Hi guys, my name's Sophie McMurra. I'm a registered veterinary nurse and a veterinary technician specialist in small animal internal medicine. I work at a referral hospital called North West Veterinary Specialist, which is part of the Linnaeus Group, where I make up part of the internal medicine department and I'm one of 4 head nurses.
So today I'm gonna talk to you about nursing the protein losing enteropathy patient. And what protein losing enteropathy, also known as PLE actually means, is just a condition which causes you to lose protein through your gastrointestinal tract. Now you can see this image here of a Doberman who, as you know, usually have a really long slim face.
It's full of peripheral and facial edoema. Now this was the first PLE case that I ever saw in practise, and I found it fascinating that this can be caused by a gastrointestinal disease and wanted to delve deeper to find out more about him. Now PLE is not a specific condition, but it's a symptom of many different gastrointestinal diseases, so it can come alongside many of the GI diseases that we'll talk about in a moment.
There's vary in severity. Some patients will have gastrointestinal disease and have no signs of protein losing and uropathy at all. Whereas others can come in with really severe peripheral and facial edoema, they can have leakage of fluid into their cavities such as the thorax and their abdomen, and they can become really, really poorly with it.
It does carry lifelong, life-threatening complications and the most common one being a thromboembolism, and it's much more common in dogs than it is in cats. So for this talk, I'm going to focus on dogs mainly. Now Purely is caused because plasma proteins are lost via the gastrointestinal tract at a quicker rate than the body can keep up with.
So we're losing them too quickly and we can't maintain that level of protein that we need, and that causes a hypoproteinemia or a low protein level within the bloodstream. Now, we have many different proteins within the bloodstream and albumin is the largest one. So albumin and globulin are responsible for the colloidal oncotic pressure.
So we know the proteins have that oncotic pull, to pull the fluid into the vascular system. If our proteins start to become low, there's less of that oncotic pull, and then the fluids can start to leak out into different cavities such as your pleural space. And this does cause some alterations in your fluid balance.
And that's why you may start to see peripheral edoema, particularly in the distal limbs and also around the face in patients with hypoproteinemia or any low protein levels. Whether that be caused by a PLE or some other conditions, that's there are some of the typical signs. So before we can diagnose a PLE, we need to determine the origin of the low protein to start with.
So there's a few different reasons why a patient may have low protein. So we can lose it via our gastrointestinal tract with certain conditions, and that's called protein losing enteropathy, which we're talking about today. But we can also lose it through our kidneys.
So we know with normal kidneys, if they're functioning well and there's no damage to them, the kidneys should retain those proteins. Now if that glomerulus is damaged by any maybe the patient has an acute kidney injury or they've had one in the past and there's now lesions in the kidneys, that can cause some leakage of proteins and they can have a glomerulonephritis. So that one is called protein losing nephropathy because we're losing it via our kidneys.
And then we have liver. So our liver is responsible for making these proteins and synthesising them. So if we have a liver dysfunction and it's not functioning correctly, it may not be making those proteins to start with, and therefore our levels will become low.
And there are some other issues like blood loss, so we know that if we lose blood, then our proteins become low and so does our PTV. So they both go low at the same time because they're both being lost at the same time. And also burns, so luckily we don't see burns very often in veterinary, but you do have a patient who has quite severe burns.
They lose sebum on the skin. And that contains, it's very protinaceous, so it contains quite a high number of proteins. And that's why we need to do further investigations so that we can pinpoint where this protein deficiency is coming from, and we can try and target that specific disease.
So the most common cause of PLE in dogs is inflammatory bowel disease or lymphadectasia. So that's quite a big word. If you haven't heard of it, it basically means the dilation of the gastrointestinal lactals which line your GI tract.
They dilate and they leak lymph which contains proteins. So the proteins are leaked into the into the gastrointestinal lumen, where they're excreted with the faeces and they're taken out of the body and they're lost that way. So they are the two common causes of purely in dogs.
Whereas cats gastrointestinal lymphoma is the most common cause, and you can see this image here, it's an endoscopic image of a patient with inflammatory bowel disease. Now this duodenum is supposed to be nice pink smooth tissue, and you can see it's really inflamed, really knobbly, really edematous, and as you can imagine, that edematous tissue is. Quite likely to be leaking some proteins and some fluid into the lumen itself where it becomes lost, so you can see quite easily why they would lose proteins with such an inflamed gut.
And you can have some other conditions like lymphatic disorders. Maybe you have a really high parasitic burden or an infectious disease, or maybe there's a gastrointestinal obstruction, young patients with interceptions, if there's an obstruction there and the blood becomes really inflamed around it, then you can start to see leakage of proteins. OK, so depending on the severity of the condition, the clinical signs can vary quite significantly.
So if this is from the gastrointestinal tract, we're likely to see vomiting and diarrhoea. Maybe some Melina, so your black tarry faeces or hyperexia, they may be anorexia, so completely off their food or they may just be eating smaller amounts. Weight loss as well is quite common and hematemesis may be seen, so blood in your vomit.
And any acute GI signs can come along with a gastrointestinal obstruction, so signs like abdominal pain, vomiting, diarrhoea, and anorexia. So that's why it's quite important to triage these patients and make sure that we can do the correct diagnostic aids to find the cause, especially if we are dealing with a gastrointestinal obstruction that will need to be rectified pretty quickly. So we may also see signs that fluid is starting to move across our our cavities and enter the third spaces.
So we may have an acitic patient in front of us, a patient that presents with a really round abdomen full of ascites and full of fluid. It can also leak into the plural space, so all of the clinical signs that come along with a pleural effusion such as tachypnea. Dyspnea, paradoxical respiratory patterns.
So that's just where the thorax and the abdomen work alongside each other. So as the thorax expands, the abdomen will almost suck in, and that's because there's so much fluid in that pleural space, the lungs are unable to fully inflate and fully ventilate. So the abdomen is being forced alongside it in order to aid ventilation.
We may see peripheral edoema as you see in so in the original image, and clinical presentation can vary massively just depending on the condition, how severe it is, and each patient is different. So as an RVN it's really important that we are able to triage these patients on presentation. So if you have a triage sheet, a triage record in your practise, they're really, really useful.
If you don't have one, maybe consider making one. And it's it's just an easy sheet, similar to a general anaesthetic record and have it on a clipboard ready next to your crash card so that you can just grab it and you can start filling it in for any patient that comes in. So you should have an area for your TPR.
So we need to perform a full TPR in this patient. Check its heart rate, check its pulse rate, see what's going on with that temperature. Let's try and figure out what's going on with these patients.
Look at the respiratory rate and effort. Is it really tack near? Is it really struggling?
Does it have a paradoxical breathing pattern? And if so, provide oxygen to that patient. If they'll tolerate a mask, ideally tight fitting so that the oxygen can't escape.
Perfect. If not, you can use nasal prongs, have a few different options there so that you can tailor it according to your patients and what they will tolerate. IV access.
So this is a really important one. We need IV access to administer any emergency drugs. And if you have a patient that comes in with peripheral edoema or facial edoema, we know that there's a good chance that more of this edoema may develop as the patient stays with us.
It's a good idea to consider placing a second IV catheter because the amount of times you've placed an IV and then it's become dislodged maybe the day after. By that time, the patient is full of peripheral edoema, and you're trying to find a vein in a really poorly patient who has peripheral edoema over every vessel and every limb is really difficult. So if you can gain that IV access, it just gives you that extra level of security and puts you one step ahead of the game for if they do deteriorate and if you were to lose an IV access, which commonly happens.
Attach any of your monitoring equipment to the amount of practises that I know have monitoring equipment and they just sit in a drawer, use them, attach that ECG we don't know what this patient's in for yet. Check its heart rate, is it normal? Check if there are any abnormalities.
We may not know how to read an ECG. But the more we use it, we, the more we will get to know what is normal. We don't expect anybody to say, ah, this patient has this cardiac condition or this abnormality is a VPC or, you know, any other cardiac issues but.
Once we get used to what is normal, the important thing is that we can point out when there is an issue. And if there is an issue, we can alert the veterinary surgeon, and that will help the patient massively. So we don't need to be able to diagnose what's going on on the screen.
We just need to know when it rings alarm bells. And if you have blood pressure, link it up. If you have a patient with peripheral edoema, the piece of the tail is a really useful area to pop a blood pressure cuff on because they don't tend to become edematous here.
And if you have ultrasound, this is a great opportunity to perform a point of care ultrasound, and this can absolutely be performed by nurses. If your vet or your clinician is in the consult, they're dealing with the owner, you have the ultrasound probe there and you know what to do. Pop it on the tho.
If you can see a massive pool of fluid in that pleural cavity, then that's great. You can let your vet to say this patient has a really severe pleural effusion, we need to drain it. You can alert another member of staff to start getting things ready while the clinician or the vet is in.
Consultation and as they walk through, it's all there ready, they can just pop the robe on to confirm it and then Seracoentitis can go ahead. So all of these things just allow us to triage the patient that little bit more smoothly and successfully. And at Northwest we actually held a, we have a wonderful human ultrasonographer who works with us called Angie, and she holds courses for, Specifically for veterinary nurses to train, to learn about point of care ultrasounds, and I've done this myself.
It was over a couple of days, and it's practical she has dogs in there, you practise all your different techniques, and it's really, really useful and it's tailored around the emergency settings so that you can just do that point of care ultrasound. And then most importantly analgesia. So your pure opioids are a good choice for this.
So maybe your methadone, or I think the most important thing is when we're thinking of analgesia is performing a pain score. So how painful does this patient seem? What drugs are we going to give, and is that drug effective?
So give some pain relief. Ascites is really uncomfortable if you have a really tight abdomen full of fluid, and also peripheral edoema is as well, so that's also alongside a gastrointestinal disease, which I think we quite commonly underestimate how painful it can be. If you think of human patients with the likes of ulcerative colitis, you get quite severe abdominal pain, so always try to do a pain score on these patients as and when you can and remember that they are likely to be quite uncomfortable.
OK, so as part of the triage, if your patient is suffering with a pleural effusion, this will reduce the patient's ability to ventilate. So if they can't breathe effectively, that's going to cause them to really start to decompensate. And it reduces the capacity of the alveoli to expand.
So if, if those lungs can't expand properly, the patient can crash and burn at any time in front of us. So we need to really start looking into what we can do to help these patients. We need to first of all, make sure the patient's on oxygen.
So if we provide oxygen to these patients, all of those red blood cells that are swimming around our bloodstream are becoming 100% saturated with oxygen. And that's great because if the patient starts to deteriorate, it buys us some time, it may buy us 5 minutes before they get to a really dangerous level of desaturation. Whereas if our, if their oxygen level is only Maybe it's quite low already, and then they start to desaturate, then we're getting into dangerous territory because they may start to deteriorate even quicker.
And then once the patient is saturated effectively to ideally 5 to 15 minutes, however long you can and however much they will tolerate it, we want to perform thoracotenittis. Now, ideally, thrachocentesis will really benefit the patient if it's done prior to any sedation or GA because those lungs will then be able to expand properly. We'll be able to breathe and we'll be much more stable under the sedation, under the anaesthetic.
So ideally perform it consciously just under . With maybe some local anaesthetic, which we'll mention in a moment, and with analgesia on board, they tend to tolerate thoracoentheis quite well. Just get that fluid out and then we can look at sedating or anaesthetizing the patient if we need to, depending what diagnostic aids and how quickly we need to move.
Now there are some risks of thoracocentesis, however, the amount of these I've seen and you very, very rarely see any issues. A lung laceration is always potable, pneumothorax or some haemorrhage if they pop a vessel on the inside on the way in. And if you do have that ultrasound, do an ultrasound guided, you know, grab the ultrasound so that your vet can pop the probe on and watch where their needle is to try and avoid any large vessels, try and avoid any long globes, and they can go exactly to where that fluid is.
So it just improves the safety. OK, so if we need to perform thoracocentesis, ideally, as we've just mentioned, pre-oxygenate for 15 minutes and then remember to give them oxygen throughout as well. It should be in sternal or lateral recumbency depending what your vet prefers, and we need to clip and prep the area, so it should be between the 7th and 8th rib.
We can use local anaesthetic such as lidocaine, and you can just infiltrate this around the area. So that just means you pop the needle in and out, in and around circular motion around the area where the needle is going to enter the thorax, and it just infiltrates lidocaine around that area. And that works quite well.
Or you can also perform an intercostal nerve block, and there's a really useful website that you can use called the Zero Pain philosophy. And this is set up by two specialist anaesthetists that I used to work with, Matt Gurney and Carl Bradbrook. They record videos of themselves performing these nerve blocks, and they talk you through it.
So it will just give you that little bit more confidence than reading it in a textbook and having to go off your own back. So zero pain philosophy. They have a website you can also contact them if you have any queries, and they have a Facebook and Instagram page as well, so really useful resource if you want to start using things like nerve block.
So depending on the size of the patient, we need to gauge which, which technique we're going to use. So if we have a really small dog or a cat, we may just want to use a butterfly needle, just pop it in and get that fluid out quickly. Whereas if we have maybe a bigger dog or this chest drain is likely to to stay in longer term, we can place a chest drain and chest drains are usually penetrated, so they get out every single last drop.
So they're really useful and they're really well tolerated by the patient. We then need an extension line with a three-way tap and a syringe so that we can keep on aspirating this fluid and we don't need to keep disconnecting that syringe to get the fluid out. We can just use that three-way tap and keep on aspirating all of that fluid out of the cavity.
Now with the CITES, we treat this slightly differently. So we only tend to drain ascites if it's causing any respiratory issues or if the patient is vomiting from the pressure on the stomach. So this does cause an increase in that abdominal pressure and it may well impair the patient's ventilation if it's quite big.
It's very likely to be uncomfortable and it may reduce their appetite as well, because that stomach may be really there's a lot of pressure around the stomach, so they may not be able to fit in a large meal. Now bear in mind the position that we put these patients in. So if we were to need to put the patient in dorsal recumbency and they have an abdomen full of fluid, it's like a patient with when we performing a caesarean.
If you pop them on their back, that can compress some of the venous return to the heart and it can cause severe hypotension. So ideally, we don't want that these patients in daughter recumbency if we can help him. And if we do need to drain the abdomen, it can cause hypotension or cardiovascular collapse if we remove that fluid too quickly, too quickly.
And the reason for that is because the patient starts to compensate for that increased abdominal pressure, and if we remove that fluid too quickly, they simply can't cope. So their blood pressure will plummet and also their cardiovascular system will really struggle to keep up with the sudden reduction in pressure. Just go nice and slowly and monitor as you, as the vet is removing this fluid, just monitor them, keep an eye on the heart and respirate, keep an eye on blood pressure and ECG, any monitoring equipment that you can have.
So when we are taking fluid, we always should get samples. So get yourself two EDTA tubes and a sterile plane tube from each site. And this allows us to see what's going on.
There's no point draining that fluid and then not testing it. We can have a look in-house under the microscope, look for bacteria, we can pop it on the refractometer that we use for our urine every day, look at the protein level. So if it has a minimal protein level, it may well be a pure transitate.
And that's what, that's quite common with low protein hypoproteinemia, which is causing the fluid to leak out. We can also send it off for cytology, bacteriology and a protein analysis in the in the the lab. So it's really useful, we need to always take samples of our effusions.
OK, and then we need to delve deeper into how we're gonna diagnose this, what's going on and why is this patient presenting in this way? Where are those proteins being lost? So on your biochemistry, you're likely to see a low albumin and a low globulin level.
Now the other values on your biochemistry may help you determine the origin. So if you have an elevation in your liver enzymes along with low protein, we may think, ah, the liver is struggling to produce these proteins. So it may be the origin may be a liver disease.
If we have really increased renal parameters, we may think we're losing this via the kidneys. And if it is a liver problem, we can do a bile acid stimulation test, because this is the only test that truly tells you about the liver function. So you can have really elevated liver enzymes that can be from other areas.
It doesn't necessarily always mean it's the liver, it could be the bile duct or it could be from other conditions. And the liver can still function perfectly well, so we need to know is it functioning? Because if it's not functioning, that's when the albumin and globulin will start to decrease and a bile acid stimulation is the test, perform to check the the liver function.
We can also test folate and carbalamine. These are both produced in the small intestine. So if we have low protein along with low folate and carbalamine, we may think, I think we're losing this protein via the small intestine, so it may point towards the protein losing enteropathy.
And then there's also other things that we can do. So look at our urinalysis. The protein urea, are we losing protein in our urine?
Normal urine protein creatinine ratio is less than 0.5 in the dog and 0.4 in the cat.
So if we're losing protein, it may indicate that we could have some, some renal disease here. So all of those tests will all help us pinpoint where this protein deficiency is coming from, so they're all really useful. And then to further diagnose what's going on after you've performed your pocus, your emergency ultrasound, you need to ideally do a full abdominal ultrasound.
This allows us to assess anything like lymph nodes. We know this is the most common condition that can cause PLE in cats, GI lymphoma. So look at those abdominal lymph nodes, look for a GI obstruction, assess all the different organs, and then we can pop a needle into anything that looks alarming.
So any of the organs maybe want to FNA the liver, any free fluid and the lymph nodes as well to aid our diagnosis. And if you have an endoscope in your practise, this is the ideal case for it. So endoscopy is minimally invasive, it's a really useful tool.
And every time we do an endoscope, so we pop the, we can do an upper GI scope, we can pop the scope down into the stomach and the duodenum and sometimes even the ileum. And we always, always take samples, so we never just visualise the gastrointestinal tract need samples in order to get a diagnosis. So you can biopsy samples, small particles of the stomach and the duodenum or any other area of the the GI tract that you can gain access to.
And we say take on average between 10 and 20 samples per area so that you have the better chance of diagnosis, and you don't want to end up going in again because you don't have enough samples. And it just allows multiple small biopsies along that gastrointestinal tract. If you just do, if you just look at the stomach and you think, oh, that doesn't look too bad, you can then take the duodenum, you can take the ilium, you can even do a lower scope and start looking at the colon, as well to see what's going on in the the full GI tract.
Now, I've been, I've assisted with many, many GI endoscopies and it carries an incredibly small, small risk of GI perforation. Now, if you have a patient with really severe gastrointestinal disease, and it's really edematous and really inflamed, there is slightly higher risk of a GI perforation because of all those samples, but it is very, very small a risk. Also, the other benefit is if you don't have a wound, so the patient hasn't gone to surgery for these biopsies, you can start the medication sooner.
So steroids are typically a drug of choice for a lot of GI issues, and we know that you can't give steroids if you have a big surgical wound. So this just allows therapy to start a little bit quicker. Now as nurses, we're likely to be performing the general anaesthetic alongside the endoscopy, so there's some things we need to look out for.
So they need to be starved overnight, as with any GA, whereas with a lower GA GI scope, they need to be starved for at least 24 hours, ideally to try and get rid of anything in that lower gastrointestinal tract so that we have a clear view. If the patient is young, i.e., less than 12 weeks old, then we don't need to starve them for any longer than 2 hours ideally, and we need to monitor their blood glucose throughout the GA to test their blood glucose before we give any anaesthetic drugs tested throughout and.
And on recovery as well. We know that young patients and small patients can become hypoglycemic very quickly, and especially if they are hypoorexic and they have vomiting and diarrhoea. So keep a very close eye on their blood glucose.
We always give gastroprotectants or antacids prior to endoscopy. Patients that have been starved are more likely to have gastroeso reflux. So an antacids will just help these patients.
And omeprazole IV before the anaesthetic is the drug of choice. So reflux and regurgitation in these patients could be slightly higher a risk, so we want to anaesthetize the patient to keep their head elevated, and once that ET tube is in, inflate it and check it to give them a breath and make sure you cannot hear any leakage and just inflate that cough. That if they were to regurgitate, there's a minimal risk of anything being aspirated into the lungs.
Now GI or gastroesophageal reflux can be clinically silent and it can cause esophagitis. So any starved patients, regardless of whether it's getting an endoscope, an endoscopy or any other procedure. Have an overproduction of gastric acid because the stomach starved and it hasn't been used, so that gastric acid can flow up the oesophagus and can cause really severe really severe inflammation.
It's really painful. They don't always show signs of it, and you may well see it when you pop the endoscope down. You may see it's red and looking a little sore.
So bear that in mind, and that's why the gastroprotectant and antacids really help with this, especially if we're popping something into the stomach that can encourage that stric acid and reflux. Now be aware that opioids may cause gastric reflux because they relax the sphincter. Although you are safe to use these, just, just use them with caution and be aware that if it's a patient with severe reflux already, we may want to alter the dose and maybe use something else while they're anaesthetized.
And if the patient has any electrolyte abnormalities or metabolic state issues, we want to ideally correct this before we do the anaesthetic. So if the patient has low potassium hypokalemia because they're not eating as much and they're losing it through their vomit and diarrhoea, we want to correct that ideally before we go putting them under an anaesthetic for an endoscope. And if you have an overweight patient, they're at higher risk again because once they're, well, once they're overweight in general, but once they're lay down, they are at risk of desaturating because they, their ability to breathe is impaired.
So they may have hypoventilation, they can only take really small breaths because of the, the increased pressure on the thorax. So these are even more important to pre-oxygenate, ideally use a tight fitting mask and pop your your pulse oximeter on there. Look at the patient's SPO2, it should stay above 95.
If it drops below, then you need to have a look and see what's causing them, and always consider the position that this patient is in. Now, specifically for endoscopy. There is a risk of causing gastric overinflation.
So with the endoscope, we need to put air into the stomach and the GI tract so that we can dilate it and we can see what's going on. So we do this with every single endoscopy. Now there is a risk that we can cause overinflation.
And if that happens, it can reduce your venous return to the heart and it can also cause a vasovagal response. So that can cause bradycardia. So you may start to see changes in your heart and respiratory rates, so quite typically they may go up to start with, while the patient's starting to compensate.
And then if it is maintained and we don't reduce that overinflation as they start to struggle and that venous return is compromised, they may start to then dip, so the heart rate may start to become low and the respiratory rate may start to become low, and that is a really serious issue. We may also see drops in our blood pressure as well because of that lack of venous return to the heart. So if this does occur, keep an eye on it.
Keep your hand on the patient's stomach. If you do feel like it's overinflated and you're seeing any of these signs, alert your vet straight away because they need to suction that air from the from the stomach, and they can do that with their endoscope with the the suction button. It just gets rid of the air and it will just decompress that stomach and that should fix these.
Keep an eye on it and also monitor it in recovery as well. Make sure that air has been suctioned out, even if it's not overinflated now, always suction it out before you recover the patient. You don't want to send the patient to recovery with a massively dilated stomach and gastrointestinal tract, always just remind them to deflate it before we finish.
Now, some patients need surgical biopsies, and this may be necessary if on the ultrasound, the lesion seems to be on the submu mucosal layer. So it's not necessarily on that layer that we can reach via an endoscope. So this also allows for full thickness biopsies, which you need for certain conditions.
And if it's in an area that is beyond our reach from the endoscope, so maybe we won't be able to reach it, we may need to take the patient to see it again. Now this is an invasive procedure and the risk of surgical biopsies carries higher risk, so poor wound healing, delay in therapy if we need steroids, and the enterotomy sites can also dehis and break down, which would carry a much higher risk. Now, regardless of where you've got those biopsies from, we need to put them in formalin and send them off for histopathology.
And if we're looking at grading inflammatory bowel disease, there is a set criteria which you can find online. It's called the WSEVA grading system, and that tells you exactly what you need in order to diagnose and grade the level of IVD. We can also send it for something called immunochemistry, and this just differentiates between IBD and gastrointestinal lymphoma, which you can get in both species.
Now, for treatment and monitoring these cases, it just depends on what the diagnosis is. But quite commonly we use prednisolone steroid therapy for a lot of different GI conditions. And if we are looking at a PLE then we may have a low carbalamine level because it's being lost from the small intestine, so we may want to supplement the carbalamine as well.
We can give supportive therapy if the patient's nauseous or being sick. We can give antiemetics and remember that analgesia. Now these are often lifelong conditions, so educate the owner to say this is a lifelong therapy, we're likely to need steroids long term and look at the appropriate diet, so does it need a hydrolyzed protein diet or an ultra low fat diet, because a GI diet doesn't fix all.
Certain conditions like lymphaectasia need a low fat GI diet to make sure we're using the appropriate diet for this condition. And you can go on the Hills or Royal Cannon website and they often have a list of different conditions. If you click it, it'll tell you exactly what diet is appropriate.
So it's really easy to find. And then finally, if our albumin level is quite low and it's staying quite low, we may need to supplement it. Now this is called Zenalb, and it's a human albumin.
This is the drug that we use at Northwest. And it's used for patients with a low albumin level, so not only PLA maybe it has liver disease, severe burn patient or septic peritonitis where it's losing those those albumins into the gut. Now it does carry a higher risk of anaphylactic reaction because it's a human drug.
So we always, always give chlophenamine, which is an antihistamine, IM 5 minutes prior to the infusion. And then we need to closely monitor these patients during the transfusion. So I mentioned earlier that albumin carries that high oncotic pressure.
So if we're given concentrated albumin, there is a risk of over infusing these patients because of that automatic pressure that we're putting into the vascular system. So monitor the heart and rest rate and just keep an eye on them throughout. Now, we need to treat this in a similar way that we would a blood transfusion, to perform a baseline TPR immediately prior to the infusion, not an hour before, not 2 hours before, because they can change drastically in their condition.
So immediately before, perform a TPR. The dose of albumin is 5 mL per kilo, and it's typically given over 4 hours. If the patient does have real issues with its blood pressure and they're hypotensive, you can give it quicker, but we must not change the initial test rate.
We need to test these patients to check they're not gonna have a reaction before we give this drug. And how we do that is we give a test rate of 0.25 mL per kg over 15 minutes while we're monitoring the TPR every 5.
Now we're looking for drastic changes in that TPR. So has the heart rate almost doubled? Has the rest rate doubled?
Are they now pyretic? Are they becoming, have they got hives on their face and they're really itchy? If so, that could be a sign of an anaphylactic reaction and we need to stop the albumin transfusions straight away.
I've given many of these and I've never actually seen a reaction yet. So it is still low, but it is there, so we need to monitor closely. And then after that 1st 15 minutes, if we're happy, double the rate to 0.5 mL per kilo, give that for half an hour.
So we can now start to reduce our CPRs slightly, so perform 2 in that time. If still no reactions, then give the rest over 4 hours, and the 4 hours should be from the start of that initial test rate. So remember, hypertensive patients, you can give it faster but do not change that test rate.
Check that it's safe before you give it. OK, so I've given you a lot of information there. So just to quickly summarise, we need to look at The different symptoms and we need to pinpoint where the hypoproteinemia is coming from.
The symptoms vary massively, so some patients are really stable, some patients come in moribund and collapsed. As nurses, we need to triage those patients, assess their vital signs, and care for them appropriately depending on what signs they're showing. We may need to perform thoracocentesis and give an albumin transfusion.
Another thing to mention is if you are going to give albumen, you want to give it ideally 4 hours before your general anaesthetic. So if you give your albumen, once it's finished, anaesthetize your patient, your blood pressure will be better, your colloidal oncotic pressure will be better, and it gives you a much more stable GA. It also gives the body less chance to get rid of that albumin if it's going to do so.
So if you wait 10 hours before you anaesthetize the patient, those proteins could have been lost again. So to make best use of that albumin, give it 4 hours before the GA and then anaesthetize the patient once they're at their most stable level. And then we need to do further investigations, so bloods, ultrasound and endoscope, ideally, sometimes surgery.
And then remember our nursing care that we can give. So give oxygen when they're back in their kennel if you have the facilities to do so, use nasal prongs. Put a monitoring machine outside, they cannot look at their vital parameters, your ECG and your blood pressure.
You can also perform physiotherapy, so gentle massage of those limbs to try and encourage that fluid back up towards the heart. Remember your general anaesthetic considerations for a PLA and also for an endoscope. And educate the owner that this is going to be a lifelong condition needing lifelong therapy.
An important thing to point out about prednisolone steroid therapy is alert the owners of the side effects. The amount of times the owners come back in because the patient is urinating in the house, urinating in its bed when it didn't used to, it's drinking more. And they think it's a welfare issue and that you're not fixing the problem.
We don't want patients to be put to sleep because the owners misinterpret these symptoms. Educate them to say it doesn't mean that it's not fixing the condition. It just means that it often comes alongside steroid therapy.
So if they know to look out for it, they know it doesn't mean that the patient's suffering, then we're much more likely to have a successful outcome. OK, that's all from me on PLA. Hope you've enjoyed it.
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