Hi, my name is Sophie McCora. I'm a registered veterinary nurse and a veterinary technician specialist or BTS in small animal internal medicine. I work at a referral hospital called Northwest Veterinary Specialists in Frodsham, where I make a part of the internal medicine department and I'm also one of 4 head nurses.

And today we're going to talk about, talk about an acute kidney injury, and I've chosen to focus on the skills that we can utilise as nurses to to nurse these patients back to health, hopefully, and Usually they're long stay patients, so there are many things that we can do while we're in the hospital so that they can have all the benefits that they need. So first of all, we'll talk a little bit about what an acute kidney injury is before going on to treatment. So fluid therapy is the most important treatment that we can provide, and we'll discuss what electrolyte changes we should see and how we can rectify them.

We'll then go on to the placement of the ordinary catheter because measuring the urinary output in these patients is really important. And then placement of feeding tubes. So typically these patients can be quite long stay patients.

The sooner we can get enteral nutrition on board, the more we will support their nutritional value. And any patient in the critical care setting should have nutrients going in. It's really important and it has been shown to Improve mortality rates.

So the sooner we can start feeding these patients alongside their treatment, the better the likely outcome. And we can place nasal esophageal tubes in these patients from day one while we're stabilising the patient enough in order to have a GA to have a more long stay patient tube placed. So there's many things that we can do as nurses.

OK, so the kidneys themselves are really important. They play many different roles within the body. They play a really important part of the RAS system, so the Renin angiotensin aldosterone system.

And if you haven't heard of that before, it's the system that controls our blood pressure. And the kidney plays an important role because it's the kidney that detects any changes in blood pressure. So if we do start to see a hypovolemia and our, our fluid value starts to go down, the kidneys will Quickly detect that and we'll start to retain our sodium and our water so that our blood pressure can start to increase again.

And this is vital so that we can carry on perfusing our organs adequately, . Just to maintain normal daily life. They also excrete and retain electrolytes.

So depending on what the electrolyte is, they play a really important role in maintaining our electrolyte balance. They also excrete waste products. So a urea and creatinine, they are no nitrogenous waste products, and they are responsible.

The kidney is responsible for excreting these waste products out of the out of our bloodstream. And also toxins as well, quite a lot of toxins will go through the kidneys where they're excreted and sent out of the body. We know that the kidneys produce urine, and they also produce some hormones, which we'll talk about on the next slide.

So Kidney dysfunction can really severely impact the health of our patients because of all these important mechanisms that they have within the body. Now the functional unit is called the nephron, and inside every nephron, there are many different things going on. So we have the glomerulus, which is a little bundle of capillaries inside the Bowman's capsule.

We have the loop of Henley, and we also have the distal tubule and the collecting duct. So our water balance is maintained within the nephrons, and also this is where our electrolytes are excreted and retained as well. And also those nitrogenous waste products that we've just mentioned.

So the nephron is the functional unit and it's really important that we can understand that all of this happens within the the nephrons themselves. Now the hormones that we that are produced in the kidneys, there's the first one we'll talk about is erythropoietin. And this is responsible for the production of our red blood cells.

So as our blood flows through the kidney, it will quickly detect if our red blood cells are starting to dip or become low. The kidney will then produce erythropoietin, which then stimulates the bone marrow to produce more red blood cells. And this happens on a daily basis in order to maintain a normal red blood cell value.

So if we start to see issues with our kidneys, they may not, they may struggle to produce erythropoietin, and we can quite often see an anaemia of chronic disease or anaemia of renal disease. And we typically see this in maybe your older cats or any patient with chronic kidney disease, and that's just because of the erythropoeating. And the reduction of The kidneys also produce renin, which is the first part of the RAS system, and this controls the body's blood pressure.

And then we also have Calcitron. So this is responsible for the calcium absorption from the small intestines. So you can see why a kidney injury or kidney disease can quite often go from a disease of one organ to a systemic disease, and it can have knock-on effects to other systems within the body.

Now an acute kidney injury itself is defined as an abrupt reduction in renal function. Now this can be structural, or it can be functional damage that we see. So we will see a sudden onset of potentially life threatening kidney dysfunction with this condition.

And we'll see a reduction in the excretion of those waste products, to the urea and creatinine and also the electrolytes. So usually the potassium and calcium, they're excreted as waste products so that they don't build up and we don't start to see increases in those electrolytes. So they're excreted by the kidneys.

If we start to see an injury, we may not be able to excrete them as effectively, so they may start to build up. And your potassium in particular is one that we do tend to see increase pretty quickly and can be very dangerous. And we'll see alterations in our hydrogen ions, so we may start to see metabolic acidosis with an acute kidney injury as well.

And as we mentioned before, it can quite quickly become a systemic disease, and we can typically see multiple organ dysfunction syndrome, which is also known as MOS. Now the 3 things to remember when we're looking at an acute kidney injury, is it causes fluid retention. It causes electrolyte abnormalities, and it also causes acid-based abnormalities.

So they're the 3 things that we need to remember and the 3 things that we need to try and rectify in order to help these patients. OK, so when we see azotemia, and all azotemia means is just an increase in your urea and your creatinine. So once your kidney values start to go up, that's called azotemia.

Now there's many different reasons that azotemia can occur, and it doesn't always have to be caused by the kidneys. So it's important that we need to assess the origin, where is this azotemia coming from and why is it being caused. So the first one that we can look at is pre-renal cause.

And Pre-renal aotemia is usually caused by a reduction in blood flow to the kidneys. So a reduction in perfusion will stop those waste products being perfused to the kidneys, therefore they can't excrete it, so we'll start to see a build up. And things that can cause this are haemorrhage.

If the patient has vomiting, diarrhoea, or a poor fluid intake, maybe they've been locked in a shed and haven't had access to food and water for a little while, particularly if it's a cat. Systemic disease, so heart failure, if your heart is not pumping your blood effectively, then we may see a reduction in our renal perfusion. So, that's pre-renal aotemia.

And this is completely reversible with. The restoration of an adequate renal perfusion. So that's really important to remember.

And usually we don't see sky high azotemia with this. It will be increased, but as soon as we start to reperfuse this patient or correct the cardiac failure, whichever the cause is, then that azotemia should start to reduce straight away and they will go back to a normal value, providing there's no other kidney injuries. Or maybe it could be intrinsic renal disease itself, so the functional element of the kidney is affected.

And this can be caused by ischemic events, so maybe the patient is hypercoagulable, meaning they're more likely to produce clots. And if they've thrown a clot to the kidneys and it's caused an ischemic event within the kidney itself. Or maybe the patient's ingested a toxin.

If they've had an anaesthetic and we've given a non-steroidal before, the blood pressure has been able to correct. If they're slightly if they're hypovolemic, we've given a non-steroidal and we've had an anaesthetic as well, we can quite quite often cause an acute kidney injury that way. Or maybe they've ingested ethylene glycol.

So all of these things can cause renal functional damage. And then we have post renal. So post renal is usually something, anything after the kidney, so the urinary tract, and it's usually caused by an obstruction.

So an example of this is your blocked cat, or your blocked Dalmatians that may come in. And the obstruction could be in the urethra, the bladder, the ureter, anywhere after the kidney. And this can cause a backup of of urine.

Those waste products are retained and they're unable to be excreted because there's a blockage there. So that's why we see the increase in our blood values and it can get dangerous enough that you could possibly even cause a rupture of something like the bladder or the ureters. And all of these conditions are potentially reversible if they're diagnosed early enough and treated appropriately, and they do constitute a neurological emergency.

So this is vital and we do need to act quickly when we see azotemia, and it's important to try and determine the origin as quickly as we can. And then once we have decided, yes, this patient has an acute kidney injury, there are 3 different phases to an acute kidney injury. So, first of all, we have the initial phase, which is where the injury happens.

So the patient's just eating a tonne of non-steroidals or is just ingested some methylene glycol. We'll start to see aotemia, so those renal values will start to increase. The patient presents to the hospital and often we will see polyuria, which It's usually the sign that they'll come in with because the owner has noticed that they're urinating like crazy.

But it's then usually followed up with oligura, a small amount of urine and even anuria. So as the disease progresses and the kidney function starts to decrease, the patient gets worse and the urinary reproduction can start to can go from polyuria to anuria pretty quickly. And then we have the maintenance phase.

So this is where the important part happens. So this is where we really need to start treating this patient because irreversible damage can now be caused in this maintenance phase. So, this is where our renal function will start to reduce.

And the damage can really progress to an irreversible level. And then hopefully the patient will get to a recovery phase. And in that recovery phase, the kidneys will start to compensate, so they start to get used to what's going on.

Hopefully we've managed to excrete any toxins that may have built up and it may have caused the issue. The nephrons start to repair, the renal function improves, and we'll see that asotemia just coming down and down and down as in as the patient recovers. Now, there's many, many different causes of an acute kidney injury.

So we mentioned hypovolemia, shock, dehydration. Decrease cardiac output if the patient has heart disease. Could also be an anaesthetic if the patient maybe it's a cat who's got chronic kidney disease and it's undergone anaesthetic, .

If the renal perfusion and the blood pressure has not been monitored adequately and the patient hasn't been on fluids, an acute kidney injury could be caused. Well maybe there's. A toxin there, non-steroidals, ethylene glycol, or they could have a different disease, immune mediated diseases or infectious like leptospirosis.

Now, depending what caused the issue, an acute kidney injury, the clinical signs may alter slightly, but. Often we may see them coming in with vomiting, possibly even diarrhoea. Anorexia often accompanies that.

Ataxia, if it is a toxin and the patient starts to become a neurological, which can lead to seizures. A rapid increase in that urea and creatinine on your bloods, your polyurea quickly followed by oligura and aura as well. OK, so we need to do a clinical exam and what are we gonna find?

So this is an acute injury, so often they're in a normal bodily condition because it's not a chronic disease, it's not been affecting the patient for a long time unless they have something else going on. They may be dehydrated, or they may not. They may be overhydrated.

It depends when they present. So if they're annuric and they've started to already have a reduction in that kidney function and they're no longer able to produce urine and diarrhees, then they may start to become overhydrated. We may see some oral ulceration or we may see fever depending on what the cause is.

Quite often on abdominal palpation, you will detect that they may be painful, particularly in the area of the kidneys, and you may not be able to palpate a bladder. So if they're polyuric, they're urinating out and they're not holding any urine within that bladder. If they're anuric, the kidneys aren't producing any urine because they're failing.

So again, you may find it difficult to find a bladder. OK, so initial treatment, fluid therapy, absolutely most important thing that we can give to these patients right now. And It's important that we have a nurse with these patients who can really closely monitor them.

This is not likely to rectify really quickly, and we need somebody to be monitoring the fluid therapy because it's likely to change quite a lot, depending on the patient's response. So we need somebody there, checking the patient, reassessing the patient and altering the fluid therapy accordingly. And we also need to keep a very close eye on our urinary output.

So, we need to look at, when we look at urinary output, it gives us a good idea of renal perfusion. So if the the kidneys are being perfused, they should have a good urinary output. Unless they're starting to fail and the disease is progressing and then we need to look at rectifying our fluid therapy and our urinary output.

However, if they are becoming auric, It's important that we Don't just panic and quickly stop the fluid therapy. We need to make sure those kidneys are diarrhoea, so we may need to start diuretics, but we'll talk about that a little more in a few slides' time. We need to place an indwelling urinary catheter, which we can do.

We can do all of them, so we should be absolutely putting ourselves forward to place these urinary catheters. And then we may need to manage any electrolyte changes, so hyperkalemia and increase in our potassium value in the bloodstream, that's the most common one that we'll see. And that can be life threatening and is really dangerous.

We need to manage our metabolic acidosis. And we need to think about what's caused this. So if it is a toxin, can we induce a mess?

Do we make them sick to try and empty out the rest of that stomach before it's metabolised or ingested? Is it something that can be treated with activated charcoal, because some can, some can't, depending what it is that the patient's eating. Is there an antidote available?

And do we need to perform gastric lavage to try and flush out that stomach to make sure we can get everything out that we can before it goes down the gastrointestinal tract? Often the patients are painful, so we need some analgesia on board and depending what's caused it, gastroprotectant or antiemetics depending on the cause. OK, so we'll go on to fluid therapy and we'll also discuss electrolyte changes and what we can do about them.

So fluid therapy, absolutely most important thing that will make the biggest difference to these patients right now. So, We need to correct our dehydration, if there's any present. And we need to expand that intravascular volume to make sure we're perfusing the kidneys accordingly.

And if there's any vasoconstriction within the kidney, then this will also help by increasing the perfusion. When we give fluid therapy, it automatically promotes diuresis. So along with diuresis, we get the excretion of those waste products, the urea and creatinine, and we will also start to promote the diuresis and the excretion of potassium as well.

So it has multiple benefits. And it will also help to remove any toxic substances. So we need to give an isotonic crystalloid.

And about a third stays within the intravascular space, but about 2/3 moves out into the interstitial space. So we need to correct the dehydration as well, because if the patient is dehydrated, the fluid won't stay within the vascular space. It will go out and it will diffuse out to correct that dehydration within about 20 minutes.

So we need to calculate these patients properly because it really will make the difference between survival and death for these patients. It's really important. We do need to be careful with oliguric or auric patients and as the disease starts to progress, we need to keep a close eye out on that urinary production because they can now become very quickly to, very easy to overload.

And something important to remember is with cats, they don't always follow, they don't always read the textbook. They don't always follow the same signs as dogs, and often with volume depletion, they can become bradycardic. So if you have a collapsed or dehydrated cat that comes in or a blocked cat, and they have what you would determine as a normal heart rate within the normal range, or bradycardia, that's abnormal for a collapsed or a sick cat.

They should be tachycardic. So, if you do see a bradycardia in cats, it could be because of a hypovolemia. Now, it's important that We remember these dehydration charts.

You'll find them in every textbook that you look at, and it's something that we can use on every one of our patients. If they're getting fluid therapy, we should be looking at their dehydration chart. It's really easy to remember, and you will find it online or in all of the textbooks as well.

So you can see 6 to 8% dehydrated, you may start to see a reduction in your capillary refill time and you may start to see slightly sunken eyes. 10 to 12% dehydrated is danger zone. Extremely dry mucous membranes, sunken eye orbits, and dull looking eyes, and we may be likely to see signs of shock, so your tachycardia, your cold extremities, your weak and rapid pulses, and they may even start to alter their consciousness.

And then if we have a patient who's 12 to 15% dehydrated, this is really dangerous and they could die very quickly from this. So signs of shock and then very quickly can deteriorate. So we need to act on that really quickly if that's how our patient is presenting.

So we need to correct our intravascular volume. So when we look at a textbook, they tend to all say shock rates, dogs 90 mil per kilo, and cats 60 mL per kg. So we wouldn't ever just say right, the patient's in shock, give it 90 mL per kilo, and off we go.

There have been studies to show that smaller doses and reassessing regularly have been shown to have drastically improved mortality rates. So with a dog, you can give 10 to 20 mL per kg bolus, reassess with a cat, give a 2 to 10 mL per kg bolus and reassess, constantly reassess after we've looked at the patient after the bolus, has the tachycardia come down? Has the demeanour changed?

Are they a little bit brighter? Are the pulse, is the pulse quality improved? Does the patient need another bolus?

Do they need another 2 bolus? It's important that we just give increments and stay with the patient and reassess because If you just give 90 mL per kilo, it may only need a 50 mL per kg bolus, and then we. We're reducing the risk of overhydration, especially in patients where anuria could start to creep on very quickly, we can over profuse those patients very quickly if we're not careful.

And we do need to give large volumes of fluid therapy to correct hypovolemia and dehydration at the same time. OK, so this is why it's so important to look at our dehydration charts, because it plays an important role in our dehydration, calculations for our fluid therapy. So whatever percentage you deem the patient at, so say 8% dehydration for this as an example, you times it by the body weight in kilos.

So 8% dehydration times by 10 kg is an example, and then you times it by 10 again. This gives us 80 800 mL of fluid to correct. We then need to give that alongside the maintenance fluid rate of 30 times the body weight plus 70 mL per kg, so mL per day.

So again, 10 kg dog, 30 times 10 kg equals 300 mL, plus 70, 370 mL, and that's your maintenance rate. So we need to correct dehydration and give the maintenance rate, so we need to add those together. So 800 mL, plus the maintenance of 370 gives us 1170 mL per day.

And that comes to just under 50 mL per hour, which is only 2.5 times maintenance. And then we need to calculate any ongoing losses, so if the patient's still vomiting and has diarrhoea, we need to measure that.

And we need to add it on to our fluid therapy rate. Otherwise, we're given these rates of fluid to try and rehydrate the patient, yet they're just dehydrating themselves by having vomiting and diarrhoea. So we need to keep up with that.

We need to keep up with the patient and make sure that we are looking at any ongoing deficits. And when we're weighing, if they've puked on an incho sheet, 1 gramme equals 1 mil, so it's nice and easy to remember. OK, so to form a fluid therapy plan.

So if the patient's auric or oliguric, we need to administer bolus, we need to get that patient urinating again. We can give a 20 mL per kg bolus if it's a dog and 10 mL per kilo bolus if it's a cat over 10 minutes. And then monitor that patient's response to the fluid therapy.

We cannot monitor these patients enough. If you have an ECG, if you have blood pressure monitoring, get them out, use them on this patient. This is definitely the patient to use it for.

Look at your heart rate, is the patient's heart rate coming down with the fluid therapy plan? Is the patient responding? Are the mucous membranes nice and pink?

Is the capillary refill time improving? Are the pulse quality, is the pulse quality now feeling better? Is the patient's demeanour improving?

And if there's no signs of overload. And the urinary out is not restored, we may need to give that remaining deficit over 1 to 2 hours to try and correct that hypovolemia and correct that dehydration, because otherwise, if that dehydration continues, that's putting real strain on injured kidneys and that will progress the disease even quicker. If you do have a patient with cardiac disease or a high risk of fluid overload, you can administer the fluid over 4 hours and just monitor them very carefully.

So, if you're looking at a patient and looking for signs of over infusion, you can listen to their chest. So pulmonary edoema may start to occur. You may hear some harsh lung sounds and you can also see peripheral edoema starting to form as well.

So we want to avoid all of that. And then it's important that we match our ins and outs. So if you do have a polyuric patient and the patient is urine out and really high, has a really high urinary output, the normal rate is 1 to 2 mL per kg per hour.

If they're polyuric and it's double the normal urinary output, we need to make sure we're putting that level back in. So we need to look at, calculate how much our urinary output is, and make sure our fluid therapy rate is as high as that, if not higher, because if, if we're urine out, urinating out more than what's going in, the patient will become dehydrated quickly. So even though this can lead to very high fluid rates, if the patient is diarrhezing really quickly and getting rid of a lot of it.

It will cause dehydration, and that's not what we want in these patients. So the fluid rates can be quite scary in these patients and they can get really high. And our goal with fluid therapy is to increase that intravascular volume.

Restore any deficits that we may have and initiate your production. So 1 to 2 mL per kg per hour or 25 to 50 mL per kg per day, however you like to calculate it. It's easier to do mL per kg per hour because quite often we will be emptying that ordinary bag every 1 to 2 hours initially, depending on the ordinary output.

And close monitoring, you cannot monitor these patients close enough. We need to look for signs of over infusion, and we need to maintain that urinary output and match it with our fluid rate. So the electrolyte changes that we often see is hyperkalemia.

And we may also see, well, we're likely to see a metabolic acidosis. So hyperkalemia just means an increase in our serum value within the bloodstream. This is a life threatening emergency and it tends to affect the cardiac muscle.

So the signs that we may see is bradycardia. We may see a ventricular tachycardia or fibrillation. If you have an ECG.

Link it up to this patient. And on your ECG you may see peaked T waves. If you're not very familiar with looking at ECGs, this may be a little bit confusing to to understand.

But the only way of getting to know what a normal ECG looks like is just repetition. So the more you use it, the more you'll get used to the normal complexes. You're not expected to be able To diagnose every abnormal complex.

But what you can start to do is know when something's normal and then know when something's not. Whether you know what it is or not, it will alert you to be able to tell that to tell the veterinary surgeon. So the more you use it, the better you will become.

So peak T wave, and when we say a peak T wave, it's usually as tall as the QRS complex, if not taller. We may lose our P wave, and then we may start to see wide QRS complexes, which is real danger zone. Now, to treat hyperkalemia, it depends on the value.

So normal potassium value. Is 3.5 to 5.5 millimoles per litre.

So if it's increased to 7.5, we can treat that with fluid therapy because as we start fluid therapy, we mentioned that fluid therapy promotes diuresis and when we promote diuresis, we promote ordinary excretion of things like electrolytes. So your potassium will start to be diarrheed and excreted out and it will also promote.

The excretion of those waste products as well. So when we diaries, all of those things go, go with it. So your on creatinine will come down and so will your potassium.

So it has multiple benefits. Whereas if it's over 7.5, that's when we're likely to start seeing our cardiac changes.

So we would need fluid therapy to promote the urinary excretion, but we would also need calcium gluconate. Alongside it to 1 mL per kilo, we usually dilute this and give it slowly over around 5 minutes. And this won't bring down the potassium value, it will just stabilise the myocardium and stabilise that heart muscle.

So it will just stabilise our patient. Whereas we can give insulin alongside and this will bring down that potassium value. So the mechanism for insulin, we know that we use insulin in diabetic patients, and that's to bring down glucose.

And it brings down glucose by sending it into the cells. So glucose is a co-transporter with potassium, so when it sends that glucose into the cells, it also takes potassium with it. So we can give insulin to treat hyperkalemia.

But we need to be aware that we could then start to cause a hypoglycemia, so our glucose level can start to decrease as well. So we often give glucose alongside this just to prevent hypoglycemia. So insulin and glucose.

And then if we do have a severe metabolic acidosis, we can give sodium bicarb as well. I've been lucky enough to not ever need to give bicarb to a patient. Usually the, the fluid therapy changes will be enough, but it depends how severe the patient's acidosis is.

And then we need to repeat electrolytes every 1 to 2 hours until the patient is stable. So if we're looking at treating electrolyte abnormalities and acidosis, then we do need to keep a very close eye on the patient's electrolytes. So, 1 to 2 hours may seem overkill, but it's absolutely essential.

We don't want to send it too far the other way, and we want to make sure that we are that our treatment is actually having its benefits and doing what it's supposed to do. And then once we've reached normal levels and we're happy with it, we can then go to every 6 hours once the patient is stable. OK, so we'll move on to the placement of a urinary catheter and depending on the sex and the the species, obviously, the many different skills and different techniques for placing urinary catheters, but I've chosen to focus on the bitch urinary catheter for this one, and that's because it's notoriously difficult.

So I'll talk you through how to do it. OK, so if you have a dog. A male dog, then they can absolutely be placed conscious.

You do not need sedation, really easy, pop the catheter in, indwelling, off you go. Whereas a bitch and a tomcat is a little bit more difficult, so they may require light sedation or even anaesthesia depending on what the the cause of the AKI is. Now the female urinary catheter can be tricky to place and that's because of the position of the urethra inside that urethral orifice.

And there's many different reasons why we need to place a urinary catheter. So one, we need to look at calculating that urinary output so that we can match it with our fluid therapy with an AKI. It maintains a patent urethras, if the patient has come in with an AKI from being from a blocked urethra, then we need to maintain patency.

Often these patients, particularly if the disease does progress and they are recumbent, they can be recumbent for quite some time, so it will prevent urinary scaling. It will also allow us to collect urinary samples if we need to and do any contrast mediums if we need to. And it is a necessary skill of the RVN.

So once you learn how to do these, then it's a really useful skill to take home and to to utilise regularly in practise, as and when you need it. And there are a few complications or contra contra indications and that may be if there's a urethral mass present, any urethral trauma, we don't want to be poking a catheter in there. And if the patient has a urinary tract infection, then we don't want to give that bacteria a nice direct route up.

So, Before we go and give our patients any sedation or general anaesthesia if we need to, beforehand, we need to stabilise their cardiovascular system. So, make sure the patient is normal volemic before any sedation or GA drugs are given. We need to restore norvolemia and correct those electrolyte abnormalities alongside metabolic acidosis.

So we don't want to be given, if a patient has hypovolemia and is hyperkalemic and it doesn't have a stable cardiovascular system, the last thing you want to do is sedate it or give it an anaesthetic. We need to make sure all of these are stable before we go ahead and place the catheter. So a good drug choice to use is midazolam and borphenil.

If the patient is painful, you can switch that out for methadone. And It's good to use lower doses in acute kidney injuries. We don't need to give them any more than they need, so the lower the dose, the better, and we can just titrate it to effect.

So particularly with our opioids, you can give a smaller dose, start off the lower end of the dose range and titrate to effect. So if we need more, you can top up with more, but don't quickly just jump to the middle of the range or the higher end, titrate to effect. And with uremic animals, it does increase the blood brain permeability.

So they are more likely to be overdosed and it's more likely to have a more profound onset. They absolutely need fluid therapy throughout, even if it is just a sedation, we need to support those kidneys throughout and give them the best chance of excreting the the anaesthetic or the sedation drugs. And we absolutely need to be monitoring these.

You get every piece of equipment out that you possibly have. If you have an ECG, if you have a Doppler blood pressure machine. Everything that you have, use it on these patients.

The closer we can monitor them, the better. OK, so, What equipment do we need to place a urinary catheter? To get out a selection of ideally silicone foley catheters.

An appropriately sized syringe with saline to fill the bowl once we're in. Sterile gloves and lubrication, a speculum, a collection bag, usually with a Christmas tree adapter, some of them come along with them. Clippers because we need to clip that area and clean it with iodine solution, treat it like a surgical area, and we need to prep the valve and just give it a good clean.

The last thing we want to do is introduce bacteria into the ordinary tract. And then if you need any samples, then collect the sample tubes as well. Now, a little tip is you can check the balloon for easy inflation prior to the placement of the ordinary catheter, because quite often I've found some of them, I don't know if it's just a manufacturing fault or what, but with some patients I've inflated the balloon and then the next minute the patients you'll have woken them up, they'll go to walk back to their kennel and out comes the ordinary catheter.

Because some of the balloons can have an issue. So just check the balloon prior to placing your catheter, make sure it's holding OK, there's no tears in it, and then just deflate it again before, before placing. That way you know it's definitely working.

So there's 2 different ways of placing the ordinary catheter in a bit, so you can use the speculum or you can use the digital method. So everything else is the same. So the recumbency, I place them in dorsal recumbency with their legs relaxed, or you can have them up in a frog position.

Some people like to place them in sternal recumbcy with a foam wedge under their hips, whichever, as you start to learn these techniques, you will get your own preference. I personally prefer the dorsal recumbency. You need to clip and prep the area.

Remove the ordinary catheter and lubricate the end, maintaining sterility. If you're using a speculum, turn on the light and insert the blade so that the opening is at the top and the bottom, so ventrally and dorsally. And once you open the blades, you should be able to visualise the urethral orifice ventrally, and you can just feed that catheter tip into the urethra if you can see it nice and easily.

And then once you go into that urethra, you need to advance it until you start to see urine back ideally or if until you reach the bladder. And then inflate the Foley balloon and attach it all up to the collection bag. And you do need to clean and dry the patient before putting them back in the kennel, that's one of my pet hates.

Putting the patients back in the kennel, when they're all covered in in urine because it's all spilled out. Clean and dry the patients, make them as comfortable as possible. Now the other way of doing it is the digital methods, and this is how I prefer to do it.

So rather than using a speculum, you would lubricate one of your fingers, insert your lubricated finger and run it along the ventral surface until you feel what feels like a small doughnut, and it's just like a little bulge. You can place your fingertip just after the doughnut, and then when you slide that catheter in, you just need to slide it along your finger so that you're guiding it into that orifice because that doughnut is the urethral orifice. So you just place your finger beyond it and slide the catheter in.

And then once you're in exactly the same once it reaches the bladder inflate it and attach everything up and off you go. So There are monitoring things that we need to do, once this is in place, and we need to calculate the urinary output, ideally every 4 hours or more frequently in these patients, particularly if they do become anuric or oliguric. So 1 to 2 mL per kg per hour is normal.

And we need to clean and flush the vulva with dilute iodine solution, we shouldn't really be using chlorex on any mucous membranes because it's quite abrasive. So dilute iodine is useful. And you can make up a bottle labelled specifically for this patient, ordinary catheter, and then it's there for your daily use.

Clean along the catheter itself and just make sure you're flushing around the vulva to make sure you're keeping it clean. And then you can monitor the placement and prevent any the patient from becoming tangled, so you can tape it to either the back leg or you can take it to the tail. Now, again, it's personal preference.

I prefer to tape it to the leg, but some people think that that pulls a little bit more. If the patient is recumbent, you may be OK to just leave it without taping it to the tail or the leg, but please make sure that the bag isn't just sat on the floor where it can become contaminated and dirty. And pop it in something like a, a litter tray with an incho sheet inside, pop it inside or even hang it on the kennel where it's away from the floor.

Nobody's going to stand on it and pull it out, trip up, and we're less likely to get any any complications if it's nice and clean. OK, so monitoring our ins and outputs. So normal urinary output 1 to 2 mL per kg per hour.

Oliuria is defined as 0.5 to 1 mL per kg per hour, and aura is defined as less than 0.3 mL per kg per hour.

We should be weighing our patients twice a day, and they should gain weight when they're correctly hydrated. If they're decreasing weight, we know that the patient is losing fluid, so we may need to look at our fluid therapy rates. And then diuresis is a really important thing that we can do.

So if the patient is anuric, we need to promote diuresis. So we can give furosemide or we can also give Manitol to promote an osmotic diuresis. So if we increase the osmotic pressure, the patient should naturally start to diarrhoea.

And you should start to see improvements within 1 to 2 hours if you do need to administer these, and it's really important that we look at blood pressure measurements if as and when we can. And another useful tool that we can use in the critical care setting is your specific gravity. So we know that dehydrated patients should have concentrated urine.

So it's always important to look at this alongside hydration status. Otherwise the value is completely pointless. So, if we have a patient who's dehydrated and we look at this specific gravity and it's within one of these normal ranges, that's great, but it's still abnormal, because it shouldn't be within that normal range if it's dehydrated, it should be increased.

And that will give us a good indication as to whether the patient's kidneys are functioning correctly. Are they concentrating that urine like they should be? And if not, then it's something that gives us a good indication as to what we're dealing with.

And always look alongside hydration status. OK, so we'll quickly just mention about the placement of feeding tubes. So nutrition is really important to these patients, and the sooner we can start it, the better.

These patients could be in for 1 week or 2 weeks, maybe even longer, depending on what we're faced with. And it's really important that we don't forget about their nutrition. So calculate the RER, you're weighing them twice a day anyway, so you need to adjust the RER accordingly.

Easy calculation is 30 times the body weight in kilos plus 70. And this is accurate between 2 and 30 kg to most of our veterinary patients. And then if the weight is changing daily, then we need to recalculate every day.

So a nasoesophageal feeding tube is just a thin feeding tube that goes through the nostril and the tip lies in the in the caudal oesophagus, whereas a nasogastric, the tip sits inside the stomach. And there's no proven disadvantage with sitting inside the stomach, whereas we used to think it promoted regurgitation, but now there's no proven disadvantage to that. It assists in enteral nutrition, and it's really useful for short term nutrition.

So if the patient's not able to undergo anaesthesia yet, we can place these as nurses from day one and it just prevents malnutrition in these patients, and it will promote a healthy recovery. Quite often we'll need a size 3.5 to 6 French in cats depending on their size, and they obviously vary in dogs depending on their size.

So contraindications, if the patient has brain trauma, increased intracranial pressure, we don't want to increase that anymore. Any severe thrombocytopenia, or bleeding disorders, facial trauma, gastric outflow obstruction or esophagitis, or maybe if the patient is in a coma. So first of all, we need to pre-measure the tube, so measure from the nose down to the 9th rib.

And then you can just use a marker or you can see in this image here I've placed a little piece of tape as a marker so that we know where to go, how far to push this tube in. And then you need to leave enough for the tube to be curled around and either stapled or stitched to the patient's nose or head. Now we use local anaesthetic, which are the little minims tubes, put it in both sides of the nostril and.

You can also you pop it in both sides because sometimes they will tolerate one side better than the other. And you can also pop them in the conjunctival sack because it then goes down the tear duct and it can apply some local anaesthetic into the back of the throat as well as the pharynx. We need to lubricate the end of the feeding tube so that it slides in nice and easily and get a firm hold of the patient's muzzle because they are likely to just have a little wriggle because it it's ticklish when you first go in.

Now you need to gently slide the tube into the nostril, directing it ventromedy, so towards the centre of the nose. You should see the patient swallow, and that means it's gone into the oesophagus. If they cough, it could be in the trachea, so just pull it back out and have another go.

Once they have swallowed, advance it until you reach your pre-measured length. And if you do feel any resistance or the patient is really resisting, then just stop. And to confirm your placement, typically we'll just do a lateral thoracic radiograph.

But you can also attach a syringe and look for negative pressure. So there shouldn't be a load of air coming back if you're in the stomach. If there's a load of air coming back, you may well be in a lung or in the, in the airway.

So that's a good sign of . Check in correct placement and you can also inject 5 mLs of sterile sodium chloride just to see if the patient coughs with the first few drops then just stop and remove it. Prior to each feed, you do need to flush it with sterile, sterile water.

It does need to be sterile because if it's not in the right place and it has gone into the airway, then we don't want to be introducing any bugs in there, so sterile water to confirm placement before we go popping food down this tube. And then we also need to make sure that we're flushing it after the feed as well, because these tubes are very thin and they can become blocked very easily. Now the tubes can be sneezed out, which is quite common, they can be coughed up.

They can be regurgitated, they can chew the end off, they can be inhaled, anything they fancy. And you can also get local irritation to the nostril as well, and a small amount of bleeding occasionally. It's a daily tube care, you need to just clean and flush the tube, check the attachment site so you can either attach it to with a staple or just one little stitch.

I personally prefer to staple it. I think it's quicker, easier, and it's less painful. And you can just do it to on the centre of the head.

Some people like to glue them with a little bit of tape as well, just glue the tape down, but I don't think it it sticks very well. You will get your own preference gain. And just remember to do the patient's daily RER and change it according to the patient's body weight.

You will need a buster collar to stop the patient from clawing this out, and liquid diets are ideal. If you need to stop blending diets, you guarantee it will block this tube. So the liquid diets like the Royal Cannon, gastrointestinal diet or enteral care, things like that, they're all ideal.

You can also use it if the patient is eating but only small amounts. It's important to top up the feeds with the liquid diet to maintain that RER and prevent any malnutrition, eating tiny amounts each day. It's good that they're still eating, but it's not good enough.

They will become malnutritioned and it will not help with their recovery at all, so we need to top it up, make sure we're giving that patient the RAR. And the prognosis of an acute kidney injury is variable, completely depends on what's caused it and the severity of the disease, and also the treatment options that we have available. The recovery phase can last up to 12 weeks, so don't give up on these patients too early, and also the degree of aoemia does not correlate with the patient outcome.

So if this patient has really sky high off the scale, urea and creatinine, doesn't mean they won't recover. Depends what's causing it and if we can rectify it quick enough. So don't give up too soon and hopefully we have good output outcomes with these patients.

And I hope you've learned a few different things that you can utilise in practise when looking after the patient with an acute kidney injury. That's all from me. Thank you very much.

If you do like internal medicine, I do have my own Facebook or Instagram page called Veterinary nurse Medicine Geeks. You can follow me on there. Thank you very much.