hours to ensure that appropriate fluid therapy response for weight loss or weight gain.

So we think about our, management, of fluid therapy. I've talked about those balanced, isotonic crystalloids in shock aloquats. I'm thinking about reassessing that profusion in cardiovascular status every 15 minutes, or every time a bolus is administered, .

And this fluid deficits should be replaced within about 6 hours if you've got shock deficits. For dehydration, we might replace anywhere between 6 to 48, depending on your patient. Think about combi comorbidity, so older patients and potentially cannot handle as much fluid, therapy like like replacement in such a short time, so you might lengthen that against smaller patients like cats, young dogs.

Aren't going to cope with so much fluid. They're going to quickly get overloaded. So increasing the length of your dehydration, rehydration plan.

But a young, healthy, you know, Labrador, for example, they might be able to have it within an 8 to 12 hour period for that, rehydration of that dehydration parameters. Think about as well when you're calculating your dehydration plan. So I'm Remembering that we use that calculation, which I think is on another slide as well.

But we do our dehydration deficit as a percentage point. So for example, 7% is 0.07.

Times by our body weight and then times by 1000 and that will give you your mils of deficit. So then you divide that deficit by however many hours that you're gonna replace that over. And then, And then you will give that plus your maintenance.

So for example, 2 to 3 mL per kilo, per hour. So, often see quite high, but that should then be reassessed. So again, we don't just leave that for the full 12 hours if we're replacing it over 12 hours, we check it every 4 to 6 hours within that.

I So these patients are gonna have high volumes of diarrhoea. We need to think about, accounting for that. So for example, when we think about our urinary obstruction cats, we get that post-obstructive diuresis.

We measure the ins and outs, we account for losses that that patient is putting out, and we start to give more fluid to compensate for that. The same for our patients with diarrhoea, if they're putting out tonnes of volume of diarrhoea. We're not just going to give our dehydration plan plus our maintenance.

We're also gonna add on, OK, on average, this patient is producing 50 mL per hour of diarrhoea. So that's gonna be your ongoing losses that you're gonna replace, and that might reduce as you go on, and again, looking again for your fluid overload signs, thinking about the weight of your patient. If your weight of your patient is really increasing quite rapidly, you're maybe not gonna be adding as much replacement for that those ongoing losses.

So in severe cases with distributive shock, where they don't respond to fluid bonuses, I mentioned those vasopressors and they should be used. I'm, again thinking about electrolytes. So thinking about what's in your fluid, but also potentially that we might need to, we might need to supplement, for example, hypovolemia, we might supplement with the potassium supplementation.

So. We've talked about potentially a breakdown in that gut mu mucosal barrier. I'm, and these patients potentially at risk of loss of clotting factors, platelets, albumen from losing those plasma proteins within that diarrhoea.

And so I'm is in these patients, I'm plasma, I'm fresh frozen plasma or frozen plasma, more superior to Hartman's as a replacement solution. We always talk about replacing like for like so. Again, if your patient's now anaemic, or we're monitoring our, PCV total solids, and initially, we see that dehydration, we see a normal or increased PCB and an increased total solids.

But then all of a sudden, they both start dropping. That might be because we have that, those plasma protein losses. So albumin is being lost.

We're losing lots of red blood cells from the, the sheer volume of that hemorrhagic diarrhoea. And so we replace like for like, just the same as if we lost blood from a spleen. And we'd start to think about doing that.

If we're doing rodenticy toxicity, we've lost all clotting factors. So we start to replace with plasma protein. The same goes for this condition.

It's not a benign condition. It can kill these patients. And so, supporting them in the best way that we can.

So we'll talk in a minute about nutrition, but this is another way that we can support them, by increasing that vascular, intravascular space, with like for like, you know, it's it's lost plasma proteins. That intravascular, that, that balance crystalloid solutions only last for about 45 minutes, whereas this plasma, is gonna last a bit longer. I So, profound hyperalbinemia is often seen in these patients that have this ongoing loss of these plasma proteins.

In the UK we can't replace those unfortunately with Alins and in the US they have human albumin that they can use, but it's obviously it's still even in the US isn't commonly used. So the way that we're going to do this, is through the use of nutrition. So as long as that patient isn't vomiting, I'm placing a a nasogastric tube or a nasoesophageal tube is relatively simple, and it's gonna provide the immediate nutrition to those patients, and aiming those andterocytes.

So, . The difference between placing our NG tube and our our our NO tube, like our IO tube, we might place an NG tube if we have a patient that's nauseous or has ileus. So it seems kind of funny to say this patient might have ileus, even though they're having horrific diarrhoea.

But often that diarrhoea is a symptom of necrosis or bacteria presence in the intestines that's causing that sloughing and kind of diarrhoea. And that, you know, the, the water's being taken. I'm from other spaces, like the intravascular space, and the extravascular space I'm lost, but there's still a decreased gut motility, so we often have a lot of fluid in the stomach, so.

Having a way to remove that volume is ideal. That's gonna decrease our risk of regurgitation and the risk of aspiration pneumonia, and also increase patient comfort. Like, I'm, I don't know if you know, like if you eat a big bowl of soup, and then you kind of, it feels like you sloshing around.

It doesn't feel comfortable. That's maybe it's just me, but . They, it's not comfortable, and those patients feel nauseous, they feel lethargic.

They don't want to move because it's, you know, it's making them feel even worse. So having that, tube there is going to help us. But it's not, again, without risks of leaving an NG tube and is that we can sometimes still have a little bit of, fluid that passes through that, cardiac sphincter.

Obviously, NGO we would like these patients to eat by mouth. And so thinking about what that patient eats at home, and how we can make them feel comfortable in in the hospital. So are we feeding them in a room, and we have a visitor's room for owners that has a couch in it, so that the patient can go sit in there with them.

Feeding them in different types of bowls. So again, like thinking about cats, ceramic bowls, having water away from, from the, food, having a height for some patients if they're used to that thinking about again when we're doing that good history taken at the beginning, asking them when we're admitting them kind of those questions so we know what they like to eat at home, how they like to eat, if they have any plans to eat. Tasty junk food.

I'm, again, thinking about whether it's been a dietary indiscretion. So if it has, we're not going to be start thinking about junk food for these patients. But things like, I'm chicken applauses, I'm especially warmed up, kind of feels a bit junk food to them, but it's not as bad as like feeding them, you know, something else with lots of jelly that might make them feel worse.

I'm Probiotics, in these patients, have the potential to be helpful. So often systemic antibiotics are steered away from, because we don't know what causes it, and because, and we haven't done a culture on these patients unless we send the, you know, unless we send the faecal samples off. But at that point, we've already treated that patient for several days.

So I'm really start to think about systemic antibiotics if these patients start to slip into that septic kind of, area. But the probiotics, they modulate intestinal immune function, they promote epithelial cell homeostasis. They also exert neuromodulatory effects.

They block the effects of pathogenic bacteria and have really good nutritional benefits as well. So, . They're over the counter, or we can prescribe them.

But they often have been shown to shorten that acute diarrhoea. And this is seen in shelter cats that they had a shorter duration, . In, in that acute diarrhoea.

And there was another one for faeces and dogs as well, that, the, the first, the time to first normal faeces and these are reduced as well. So, we have been in for 2 to 4 weeks, and so often we get these patients start them pretty quickly. I'm And then we might think about our patients we've thought about our nutrition, so we're gonna feed.

High quality protein, potentially low fat if they've had a dietary indiscretion, and they've got concurrent things like pancreatitis, but thinking about replacing that. So again, if they've got lots of fluid or they've got poor gastric motility, not overloading with feeds, we might do, split them into 8 feeds as opposed to 6 feeds. We might We do it as a CRI if they, they are constantly kind of regurgiting and burping.

Or we, are gonna cut their feeding. So again thinking about anorexia and refeeding. So how long, are we doing it over?

We're doing over 3 days or 5 days of replacement, to full RER? Potentially with these patients, if they have been anorexic for a while, we don't just bung them straight onto liquid feed in their nasogastric tube, or nasoesophageal tube. We often do things like or related to that microenteral nutrition.

So very, very small amounts, but what that does is kind of prime those andterocytes, and the microvilla ready for, proper nutrition, because it's not really had any nutrition for a while. So, I'm often I find that this is more successful in these patients. And we, we continue to feed them until they're starting to eat, potentially 2/3 of that RAR by themselves, and we know that they're doing that consistently.

I'm thinking about reducing that nausea, we've done that potentially by syphoning gastric fluid, but we might think about Oopin, gastric antacids, . Omeprazole potentially if our patients are doing lots of regurg and at risk of esophagitis, . Again, I'm thinking about our gastric motility, so this hyper perfusion can cause decreased motility.

So metoclopramides, CRIs, and they help stimulate motility, and metoclopramides also works as an antiemetic. Ondansetron, as well as an antiemetic, and that decreases that nausea and vomiting. Ondansetron can be quite expensive.

So again, thinking about your patients, and the the financial concerns of your, of your owners as well. It's very important. I'm And yeah, just keeping an eye on this and making sure your patients get full RAR.

We know that nutrition is vital to, keeping the microvillin the enterocytes healthy and working. And again, we don't want those to die or to, to decrease in motility because that's going to potentially cause more, acute hemorrhagic diarrhoea syndrome. Patient comfort is gonna be, you know, should not be overlooked.

There's gonna be cramping from these patients, that pain that's associated with the hemorrhagid diarrhoea. Potentially, we're gonna be giving these patients opiates, ones who use validated pain scoring systems. So again, if you have changeover of staff, make sure it's a consistent pain scoring system that you're all up to date with that.

And that you're on the same page. I'm, I whether that patient has like abdominal tendon, so I'm, you know, whether they're tensing on abdominal patient palpation. So opiates can cause ileus.

They're still commonly used in the early treatment stages of these cases, but then we might switch them to something less, you know, less potent. So often concurrently what we do with these with our patients with the acute hemorrhagic diarrhoea syndrome is we'll start them on, Our methadone and paracetamol potentially might add ketamine in there, that has less effect on our, obviously our gut motility. We might add lidocain in, but this sometimes can swing over the gut, Cramping, so we kind of steer away from this in our hemorrhagic diarrhoea syndrome.

We then might stage down the, the methadone and then the ketamine and then that patients just some paracetamol and steer away from non-steroidal anti-inflammatories, and we know that these are cocks, enzyme specific, but when we have diarrhoea or especially blood. Loss, or changes to our blood pressure and hypertension. This means that they're not co specific, and then that can start to cause things like acute kidney failure, and more problems for your guts as well.

So we steer away from non-steroidals until our patients. I kind of have a normal poo if they've still got pain or they've got concurrent disease, for example, or an old arthritic dog that happened to get acute hemorrhagic diarrhoea syndrome from having NSAIDs, whether we staged them back onto NSAIDs or changed them onto something else. But really thinking about that multimodal, there's so many other drugs that we can use other than just opiates are gonna cause that LES.

So thinking about things like ketamine CRIs, and lidocaine, potentially, and when we're using multimodal, we can use opiates, and that just means we can use less of them as well. . Thinking about patient comfort, not just in the sense as well of having this cramping and this gut pain, but these patients have diarrhoea, so.

And when there's diarrhoea on the skin, it can really irritate and burn the skin. So it's a, it's really acidic fluid. And what we often get is this almost like scolds, these diarrhoea scolds.

And so the nursing care of these patients is really intensive for these dogs. Keep them clean as, keeping them clean is the most time consuming care. So potentially might use this, diarrhoea, .

Kind of chart and category, of whether they've got a mild, moderate, or severe, kind of, problem, and, and use it as a protocol as to what you do, whether you slip the fur, and whether you're placing, things like dermisol on a light barrier cream, or whether you're starting to think about, things like Sudocrem that has lidocaine in it because that local anaesthetic is gonna provide some form of pain relief to that. So clipping it with feathers, is fine in these patients, we're trying to if we're shaving them to the skin, we're gonna potentially lead to, clipper rash, more intense irrigation, irritation, and again, that frequent bathing and caring for the skin is and perineal region is going to be necessary. So often with these diaper rash products and mta and things like that.

So once they're eating and their diaries cease, you can return home. So we can use regular bathing and scoring, . Taking pictures is vital as well.

I see the progression again. These clipper rashes that, that picture with the faecal catheter, sorry, just the dog bomb holes, but that, that one is severe and that potentially that patient is at risk of sepsis again or a hospital acquired infection, things like MRSA, things like that, we'll talk about infection control in the next slide. But I mentioned these faecal cat.

They're really, really useful, and so we just place a foley catheter we fill the balloon up with like 1015 mLs of water, and we place a collection set on the end of it, so you you'll need like a Christmas tree. To put them in. And yeah, we basically just take these to the patient's tail, and then you just have to deflate that balloon and move it around every 4 hours.

So there's several tips, in doing this. Some people just cut the end of the foley off rather than just having, a small hole. Some people cut holes in.

I find the most effective is you just cut the end. And then the diarrhoea can flow freely through. And the problem is once it starts thicken up is that sometimes it won't go through and you and you have an issue.

And the other thing is when you take patients out to the toilet, if you are taking them out, you know, for stimulation to be outside, . Then often if they like sit and squat, and they thrust, they will often hoop these out. So what I often do is take that opportunity, when I'm taking them outside, is that the, that's the time when I deflate the balloon, and, and, avoid that necrosis of the tissue from having that balloon inflated for more than that.

There are human ones, that you can sort in for the veterinary world. And rather than placing a foley catheter inside, the, the, the anus, they have like, almost like little doughnut rings and they suction and kind of have a sticky spray that you put on and they suction to. The bumhole.

And it's a much thicker, like hose pipe, so that it collects the, faecal, matter in there. Again, from an infection control point of view as well, placing a Foley catheter is gonna be much more effective. You're not gonna be cleaning your kennel 5000 times a day.

You're able to get rid of that faecal matter into a clinical waste bag without touching anything else. No other patients are at risk of, that spore. Remember that Clostridium is a spore.

And so, it's potentially, I'm going to be passed to other patients. So you're thinking about. If we have lots of incidences of hemaic gastroenteritis in your patients, that have been housed with surgical patients or dental, you know, your dental patients are a bit older and a bit more susceptible to that, they might then post-surgeries start to be getting things like hemorrhagic diarrhoea.

So finally, infection control, is really, really important. And so we just have to make sure that these patients, are housed away from other patients. So not necessarily in isolation, but thinking about the layouts of your practise, if, if that's impossible to house them, any distance from, the patients, we know that it should be distance anyway.

But if they're not housed any further apart, then I would consider putting them in your isolation, unit. We have things like these infection control signs that are printed, laminated, we put them on the kennel on the front of a kennel of a patient. When they come in, so we know what kind of PP we're gonna wear, so.

Thinking about that we need fresh gowns and gloves, and potentially masks, and potentially new footwear, each time, so. I'm, I am, I'm very much for green, like initiatives, and we have a a great implementation at our hospital. And but unfortunately for these patients, it is not appropriate to take the the The apron off and hang it on the door.

If somebody else comes along and they brush up against it, they're potentially, you know, they're potentially now a foam mite. That door is now a foam mite. If that patient, you know, even though we've not got any visible diarrhoea on it, that, that is now a foam mic, we get rid of it.

No, you know, no exceptions to the rule and doesn't matter whether we write from on it or not. That's unacceptable. And we just put an extra charge on our patients that have barrier nursing, on there.

It's a different charge for isolation, but we just have a barrier nursing, so that accounts for the amount of gloves and gowns that we're gonna use each time. Hand hygiene is paramount. So, I see a lot of people, they put the gowns and the gloves on.

And they think that that acts as their infection control. But our hand hygiene is paramount. So remember the 5 points of hand hygiene.

So, before touching a patient, after touching a patient, after touching a patient's bodily fluids, after touching a patient's environment. So again, like I say, if you've got, a gown that's hanging on the side, that's a, that's now part of that patient's environment. So anytime you touch that, you're gonna have to change all your clothes and wash your hands.

So it doesn't make sense to keep them. And before any surgical procedures or other procedures. So for example, when we're looking at our catheters, make sure that we're looking at those first before we start looking at the patient, or cleaning up any faecal matter, and many of that hemorrhagic diarrhoea.

So think about how we're going to dispose of that diarrhoea. So again, we use less and less of our, incontinence pads, where the patients have large volumes of diarrhoea. Maybe think about using it in constant pads if it's doing it in the kennel quite frequently.

If it's doing it quite frequently in its liquidy, stick a Foley catheter in. It will change your life if you haven't used one, because you're not constantly having to think about cleaning and disinfecting the kennel every time that patient's diarrhoea in there, because You know, whilst you're cleaning that the patient's got to be somewhere else and that might be near other patients, or again, dirtying up other areas of your of your practise. Try and have somewhere separate to walk these patients.

So you might have things like astroturf, or just concrete areas that then you can scrub down, that you can wash down and scrub down, so you can clean and disinfect them. So you're not exposing other patients to that diarrhoea. Make sure it's not near a client area.

And again, grass is really difficult to clean. And, and to get rid of those bacterial spores. We know that that Clostridium lives in the soil, but if we're adding potentially more Clostridium to the soil, there's, there's other patients that are walking are at more risk as well.

. Disposing of bedding, so, we often will have a bag for the patient, so just put that patient's bedding in there. So it all gets washed separately and it potentially will get soaked if it's got diarrhoea on it or vomiting on it, but vomit on it. We soak it in, our allogene, or bleach before we put it in, with our wash.

So our washes are all done on 90 degrees. So it should be 60 degree minimum, but often with these patients that have infectious, diseases or, or hemorrhagic diarrhoea, we'll do them at 90%, 90 degrees. Sorry, I don't know why I put 90%.

I meant to say 90 degrees. I'm knowing the difference between cleaning. And disinfection.

So, things like our Agen are great, especially we use them for the correct contact time. So remember, and if it's useful for your practise, . Put the contact times up in visible areas in the kennel areas so people know how to, how long to leave it on and when to wash it off, .

So allergene is a disinfectant. Disinfectants will become, what will basically be not of any use if they use if if there's organic material. So for example, diarrhoea or vomit, once you put that allogene on there, it's not effective anymore.

So we wash the. Diarrhoea or the vomit away with water, wipe it up as much as possible, and maybe just with hot water, and cleaning, so cleaning will break down those organic materials again. So when the patient leaves the kennel, and before we have anything else in it, we're going to clean it and disinfect it.

So potentially using things like I'm flash. I'm as a cleaner. I'm, and then I'm allergene or bleach.

But Agene is safer as a, as a disinfectant. There's other, there's other things in the, in the market that are cleaners and disinfectants and are really environmentally friendly as well. So I recommend that you look those up.

But again, always thinking about the appropriate contact time for disinfection. Spray bottles, a massive bugbear for me. Think about you're spraying that, and not only you spraying anything that's like just been sat on the bottle, but now you're spraying any kind of the, that bacteria, and the spores from the diarrhoea everywhere.

So clots and buckets, make sure that we're getting rid of the bucket and the cloth and not leaving it sat around. I'm really thinking about the infection control, so not just for this patient, but the whole of your hospital about cleaning audits. Making sure that you're doing, you know, weekly or monthly deep cleans, as well as weekly themes, so there's less risk of hospital acquired infections that, this, this already, infection compromise like, compromised patient.

And again, think about the patients that are slightly older, they're gonna be even more risk for the younger patients. Think about those patients. And the fact that they're already immunocompromised.

And if we're not cleaning up areas appropriately of the hospital, that we're putting those patients at more risk. So, it's boring. I, you know, there's no, there's no fun way to talk about infection control, but it is a key part of our jobs.

It's a key part of keeping those patients safe and healthy, allowing them to rest and recuperate and, and, you know, and become normal. So again, I'm having things like a dedicated nurse. Making sure that they're handled last, and.

You know, making sure that you don't go home in your uniform, or come to work in your uniform, because there's things, again, more so when we're going home, we've dealt with a patient with hemorrhagic diarrhoea all day. Like, we might not necessarily see any diarrhoea on us, but are we going home to our pets and taking that, you know, potentially taking sport, we have firmite for our pets, and we have for for us to get, you know, for our own personal health as well. So everything to do with infection control is really important.

I could talk about it all day, but I'm not going to because I, I don't want to send you off to sleep. So thank you very much for listening. If you've got any questions, feel free to email me at [email protected].