Hi everybody, my name is Sophie McMurrough. I'm a registered veterinary nurse and a veterinary technician specialist in small animal internal medicine. I work at Northwest Veterinary Specialists where I've been the medicine nurse for 12 years.
I'm a recovery rescuer and author, and I also have the Facebook and Instagram page Veterinary Nurse Medicine Geek if you do like things internal medicine. I have the honour of speaking to you tonight about the triage of medicine emergencies. So I'm going to talk to you first of all about general triage as a whole, so what to do when an emergency patient presents to you, and we're going to go through some major body systems.
I've then chosen two different types of medicine conditions to talk about so that we've got a bit of a contrast. But the general overall triage should hopefully set you up for every patient which presents to you in the emergency clinic. So first of all, we'll talk about major bodily systems, and when you are presented with an emergency, we do need to act quickly.
We do need to be decisive, and we need things in a systematic order. Now I've written here cardiovascular, respiratory, and neurological, because these are the three main things that spring to mind when we first are presented with a patient in front of us. But we don't necessarily do them in a specific cardiovascular first, respiratory second, we almost do them at the same time.
So first of all, we would pop the stethoscope straight on, check the heart. Is it beating? Is it beating regularly?
What is the rate, what is the rhythm? Is it irregular? Is there a heart murmur present?
And then we would be also looking at the respiratory rate and effort at the same time. And then we can move our stethoscope up and auscultate the lungs to have a listen for any changes there. Neurologically we're looking at whether this patient is conscious, whether they're able to come around when we speak to them, how are they, are they weak, are they collapsed?
Are they recumbent? So I've written them in a list, but we kind of do it all at the same time, if that makes sense. But the most important thing is that we are quick in our decisions and we are decisive so that we don't stand and you know, wonder over things for quite some time because time really is of the essence when it comes to a medicine or any emergency.
So we'll start off with cardiovascular. So when we look at the cardiovascular system, we can find changes whether from the, whether they are from the cardiovascular system specifically or whether they have an extra cardiac origin. And what I mean by that is.
Everything that happens to the body will affect the cardiac system, so it will increase your heart rate or decrease your heart rate. So if we are in shock or we have sepsis, we can start to see changes on our ECG, but that doesn't mean it's cardiac in origin. The heart often just changes and adapts in order for the body to survive in these environments.
And the thing that we want to know is do we have a decreased function? So is our heart functioning as it should? So we need to look at heart rate.
We need to look at heart rhythm. Is it regular? Is it not regular?
We can, we'd need our stethoscope to listen to the heart to check whether there are any murmurs or gallop rhythms present, and then we should have our finger on the pulse as well, ideally peripheral pulse if you want to check about perfusion, although it's not the most accurate way. Of of knowing about perfusion, I do feel that it is helpful in the emergency patient just to give you an idea about what, what kind of place they're at right now. Are they bounding pulses, are they incredibly weak?
So it doesn't give you a definitive answer, but it will give you an overall idea on how the patient is currently compensating. If we are checking for a heart rate and we don't have a stethoscope maybe because the patient's presented and we didn't expect it, then the femoral pulse should be the one that we're we're using and we're checking. Look at mucous membranes.
Are they pink? Are they tacky? Are they muddy or very congested?
And how is our capillary refill time? Is it prolonged? Abdomen, do we have fluid distention, which could be suggestive of congestive heart failure or a multitude of different conditions which could er distend the abdomen like er your splenic bleed for example.
And these patients may require oxygen therapy. We should link up the ECG if you have a multiparameter, ideally, hopefully you do in your triage area. Link up the ECG, your blood pressure.
Blood pressure will give you a good idea on the cardiac output and whether that patient is perfusing the tissues correctly. Pulse oximetry, if you have one, just to check whether the oxygen, whether the red blood cells are saturated enough with oxygen. And if the patient ends up being intubated with an endotracheal tube, we can check our carbon dioxide as well.
And then respiratory rate, so we need to look at the rate. Is it increased? Is it really slow?
Are they about to arrest? We need to look at the effort as well. Is there an increased effort there?
Could it be a cat with a pleural effusion, for example? Do they have a respirator abdominal effort where the abdomen is sucking in as they're trying to, to take a breath? Mucous membranes I've put on there as a something to check, although they do have their limitations, and the same with capillary refill time as well, they don't often.
Mucous membranes give me a good idea about how the patient is compensating, but it doesn't necessarily mean that they are doing well if the the mucus membranes are nice and pink. Auscultation, we need to pop our stethoscope on the lungs, have a, have a listen to the different sounds, have a listen to the inspiratory noises as well as the expiratory noises. Are, are there squeaks there or crackles?
Is it wheezing? If the patient is in respiratory distress before doing any of this, we should just pop them in an oxygen rich kennel before investigating and checking them further, because the respiratory patient can decompensate incredibly quickly, and we need to keep the stress of the environment to a minimum. They've already been put in a car, they've already been brought in, probably by quite panicked owners.
And we could be the tipping point if we're now poking them and trying to assess them. They don't know where they are. They could easily decompensate at this stage.
So pop them in an oxygen kennel and leave them to rest until they seem a little bit more rested and stable. If we do suspect some changes in respiratory effort or rate we can pop the ultrasound probe on. We can do this as RVNs and just do what we call a TFAST or a point of care ultrasound I should say.
And you can do this off the thorax just to check if there is any fluid there. And then neurological systems. So when a patient presents into the emergency room, we need to think what can endanger their life, what can we do which can prevent that and help them, and often it is progressive, especially when we think of internal medicine conditions.
Often they will present with an illness or a disease of some sort, and that's not going to go away quickly until we figure out what it is, get a diagnosis and start treatment. So often it is progressive unless we intervene. We need to look at the patient's mental status.
Are they awake? Are they alert? Are they responsive when we're talking to them?
Are they seizuring? Have they had any seizures? Are they head pressing, which could be a sign of neurological issues like encephalopathy?
Do they have nystagmus? Are they hypoventilating? And if the patient were to present with seizures, they can become hypoxic very quickly.
Often every single muscle in their body is tense, so they can become hypothermic because if you imagine all of those muscles, not only tense but also twitching and spasming as well, the temperature can go up. And if they can't open their mouth to breathe because they are seizuring and often they will have their mouth closed, they're just not able to thermoregulate and cool down as well as they normally would. They can become quite acidotic as well, and all of this takes a lot of energy from the patient, so their glucose could become low from seizures and they could be presenting now with a hypoglycemia.
Metabolic disturbances can be quite common in a multitude of different conditions, and we may see a depressed consciousness, is the patient in a coma, or can we stimulate them when we talk to them. So again for these patients we need to be checking blood work, any patient that comes in with any signs of seizures or twitching or anything that looks neurological, we should be checking her blood glucose. It's super quick, it's easy and it could give us our answer very quickly.
Electrolytes to check for any metabolic disturbances and also blood gases as well. OK, so we've checked the major body systems. Another thing to just mention before we move on to the actions is if you do ever have a patient in shock or presenting to you which could could become a patient in shock, we do need to be careful with temperature regulation.
The body goes into a state of er stress and they will, the body will redirect the blood. To the vital organs where you really need to preserve the perfusion to those tissues, if we go and then place the patient on a hotdog or a a heat mat I should say, we're redirecting, we're vasodilating those vessels which are touching that heat pad, and we're redirecting the blood to that area. And away from the vital organs, so in any of these circumstances, I would always go for indirect thermoregulation, so using blankets and trying to warm the patient up that way rather than using direct heat.
OK, so we've assessed our patient, now what do we have to do? So hopefully you've got your multi-parameter there, hopefully by this point you've already got your ECG on. We have a few blood pressure readings, we've got a pulse oximeter measuring the saturation of our oxygen in our cells.
Capnography, if the patient is intubated, you can put the, if they have a tight fitting mask, you can put the capo line into that mask. However, I would never rely on that number. It's good to know that there is one present and get an idea of a number, but I would never rely on that as a trend to.
Kind of use as a. As a guide to treatment. It's just another, another thing to consider.
Temperature, we should be checking their temperature, see if we need to change anything. Hypothermia has been shown to reduce er sorry, increase the patient's mortality rate and reduce survival to discharge. Or the patients, especially with the amount of brachycephalic that we see now, they could be hyperthermic and we may need to cool them down.
We then need to place an IV cannula, providing we have consent for treatment. And we need to pull blood work as well. So when we look at what diagnostics we may see, I've actually created at Northwest, I've created a medicine emergency triage tool, and it's, I say tool, it's it's basically a sheet which tells you what blood work the vet is likely to request for each different condition.
And it will have a multitude of different medicine conditions on there and so that the vet can then go back to speak to the owner in these situations, we then have it and we're not gonna miss anything in that high paced, fast paced situation. So blood glucose, again, as I mentioned, especially if there are any neurological issues. Renal baseline, so we need to check our kidney function, liver, so hepatic baseline as well.
We want to check electrolytes, and we also want to check our PCV and total solids. This can give us an indication about not only anemias, but also the hydration of our patients as well. Or if there's any bleeds there.
So a summary of triage is to look at any major concerns that we may be, we may have concerns about when it comes down to our major bodily systems. So if we assess those body systems and we intervene and we. Help the patient or prevent them from progressing and getting any worse, then that could be life changing to that patient.
We need to be questioning whether signs are continuing to progress or whether what we're doing is working. How is the response to therapy? Is the patient's blood pressure improving to the fluid therapy?
If not, what can we do to prevent any further progression? And everything that we should be thinking of during that triage is how can we prepare for the next step. This is where we are at the moment.
If they deteriorate, it could go to X, Y, or Z. How can we prepare for any of those outcomes or eventualities? I'm just gonna touch on fluid overload because quite often we hear that we should be using shock rate fluids in many of our conditions who present.
And actually, there's been quite a lot of discussion over the last few years whether that is the correct thing to do. When the patient has an illness or an injury, the body naturally goes into a state of, . Depends on what you're dealing with, but a state of shock and survival mode.
In that survival mode, the body changes to retain sodium, which also retains water. And the whole reason for doing this is that if you're ever stuck in a desert island, our body will try to survive as long as possible by retaining that sodium, retaining that water, and therefore maintaining perfusion of the tissues and increasing survival. But our patients are not stuck on a desert island, they're often in a HDU or an ICU clinic where we have plenty of fluid therapy, sodium chloride, Hartman's solution, and anything that we may require.
But that doesn't mean that the body is instantly out of that state of survival. So when we give an absolute load of fluid therapy, We could be putting them at greater risk, depending on the condition, some of them absolutely need it, but not all of them do. And with a body that is retaining more sodium and more water, they are at much greater risk of going into fluid overloads than your standard patient.
So we definitely need to err on the side of caution and we need to be very good at our monitoring and our . Checking that these patients are not gaining any of the signs or symptoms that may suggest fluid overload. Fluid overload has been shown to have an increased mortality, and with fluid therapy, we should be giving incremental doses so we don't just start off with a massive fluid rate.
We give boluss of say 5 mL per kilo to a cat or 10 mL per kilo to a dog. You can increase that to 20, reassess how are they going, Has their heart rate increased, has their blood pressure increased? Do they seem like they need another one?
Is it working or do we need to find something else? And are they genuinely hypovolemic? The reason that we give fluid therapy is to try and preserve cardiac output and perfusion to the tissues, and there are many studies out there now, mainly in the human field, to say that actually some clinicians will give enough fluid therapy to preserve cardiac output, but then let the body do the rest.
Now This can be a very controversial topic and it's far beyond the scope of today's talk, but it's something just to consider the next time you're presented with a patient who you would naturally just grab a bag of fluids and give bolus after bolus. So there's just a few things to to consider and to take home and think about. Another way of checking whether the patient has signs of fluid overload is check the body weight.
If there is an increase of 5 to 10% in body weight, this can be suggestive of fluid overload. They can become hypertensive, they can get peripheral edoema, the conjunctival edoema, so they get really swollen eyes. You can see jugular distention and even respiratory signs if they start to spill over and get things like pulmonary edoema or pleural effusions.
Now that almost summarises the the general triage and a few points to think about. Now I'm gonna talk first of all about the anaemic patients and the triage of these patients, and then we'll go into Addisonian crisis. I've chosen two quite different scenarios so that we can hopefully cover a wide range of different situations over this talk.
So when we think of an anaemic patient, anaemia is the reduction in red blood cells. So whether that be from haemorrhage, whether that be from hemolysis, maybe the patient has an immune mediated hemolytic anaemia where the immune system is just attacking all of the red blood cells. They often present with pale mucous membranes, but a tachycardia and a tachypnea, and we'll talk about why they may get this in a moment.
They have a decreased circulating red blood cell count, and if you think of what your red blood cells do, they carry our oxygen and deliver it to the tissues around the body. So if we have a reduced red blood cell count, we have therefore a reduced oxygen carrying capacity. The patient may have bounding pulses depending where they're at in their own condition.
If they are compensating well, they may have bounding pulses on presentation. And that's because the one of the heart rates has gone up to try and improve circulation and improve perfusion to the tissues. But also if the red blood cells have reduced, we don't have as much oxygen carrying capacity, so we have to increase the rate at which they flow around the body before we start getting hypoxemia.
Or hypoxic damage, ischemic damage. So the body will almost go into a fluid retentive state so that it retains more water to help with that perfusion. You think if your perfusion goes down and your circulating red blood cells go down, that's a real danger zone.
So the body will naturally start to compensate, increase the heart rate, retain more fluid. And more water so that we can hopefully maintain perfusion to those vital organs and vital tissues. The patient may be jaundiced, and that's because if you have hemolysis, so the lysis just meaning the breakdown or destruction of the red blood cells.
Red blood cells break down, they release haemoglobin. Haemoglobin goes to the liver where it's converted into bilirubin and therefore the patient becomes jaundiced. The patient may be weak and could even present in a collapsed state because they just don't have that tolerance because of the, the reduced oxygen carrying capacity.
So they will have exercise intolerance and even just the tolerance for normal daily activities can become a challenge. Often the patients with quite a sudden onset anaemia can have a low grade heart murmur, typically it's only about a grade 1, absolute maximum 2. And this is just because of the change in viscosity of the blood, so it's not a cardiac origin and typically once you treat the anaemia, then the heart murmur will resolve.
So we need to provide oxygen to these patients. So we've mentioned that the red blood cells, they often, well they have a biconcave disc shape so that it. Gives a greater surface area to carry oxygen on those cells, they not only become destroyed, but some of them almost pop and become spherical so that they lose that biking cave disc shape, and they're no longer functional.
So the ones that we do have may not even be functioning very well. So we need to provide oxygen to these patients so that the, the few viable cells that they do have left can be fully saturated with oxygen. But don't be fooled if you look at a pulse oximeter and it says 99 to 100%.
That is measuring the percentage of oxygen in that individual cell. It does not mean that the patient is not becoming ischemic, is not becoming hypovolemic, and is not having a reduced oxygen delivery to the cells. It's simply telling you about the saturation of that one individual cell.
Have a look at blood pressure, this can give you a really good indication about how the patient is compensating, it may be increased because of that, the change in vascularity and the change in heart rate and pressure because the patient is currently compensating. But then if they start to decrease that blood pressure may plummet. We need to correct the patient's circulating blood volume or red blood cell volume with fluid therapy if required or with a blood product, depending on what we're faced with.
And then sometimes patients can present with hypothermia, which again has been shown to increase mortality, so we often we do need to be checking temperature as well. We know that our blood plays a very important role in thermoregulation, so these patients may struggle to maintain that body temperature. OK, so we've done an initial triage, we know that we're now faced with an anaemic patient, we need to start thinking about blood work.
So PCB and total protein. This can tell us a few different things. So if we have a low PCV but a normal total protein, that indicates that it's only the red blood cells which are starting to diminish, and that may indicate hemolysis, so that something is breaking down the red blood cells.
Cos the proteins are absolutely normal. But if you have a low PCV and a low total protein, that's a whole blood product being lost and that may indicate haemorrhage. So the whole blood product is being lost through a bleed.
So we need to look at haematology and alongside every haematology that we do, we should be doing a fresh blood smear. And we can look at a platelet count in-house. I must do this about 4 times a day in my clinic at least.
So we can do this as nurses. We can look at, once you start getting used to looking at blood smears, you can differentiate whether this is a regenerative anaemia or a non-regenerative anaemia and, That is the way of looking at that is whether the, the cells are all kind of a similar size and a similar hue or a similar colour, or whether there is a variation between, look at the the biggest cell on there, red blood cell. Compare it to the smallest cell on your on your field and see whether that indicates some regeneration.
And then we can do an insaline agglutination test, so this does make up part of the diagnostic pathway of immune mediated hemolytic anaemia. So what we do there is we would get a blood sample in an EDTA tube, and it does have to be in EDTA with the anticoagulant. We would then take out one drop of blood, pop it on a microscope slide with 4 drops of saline.
Which is different to what I learned when I was in college or uni, that was one drop of blood to one drop of saline, but the 2019 consensus statement says now it's much more accurate to use four drops of saline. There's an image of it here on the on the screen, and this is, you would basically just mix it together, mix the saline with the blood, it should just stay as 11 colour and it should just mix in nicely if that's a negative. Agglutination test, whereas these that you can see here, it almost has what we call a sandstorm effect, and that is the individual red blood cells starting to agglutinate and clump together, which gives it this sandy, grainy appearance.
And you can also see that it's jaundiced there as well, which we mentioned earlier on. So blood work doesn't stop there, this is internal medicine, we love to do bloods. Coagulation panel, so if you do have a coagulation machine in your practise, this is absolutely one that we should be checking.
And a tag, so I appreciate not many clinics will have this, but just briefly to touch on what that is, it will look at the formation of the platelet plug or the platelets activation, so it looks at whether the platelets, Plug is forming appropriately and then is it also being broken down appropriately as well, so this is a really useful, tool to have in practise to see whether the patient has a primary coagulation issue with the formation of platelets, or the function of the platelets. Angiostronginus, so a snap test or a faecal analysis, looking under the microscope, angiostrongulus can cause er coagulopathy, so it can stop the patient from being able to bleed because it can interfere with that coagulation cascade. Sorry, I should say the patient being able to to clot and stop bleeding.
And then of course we need biochemistry, check for any concurrent diseases, check the liver, check the kidneys, check the gallbladder, especially in a jaundiced patient. Have a look at how they may all be functioning. Your analysis can give us can just complete the picture, so sometimes your analysis just gives us a bit more information which may complement some of the blood work changes that we may need for a diagnosis.
And then depending on the patient, we could send off an infectious panel so looking at things like Mycoplasma hemophalus in the cat or Borrelia, especially in patients if they have been abroad. So before we deem a patient as. Requiring a .
A patient requiring a blood transfusion, we need to look and assess a few transfusion triggers because this is not a benign procedure and it's not always appropriate to give blood to every single patient that that presents with an anaemia. We need to assess a few things first. So first of all, is it acute or a chronic anaemia?
And I'm often asked when we do talks, what's your cutoff for a transfusion, and actually, you can't really put a set number on. If it's below this number, you would definitely transfuse because actually if you've had a chronic anaemia, that patient's PCV can go much lower with less clinical signs, because the body has had much longer time to adjust or adapt. Whereas an acute has been rapid in onset.
And the patient hasn't had time to compensate and get used to those changes, and therefore they can often present collapsed and really, really poorly. So it just depends whether the patient is acute or chronic with with their anaemia. What is the rate of ongoing loss?
Is this a massive haemorrhage that you're looking at in front of them? Is it er an anaemia of chronic disease? Is it something which we are likely to be able to treat now and stop the progression, or is it likely to continue?
Tissue perfusion, so we can use lactate, a lactate monitor of the little handheld devices if you have one. This gives you a really good indication about tissue perfusion. So a lactate is produced with anaerobic metabolism, so that's the body's natural survival mechanism, if we do have a reduction in our perfusion or oxygen delivery to the tissues.
The body will produce lactate, as a a response to, Convert the body's metabolism to an anaerobic state so that they can hopefully just survive that bit longer, without the oxygen supply that they would usually have. So a lactate level, if that is increased, it tells us that we may have a reduction in our tissue perfusion. Ongoing treatment, is the patient likely to have an anaesthetic soon?
Does it require surgery? Is this a bleeding splenic mass, for example? If it does require ongoing treatment, the patient may really be dependent on the packed of blood cells, for example, in order to survive the anaesthetic to make them that bit more stable prior to anaesthetizing the patient.
Or is this a patient with a concurrent disease or a comorbidity? Is this a 14 year old Labrador who actually has chronic kidney disease, heart failure, and now he has anaemia? What are the chances of this transfusion being successful in that scenario?
And is it appropriate to give this product to a patient with those comorbidities, what will the outcome likely be? So we need to treat the individual rather than looking at just numbers on the blood result. And we need to transfuse according to clinical signs, so look at the individual in front of you, how they're coping.
And how the rate of progression. Seems to be going because if they really do need a transfusion and you think the prognosis is quite good, then absolutely jump on that the blood transfusion if required. And just briefly, this is not a talk about blood transfusion, so I'm not gonna go any further into this, but before you do go reaching for that blood product, remember that if you have a dog and they've never had a transfusion before, negative blood is a universal donor.
So they can have a bag of negative if it's their first transfusion, and only for their first transfusion. They then must be. We must blood type them beforehand so that we know what to do for any future transfusions.
And then with cats, we absolutely must always blood type a cat and cross match because cats have naturally occurring aloantibodies against the other blood type and if you give the wrong blood type to a cat, even just a few mills can be fatal. So they absolutely must be blood typed and must be cross matched. So in the anaemic patients, if hemolysis is what's causing the issue, packed red blood cells are more likely to be your bag that you're gonna reach for.
This contains red blood cells in an anticoagulant. It does not contain plasma. So normal bulimic patients who require those red blood cells for the oxygen carrying capacity, this is ideal.
It doesn't have any platelets or any clotting factors, and it can stay viable in the fridge for 42 days, so it's really useful to have a bag of this in. OK, so that's all I'm gonna mention about blood, about anaemic patients and transfusions. So we'll go on to the Addisonian crisis now.
So first of all we need to understand what we're actually treating so that we can jump on successful treatment of this patient. So primary Addison's disease is the most common form, and this is the bilateral destruction of the adrenal glands. It's classed as idiopathic, we don't really know what the cause is, we think it may be immune mediated, but there could be a list of potential causes in these patients.
And when they've done autopsies on these patients after they have passed away. It's shown atrophy of all layers of the adrenal cortex when they've done histo histopathology, so it really does destroy the, the adrenal cortex completely. We do believe that it is immune mediated, but it could also be seen with certain types of neoplasia, or cancers, or it could be an iatrogenic cause, so maybe the patient has been put on mitota if they are, this is more for the American listeners.
Mitota is not available in this country anymore. But miota destroys the adrenal tissue, and if they become, Addisonian with that, there's no going back, so they will permanently be, an Addisonian patient. But it can also happen in this country with the likes of your riosta.
If you are putting the patient on that therapy for Cushing's disease and we suppress the production of those steroids too much, then they can become Addisonian as well. Or if somebody just stops stops giving the patient who's been on long-term steroids, they stop giving the the steroids, abruptly and that can also cause an Addisonian crisis because the body's just not used to being. Well, having to produce those steroids by themselves.
So primary Addison's disease is a reduction in both glucocorticoids and mineralla corticoids, and we'll talk a bit more about what that means. So in order for clinical signs to occur, we must, we will have about 90% loss of our adrenal function already. Mineral or corticoids control our sodium and also our potassium.
And we know that whatever our sodium does, our water tends to follow, so it plays a very important regulation in our sodium and water regulation within the body. So the loss of aldosterone leads to renal loss of sodium chloride and the retention of potassium, so the hallmark signs of an Addisonian patient is hyperkalemia, so high potassium and hyponatremia, so low sodium. So potassium goes up, sodium goes down.
And if we, if our sodium goes down, we're gonna really struggle to keep hold of our water as well, so these patients present with quite a profound hypovolemia and that is often what is causing the main crisis signs. With the Aonian crisis, they will often present in an acute collapse. They're hypovolemic typically, so they may be in hypovolemic shock.
If they are in hypovolemic shock, they may be hypotensive, so have a low blood pressure. This may be indicated with a weak femoral pulse, and they may have profound weakness overall. They could even come in collapsed or moribund, and unconscious.
And With hypovolemia, the heart rate typically increases in order to maintain perfusion and try and try and compensate for that lower circulating blood volume. But if these patients present with a hyperkalemia, so a high potassium value, that can cause a bradycardia. So if you're ever presented with a hypovolemic patient or a patient who is collapsed and in this state, and they have a bradycardia.
The two main things that I would think of would be hyperkalemia, so a possible Addison's Addisonian patient or a blocked cat maybe. Or a Cushing's triad, so a patient with an increased intracranial pressure, but that's a whole different topic, and I'm not going to mention any more about that. So these patients can quite often present the same as any other emergency, but there could be a few little indications that may point to an Addisonian crisis over the other ones, and the main one of those is the bradycardia in a, in any collapsed patient.
So of course we need to try and diagnose Addison's disease or hypoadrenal corticism, and we would do that usually with an ACTH stimulation test. So we need to take a basal serum sample. We need to administersinactin.
Which is a synthetic man-made version of ACTH which is produced by the pituitary gland in the brain. We give that IV and then we take a post ACTH sample one hour later. So if we have a low basal cortisol and a low post ACTH cortisol, that could be consistent with Addison's disease.
But we do need to make sure that the patient has not been receiving steroids for any other reason because this will interfere with the result. So the main treatment of an Addisonian crisis is to correct the hypovolemia and the hypotension. We need to look at electrolyte imbalances and see what we can do and how we can alter these, especially if there is a hyponatremia and hyperkalemia present, they can both be quite a, a dangerous combo.
We need to look at metabolic disturbances. Is the patient acidotic, and if so, how profoundly. We need to improve our vascular permeability and administer glucocorticoids if the vet is certain that this is an Addersonian crisis.
Rapid fluid therapy is the most important treatment for these patients. So if the patient is going to die from an Addisonian crisis, it's likely to be because of the hypovolemia, an increase in our vascular permeability, and hypovolemic shock. So the main thing that will save an Addisonian crisis is fluid therapy.
So how are we going to treat this fluid therapy, how are we gonna treat the hypovolemia with fluid therapy? So an Athertonian crisis is an emergency and it does require intensive care, so these patients may be required to go to an overnight clinic if you are not, if you're in a general practise which doesn't have overnight care. When we treat hypovolemia, we are then improving.
Perfusion to the kidneys, so renal perfusion, that will promote diuresis and start to diurese the potassium out and naturally bring that down. It will also promote the movement of electrolytes into the cells as well, which will help in this situation. If you read any textbook, it will say if your sodium is low in the Addisonian crisis patient, you should administer sodium chloride IV.
And this is often preferred in these patients because of the hyponatremia. And it aids in just correcting the the low sodium and the low chloride. However, some patients, if they are really profoundly acidotic, often some clinicians will reach for Hartmann's solution.
To try and counterbalance or correct the academia. Prior to correcting the sodium changes, because it just depends how profound, each of those things are, and what, which one is more likely to, Cause harm quicker, so which one do we need to treat that bit more rapidly. So as we mentioned earlier about the risks of fluid overload, this is a really hypovolemic patient, so fluid therapy is going to be the thing that can save this pet's life.
But again, we still don't want to go silly with it, we need to be careful. And we need to be monitoring and checking our response to therapy regularly. So give, start off with maybe if it's a dog, a 10 mL per kg bolus.
And you can go up to those shock rates which are stated in the In the textbooks, but you would do it incrementally rather than just putting a patient on 90 mL per kg, you would do it as 10 or 20 mL boluss and reassess after each bolus. So once we've given a bolus, we need to look at monitoring hypotension, so blood pressure measurements, we need to look at those every 5 to 10 minutes to see how the patient is responding to that bolus. What's the heart rate doing?
Is it starting to come down because the, the perfusion is improving, so the heart's having to work less hard, there's less demand. How's the pulse quality? How is the mentation?
Is the patient becoming brighter with better better pulse quality and therefore better perfusion? And then we've mentioned about hyperkalemia, so we'll just touch on some of the electrocardiac or the ECG changes that you may see with a hyperkalemic patient. So an increased potassium slows the conduction.
Excuse me, the cardiac conduction and excitability of the souls. And you may not see a bradycardia unless the potassium goes over 8 millimoes per litre. Normal depending which lab or which machine you use is between 3.5 to 5.5.
So once it starts going to 8 or above, we may start to see a bradycardia. The hallmark sign that we think of when it comes to hyperkalemia on our ECG is the tall peaked T waves and the widening and flattened QRS. And when I say tall peaked T waves, look at the, you've got your P wave, your small one, your big spike, QRS, and then your T wave afterwards.
And that T wave is around 3/4 or almost the same size as that QRS. So that is what the the T wave would look like with a hyperkalemia. But take caution with cats because they often have a smaller QRS complex, and this can often be mistaken as a tall spiked T wave, but it's actually just the QRS which is smaller.
But we would never look at this and. Use this solely as a. A way of diagnosing hyperkalemia, we of course need blood work alongside it to give us a figure and give us a number to er diagnose hyperkalemia.
But it is very useful to be aware of what we may see, and that it can cause other changes like atrial standstill, they can eventually become wide and bizarre complexes and it is a life threatening emergency which can cause cardiac arrest. So when we look at the treatment of hyperkalemia, when it comes to the Addisonian patients, we need to think of what's causing it. So we mentioned that we get a reduced mineral or corticoid, which is aldosterone, which causes potassium retention.
And it then increases the secretion of sodium, which is contributed to our hypovolemia. So the patient needs fluid therapy, but it also needs steroids as well in order to keep hold of that fluid therapy. And keep hold of the correct electrolytes rather than carrying on getting rid of the important ones and retaining the toxic ones.
Glucocorticoids that we can administer, dexamethasone can be given without altering an ACTH blood result, and therefore it can be administered in the acute patient, providing the vet is certain that this emergency patient is likely to be an Addisonian and the steroid is required. For a mineral corticoid, we can give hydrocortisone, which is a human drug and this can also be given prior to the ACTH testing, so we don't need to wait until after we've taken the bloods for the ACTH. So to treat the hyperkalemia itself, if required, often we would use fluid therapy first.
If the fluid therapy is not enough in diaring the patient and excreting the potassium, and we're still seeing changes on our ECG and a bradycardia, then we may need to intervene with some more treatment. We could give a 50% dextrose to make a 5% solution, which is 100 mL of the 50% dextrose per litre of fluids. And we would give neutral insulin, so your soluble insulin IV.
And we know, I think if you're a diabetic patients, this sends the glucose into the cells. Well glucose is a co-transporter with potassium. So it will also send the potassium into the cells as well.
And that's why you need your dextrose and glucose solution alongside because this patient may be normalglycemic, but we need the insulin to act on the potassium in this instance. But it, it can't pick and choose between the two, so it will send both into the cell, and if we don't give a glucose solution, you will then have a hypogalemia, hypoglycemia to deal with. We need to monitor our ECG closely and do not.
Do not use potassium containing fluids, . If we do have a hyperkalemia. So that would be the likes of your your Hartman's solution potentially.
And ideally, usually once the patient is on all of this treatment and on all of the fluid therapy and we've corrected the metabolic disturbances, we've corrected the electrolytes, typically these patients will stabilise over about 12 to 72 hours, so either ideally the first day, but it could take a few days depending on how profoundly unwell these patients were at the time of presentation. If the patient does continue to have cardiovascular or cardiotoxic effects from the hyperkalemia, we can go on to give calcium gluconate. This is 1 mL per kg, it must be diluted and given slowly IV.
This will treat the cardiogenic side effects of the hyperkalemia, but it will not change your potassium value itself, so it just stabilises the myocytes of the heart and puts the patient into a more stable, Position, but your patient will remain hyperkalemic if you don't give it, the other forms of treatment which will actually lower the potassium value itself. So just to go over again, we need to supplement glucocorticoids, ideally until oral can be administered when the patient is much more stable and they have a diagnosis. We need to correct acidosis and fluid therapy to treat hypovolemia.
Very, very occasionally, very rarely, we may need to use bicarbonate to correct acidosis, if it is severe and prolonged and it's not responding to our treatment. But we need to be aware that cerebral edoema can cause fatal complications of bicarbs, so I've personally never used it, but it's useful to have it on your radar just in case. And then hypoglycemia can be prevented with a 50% dextrose solution IV.
So just to summarise what we would do in our triage situation, we must be rapid and decisive with any of our decisions that we make. We need to look at the major bodily systems and any of these actions that we take can really be life saving for these patients. I'm hoping that this talk has covered a broad range of different scenarios that you could be presented with in the veterinary clinic and has allowed you some of the tools that you can then use to tackle many different medical conditions that you're faced with.
We do have a range of specific conditions which require specific actions, but generally if you start off with those triage tools, you are on the successful path to saving this patient's life, and any of those findings that you get from that initial summary of those major bodily systems can point you in the right direction as to what the next appropriate step will be. RVNs are absolutely invaluable when it comes to the nursing input of these patients, and I know in my clinic, the vet will often bring these patients into the prep room, leave the patient with us while they go and talk to the owner. You are a nurse, you can do most of these things that I've talked about today, and it's teamwork alongside the vet and the owner to get their input on what treatment they want to do.
So RVNs can massively improve the outcome for many patients, and I'm hoping that you've learned a thing or two from this evening's talk on triage. That's all from me, thank you very much, I hope you've enjoyed it. And if you do like internal medicine, please pop along to my Facebook or Instagram page, Veterinary Nurse Medicine Geek where I update.
Lots of things there regularly. Thank you very much.