Well, hey, welcome everybody. I'm really glad you're here today to spend the next hour talking about how we deal with our emergency patients. I'll tell you what I'm gonna do.
I'm gonna try to minimise or get rid of me so we can focus on what's really important, which was the information we're gonna share. So obviously, we can't talk about all the emergencies individually in one hour. So I thought what we would do would be to cover what we should be focusing on in all emergency patients regardless of what they have.
And I think We really only have one goal when we're dealing with any unstable patient, and we don't need to know what's wrong with the animal to achieve this goal, and I think that can help us. Avoid adding additional stress to the patient and the staff by reaching for diagnostics when what we ought to be doing initially is this, just focusing on getting as much oxygen as possible to the cells in the body. So deliver oxygen to the cells.
Basically the formula for life, OK? And The formula for oxygen delivery DO2 is The product of cardiac output times how much oxygen is in the arterial blood, so arterial oxygen content. Cardiac output is the sum of stroke volume.
And heart rate. OK, stroke volume times heart rate is cardiac output, and the amount of arterial oxygen in the blood is basically Primarily that bound to haemoglobin, right? So over 98% of the oxygen that's carried in the arterial blood is bound to haemoglobin and there's a small percentage that is dissolved.
That's the PAO2, that's the value you get on your arterial blood gas, minor component of arterial oxygen content, but important because it's kind of the driving pressure to get that oxygen in the blood into the cells. So, The things in red basically are all we need to focus on clinically to optimise oxygen delivery. So to sort of maximise or optimise stroke volume, that's the rationale for which we give subcu fluids.
Controlling the heart rate is necessary in some instances, and that is when there is a change in rate or rhythm that is hemodynamically significant. OK. If profusion and blood pressure are OK, we don't really worry too much about arrhythmias.
I think the most common arrhythmia that we see in most of our standard emergencies is a sinus tachycardia, which is an appropriate response, response to decreased perfusion and cardiac output. So if the stroke volume goes down, say from haemorrhage, then heart rate must go up to compensate and that's a normal response. We wouldn't treat with a specific anti-rhythmic drug sinus tachycardia, we actually just control that by eliminating pain and making sure we have adequate fluid volume.
However, if we do have a profound bradycardia complete heart block or a malignant ventricular tachycardia that is causing poor profusion, hypertension, we reach for our anti-rhythmic drugs there. The key though, when it comes to dealing with maximising arterial oxygen content in the blood is to ensure adequate haemoglobin. Translation, we don't treat severe anaemia with just oxygen.
We're going to give those anaemic animals oxygen. They will feel a little better, but they will feel much better when we normalise or get as close to normal as possible, their haemoglobin by giving them, you know, pack red cells or other blood products. And then just because we want to give them every benefit of, of therapy possible, we reach for supplemental oxygen in all of the unstable patients.
And this optimising oxygen delivery is where the ABCs of core stabilisation for all emergency patients come from. So the A and the B airway and breathing, the point of that is to get oxygen into the blood and to do that, we have to make sure the airways are patent, no upper airway obstruction, that we've got lungs that are functioning OK. So if you've got pulmon left side of congestive heart failure, lungs are full of fluid, we get diuretics so that they can participate in oxygen exchange.
And then whenever we suspect there might be pear space disease, we tap the chest. OK, that's to. Do the A and the B of the ABCs get oxygen into the blood and then C, circulation, we've got to get that blood circulated to the cells in the body, and this requires, if you look back to that last slide, as normal cardiac output as we can achieve in that emergency setting enough haemoglobin to transport the oxygen and in trauma patients, making sure we have intact blood vessels.
Common sense, huh. And so this then directs us further to which of the, which organ systems are most critical for us to focus on and we're presented with a patient that's unstable. We're not sure what they have.
So first and foremost, the respiratory system trumps all others. Any animal showing any respiratory signs gets treated first in that sort of triage. You know, ranking, because without oxygen in the blood, we're not gonna have a patient to deal with.
So we want to look for signs of respiratory distress, changes in heart rate, changes in effort, loud breathing, which usually indicates an upper airway problem and certainly cyanosis, OK. To assess the respiratory system, first, we just wanna, without stressing the patient, just watch and listen, OK? Knowing that, say in a hospitalised patient, a change in respiratory rate could be an indicator or an early sign.
That we need to address what's going on with that patient. Usually upper airway obstruction, kind of is associated with increased inspiratory effort, and you can confirm that if the animal's really unstable and you're not getting anywhere, relieving that increased inspiratory effort with just giving supplemental oxygen, nasal or flow by, whatever least stressful method you choose, then intubating that patient will tell you if when you intubate the patient. The respiratory rate improves, that confirms upper airway obstruction, thinking laryngeal paralysis type scenarios here.
Lower airway disease, asthma, for example, usually increased respiratory efforts. So just by visualising the patient's breathing, you can sort of localise where the respiratory tract your problem is. With plural space disease, often the animals just do this rapid shallow breathing.
So that creates a problem for us. Are they just not moving enough air for us to hear it with a stethoscope, or is there truly something in the plural space that's muffling those airway sounds? The trick here is, if you're lucky enough to be a sculpting the animal when they take this compensatory inhalation just to try to expand the lungs as much as possible.
If you don't hear lung sounds when they take that big chest excursion, that's more convincing that you have plural space disease and certainly cyanoticous membranes are a sign that we all know are an indication of imminent respiratory failure. This means that there is less than 50%, 50 millimetres of mercury of. Arterial oxygen in the blood.
So your arterial blood gas would reveal a PAO2 of less than 50, and that is a critical cutoff. We think below 60 is when animals need to be kind of on ventilation if they're not responding to supplemental oxygen. This patient has exhausted all compensatory mechanisms that's on the verge of respiratory arrest.
The key here is, you need to have over 5 mg per DL of reduced unoxidated haemoglobin to detect cyanosis and With that formula of the haemoglobin times 3 is what the hematocrit should be. This means that if you have a PCV in an animal that's less than 15, that means you have less than 5 milligrammes per DL of unoxygenated. Haemoglobin, so you might miss cyanosis in that patient.
The good news for us is we usually don't have such severely anaemic patients and if we do, they just have anaemia. Luckily, most of them do not also have a severely compromised respiratory system. OK.
So that's the respiratory system, control that. Next, we focus on the cardiovascular system. They circulate that oxygenated blood in here.
We do our usual physical signs, look at for usual physical signs that we have poor circulation, poor perfusion, so pale gums, prolonged over 2 2nd cap and refill time, thready weak pulses, the animals may be showing. Sort of weakness, maybe collapse and and the very late and most obviously severe stages cardiopulmonary arrest. I want to spend a couple of minutes talking about how much information you can get from pulses.
I think if there's one thing that I want us to take away from this hour is that we should start. Feeling dorsal pedal or metatarsal pulses, OK? Because if you feel a femoral pulse, does that mean you have normal blood pressure?
It does not. It means your blood pressure is over 50 or 60. OK, that's great.
Better than having it less than that but not normal. If you detect A dorsal pedal pulse, a more distal pulse, then you have normal blood pressure. So start there, OK?
Practise on larger dogs, maybe when they're under anaesthesia, but I always recommend first pulse you take on an animal should be dorsal pedal. That way, if you feel it, you're assured blood pressure is OK. If we simultaneously auscultate the animal while palpating the pulse, if we see a disconnect, we hear a heart sound without feeling a pulse, then we have obvious evidence of an arrhythmia which should prompt us to get an ECG.
Then there's this pulses paradoxes. So if you're palpating the pulse in an animal and it gets weaker when the animal inhales and stronger when the animal exhales, so the strength of the pulse varies with respiration. In fact, you don't have to remember which way it goes, but if you can detect a variation in the strength of the pulse with respiration, that is pulses paradoxes, and the thing that should come to mind, there are more than one cause of pulses paradoxes, but Pericardial fusion should be the first thing that comes to your mind because it's really easy to rule out just putting a probe on that patient.
The other thing is we never want to delay CPR. While determining whether or not the animal has a pulse, it's really hard to tell whether a pulse is present and while we're wasting time to do that, or actually it's even harder to convince ourselves that it's absent because we really want there to be a pulse. So we might spend 1530 seconds just fiddling around trying to find a pulse while the animal should be getting chest compressions for basic life support.
So if you think the animal Has no pulse, maybe 10 seconds max to try to assess that if you're not convinced it has a pulse, start basic life support with chest compressions because the chance of doing harm to an animal that doesn't need it, very minimal, the chance of delaying CPR in an animal that does need it devastating. OK. Then the next of the critical organ systems is neurologic system.
Now this is obviously very important for our patients as well, but mostly on the human side. So there's another letter in the core stabilisation of emergency patients on the human side, which is disability. Do they have any evidence of mentation changes?
So we want to assess our patients for that as well because it's certainly indication potentially of significant head trauma or other intracranial problems, but also a consequence of severe hypoxemia or poor profusion, OK? And then the urinary system is the other of the four critical organ systems here mainly because we don't have a. An animal who has an ability to eliminate your normally, then what happens, we're concerned if it's obstructed or has a disruption in the urethra or bladder that we might develop severe hyperkalemia with, you know, consequences, you know, that can be certainly serious with cardiac arrhythmias.
So those are the four key systems then in trauma patients, clearly here we want to have a whole separate little set of things we want to assess for active haemorrhage which must be stopped to, you know, get the sea circulation under control. Check for open wounds, open fractures, you know, ocular changes that might require emergency therapy, and here is where the E, the final of the letters of core stabilisation for emergency patients exposure would come in handy. So for example, cat comes in, not eating, you feel it, you detect it, the animal has a fever.
Maybe some discomfort around the base of the tail, but you don't really feel anything, no abscess yet, right? So clip the area to see if there are puncture wounds. Maybe that would be the only indication of a cat bite injury.
You get the picture. When we're not sure, clip the hair, find out if there is any underlying issues that would help us determine what's going on with our patients. OK.
We have an unstable patient, especially one with respiratory issues straight to the treatment area. Where we start oxygen by the least stressful method. These guys are fragile.
We don't want to spend a lot of time holding them down, restraining them, doing a lot of diagnostics, just get oxygen near their face. OK? This may be flow by with the end of the endotracheal tube, sorry, with the end of the anaesthetic tubing or a mask that's not tight fitting, so we don't have resistance there, get oxygen going, and then as soon as possible establish IV access.
You might not need to give fluids initially, but, at least you want venous access in case, the condition deteriorates and you need to administer emergency medications most effectively give an IV and the clue here is when you place the catheter, before you hook up the fluid line, fill 4 or 5 inadequate tubes with a flashback with the blood you get back in the catheter hub. This, these tubes of blood are basically all you need to do the 4 sort of core. Diagnostic blood tests we want in all emergency patients.
So don't waste the opportunity to get that blood cause it's not stressful. You've got the catheter in already, so all you do is fill up those tubes setting aside. We'll talk about what to do with those in a minute, but get that blood.
And then we want to assess by monitoring the the organ systems we've been talking about. So pulse oximeter, how we're doing oxygenation wise, ECG, how we're doing heart rate and rhythm wise, and blood pressure, how are we doing, you know, circulation wise. OK, if the animals are gonna be on nasal oxygen for a while, clearly this is where nasal oxygen comes in.
Most of us are using the red rubber catheter, measuring it from the tip of the nose to the lateral campus of the eye, marking the tube. Applying a little topical anaesthesia, kind of making sure the head isn't tipped up so that we direct the tube ventral medially and get it into the right space there, OK? So, kind of Standard therapy there and we get pretty good increases in the fraction of inspired oxygen in these patients.
And if you have a say a brachiocephalic breed or a a dog who's really tolerant, trying human nasal prongs may be a really quick way to at least get some oxygen going until we can, you know, maybe consider if we need to put in a nasal catheter. Or not. And then here we want when we're sort of glueing it in place or suturing in place, make sure we avoid whiskers, do everything you can to minimise the irritation factor of these cause sneezing is the enemy of nasal oxygen administration.
We have those tubes in place. We mentioned this earlier, if you have any suspicion that your animal has something in the pleural space, air or fluid, then tap the chest, because here again, the chance of causing harm if they don't have a plural space problem, minimal. The chance of causing harm if they do, and we don't tap the chest is much higher.
OK, so we want to do this. Internal recumbency in most instances or if they're in lateral, that's fine. What position they're more comfortable in.
Again, minimal restraint, often they don't need sedation, but if they do, just keep it light with butorphrenil or buprenorphine, maybe apply some topical anaesthetic there. And then we want to introduce the needle or the catheter between the 7th and 9th intercostal space, aiming for the Back of that space, the caudal aspect of the space, OK, because we know that the veins, arteries, and nerves run along the caudal edge of the rib, so we don't want to hit that spot. So aim with your needle, the caudal half or so of that intercostal space you choose, and then even though the media sin is perforate in dogs and cats, tap both sides of the chest.
All right. Get an endpoint one side, go to the other side. You may have already removed all the fluid and all the air.
It happens because again, the mediasinum is perfrate so things slide back and forth. However, sometimes there are pockets of air, pockets of fluid, so tapping, tapping both sides of the chest is important and you will see that your patients will thank you. They will take that big compensatory breath to re-expand the lungs, and now you've got a much more stable patient to do further diagnosis and treatment on.
Next step in all stabilisation of emergency patients is almost always with therapy, but we got some changes here to talk about. The awareness these days that hypovolemia, overdoing fluids. Can be as bad for the patient as underdoing it.
All right. So we wanted to use basic principles of fluid therapy. If the animal, our goal, is it hydrated?
Is there normal perfusion, is there normal volume? Are we keeping up with ongoing losses? If we are, then the animal needs basically no fluids, especially if it's eating or drinking or only maintenance.
Fluids. The problem with overdoing it is that we can develop fluid overload, and I think we mostly think that the initial organ affected will be the lungs. So we're looking for tachypnea, serous nasal discharge.
Certainly, if that happens, assign a potential volume overload to many fluids. However, it's the filtration organs that are affected first. The lungs, luckily.
Are designed to handle a little extra fluid volume. The venous capacitances can handle that to keep the airways dry. Filtration organs, gut and kidneys, not so much.
So your first signs of volume overload might not be related to the respiratory system, but to the gut or the kidneys, meaning you might have the cat, for example, that's regurgitating that sort of burpee in the back of the throat thing, or you might actually see kidney function get worse on fluid therapy. This is confusing. Most of us think.
And it's true in a lot of cases that if kidney function is getting worse, a patient needs more fluids, but that may be the absolute wrong call. And worsening kidney function on fluids may be a sign of volume overload, and the reason there is if we're giving crystalloids our most common fluid, in a half an hour, only about 25 to 30% remains in the blood vessels. The rest is in the interstitial space because that fluid equilibrates easily.
Therefore, you've got increased interstitial fluid. The kidney is surrounded by a rigid capsule. So if we increase the amount of interstitial fluid in the kidney, then we also increase the pressure, intrarenal pressure increases, which decreases perfusion, also kind of compresses tubules and blood vessels, and can therefore cause worsening kidney function.
And our goal with fluid therapy is to minimise the risk of that, excuse me. By protecting this thing called the endothelioglycocalyx. Electron micrograph upper left, it's this sort of sieve-like wispy coating of the endothelial cells in the blood vessels which mainly functions to keep things where they belong, large proteins albumin in the blood, not in the interstitium, and make the surface of the vascular endothelium inert so that white cells and platelets don't adhere or traverse through.
There's a hyaluronic acid layer of this . Of this, Glacocalyx. And glycocaly that sort of coat spreads over all the cells and kind of coats the gap junctions to keep proteins and white blood cells and platelet receptors from being exposed.
Therefore, when the endothelial glycocalyx is intact, we don't have problems with The fusion. We don't have problems with thrombolysis. We don't have problems with increased inflammation, OK?
The things that damage the endothelial glycocalyx are usually severe inflammatory states or trauma. OK. However, overdoing fluid resuscitation with clear fluids, getting too many too fast also damages the endothelio glycocalyx.
Of the fluids that we use, sadly, the most common one is the most damaging to the end. The glycocalyx. And when it is damaged, then we have all those consequences that we talked about on the last slide.
So our goal now when we're administering fluid therapy is think about how to preserve this glycocalyx. OK. And here is how in an emergency patient, we're giving less crystalloids and more slowly, less to minimise the destruction of the endothelial glycocalyx.
So we were, we're giving now in dogs 10 to 15 mL per kg in bolus. And cats 5 to 10 mL per kg. We're doing that 2 to 3 times and we're giving each bolus over 20 to 30 minutes.
If our patients critical at onset, we'll give one dose of hypertonic saline and if then we need to do any more after 2 or 3 crystalloid boluses after a potential administration of one dose of hypertonic saline, then we need to reach for natural colloids, fresh roils and plasma or in dogs canine specific albumin. All with the intent of sparing the anaesthetic glycocaly, why go slow if we give fluids at a rapid volume that increases the venous pressure. And the heart thinks, 00, I'm going into failure here.
So it secretes something called ANP atriomaturitic peptide, which is toxic, damages, nudes the endothelial glycocalyx. So if we give fluids more slowly, we give the vascular space enough time to sort of compensate. For that increased volume with therefore less ANP secretion and then therefore less damage to the endothelial glycocalyx.
OK, so we are resuscitating our patients in this kind of new way, slower and lower volume of fluids. How do we determine if we're reaching our end points? Well we use Again, what is our goal?
We would love to know if we're getting enough oxygen delivered to the cells, which we can't directly measure. We can indirectly measure it using distal indicators, so things that are far away from the cells. These are fine.
These are not gonna be discontinued. We're gonna continue to use them. These are our standard ways we assess for perfusion and blood pressure.
How's our heart rate? What's our pulse, our pulse quality? Do we have a normal capillary refill time, blood pressure normal?
OK. These things we want them to be normal, but them being normal in people and animals does not mean that we have adequate oxygen delivery to the cells. How close can we get to the cells?
Well, our best indicators are lactate. If we aren't getting enough oxygen to the cells, then we switch to anaerobic metabolism oversimplification with increased production of lactate. And based excess on your venous blood gas is another indication of whether or not we're getting enough oxygen to the cells, urine production as well.
A decrease in urine production is an early indication of a decrease in core perfusion. Which means in order to determine whether or not an animal's urine production is decreasing that we are putting in urinary catheter is aseptically closed collection systems in animals that are critical in which we can do that. So, you know, medium dogs and the male dogs, the easiest patients to do that.
OK. These guys are dynamic, so once we have established, you know, our end points and we're gonna sort of back off on our resuscitation efforts and go to more maintenance type fluid therapy, patients might not remain stable, so we want to continually reassess these factors, these parameters to make sure our patients are remaining stable. OK.
How can we Quickly assess our patients for the most critical parameters that we need to fix if they're not normal. Well, I think you can make a case that in all emergency patients, immediately we want to get a packed cell volume and a total solids, and I know. In some countries, using those microhematic tubes and the microcentrifuge for a PCB and total solids isn't common.
If that's not common, then you look at your PCV or hematocrit on your CBC and your total protein on your biochemical panel, OK, but the PCV total solids, blood glucose and lactate can all be done on those little tubes. Filled up when you put the catheter in, by getting the flashback of blood to, you know, fill up those 3 or 4 tubes. So immediately grab the PCB total solids, blood glucose and lactate.
Why? Because if you don't fix these quickly, you won't have a patient to deal with. As soon as possible, then expand the rest of your laboratory diagnostics.
Electrolytes and all, a venous blood gas, you can make. The case for venous blood gas and all, C-reactive protein to give you some prognostic information and to detect if in a dog systemic inflammation is present. And then it's, again, we want to to assess both the extent of disease and severity, get our the rest of our minimum laboratory database, CBC biochemical panel urinalysis.
If you suspect a coagulopathy, coagulation testing, and we'll end the lecture with a quick review on how to interpret those tests. And then if you can, without stressing the patient, get extra blood, save it so that you might want to consider sending in blood for further testing once you get your initial round of diagnostic. Back.
OK. We have a trauma dog here. And here we see what I like to see in all my trauma patients or any unstable patient front of the cage where I can look at it, what their vital signs are, their temperature, pulse, respiration, and what those critical laboratory parameters are.
The question here is, this dog was hit by a car. Is it bleeding? Could it be bleeding internally?
Well, it's not anaemic. Could it be bleeding? There's a clue that it might be, and that is the low total solids.
If you have an animal that's acutely traumatised, say it has a lacerated spleen, yes, that's bleeding, and you're gonna lose both red cells and total solids from the bloodstream. However, the animal's epinephrine level is also sky high. It's shocky, and that epinephrine will squeeze the spleen, cause planic contraction, and then squeeze out their maturing red cells masking the anaemia.
So that's an important clue because if you find this pattern of a normal hematocrit with low total solids. In a trauma patient, Easy on the fluids because there might be an unstable clot that's trying to stop that bleeding on the spleen. And if we blast in a large volume of fluids too rapidly, we may disrupt that clot and end up with this.
This is that same dog two hours later who did get The standard one blood volume less than an hour as quickly as you can get it in, and then we ended up with a much less stable patient. All right. Now I just want to show you this.
This would be again, we wanna reassess our patients frequently until we're convinced they're stable, and this means having a flow chart. Easily accessible so that anybody walking by, any nurse, any doctor can determine if things are improving or not, and if not intervene quickly. We don't want to have to be shuffling through a medical record to determine what we need to do next in these sort of unstable changing patients.
So let's just quickly review how You can use the PCV in total solids or the hematocrit and total proteins to sort of determine what's going on with your patient. If the PCV is normal, usually that means the animal is not anaemic and not bleeding, except as we just discussed in that acute patient. So what will happen eventually is you will unmask the anaemia with fluid therapy, even appropriate fluid therapy, but initially a normal hematocrit usually means that we don't have anaemia or haemorrhage.
And if our proteins are low, that might be acute haemorrhage like we just talked about, or there might be some low protein condition, you know, who knows, GI, liver, kidney, glomerular. If our hematocrit is normal and our total cells increases normally means we have no problems with the red cell picture. We just have a paroteinemia like a multiple myeloma or say ligiosis, yeah.
If the hematocrit is low, that's usually anaemia, and that can be haemorrhage, in which case we'll see the total solids also being low, or it can be hemolysis, in which case the total solids or total protein will be normal. This is really important. Look at the total protein or total solids in an anaemic patient to determine if you have haemorrhage or hemolysis.
If both are increased, that's normally just chemo concentration, dehydration. OK, and again, how often you repeat this depends on the condition of your patient and how it's responding to your treatment. Certainly very frequently, initially in severely anaemic patients, and then as you stabilise them once, twice, you know, a day while they're in the hospital.
We talked about lactate being one of the more proximal indicators of oxygen delivery to the cells. If there's poor profusion and less oxygen delivery lactate goes up proportional to that deficit, so the higher the value, the worse shock your patient is in for all intents and purposes. What's really important is, yes, in some diseases, studies have shown that the initial value may have some prognostic value, but regardless of the initial value, if it is returning to normal, that's what matters, that's what's telling your patient is on.
A good therapeutic plan. If not, then you need to change something, investigate further, treat more aggressively. This is a really good way to monitor whether your resuscitation efforts are successful and whether they're staying that way.
You could make a case for any hospitalised patient who's unstable at presentation. That a lactate be done on a daily basis to detect cult profusion deficits that will appear prior to you being able to tell by a change in capillary refill time or pulse strength or quality or blood pressure. So just we mentioned that what really matters is not the initial value is what happens with therapy.
Some animals that shouldn't live because their values exceed these sort of cutoffs that you read about in the literature. Some do survive. So I say regardless, you got a trauma patient who's got a lactate, initial lactate over 4.
In one study that was predicted of non-survival, you're gonna not treat because it's 6. No, you're gonna treat as long as it's going down, you're, you know, you're heading in the right direction, but It does help us keep in mind, like if we do have values that exceed some of these cutoffs, then at least we can have a conversation with the owner that there might be a longer course of treatment, might be kind of more expensive, we might need to be that sort of thing. So useful to have some of these guidelines in mind, but remember, as long as you are seeing an improvement in overall clinical condition of the patient and lactates improving, and it should come down about 50% every 1 to 2 hours, keep going.
OK, blood gases, when it comes to initially assessing most of our critical patients, you want a venous blood gas. It's not just that, yeah, you can get by with one, you don't have to stick an artery. No, you want a venous blood gas because it's a better indicator of the thing we care most about, which is oxygen delivery of the tissues, and here the parameter is the base excess.
And with the venous blood gas, you can assess ventilation because the venous PCO, the venous CO2. And the arterial CO2, that should be a CO2, not 02 there. I'm sorry about that.
So they're equivalent. So the venous CO2 can be a surrogate of their arterial CO2. It's a little higher but not enough to really change your interpretation, but you could ignore, and you should ignore the venous oxygen.
It tells you nothing about the lungs oxygenated ability. This oxygenating ability, this is where you need an arterial blood gas. In patients who have respiratory signs and you're concerned about their lungs ability to oxygenate the blood, that's where the arterial sample is required, OK?
Otherwise, you really do want a venous blood gas trauma, diabetic ketoacidosis. Chronic kidney disease. Venus is a better indicator of what we really care about DO2.
And to make interpreting blood gases simple, I like to just remind people of the rule of four all normal values for your blood gas have a 4 in them. OK, so PH 7.4, PCO240, bicarb 24, base excess minus 4.
In dogs, you know, C-reactive protein is a very sensitive and specific indicator of systemic inflammation that increases really early after the onset of inflammation within 4 hours, peaks up to 24 to 48 hours after the onset. So a very early marker that your canine patient has systemic inflammation. And because of its short half-life, a really nimble monitoring tool.
If your treatment is working on a, you should see on a daily basis, your C-reactive protein normalising. Many, many causes, many, many diseases, in which C-reactive protein has been looked at in dogs. We're gonna talk about basically the over view of how you use this tool in our, in our canine patients, basically.
At presentation, grab a C reactive protein which can be done in clinic now. If it's normal at that time, no evidence of systemic inflammation, so go down another diagnostic, you know, pathway. However, if things change, you might want to reassess that for the development of systemic inflammation.
If CRP has increased at presentation, you've got it. So that dog who's vomiting. With an increased C reactive protein, pancreatitis, you know, with sort of that systemic form of pancreatitis would be one thing to consider.
These patients may be a little sicker, may be more expensive, may require longer hospitalisation times. We we'll have time to just focus on one of the sort of the newer indications for C-reactive protein. It can both determine if a dog with any kind of respiratory signs or issues with lung infiltrates.
You're not quite sure what they are. If the C-reactive protein is increased, the dog has bacterial pneumonia and Now we can use the C-reactive protein to determine the length of antibiotic therapy. Old school, we would give antibiotics for 2 weeks beyond resolution of radiographic signs to dogs with pneumonia.
That takes a very long time. And sometimes you're left with scarred lungs, so you're not sure if what you're seeing in the lungs is residual pneumonia or just like inactive scar tissue. So it can complicate this old rule of like how long do we need to give antibiotics.
We now have two studies in dogs that have shown if you have a dog with pneumonia, following C-reactive protein, once the C-reactive protein is normal, treating for 5 to 7 days and stopping is effective therapy, even if lungs aren't normal radiographically, the dogs improve without relapse. In humans, they stop antibiotics when the C-reactive protein is normal. We're a little more conservative there.
So go for a week sometimes too there are some veterinary schools in the United States that use this rule, but they are a little more conservative and treat for two weeks beyond resolution of radiograph treat with antibiotics for 2 weeks after the C-reactive protein is normal, even if the films haven't normalised and the dogs tend to do well. OK. So let's put this to use in, in a patient who just to, you know, cut to the chase here.
This is a dog that was boarding, vomited, developed respiratory distress, comes in to see you as the emergency clinician in severe respiratory distress. This dog has a history of sort of muscle weakness over the last few years. And so, you know, with a dog who's has an acute onset of respiratory distress after vomiting, a working diagnosis is aspiration pneumonia.
Yeah. Now, could it tie into this gradual muscle loss thing? Maybe now there's a progressive neuropathy or myopathy that's affecting the oesophagus or the pharynx, and so we've got an increased risk of aspiration pneumonia.
So that's what we're gonna be focusing on and we, you know, want to assess our patients. So clearly here we've got, the white blood cell portion of the CBC white blood cell count is normal, which is the case in 50% of dogs and cats with severe infection inflammation. We don't look at the total white blood cell count.
Only to determine if we have infection inflammation, it's normal in half of the animals that do. So we need the differential obviously in here. Probably what we're looking at is white count's normal because we have a profound neutropenia and increase in the number of banned neutrophils.
OK. So how do we assess this patient going forward? There's a couple ways to do it.
This is, you know, we've got on the far left is the dog. Months ago when he was normal in for normal blood work, and we see that that dot plot, the graphics that you get with your CBC report looks like a normal dot plot, which is to the far right. That's him when he was basically normal.
OK? And we can see when he presents, which is the second dot plot from the left, he has, the report said very few neutrophils. Neutrophils are purple and there are very few dots.
So yeah, that's true. And then the report suspected an increase in the number of bands. And I'll just tell you.
That there are, and you can tell that because band neutrophils live in the area where the monocytes and lymphocytes are. OK, the machine's not not not sure what they are, but they are more complex and bigger than a mature neutrophils, so they're up and to the right. On this dot plot, and that's in the red monocyte and blue lymphocyte cloud.
So the machines like I gotta call you something, gotta put you somewhere. I'm putting you there and then it lets you know with the asterisk you better go looking for what these cells are. And then when you see that sharp distinction between the Red in a blue cloud, we call that the shark fin sign.
That's a sign of a left shift. Every day, the dog is with us. We can see, even though the white cell count is always normal, that the graphics, the dot plot is looking like a more normal dog.
And obviously, C-reactive protein is another very useful way to assess this patient. And we can see that on a daily basis it's returning to and ends up being normal after 4 days in the hospital, letting us know we're on the right track. You still need a CBC, all right, because they complement each other.
So the C-reactive protein is more sensitive. Then the white blood cell count is it will change, go up faster than you might see a change in the white blood cell count, and it is specific for inflammation, systemic inflammation, dogs only, and you know, we know that changes in the white blood cell count, you know, an elevated white count isn't always inflammation infection, it could be stress leukogram or it could be chronic lymphocytic leukaemia. A low white blood cell count, though it can be a sign of overwhelming acute infection like our dog here, can also be a bone marrow problem.
So we want to assess both, but I think including C-reactive protein in these guys can be very useful, especially because some of the diseases for which we use C-reactive protein as a diagnostic and monitoring tool. Are immune-mediated diseases. So IMHA ITP, immune immune-mediated polyarthropathy, C-reactive protein is up in all of those.
Those dogs need corticosteroids. C-reactive protein is not affected by drugs, an inflammatory drugs, surprisingly, like corticosteroids or non-steroidals. So we can use in dogs on prednisone, immunosuppressive doses of prednisone or prednisolone.
We can use C-reactive protein to determine if we're going into remission, staying in remission, and coming out of remission. So very useful that it isn't affected by the medications we want to treat these patients with. OK.
A couple more tips and then I think we'll wrap it up here. So, we talked earlier that if a if a kidney function gets worse on fluids. It might be because we're in a situation where we have hypervolemia, and the right thing to do maybe to decrease the fluid.
So how do you determine if an animal was getting function is getting worse on fluids needs to have more a kind of knee jerk reaction or less. Two ways weighing the animal. If the animals gaining weight, you know, acute weight change is a change in total body water.
So if the animal whose kidney function is getting worse, is also gaining weight over that time, consider backing up or stopping the fluids, or figure out the total amount of fluids the animal has received during the time that the kidney function has gotten worse, and compare that to maintenance. And if the total volume far exceeds maintenance, you gotta stop the fluids that's usually sufficient, but if not, then you might need to give a diuretic. OK, so let's take an example of that.
We have a cat, went to surgery for a nephrectomy for like a renal abscess, just pyonephritis that we could not resolve, OK? Got worse after surgery. Like 6 to 8 hours after surgery, kidney function is getting worse.
So we looked at the total amount of fluids that cat got in that period of time. So during surgery, it got sort of the standard rate of 5 mL per kid per hour. So that was 80 mLs, couple of hypertensive, episodes, got some bonuses there.
After surgery, 3 times maintenance. Then you have to take into account. All the other fluids the animal might be getting, so flushing the catheters, antibiotic or other medication, menstruation, consider adding those as well.
If there were any, if there was any liquid and nutrition given, that's part of the calculation. The total volume that this cat, particular cat got in 10 hours, during which the kidney function got worse was 240 mLs. Maintenance during that same period of time would have been 88.
So what's the call here? Not more fluids, less. Stop the fluids and then watch a couple hours if you're not seeing any improvement, you give Lasix.
OK. Another tip, if possible, in the clinic, get reticulocytes in all of your patients, especially the unstable ones, right? So the ability to have a ticks in in-house on your in-house like real-time care, CBC, you know, in your unstable or practically all patients can be really helpful in both classifying anaemia and then as a clue to some occult or early disease.
So. Let's look at a dog here who's like profoundly anaemic, hematocrit is 16. OK.
Is it regenerative or non-regenerative? Well, we kind of are taught that you can use the red blood cell indices to classify the anaemia cause that's your next job to determine regenerative or non-regenerative because the ruleouts work up and treatment completely different, OK? We're taught that you should see an increase in the MCV and a decrease in the MCHC, so microcytic hypochromic anaemia.
Should be present, indicating regeneration. Turns out two different studies over a couple of years' time, like 10 years ago, 90% of dogs and cats with regenerative anemias have normal indices. So if you do see a microcytic hyperchromic.
Change in an animal that's anaemic, supportive of regeneration, but you see that 1 out of 10 times. The reticulocyte count is the best way to classify the anaemia, so having that right off the bat, not having to wait for it to come back from the lab the next day and your unstable patient super helpful. Here we have a dog with a sky hybrid t count profoundly.
Regenerative. What does that mean? That he's got either haemorrhage or hemolysis.
Those are the two causes of regenerative anemias. You can use the magnitude of the tick count to help you to differentiate. If you have a ret count that's 200, 250,000 or higher, that's hemolysis.
The highest tick counts are seen with hemolysis. So knowing that and having all this information right off the bat in our patient, we can say profound anaemia, markedly regenerative, and tick count higher than 250. This is hemolysis.
What's the most common cause of hemolytic anaemia in dogs? IMHA. That's our working diagnosis here.
So that's an anaemic animal reticulocytes super useful. What about non anaemic animals? So here's a dog that comes in, 10 year old spayed female, just not looking great the last couple days, nonspecific signs, nothing to go on physical.
So we're kind of looking at the lab results, which are the voice of the patient to help us out here, and her red cell picture looks good. Nothing to see here. 00, high ret count.
So now we have something to get our attention, right? Without retics, we're not concerned about anything going on with the red so picture in this dog, but now we have a high index of suspicion that there's something going on that we need to worry about. Is there some low grade loss of blood or hemolysis or some other cause of hypoxia.
That's stimulating the bone marrow to produce more retics, and that's keeping up with this gradual or mild change, so we don't see the anaemia. We have to start thinking about those things, which we would not be thinking about if we had not had the ret count. The other thing to think about is, if you have say, previous results on this dog, it's really good to establish each patient's normal values when they're young and healthy, because, yes, this is a Normal range for all dogs, essentially, but a given patient may be slightly to 2.5% live above or below, you know, these are 95% confidence intervals, and then some dogs like live high in that normal range, some low.
It's good to know where your patients are, because the value just because it's normal for all dogs, doesn't mean normal for your just a big dog or cat for that matter. So let's say looking back at this dog, she's 10 now, but let's say that her hematocrit, today is 43, that's normal for all dogs. But what if hers has usually been in the mid-50s?
This is now not normal for her, so the combination of a dropping hematocrit, though still normal, and increased retakes really gets our attention. Are they actually reticular sites? We can look at the graphics to confirm that maybe the machine just made an error.
Well, the reticular sites are purple and a normal dog on the right should have some. Well, 1% of red cells die every day, so you have to replace those that always retake circulating in the blood, but our report said. The dog had a lot more, and our dog has a lot more, a lot more purple dots there.
We can trust that. Also, if we look back between the big red cell cloud and the blue platelet cloud and the normal dog on the right, there's some cells of different size, some smaller cells. Our dog has a lot more.
Red cells that are varying sizes smaller than normal, and that's like basically what anisocytosis looks like difference in the size and the shape of red blood cells. So now we look at the blood film to complete the assessment. Does she have acamphocytes or schistocytes indicating maybe splenic or liver disease?
Are those small cell spherocytes indicating some early compensated hemolytic disease. So bottom line, even in no anaemic patients, it could be helpful to get the ret count. You'll see it increased in non-annemic patients and up to 10%, 1 out of 10 dogs and cats worldwide.
And again, here we can use the magnitude of the ret count and these non-annemic guys. To determine how bad the situation is, just being excited, having your epinephrine level go up, causing splenic contraction can increase the retic count slightly. It could just be a normal physiologic change.
However, if you have a ret count that's significantly elevated in a no anaemic patient, meaning above 125, 130, then go looking for some underlying disease. And in our dog here, who's got a drop in her hematoate from normal and a higher rate tick count, and she's 10 years old, I'm gonna image her belly. And maybe we'll be able to find a splenic mass before it ruptures, or look at a blood film.
Do we have any evidence of early compensated IMHA with the presence of errocytes and gallstones? And it's estimated that in most, you know, busy practises of average, you know, case load, having the ticks on all CBCs maybe about 10 to 12 times a year, you're gonna find something that you otherwise would not have found preventing an animal from getting more critical before you address it. OK, we're gonna end up with, we talked about this earlier, interpret interpreting coagulation test results.
When would you consider getting a coagulation assessment in a critical patient? If there's any concern about excess bleeding, if you've got peticia ecchymosis, if you've got sort of excess bleeding from vene puncture sites or catheter placement sites, you've got severe Sepsis, inflammation, fever, you're worried about DIC. Lots of indications for considering coags or if you're suspicious of anticoagulantrodenoide toxicity, that's what the animals brought in.
So let's first talk about what that is. OK, so with these suspected coagulopathy, we need to get a platelet count and clotting factor assessment, PT and PTT in all of them. So our platelets are the primary hemostatic section of coagulation, the first.
Line of defence to stop haemorrhage and animals with platelet problems or primary hemostatic problems have surface haemorrhage, piticia ecchymosis, epistaxis, hematuria. Due to either a decrease in platelet number, the poster child there being immune thrombocytopenia, or platelet function and the most common cause of that in dogs and cats, at least the inherited form is is vomolibrand's disease. Then we have to assess secondary hemostasis, and this is where the clotting factors come in.
And here, animals with secondary hemostatic problems have deeper haemorrhages, so hematomas. Plural haemorrhage, hemothrosis, deeper haemorrhage, and we look at our good old coagulation cascade, mostly because of its diagnostic utility and localising where the problem is. We know that You know, there's the cell-based model of coagulation, there, there are probably more complete sophisticated models of exactly what happens rather than these very step-like ladder like changes.
However, this for us in clinics is the most diagnostically useful way to think about factor or secondary hemostatic problems. OK. So all animals will be suspected.
Coagulopathy, even if it's a dog we suspect has ITP because it has all the signs, we want to get the PT and PTT as well because you may have more than one coagulation problem. So let's practise. We have a dog.
That has haemophilia A or B. What would be the expected results of our coagulation assessment in that patient? So factor haemophilia A is a factor 8 deficiency inherited and factor haemophilia B is a factor 9.
Issues. So those factors are both in the intrinsic pathway. So what would our expected results on our coagulation assessment be our platelet count, PT and PTT.
Elevated ATT only, right? Platelet counts not gonna be affected. It's not a secondary primary hemostatic problem.
And because both of our factors of concern are in the intrinsic pathway, our prothrombin time will be normal. So if you have an animal, you have your coagulation results back with a prolonged APTT as the only problem, think about a congenital factor deficiency and send blood citratoplasma in for factor assessment. OK.
What about anticoagulant adenocyte toxicity? Well, with, with sort of warfarin type products, those products inhibit factors 2, which is prothrombin, factor 7, factor 9, and factor 10. So what we would be what we expect to see with our coagulation test, platelet count, PT and PTT with anticoagulant ordenoy.
We would see both the PTT and PT elevated because the factors involved are in all of the pathways of our clotting cascade. Now, some animals, if they're haemorrhaging, will have a decreased platelet count, a moderate decrease in platelet count from consumption to try to stop the haemorrhage, but our main abnormal values will be our PT and PTT. What about early rodeo rodenoide toxicity Factor 7 of those four factors has the shortest half-life, 4 to 6 hours.
So it is inhibited first. Early in adenoy anticoagy adenocy toxicity, you might see just an increase in prothrombin time. If an animal that you suspect has a coagulopathy has, as we, as The only abnormality in our platelet count, PT and PTT, an increase in the prothrombin time PT that is factor 7, and since it's uncommon to have any other thing affect that besides anticredenoci, you've got evidence of early rodenoide toxicity.
So this will be, say 24 to 48 hours, maybe a little earlier after exposure, you might see just a PT increase. OK. What about mullobra disease?
Mombulobra disease is a platelet function defect. So what would you see? On the results of your coagulation assessment, platelet count, PT and PTT with Bobulabrand's disease, they'll all be normal.
So having normal coagulation tests does not mean you do not have a coagulopathy. And if that's the case, your animal's bleeding excessively and all those factors are all those parameters are normal, you think about a platelet function defect and here you would send in pla. Again for Len's assay.
OK, I think that's plenty for one day, a crash course. Happy to be here, and hopefully we'll be able to find some interesting topic to come with in the future. Thank you so much.