OK, so tonight we have Louise O'Dwyer. She's speaking about emergency and critical care nursing, applying Kirby's rule of 20. Louise is an RVN.
She currently works as a clinical support manager for Vets Now and is based in the 24 hour emergency and Specialty Hospital in Manchester. Louise gained her diploma in advanced veterinary nursing and surgery in 2004, and medical nursing in 2007, veterinary technician specialty in emergency and critical care in 2011, and anaesthesia in 2014. Louise has contributed to over 45 books, journal articles and book chapters, and lectures regularly worldwide.
In 2016, she was the recipient of the prestigious Bruce Vivash Jones veterinary Nurse Golden Jubilee Award by the RCVS for exceptional contribution to veterinary nursing. And Louise has taken over the role of president of the Academy of Veterinary Emergency and Critical Care Technicians in September 2018. So I'm sure you'll all agree that's a pretty impressive biography.
Thank you, and over to you, Louise. Thanks very much, Sophie. So I've known Sophie for what we say now 7 years, Sophie?
Yeah, about 7 or 8 years. So I'm gonna embarrass her because I've got a photo right at the end of a photo of, of Sophie, obviously quite a few years ago now. I highlight that in the presentation.
Thanks. Kirby's rule of 20 I think, is something that unless you work in emergency and critical care medicine, you're probably not aware of. So the rule of 20 was, developed several years ago by Rebecca Kirby, who was an American, diplomat in veterinary internal medicine and emergency and critical care.
And I think it's a useful application because we can use it as a guideline for monitoring parameters in our patients. It helps us to try and prevent, any morbidities. It helps us to try and prevent, patient death.
And also for me, it gives us a little bit of a degree of autonomy, because we can actually apply some clinical parameters when we're looking at ruler 20. And that stops us having to go back to our vets all the time. Now, I'm not saying that allows us to make a diagnosis.
What I'm saying is it can give us kind of alert parameters. So if a patient's heart rate gets above or below a certain range, then we know to go back and, and, and feedback to that vet. It means that, you know, we, if we're concerned about abnormal heart sounds, then that vet is happy for us to go and run an ECG on that patient.
We're not diagnosing, but we can actually, we've got that pre-approval. From vet, from that vet beforehand. It just saves time, you know, we've all been there.
We've got to spend time waiting for them to come out of a consult, to wait for them to come out of theatre, to wait for them dealing with whatever they're dealing with. And it just allows us to that degree of actually knowing what that next decision is going to be in this patient's treatment plan. So for me, it's a useful thing to look at applying to those, that, that sicker group of patients that we see within our clinics.
So, the rule of 20 is kind of obviously, 20 kind of parameters that we look at in our patients, but we can probably if we look at it, apply to many more to this, I've added actually communication onto this because I think this is really important. Particularly when we look at, if you're working in a hospital environment, looking at moving patients from one department to the next department, because it's so easy to forget about a certain aspect of communication, to tell people what fluid therapy rate you want a patient to continue at, to talk about what you want to do in terms of transfusions. It's also really important in terms of that handover system and also in terms, in terms of communicating with clients as well.
So as you can see, the rule of 20 consists of looking at fluid balance, looking at oncotic pull. I've tagged, I've moved albumin up and I, I added albumin along with oncotic pull oncotic pull, because the two really go together. Looking at electro electrolytes and acid-based balance, oxygenation and ventilation.
Looking at mentation and level of consciousness, blood pressure, heart rate, heart rhythm, contractility, looking at coagulation, looking at, PCV and haemoglobin concentration, renal function, immune status, something that often really gets overlooked, particularly in those critical patients, which may well be neutropenic, and are really at high risk of hospital acquired infections, looking at our antibiotic use, looking at addressing nutrition, GI motility, and metabolism. Looking at the drug dosages we drug dosages that we use in our patients. Looking at analgesia, and the big focus is going to be looking at kind of the nursing aspects of these things.
So looking at nursing care, looking at patient mobility, looking at wound management and bandage care, and looking at TLC, which obviously we all know is a massively important aspect. Of of dealing with these critical patients. So that rule of 20 sometimes can be a little bit difficult to look at and kind of remembering our patients.
So we've we've kind of broken it down to a mnemonic, which is fight back, fight back now or die. And that just for me, like I've got to have a very simple way of remembering things, otherwise I completely forget things all the time. And you can see looking at this, it applies those 20 rules, and some of them we've combined together because they, they logically go together in our critical care patients.
So fluid balance is one of the first things that we're looking at. So hypovolemia, particularly in our emergency and critical care patients, it was one of those things that is of a priority. You know, perfusion is massively important in terms of our patients.
If we don't get, Oxygenated blood being delivered to our tissues, they're gonna start to die off very quickly. We're gonna get cell death, we're gonna get tissue death, and eventually we'll get organ death and then patient death. So perfusion is one of those things that we look at, we look at addressing as a priority in terms of giving our patients fluid bonuses.
Looking at the types of fluids that we're going to give to our patients, I'm not going to be able to go into these things massively, but there are very, very good textbooks available. There is one textbook that entirely focuses on the rule of 20 and breaks it down into much, much more detail, that I can, I can mention towards the end. But we're going to look at the type of fluid that we give to our patients, depending on the individual needs.
Ma, we may want to address things like specialised catheters into our patients. You know, most of the patients that we're gonna deal with, we're gonna put a standard catheter into a peripheral vein, but actually, that may be more difficult in er in in some of our patients, we may need to look at putting central lines into them. So we look at, for me, I look at how long the patients likely to require cathe catheterization for.
I look at what types of fluids we're gonna give to that patient. I look at how often we're gonna need to take blood samples from that patient. If I've got an animal, That is on lots of fluids, that's on lots of different medications, particularly if they're on glucose or dextrose containing fluids, that can be a fairly high percentage.
If we're going to take regular blood samples, all these things tell me actually, in this animal, it may be much better early on to go with a place that a jugular catheter or a central venous catheter that allows us to do that as one procedure. Yes, they're slightly more expensive. But actually as a skill, it takes a little bit of practise.
It is a more specialised catheter. But actually, it stops us. We've all been there in that situation where you go through every single one of the animal's legs, and you get to a point where all those veins are pretty short.
And then we're really struggling to get venous access. So for me, particularly things like our DKA patients. Our multi trauma patients, our pancreatitis patients, for example, where we know we're gonna need them on fluids, on medications, where we're gonna take regular blood samples, it's better to go early on with that large ball, potentially triple lumen catheter, so we can address those issues.
One another Another important aspect is also looking at measuring fluids in and fluids out in our patients. You know, this we look at in terms of hypovolemia. So hypovolemia and dehydration are two very different conditions.
Hypovolemia is an emergency. We're not getting oxygenated blood being delivered to those cells and those tissues. Dehydration, we're gonna correct much more slowly, where hypovolemia we want to address within minutes or hours.
Dehydration we correct generally over a 24 hour period. But equally, both of them, we need to make sure we're matching fluids in and fluids out. And how we do that, we'll kind of touch on later, in this session, but it's something we want to address.
You know, it's easy to, for patients to get behind on fluids, particularly if we're concerned about them having things like acute kidney injury. Equally, particularly in paediatric patients, it's very easy to overhydrate them, and then for them to start to have issues. So looking at perfusion deficits, we generally classify patients as being mildly moderately or severely hypovolemic.
This applies much more to dogs than it does do to cats. Cats will tend to become brag tachycardic up to a point. And then they'll start to become bradycardic, where dogs predictably, their heart rate increases as, as hypovolemia severity increases.
So we see in dogs that increase in heart rates, that mucous membrane becoming paler and greyer, that capillary full time becoming longer, those pulses becoming reduced, that pulse duration in terms of amplitude, the duration becoming reduced. I was starting to lose peripheral pulses. And one of the things, and I'll probably mention it later on in this session, one of the things that we can actually measure as a parameter and get a value to is plasma lactate concentration.
So lactate is the byproduct of anaerobic metabolism or respiration in cells. So the more reduced that oxygen delivery is to those cells, the more anaerobic metabolism we're going to get and we reduced lactate is a byproduct. So generally, a normal lactate is anything less than 2.5 millimo per litre.
We originally started to look at lactate in dogs in GDB patients in the, in the early 2000s. And what we used to say is that if a dog's got a lactate above 7 with the GDV, it actually probably is worth considering, do we treat that patient because they're gonna have such severe reduced perfusion, ischemia of tissues that maybe, you know, the stomach's gonna have such severe gastric necrosis that it's not going to be operable. We now know it's more than just that final number.
We now know it's more of how quickly we can get those parameters down in those patients. So we look at bolusin and fluids very quickly. Generally we'll go.
It depending on that severe hypovolemia, somewhere between 10 to 20, 130 mL per kilo of an isotonic crystalloid like Hartman's or lactated ringer solution. Over about 1510 to 15 to 20 minutes, and we will repeat that as needed. And cats are a little bit more cautious with fluids because they won't tolerate fluid overload quite as well as dogs will do.
So the cats were more likely to go somewhere between 5 and 10 mL per kilo, but we both that fluids in quickly, because what we're ultimately trying to do. I restore tissue oxygen delivery. And that's what we need to keep patients alive.
We need to make sure we get an oxygenated blood being delivered to tissues. If that doesn't happen, if we don't have effective tissue oxygen delivery. Things start to go wrong.
The tissue auction delivery is governed mainly by two things. It's governed by cardiac output, and it's, it's governed by the amount of oxygen that's carried in that blood. And these two parameters are going to be influenced by other things.
So cardiac output is the amount of, of blood pumped out of the heart per minute. So it's dependent on heart rate, it's dependent on stroke volume. So stroke volume is the amount of blood ejected from the heart within each each heartbeat.
And that's gonna be affected by the amount of pre-load. So pre-load depends on how much blood is returning to refill that heart with blood. It depends on contractility.
So you've got a patient with severe cardiac disease or severe arrhythmias, that's gonna reduce contractility. And it also depends on the amount of after load as well. So the amount of afterload is the amount of resistance that heart's got to pump against to pump that blood out.
So if you've got a very vasoconstricted patient, That makes it more difficult for that heart to pump blood out. It also depends on heart rate, and as we said, dogs predictably will become more tachycardic as they become more hypovolemic, because what they're trying to do in the face, often of reduced stroke volume, is they're trying to maintain cardiac output to maintain tissue oxygen delivery. We also have that aspect of oxygen content in blood.
So the oxygen content of blood mainly depends on the amount of haemoglobin. So, about 96 to 98% of all the, the oxygen carried within your bloodstream is bound to haemoglobin. A small percentage is dissolved in plasma, that's called PAO2.
And both of these we can influence by giving our patients some oxygen. So supplementing oxygen will help to make sure that haemoglobin is saturated with oxygen. It will also massively increase the amount of oxygen that gets dissolved within that plasma.
So that's why predictably, when we see these patients coming into the clinics, Even if they're hypovolemic, we will put these patients onto. Some some type of oxygen therapy to try and help to improve tissue oxygen delivery. So again, we can look at assessing that, assessing that patient's own way of breathing, improving things that way.
In terms of improving stroke volume, we can look at getting these patients on some fluids and that will help increase the circulation, improve the circulation in those patients. The next thing is oncotic pull. So, we often refer to this as colloid oncotic pressure or colloid osmotic pressure.
So colloid oncotic pressure is the pressure that's created by solutes in the plasma. So it's the pressure that's exerted to keep fluids within the blood vessels. In certain diseases, within certain traumas, oncotic pool will change, and those fluids will shift from one fluid space to another.
So any patient that's potentially losing fluids or is losing losing, sorry, any patient that is losing, proteins, so that would be our patients with burns, our patients with protein losing nephropathies or enteropathies, patients with, haemorrhage are gonna have problems in terms of oncotic fall. Normal, generally speaking, normal oncotic form means that there is plenty of plasma proteins. So mainly albumin, and that's what I'll talk about next, available to keep those fluids within the intravascular space.
So Albin is what the big molecule that's required to, to make that sure that that happens. So in hyperprotein, hyperproteinemic patients or hypoalbumic patients, fluid can start to leak out of that extravascular space, and that will cause, fluid will leak out of the intravascular space into the extravascular space, and that will cause edoema. So that's when you see hyprotein, hyproteinic patients where they develop lots of peripheral edoema.
This is very different than what we call hydrostatic pressure. So hydrostatic pressure is a pressure that's exerted on vessels, and on vessel walls to push fluids out into the extravascular space in order to bathe the cells in fluids. So a normal colodoncratic pressure is 25 millilitres of mercury.
Normal hydrostatic pressure is about 37 millimetres of mercury, so that leaves a net and about 12 millimetres of mercury and pressure to pull fluids out of those vessels and into the extra extra extravascular space. So this is really important in terms of feeding the cells within the body. And you can see on that slide, if that colour oncotic pressure is low because the patient's hypoalbumic, so if you measure our COP at being 15 millimetres of mercury, that creates a bigger net of 22 millimetres of mercury.
We're going to get the movement of more fluids into that extravascular space and we start to see edoema. So I realise it's quite a, Confusing concept, but it's, again, there's more details in the in the notes. And there is also, as we said, there's a textbook available that talks about this subject.
So one of the fluids that we can use that helps to maintain colloid automatic automatic pressure is what is one of the fluids we can use is our colloids. Now colloids, So in the UK have kind of, I say, gone out of fashion a little bit. There was some controversy about using colloids because of concern at the moment is they can cause coagulopathies, and they can, cause acute kidney injury.
There are studies going on at the moment that are going to prove whether that actually does happen in veterinary patients. We think that happens in human patients, but we've got two different patients groups. In the UK we mainly have gelatin or starch-based products available.
So our gelatins are things like chemoel, or geliusin or jela plasma. Now, these fluids have got quite a low molecular weight. So I compare everything to albumin.
Albumin is 69 kilodaltons in size. As we can see from this, our gelatin products are only 30 kilodaltons in size. So that actually means They don't last a very long time in that in intravascular space.
They extravasate very, very quickly, not much, you know, in a, to be honest, not much slower than actually our crystalloids do. So we predominantly tended to use our starches. Our starches stay in that intravascular space for a longer period of time until they're broken down by enzymes in the body and then filtered out in the kidneys.
So, in the, I don't want to sound old, but in the 90s, we started to use heterarches much more. And then we've moved over in more recent years to using our tetras starches. In the US, I know they still have heta starches that are veterinary licenced available to them.
And these are, these are molecules have got a much bigger molecule weights, so our tetris arches a whole 130 kilodaltons. And he starches are 450 kilodaltons. So they, as we said, they have to be broken down by enzymes and filtered out in the kidneys, which means they last longer, they've got a much longer duration of effect.
So they're gonna increase aquatic pull for a longer period of time. So as we said, albumin becomes more more useful. So albumin is a protein that is made in the liver.
It's our most prevalent, plasma protein, so it helps keep fluids within that intravascular space. So as you said, in times when proteins are being lost, either through things like trauma, through burns, or through disease processes, there isn't enough albumin in that plasma to keep that fluid within that intravascular space, and that causes fluid to leak into the extravascular space, that causes edoema. And our albumin has so many important, uses in the body.
It carries steroids, it carries a lot of hormones, it carries amino acids, and we need that, that albumin available. To maintain colloid uncotic pressure. It's responsible for about 70% of our colloid oncotic pressure.
And I don't know why, but I've lost all my images, so something's gone wrong with my presentations because I've got lots of pictures on lots of slides, and I've got a horrible feeling that we're all going to disappear, for every single slide that I've got. Also, sodium binds to albumin, so it's gonna draw water along with it. So again, it's gonna help in terms of improving, intravascular volume in our patients.
Glucose is the other thing that we want to look at. So we want to, and there are many different diseases that are gonna affect blood glucose levels. Even things like stress in our patients are going to affect glucose levels.
And we want to try and maintain them with these normal values, as we can see in cats. They're over just under 4 to just over 9 per litre and not massively different in dogs. We define hypoglycemia as being less than 333.33 millis per litre and hyperglycemia is 6.6 m per litre.
And as we said, these widening parameters, hypo and hypoglycemia are really poor prognostic indications for various conditions. And that we can see a wide variation in clinical signs associated in derangement. So, we can see seizures, you won't need to think about paediatric patients.
Paediatric patients will seizure, if they become hypoglycemic. We can see it in diabetic patients, we can see it in comatose patients, in head trauma patients, and they can be caused by various different conditions. They can be caused by deep diabetes, by insulin administration, because that's gonna increase glucose uptake within the cells via catecholamine released, which is why we see that stress hyperglycemia in cats.
We can see arrangements in septic patients, in patients, where steroids have been administered in our cushionoid patients. And it's one of the things that we use to monitor, sepsis in our patients as well. So it's things that we want to try and maintain within that fairly tight range.
Electrolytes and acid, balance are also something that, that we want to look at. So, the main electrolytes that we tend to worry about are sodium, the potassium, and their chloride. We can also look at magnesium and phosphorus, but magnesium particularly tends to be more difficult to measure.
In most of our clinical environments. And there are certainly times when we're going to see patients that have got changes in these parameters that we need to monitor very closely. So, again, our vomiting patients, they can lose they can have massive electrolyte losses, as can our patients with, diarrhoea.
And it's so many in patients, we know we, we get big, electrolyte changes. Our diabetic patients block cats classically. They're probably one of the, the, the patients that we see most commons with commonly, apart from vomiting and diarrhoea cases where we get big electrolyte imbalances.
So, Urinary obstruction patients can't get rid of potassium from their body. So we can see often massive and potentially life-threatening hyperkalemia in these patients, or renal failure patients. The only way you can get rid of potassium from your body is by urinating it out.
So if your urinary system hasn't, isn't working normally, if your kidneys aren't working normally, we can start to see big problems in new patients. And we can see numerous problems as a result. We can see weaknesses, we can see arrhythmias, we can see heart blocks, and as we said, The most common electrolytes we tend to look at are sodium, potassium, calcium, magnesium, phosphorus, and chloride.
And this is why if you have a patient in that's got any disorders, it's really worth having a high and low. So you know to alert your vet if a patient has a potassium that drops below a certain point, or if it elevates above a certain point, particularly in those kidney patients, in those blocked cats. And it just stops you having to go back all the time.
And nag your vets about these things. Not that it's not a good thing to nag your vets, but it stops you having to do it regularly. And it means, you know, you know at which points to be concerned.
I think it's really useful, particularly if you have less experienced staff or if you have lots of locum staff that aren't familiar with working with these critical patients. It just, it just gives you those alert flags that actually, at this point, we're concerned about this animal. Oxygen and ventilation is one of the other things that we want to look at in our patients.
So for me, this is really, really a big one, and it's a a parameter that we could devote an entire webinar to. When we see patients that have issues in terms of oxygenation or ventilation, we want to really address these sooner rather than later. So when we talk about oxygenation, these are patients, oxygenation is the amount of oxygen that's been delivered to our tissues.
Ventilation is about the exchange of oxygen for carbon dioxide and alveolar level. And we need to make sure we're able to get oxygen in because we said getting oxygen being delivered to our tissues is massive. Important.
We also need to make sure we're getting carbon dioxide out of that patient's body, because carbon dioxide ultimately has an acidifying effect on the body, and we can start to get organ system derangements if patients become massive, massively hypercapnia. We can also look at these parameters to determine, do we need to ventilate those patients. So, Again, ultimately, we would probably need to have blood gas analysis.
What we generally say if a patient has got a PA 02 of less than 60, that patient requires ventilation. But actually, if you've only got a pulse oximeter, and you have a patient whose SPO2 is getting towards 90, That patient needs some help in terms of pushing oxygen into their lungs and across that alveolar membrane and into their bloodstream. Equally, if they've got an entitled CO2 or a PACO2, more than 60, that indicates they needed additional help in terms of ventilation to eliminate that carbon dioxide from the body, because we're going to develop this downward spiral.
The other indication that patients require assistive ventilation is if they've got an increased work of breathing. So, if I've got a patient where I can see they're making lots and lots of effort, and I'm concerned they're likely to go into respiratory arrest, I would rather look sooner rather than later at anaesthetizing that patient, intubating them, and taking over in terms of manual or mechanical ventilation. I've got videos that are meant to go with this, so I'm actually, I'm gonna pause for a second in case they can edit this back together, and I'm gonna come out and I'm gonna go back into this presentation because everything isn't working perfectly.
As it should do. So, I'm going to reopen this because I've got lots of videos and my videos have to play, otherwise, the whole thing kind of doesn't work. And you can see that I've got lots of pictures that go along with these slides.
Sorry, Sophie, like making your first, one of your first sessions not work particularly well. So there we go. We're back to slideshow.
All my videos are gonna work from this point onwards, I'm sure all of this we can see. I don't know what's gone wrong. We can see how all these slides.
So level of consciousness on mentation really important. We can see changes in level of mentation and consciousness from patients having primary neurological diseases, so patients with brain tumours or head trauma through to treatments in our patients. Getting blood flow to your brain is really, really important.
Your brain demands about 15% of all your cardiac output, even though relatively your brain's quite small, it requires lots of oxygen and lots of glucose. So, assessing mentation is hugely important. We've all been there when we see those patients that have maybe had foreign bodies or severe vomiting and diarrhoea, where they look terrible.
We get some fluids into them and they feel much better because we restore perfusion back to that patient's brain. So when we see deterioration in, in in mentation and level of consciousness, that can suggest that a degree, the disease processes begin to progress. We're also will want to look at, motor function and how ambulatory those patients are and understand the differences between patients being normal, between, obtunded between being stuporous and comatose.
So when obtunded patient, It is dull, but still responsive to auditory and visual stimuli. a stuporous patient will not respond to auditory or visual stimuli, but will respond to pain and comatose patients don't respond to painful stimuli at all. So if you look at this patient, this is a patient with a hypoxic brain injury, this patient is stuporous.
He is not responding to having his name called to what's going on around him. So I'm just going to play this very quickly. And So this patient actually got his polar caught.
It was stuck in the baths of his cage and it was crated when his owners weren't out. So we basically had a hypoxic brain injury. So we treated this patient with some Manitol, which, which is an automatic diuretic, diuretic, which helps pull fluid from the extravascular space from the intertestitial space into the intravascular space.
And we we assessed him for hours. And you can see it looks like a different dog. Oh.
We didn't swap in front of the beagle, beagle. So again, we can see the importance of restoring perfusion to that brain. That patient, because his brain was swollen up, he couldn't get enough blood flow into his brain and that's why we saw such big changes in terms of mentation.
Blood pressure is another thing that we can look at. So, blood pressure helps to monitor if we are under or overhydrating our patients. It's a measurement of that cardiovascular system's ability to move blood around blood around and oxygenate the body.
So it's an indirect measure of systemic vascular resistance of cardiac output, and those two parameters help determine blood pressure. We want to make sure we're using the correct blood pressure measurement measurement technique. So most of us are going to either use Doppler or we're going to use osciometric.
So Doppler is more reliable in smaller patients. So in cats and small dogs, Doppler is proven to be more, reliable. There is an American College of Veterinary Internal Medicine consensus on hypertension in cats and dogs that looked at actually what was the most accurate, and they compared it to arterial blood pressure measurement, direct arterial pressure measurement.
Osmometric, finding those bigger patients. We want to make sure our cuff sizes are correct. So, your cuff wants to be about 30 to 40% of the circumference of that patient's limb.
And know the limitations, as we said, of those different pieces of monitoring equipment. Doppler, smaller patients, osometric, bigger patients, gold standard is going to be invasive or, you know, blood pressure monitoring, so place in an arterial catheter, which most of them are not going to have available. I start to be concerned if patients have a systolic blood pressure that is lower than 90 or mean arterial pressure less than 60, but I never actually let it get to that point.
When I see it trending downwards, particularly in those patients under anaesthesia, I'm going to do something about it to get that patient's blood pressure back up again. And again, the same as what we talked about in terms of tissue oxygen delivery. There are certain things that are gonna determine a patient's blood pressure.
Ultimately, it's cardiac output and peripheral vascular resistance. So peripheral vascular resistance is how much vasoconstriction or vasodilation they've got. Septic patients, they're the classic ones that vasodilate everywhere.
Our volatile agents, the ones that cause a dose-dependent vasodilation. And that's why we try and keep our, our volatile agent settings as low as possible to stop them from vasodilating and drop in blood pressure. Cardiac output also has an impact.
So patients' heart rate, so we can potentially sometimes see a low arterial blood pressure. Patients are very bradycardia. We can also see it if patients have got reduced stroke volume.
So those, patients, so ruptured splenic masses where they bled out into their abdomen, they've got a reduced stroke volume because that blood isn't there to return back to the heart to refill it. And, therefore, we see a a decrease in cardiac output. Heart rate and contractility also has an effect.
As we said, we need adequate blood flow. We need adequate perfusion to those organs and those tissues for them to survive. So we need to ensure that the heart's not only beating but it's doing so without problems.
We need to make sure these patients don't have arrhythmias and a lot of these patients will we see issues in terms of con con contractility. May have pre-existing cardiac problems, they may present with arrhythmias. So we see a reasonable number of of patients that do have arrhythmias, and we look to treating them.
I generally these days deal more with patients going into anaesthesia. I want to know what our patient's heart, you know, what their heart is doing before I anaesthetize them, because so many of our cardiac drugs. Can have an impact in terms of causing arrhythmias in most patients.
So again, I'd love to say that we do this in every single patient that we're going to anaesthetize, but we don't. But certainly if we think about critical care patients, our GDVs are one of the classic ones that are likely to develop arrhythmias, ventricular premature contractions, ventricular tachycardia really Commonly seen in those patients with GDV. For me as a nurse, I don't expect every single nurse to be able to say, this dog got a 3rd degree heart heart degree block.
This patient is invention for the tachycardia. I want them to go back to somebody and say, Can you please come and look at this ECG because I'm worried about this patient. This doesn't look normal to me.
It may be just that that patient's in an odd position. But I always say the best, the vets that say the best nurses, the ones that go back to them all the time and peck their heads about concerns about patients because they're picking stuff up early because we're the ones monitoring our patients and spending time with them. Coagulation, I'm going to talk about very, very, very quickly.
So, again, we could do an entire lecture on coagulation. Coagulation is something in its own right. But we want to know what to, what to watch out for, for.
So coagulation, we can see disrupted by so many diseases. We see hypercoagulation in a lot of our disease processes, full stop. And the problem with patients become hypercoagulable is they're going to use up a lot of their clotting factors.
They're going to use a lot of those patients. They can produce little embolisms that can block blood vessels, things like that, and then we can see further problems, as a result of that. One of the things that we often see in our critical patients is them developing disseminated into invascular coagulation.
So what happens in these patients is they develop these hypercoagulable states. So they, You know, that disease process activates that clot clotting cascade. They produce lots and lots of clots.
Yeah. Because often they've got, you know, if you look at heat stroke patients, heat stroke patients, they, they, they, everything starts to get cooked. They got get damaged vasculature.
They're going to use up a lot of those patients because that damaged vasculature, they're going to send platelets out, they're gonna send clotting factors out to try and heal things as much as they can do. They use up the clotting factors, they use up their platelets because everything used up at the same time with heat stroke patients because their liver is also cooked. They don't have those clotting factors available.
So then they develop these hypocoagulable states where the clotting factors have been used massively. And these are the patients where we need to start looking at things like, giving them, plasma and things like that, just to try and replace some of those clotting factors that they're then missing. And the other thing that we can see in these patients is what we call vertical triad.
So this is where we get endothelial injury, as we said, classic one being heat stroke, we get damaged to those blood vessels. We also get blood stasis and we get a hypercoagulable state. So we end up with these patients that use up all those clotting factors and then have those issues.
Temperature, again, body temperature, we want to think about as part of that overall initial clinical database on patients, and we want to measure fairly regularly in our critical patients where it's appropriate. We can see hypothermia as a result of that classic heat stroke, we've got environmental exposure, animals that I've exercised too, too much. So I've got a stupid Labrador, and even when it's the hottest day, even though today isn't.
Feels like we've hit winter. Even in the middle of summer, he would run around like a crazy thing. They don't think to cool down.
Cats are slightly different, they know to go and seek somewhere that's cool. We can see high, increased body temperatures from infection, from inflammatory statuses, from neoplasia. We also want to flag up the differences and identify the difference between hypothermia and pyrexia.
Hypothermic patients, where they've been exposed to something too hot or they've run around too much, we want to cool down. Our pyrexic patients are, have got an increased temperature for a reason, and those patients, we tend to not to cool that that body's reset that thermostat for a particular reason. We can also see hypothermia.
Hypothermia, we tend to see as a result of anaesthesia for me, most commonly, we can see it again with severe systemic, diseases. We can sometimes again see it, With, patients that are septic, we can sometimes see it in our high trauma patients, and if they've got severe brain injury, we can also see it with environmental exposure, probably less so in the UK than in other areas of the world. Red blood cell, haemoglobin concentration, we also want to address so anaemia really a common finding in our hospitalised patients, .
We can also see changes to red blood cell morphology, and they're often as important as the number of red blood cells. We want to, you know, make sure we stay familiar with looking at the blood smears in a patient and identifying abnormal red blood cells that because, because that can go a long way in terms of Flagging up patients that do actually have issues and changes in red blood cell status can occur very, very quickly. We can see it postoperatively because we've given the patients, you know, too much fluids.
You know, we've already said that we will give patients bolus of isotonic crystalloids, but equally, in patients where we're giving them lot of lots of crystalloids, we can dilute down our blood cells. We can, we can, you know, we can dilute down those clotting factors. In patients under anaesthesia, we want to make sure we've addressed anaemia preoperatively.
I generally will aim for a haemoglobin concentration of about 7 in my patients that I'm taking to anaesthesia, but a lot of the time, we can really under underestimate how much blood loss we can get around things like. Fracture sites. We know about things like patients with, you know, rupture splenic masses.
We know about keeping a close eye on red blood cell concentrations in patients with immunated hemolytic anemias. But those cats, classically with horrible pelvic fractures, with long bone fractures, they can get really quite anaemic, because we'll often spend a couple of days stabilising them prior to taking them to anaesthesia. And we, they can get spectacularly anaemic.
So again, These are one of the things that we want to look at and make sure that we address prior to anaesthetizing these patients. Renal function, so renal dysfunction we can see as a primary problem, or we can see it's secondary to trauma, or toxicity or other disease processes. So, these are often those classic patients that are in the hospital for several days, and it's very easy to become complacent about them and think that they're doing really, really fine.
Renal values really easy to check on our blood machines, but we can also, you know, do very, very simple things like BUN sticks to keep an eye, on these patients. It's really important, obviously, to maintain perfusion to our, our kidneys in order to maintain that normal kidney function. And so particularly in those acute kidney injury patients, and I tend to talk about AKM more in cats than I do in dogs.
We need to, look at addressing fluids and make sure we're maintaining those kids kidneys normally in patients undergoing anaesthesia. These are one of the reasons why we've become concerned about hypertension, because we've not got normal blood flow to those kidneys. And the kidneys are vitally important in, you know, metabolising and processing a lot of the drugs that we're going to give to these patients.
So if they're not working normally, we'll mention drug dosages later, but we can start to see drugs accumulating within these bodies. So we need to look carefully about the dosages that we're giving and the dosage intervals that we're using in a lot of these patients. Well, we have patients that have got real issues in terms of renal function, potentially, we need to look at, continuous renal replacement therapy or peritoneal dialysis.
And my understanding is in the UK, we only have the RBC in London that can offer, continuous renal replacement therapy as a treatment option. And we can see a, you know, kidney injury occurring, so acute kidney injury is very different from chronic, renal failure. So I'm going, I talk generally more about acute kidney injury.
We can see it from renal, pre-renal causes. So again, the classic one being hypertension under anaesthesia. We can see it because of intrinsic renal damage.
So, you know, access to toxins, you know, infectious disease processes, or post renal issues. So the classic one being our block cats where kind of everything backs up the way and damages those kidneys. So we can look at measuring, you know, fluids in and out in these patients, measure electrolyte changes, measure lactate levels, measure blood pressures.
Or to assess kidney function in our patients. Immune status, antibiotics, white blood cell count, all kind of go hand in hand. We need to know if patients got issues in terms of infection or if they've, if that's not a cause in our patients, so.
Again, alterations in our white blood cell levels could indicate sepsis or systemic inflammatory response in our patients. So, It's really important for me, it's really important that we address immune status when a patient presents into our clinic. We look at biosecurity.
So if we've got patients that are potentially immunocompromised, so our paediatric patients, are neonates, our patients receiving chemotherapy, potentially our geriatric patients, they're going to have reduced immune function. So we need to make sure For me, we handle those patients first. We're really super careful when it comes to, reverse barrier nursing these patients because we don't want them to develop infections as a result of being in our hospital environments.
Patients with indwelling catheters and devices are going to be a high risk of hospital acquired infections. So making sure we've got really good protocols in place to try and minimise these things occurring. And certain disease process can predispose a patient.
Classic ones, I think parvovirus, or parvovirus patients, our patients present that are very sick, but equally, we can give them further problems when they're hospitalised with us, as can certain treatments. So as we said, chemotherapy, things like that. So again, one of the things that we want to address, we want to make sure we're using an appropriate antibiotics in these patients.
This again, is a whole lecture in itself, but look at responsible antibiotic use. We shouldn't be just using, you know, any antibiotic in any patient. We want to go first-line antibiotics unless something else is indicated.
A lot of the time, we'll talk about getting culture and sensitivity results on patients, but a lot of the time our patients are sick when they present. So we may kind of start with an empirical antibiotic. And then we may get some culture and sensitivity back on that patient, look to swap in something to something else.
So we're just trying to limit the use of certain classes of antibiotics. The classic one that people talk about these days is avoiding the use of third generation cephalosporin. So things like, convenia, which, you know, so many of our patients have become resistant to convenia.
And we're going to develop, we're going to get to a point where we've got major issues in the veterinary world, if we're not more careful about what antibiotics we are using. The GI system, something that we really want to address as a priority. So in terms of, GI motility and mucosal in, integrity, again, classic one being parvo, hemorrhagic gastroent gastroenteritis, another one.
Both of these diseases can cause really abnormal, extreme abdominal discomfort. We want to make sure these patients don't want appropriate analgesia, vomit and diarrhoea, we can see with so many different disease processes. So we can see GI issues in terms of primary GI disease or secondary to profusion.
A lot of our patients that have been hypovolemic for a period of time, we will see producing hemorrhagic gastroenteritis. In dogs, particularly, the GI tract is the shock organ. So anything that will cause a drop in blood pressure will affect the GI tract more in dogs and cats.
It tends to be the respiratory system more. And as we said, we can see vomiting and diarrhoea as a result of everything. And it's very easy for these patients to become septic.
If you don't have food going through your GI tract regularly, you start to lose your, the endothelium of your gastrointestinal tract, and those, the gaps between cells will become not so tightly packed together. And it's very easy for us to start to get bacterial translocation and see sepsis as a result. So, Addressing this is really important.
Addressing nutrition, which I'll talk about very, very shortly, is really important as well. My old dog that I no longer have, he developed postoperative ileus and it was awful. Like he looked like a GDV patient.
He felt terrible. And it took us days for us to get his GI system working normally. So I think it's one of the things that we can really underestimate, and it's one of the reasons when we look at starting nutrition really, really early on in that hospitalisation period in our critical care patients.
Drug dosages and metabolism, I've talked already, it's a really difficult one often to monitor. But there are a few things that we can do to make sure our patients are getting the drugs that we need. We want to think about appropriate routes to give drugs to our patients.
You know, I much prefer to give drugs intravenously, if they can go by that route because patients are dehydrated and hypovolemia, they're not going to get. Gonna get normal absorption of drugs, you know, they're not going to get normal uptake because a lot of these drugs may be protein bound. If patients are obese, if we give an IM injection of the drug, that drug, it may not well go into the muscles.
Asidedemia, the those drugs are designed to work at a specific body pH. So patients develop, you know, a very abnormal acid-based balances, that can cause problems. Liver function and hyperproteinmia kind of go hand in hand.
A lot of the drugs that we use in our patients are protein bound. So if we don't have albumin available, we're going to give these a relative overdose. We can inadvertently open to overdose these patients.
For me, it's really important that we are happy in terms of calculating drug dosages in the clinic that I work in now. We dose everything in mix per kg. A lot of the nurses that we get in we're familiar with using that kind of, with doing those calculations.
They were used to being told to how many. To do really important if you're if you're using lots of continuous infusions in our patients. I have very simple ways.
I'm not great at maths. So I like to think I like to keep calculating CRIs very, very simple. I would generally add a CRI and on top of the fluids.
Because I may need to adjust both of those parameters differently and it helps to make it simple. And make sure on this particularly important to smaller patients, paediatric patients using burettes with fluids so that we can really adjust those, those volumes according to our patients requirements. Nutrition, again, all of these things I keep saying, this is an entire lecture in itself, but nutrition really is an entire lecture in itself.
We want to get early ental nutrition into these patients. If the gut is working, we want to use it and use as much of it as possible. Early on, we think about placing feeding tubes into our patients, particularly in the surgical patients, particularly in those patients where we know they are likely to not eat for a period of time afterwards.
We can do the whole thing, and we all do it. We still do it in our clinic, even though we place lots of feeding tubes, giving those patients a variety of foods, even things like sardines or meatballs or whatever, getting onus bringing and familiar foods from home, but often that's not enough to get to, to make sure these patients are getting normal caloric intake. For us, our patients go no more than 36 hours without some sort of nutrition.
So we place lots and lots of nasogastric tubes into our patients. And the reason why we want to get food into our patients early is if patients don't get food into their guts. That prolonged absence is going to start to cause atrophy at the gastrointestinal villa.
And as we said, we start to get potential for bacterial translocation. We get those gaps between those, those cells lining the GI tract moving further apart. We can also see protein imbalances as a result of things like immunocompromised immune systems.
We can see loss of muscle strength, we can start to get atrophy of vital organs, and we can get gastrointestinal dysmatility and atrophy. So starting nutrition is really, really early on. Feeding through the gut.
So ent nutrition is best in in most of these circumstances, using as much of that GI tract as we can, because it's going to help to reduce that atrophy. It's going to increase the nutritional absorption capacities. But again, thinking about the patients that it's appropriate to use in.
So oral feeding, we really only want to use in patients that, you know, in patients that are recumbent, we need to make sure they've got a normal swallow reflex, keep their heads elevated. Where possible, you will use solid food if those patients can actually eat themselves voluntarily, and that's going to help decrease that risk of, of aspiration pneumonia. And I could do it again, and I know I have done in the past a whole session on recumment patient nursing.
Pain is another one of the things that we want to address really, really early on. So pain, pain is defined as being an unpleasant sensory and an emotional experience that's associated with actual or potential tissue damage or described in terms of such damage. And what's important and why we are so important as advocates for our patients is that inability to communicate verbally.
Doesn't mean that a patient isn't experiencing pain and in need of appropriate pain relief relieving treatments. And that's so important in terms of our neonates and our paediatric patients. They often, and rabbits and other prey species, they won't show that they're in pain, because they're much more vulnerable if they do so.
And pain is very subjective. I'll mention pain scoring, and we should be pain scoring patients, but we're going to get a variation between species and breed. An individual patients, and if you, if you're not sure if a patient is in pain, it's better to give pain, pain relief.
To that patient. And pain has so many physiological effects on these patients. We've got some variables that we can look at.
We can see variables in terms of, you know, patients will often become tachycardic when they're painful. Tachycardia is not great news. It will drop cardiac output because your heart's not getting time to refill with blood.
It can affect respiratory rates that kind of have effect and acid-based balance. It can affect metabolic rates. It will make our patients miserable.
We've all probably been there when you feel just terrible because you've I don't know. I'll, I'll compare it to me. Do something stupid on a drunken night out, and the next morning you really know about it because you're really uncomfortable.
They're not going to move around normally. That's going to affect metabolism, and patients can start to become aggressive because they don't develop emotional distress. So ideally we want to treat pain before it occurs.
In trauma patients, that's not always possible, but certainly our patients undergoing surgical procedures. We want to provide preemptive analgesia. And we will adopt this multimodal analgesia technique where we're using.
I'm gonna say this on the next slide, where we're using different drugs from different classes that act at different points in that pain pathway to achieve analgesia. So this is why we don't just go, we're going to put this patient on some Carrofen, we're just going to put the patient on some buprenorphine because They will all work at different points. So we have basically transduction of pain, which occurs in the periphery, in our peripheral nerve receptors, we then and we've got drugs that out there.
We then get the transmission of pain up our nerve fibres. So we've got drugs that can back there, particularly things like our local anaesthetics. We get processing of pain in our dorsal horn of our spinal cord.
Again, different drugs are going to work there, and then we get the perception of pain in our brain. So we utilise multimodal analgesia to try and inhibit pain at as many points in that pain pathway, and that's going to help to achieve much better control of pain in our patients. Again, this is an entire lecture in itself.
Think about nursing care, think about mobilisation of our patients. Really important in terms of wound healing. Overall healing of patients are preventing infection.
So early on, we start thinking about physiotherapy plan. You know, can we carry out passage range of move, movements? Can we do massage in our patients?
Thinking about things like bed sores, thinking about them getting sore. We've all probably been in bed with the flu, and when you get up after a few days, you feel creaky and you're really sore because you've not moved around normally. Certainly for me, as I'm getting older, it's getting worse.
You know, I can barely get up and down off the floor without making lots of noises now because I've got more joint pain. Just addressing things like bedding in our patients, making thoughts sure we're thinking about clean, comfortable bedding, bedding that is wicking, particularly if we've got patients that don't have indwelling urinary catheters, things like that. This is so important in terms of creating these nursing care plans for patients.
If you've got recumbent patients, if you've got patients that have got reduced blink reflexes, if you've got patients that are on lots of opioids, thinking about lubricating eyes. If you've got patients that aren't swallowing normally, thinking about mouth care and dental care, can we wipe these patients' mouth out with some dilute chlorhexidine solution? Things like hexamix on a regular basis, that just makes them feel a bit better and a bit more comfortable.
Think about bladica and faecal care, making sure these patients are pressing, are able to pass urine, so thinking about can we get them up and take them out for a walk? Can we express their bladders? Do we need to place urinary catheters either intermittently or in dwelling?
And that will help to measure fluids in and out. Think about faecal care. We place not a large amount, but in patients that we've got really severe, diarrhoea, we place faecal management systems into our patients.
So you can either buy, These purpose-made ones, which is in the top right image, where basically you you place something that's a bit like a big foley into that patient's rectum, and they pass diarrhoea down that tube into a collection bag. Or in this bottom image, you can see you do exactly the same with a Foley and a urine collection bag. And this is patients that are producing basically liquid diarrhoea.
And those patients that can't get up and move out of it. So they continually, they become soiled. We've got to get them, we've got them get them washed because otherwise they're going to get urine scaling, they're going to get faecal scaling.
So just thinking about what we need to do to our patients. It's particularly important in the role of those recumbent patients because we need to do for them what they can't do for themselves. Think about tubes and drains, you know, thinking about, you know, central lines, you know, urinary catheters, abdominal drains, all those things, bacteria are gonna adhere to the surfaces of that drain, no matter what we do to try and avoid it.
So we need to think about regularly wiping them down with chlorhexidine to reduce bacterial loads because those bacteria are going to m. Great over that surface of that catheter drain and get into that patients through, you know, as via the bloodstream, so we can see, catheter associated infections. We knew urinary catheter, urinary urinary tract infections are really common in patients that have got indwelling urinary catheters.
So we're trying to do what we can to minimise these hospital-acquired infections for developing as much as impossible. Bandage and wound care. So making sure some of this have mens, it goes hand in hand, having SOPs in place.
So we're checking insertion sites for things like IV catheters, feeding tubes, urinary catheters, womb soaker catheters, abdominal drains regularly. So we're picking up if they have issues early on. If they develop hyorexia whilst you're in the hospital, thinking, could this be related to that catheter or that drain that my patients got in.
Thinking about bandages, making sure we're regularly redressing wounds where appropriate, we're redressing catheters, we redress our catheters at least twice a day. Because we want to pick up on them developing things like phlebitis, and making sure we're really careful. I've not done it, and it's a whole session in itself, thinking about hospital acquired, hospital-acquired infection and the risk of us giving back our bacteria to those patients.
So thinking about hand hygiene, massively important in patients with tubes and drains in. One of the other aspects, of, of Kirby's rule of 21 of the last things that it talks about is TLC. So tender loving care is hopefully why all of us want to become nurses, because we want to spend time with our patients.
I didn't become a nurse because I couldn't become a vet. I became a nurse because I wanted to spend time with our patients. What we do, we become patients, that's particularly important.
So thinking about what those patients can't do for themselves, regular ro grooming, talking to them. Doing things with them which doesn't involve injection or medicating them or treating them. So interacting with negative outcomes, so, so important.
Think about the behavioural and psychological considerations of being hospitalised. So, providing nighttime is so important. We will put little signs up on our wards so that he knows that, like, we're trying to avoid dis disturbing these patients, patients as much as possible.
We will try and bundle up our interventions that we need to do, so we get some nighttime. For those of you that have had babies, you know, being on a maternity ward is probably pretty awful because not only does your own baby keep you awake, but everyone else's does too. So thinking about turning off hot lights, minimising stimulation.
Although it can be a pain, allowing favourite toys, blankets, things like that to come in for me is fine. I always warn owners they may well not get back ever again. And that's why kind of having an old t-shirt or something like that can be so useful, because it's often it's something that's quite small and may not get urinated on my concern with beds and blankets as patients may pass urine onto them, then, and then they have to go into the washing machine.
Using pheromones. So feed away, feel the friends, DAP diffusers, all these things can help to minimise stress. One of the things that we have in our wards.
As we have these classical music, we have music for dogs, music for cats playing on the iPods, iPods, and it really does seem to make a difference in terms of keeping them much calmer. And I always say when you get one cat in a ward, which is mad, the rest of them seem to follow. So as I said, really important aspect.
I said, I'm embarrassed Sophie, this is a really old photo of Sophie dealing with a tetanus patient that we had in, in our previous practise. They're in a strange environment. Think how awful it is to be podded and poked and have strange smells and no family there.
And I would say, particularly in those geriatric patients where they often have cognitive dysfunction, it's really distressing for them. Much as we can say, oh, owners coming in to a visit is a real pain, but for me, I like to have owners there to spend time, quality time with that patient to get them up and get them out, if at all possible, so they get some sunshine therapy. Just to make some, make them feel a little better, better, just getting them out of that clinical environment.
And then I said, I mentioned this very, very quickly, thinking about those other forms of communication. We spend a lot of the time when we admit our patients talking to owners about what is normal for their animal, talking about the commands that they have for going out to toilet, talking about the type of bowl that they like to eat, talking about the type of food that they like to have, where do they normally eat? Just all things that can make that hospitalisation stay.
A bit easier for that patient. Think about forms that you have. So we have transfer sheets.
So when we're moving a patient from one department to another department, we know all the details that want to continue with that patient, fluid therapy rates, nutrition, considerations, analgesic considerations. We also have very specific handover charts. So we have a handover chart within vets now that is based on the ISA system.
So we have the Isobar system. Because we, we've adapted it a little bit for veterinary patients, but this is where the ISBA system is used a lot in human emergency and critical care where you introduce yourself and your patients. If you've watched 24 hours in any in A&E, you'll have seen this happen.
So they know who this person is that's talking, who the patient is, what their clinical problem is, so the situation. Observations, so vital signs and clinical assessments, the background that relates to that patient, the plan going forward, what needs to happen, the assessment of that situation, and then we do a read back to make sure everything's clarified, that everyone is happy, and that receiver will often repeat that information back to the presenter. So I said I was going to talk to, I told Sophie I'd do 55 minutes.
I've obviously gone over, which is standard for me. So, I always felt so sorry. We, so, so jealous of this bulldog.
We had this bulldog in, a few months ago, and the only way he would sleep with his head on a well cushioned stool, but never in my life have I wanted to get in bed more with a dog because he just looks so comfy. So I'll hand over for questions. Brilliant, thank you very much.
Really good talk, Louise. I've made tonnes of notes myself. So up to now, we don't have any questions through, but if you do have any, just hover over the bottom of the screen and write it in the question and answer box, and then I can ask Louise if you do have any questions.
While we wait, I'd just like to remind you to fill in your survey, just click on the link at the right hand side of the screen and just fill in that survey so we can give Louise your feedback and also tailor the webinars for your needs in the future. OK, so we've got a couple of comments. Martha Cannon just saying great talk.
And Pauletta Hamilton, thank you for a fab webinar as always, when using a foley catheter in factor for liquid diarrhoea. Do you take the catheter to the tail for security or only Inflate the Foley balloon. Do you have any guidance on sizing for cats, small, medium, and large dogs?
We tend to use them more in dogs than we do in cats. So we'll use the bigger, biggest cats are appropriate in terms of the volume that we put into that bulb, we will generally play it by ear. I don't want to overfill it too much because my concern, and we only really put them in patients where they can't get up and move out of their own faeces.
So if we think we can, they can get up and move away, we don't place them because my concern is always that we could potentially cause ischemia or strictures or things like that. So we generally will fill it and then have a little bit of a pull, because what we want to do is fill it to a point where that patient can't poo it out, ultimately. But the bigger the better.
So it's about having the biggest tube. And if you, I, I normally look at how big I think a patient's poo would be. Does that sound really technical and terrible, that, that's what I look at.
We tend to place them more in dogs because we see them in in dogs quite a lot. And we use a similar technique if we want to use retention enemas, so for lactulose, and we use it, for I got got total brain freeze, so the kind of anti-muscle activity drug that we can use, . Methylcarbonyl, in patients with toxicities as well, where we use that as a slurry.
So we tend to introduce drugs that way if we need them to sit within the rectum to be absorbed, if patients have got reduced level of consciousness and we can't give them oral medications. But yeah, the bigger catheter, we, the biggest catheter we think is practical for that patient, and just inflate that bulb to the point where they can't poo it out. That's as technical as I go.
And do you tend to tape it to the tail and we'll tape it to the tail, yeah, I mean, if they're retention animals we they often recumbent patients so they're not moving around, but we'll take them to that tail just to try and minimise it pulling out. Brilliant. I think you made an interesting point about some drugs being protein bound, and if you have hypoalbuminemia, you could potentially overdose.
Have you ever altered your dose with hypoalbuminia with patients? We do. I mean, particularly significantly in anaesthesia drugs.
So most of the anaesthesia drugs that we use are protein bound, so we'll often reduce those drug dosages by 5 to 3, of normal. And the great thing, and I particularly like to give drugs intravenously. Because I know they're going to get to work, as long as it's safe to do so and it's licenced, because I know they're going to work in the most efficacious way.
And the great thing is if we're concerned that they've not had the effect we want, we can titrate more upwards. So, particularly in things like our opioids, we see a relatively large number of paediatric patients and paediatric patients because they've got immature organ systems. Don't always have normal albin levels.
So we'll start low and we'll give them more if needed. And again, particularly in our critical patients where you may, you know, they may have altered mentation, we can give them, we'll start low and titrate upwards. OK, I suppose that's particularly important for your opioids.
If you start off low, you can just reassess with another pain score. That's that's a. So often we'll give kind of, we'll, we'll draw up a dose and give a quarter of it and then reassess and then keep giving more.
And so we're happy that patient's got an appropriate level of analgesia. OK. We've got one more question from Craig Bailey.
Do you prefer alfaxan in your critical patients? Yes, to a certain extent, we tend to use faxa more in patients where we're going to repeat anaesthesia. So a lot of our patients with wounds where we know we're going to anaesthetize them on a daily basis, particularly in cats, because we know we can get a Heinz body anaemia with repeated doses of propofol in cats.
And the reason why we tend to prefer alfaxone is you get a little bit of a tachycardia associated with it, which can offset. The vasodilation and the hypertension that you can get. Also with Alfaxam, we can bolus it in a little bit more safely than we can do with propofol.
So it's a little bit less easy, again, particularly looking at critical patients and the fact that they may have reduced dose requirements. It's, it's not as easy to overdose patients with pro with Alfaxan is, is compared to Propofol. And it's made much, much easier these days because we now have a 28 day licence for Alfaxan.
So it makes it From a financial point of view, a little bit easier to kind of use it. Brilliant. So that seems to be all of our questions done.
So I'd just like to firstly thank JHP for for sponsoring our nurses programme. Thank you very much, Louise, for your time. It's a brilliant talk and thank you to all of our listeners for logging in tonight and enjoy the rest of your evening.
