Well, welcome everyone. Thanks for joining. We know everyone's really busy these days, so I appreciate the time and we're gonna spend the next hour or so talking about anaemia, and we're gonna use these as sort of our, guidelines.
We're gonna talk about how to classify the anaemia. And then spend some time talking about reticularlytes and all the wonderful features of them and how helpful they are in helping us with anaemic patients. And then after we're gonna finish up with talking about some kind of updated treatment recommendations for some of the common causes of anaemia that we encounter in practise with the goal of maybe tomorrow having a little easier time diagnosing and managing anaemic patients.
We know when it comes to looking at the red cell part of the the CBC. These are the big questions that we want to know is our patient anaemic, if it's anaemic, is it regenerative or not? Because that helps us determine the, the likely differential list and the next steps and then, you know, we'll also look at the platelets, their number and their function, especially when we have a bleeding patient.
We're gonna end up kind of covering some review of how to deal with coagulopathies, which I think luckily we don't see very often, but for that reason, it's nice to review once in a while, how to deal with them. So kind of straightforward diagnosis of anaemia, right? Decrease in hematocrit or PCD, kind of equival or haemoglobin.
And I really want to emphasise it's all about the haemoglobin, right? Because haemoglobin is what carries the oxygen in the body, throughout the body, delivering it to the tissues, right? You can think of the red cells as just sacs that hold haemoglobin.
In fact, that's why they just measure our haemoglobin if we get a CBC done at the doctor, right? The point I like to make here as a criticalist as well as an internist is, let's say that you have a patient with significant anaemia drop in the hematocrit or haemoglobin. You don't give that patient supplemental oxygen in order to prove oxygen delivery to tissues, right?
Because that's not gonna have much of an impact. You give that patient blood products, haemoglobin containing products, mostly packed red cells. So, so don't forget that haemoglobin is really what matters and we focus on that when we're looking at anaemic patients because sometimes with hemolysis in the sample, you can have a low hematocrit.
But that's not gonna affect the haemoglobin. As long as the haemoglobin is OK, your patient's OK, OK? So, it's not hard to diagnose our patient.
As being anaemic or not. We just look at kind of these three parameters. The red blood cell count, the hematocrit, and the haemoglobin.
These are what's called the red cell mass, and they should move together. Now, they can vary a little, and when, I don't know if you can see my pointer, but when the values are at sort of the low end of the cutoff, one might be slightly above, one might be slightly below, but as long as they're trending together, that's what you want to see. So, anaemia, a decrease in hematocrit or haemoglobin.
The very next question in working up an anaemic patient is to determine whether it's regenerative or not. Rule outs are different, diagnostic workup is different, treatment is different. So with the regenerative anaemia, two broad causes your patients bleeding or hemolyzing, OK?
And that blood loss can be internal or external, and that hemolysis can be intracellular, sorry, intravascular or extravascular, right? But it's one of those two. If it's not regenerative, then it's a non-regenerative anaemia, and this is more common, by the way, non-regenerative anaemia are more common and sort of the classic anaemia of chronic disease or the anaemia of inflammatory disease.
There's something impairing red cell production of the bone marrow. That's our next question. How do we answer it?
We look at the reticulous sites, OK. So this is just how the bone marrow red cell line matures from the most immature cell, the rubiblast up to the mature red cell. Reticulocytes are the first cells outside of the bone marrow, right?
They're the first, they're the youngest red cell in the circuit. This red line is like the bone marrow barrier if you will. You shouldn't see nucleated red cells in circulation in normal patients, OK?
And I, I like to look at, I like to show this graphic because I want to point out that even with anaemia, It's a little alarming when you see a significant number of nucleated red blood cells, unless you have a really profound anaemia that's highly, highly regenerative but a lot of reticulocytes. You know, seeing NRBCs in circulation, reported on your CBC, you don't want to be thinking it's a regenerative anaemia. You want to be thinking there might be damage to the bone marrow along these immature cells into the circulation when they shouldn't be.
OK, now, reticular cytes, you know, there's always some in circulation because there's always some mature red cells dying and they have to be replaced. So about 1% of the red cells in the body get turned over every day, so there are always some reticular sites. The question is how many and can that help us determine whether we have regenerative anaemia or not.
I also want to point out one other thing before we move on that. Reticulocytes only really circulate in the blood for a couple of days and then they go to the spleen to mature. So seeing them in the blood tells you what's happening in the bone marrow now and seeing qualities of them, one that we'll talk about later, the reticulocyte haemoglobin.
Anything attached to reticulocytes means real time and like an early way to identify changes in the bone marrow. So when we want to answer the question in our patient, is it the anaemia regenerative or not, we really only need to know the absolute reticular cy count, OK? And we, we used to have these formulas with correcting for the degree of anaemia, etc.
Not necessary. Look at the absolute reticular cyte count. There's a really useful open source website that is managed by Cornell University that school, and it is EleanPath.
And here are the tables lifted straight from Elin path, that kind of characterise the strength of the regenerative response, OK, based on the degree of, the increase in the reticular sites. Now, how can this help us classify regenerative anemias? All right.
Here's how. Bottom line, the higher the reject count obviously, the more regenerative the anaemia. Well, what type of regenerative anemias are associated with the highest retic counts?
The hemolysis kind, the hemolytic kind. So, this is a patient, this is a dog who we saw the red cell picture earlier, profoundly anaemic, and the reticulocyte count is sky high, so above 300,000, which is a marked regenerative response, OK. And the highest ret counts we see, we see with hemolytic disease, OK, versus haemorrhage.
So up above 200,000 when it comes to the tick count, think likely hemolytic disease. Is it autoimmune? Is it zinc toxicity?
Is it a blood parasite? Who knows, but it's likely. Hemolytic.
Below 200,000, it could be either, it could be milder hemolytic or haemorrhage, but the point is these values up in this range of reticular cyte counts, yeah, for sure regenerative, but, and likely going down the hemolytic disease diagnostic path. So, we were taught in that school that we can use those red blood cell indices to determine if our patient had a regenerative anaemia or not. And with the regenerative anaemia, classically, what, what we would expect based on history, basically is that we would have an increase in the MCD mean corpuscular volume and a decrease in the MCHC mean corpuscular haemoglobin concentration.
OK, that is true. OK, you will see that with regenerative anemias, but based on recent Evidence, only 10% of the time on average. So if we're relying on the indices to tell us whether or not our anaemia is regenerative, we're gonna be wrong 90% of the time.
So it makes our job easy. Look at the absolute retigulocyte count, get a reticulocyte count in all anaemic patients. Now, why, why?
Did we think in the past that we would see increased MCV, so a macrocytic and a decreased MCHC, so hypochromic anaemia with regenerative anemias. Well, because we didn't really have much in the way of, of reliable, ways to counterticular sites. Number one, it was, you know, looking at a stain and it was kind of complicated.
That got better with automated analyzers, etc. But the key, the key to understanding what's really happening here is number one, things other than And regenerative anaemia can change these values. So some dog breeds just have, like Japanese breeds just have small cells with decreased haemoglobin concentration, normally, right?
Cats with FELD that aren't anaemic may have a high NCV. So they're not specific for regeneration. And because these are mean values, and there are 25 trillion red cells in circulation.
It takes a long time for the mean, the average size or haemoglobin concentration to change once the bone marrow starts kicking out new cells. Bottom line here, all you need to classify your anaemia as regenerative or non-regenerative is an absolute reticulocyte count. And this is that patient again, we're kind of, you know, exposing more and more of his red cell picture as we go along here to illustrate our points.
Yes, he's anaemic, we know from looking at the hematocrit, super low. By the way, there's an interesting formula I want to remind you of. There's a, there's a connection between the haemoglobin and the hematocrit.
The haemoglobin concentration times 3 is what hematocrit should be, OK? And that's because red cells are composed comprised of, you know, 30% haemoglobin. So in this patient, 5, haemoglobin times 315 is the math works.
Let's say that this patient's hematocrit was 10, so we have haemoglobin of 5 times 3 is 15, but the hematocrit is lower than that, it's 10. What is that? That's he.
Lysis in the tube in the sample, OK? Affecting the red count doesn't affect the haemoglobin and that's why haemoglobin always wins out. You base your decisions on what the haemoglobin is.
OK. Now, then we looked at the recyte count in the ky, sky high, likely a hemolytic process causing the anaemia, and here the indices are normal. So this fits that 90% of regenerative anemias that have normal indices don't.
Focus too much on the indices. If they follow the rules, that's just one more bit of evidence. High MCD low MCHC that you have regeneration, your reticulocyte count tells you that.
So, with our patient here with regenerative anaemia, we have either bleeding or hemolysis. How do you differentiate those two? Well, like we've mentioned, you can look at the magnitude of the reticulocytosis, above 200,000, certainly above 300, you're likely dealing with hemolysis like our patient.
With haemorrhage, you're gonna see it. If you have significant enough haemorrhage to drop the hematocrit, in most instances, you'll find it. Now, it might not be external haemorrhage, right?
You might have splenic, you know, hemo peritoneum from a splenic mass that's bleeding or pulmonary haemorrhage, or you might have GI bleeding, and you can pull about a third of your blood volume in your intestinal tract from the GI upper GI bleed before you see it in the stool. But with haemorrhage that's significant enough to cause anaemia, you're likely going to find it, right? Also, look at the total proteins.
With haemorrhage, you're not only losing red blood cells, you're losing plasma proteins. So if your proteins are low and you're anaemic, you're likely losing blood, OK? Also, you can look at the changes in the red cell morphology and we're gonna focus on this more when we talk about how to deal with diagnosing and treating, diagnosing and treating.
Immune mediated hemolytic anaemia, but if you find on a blood film review either spherocytes or ghost cells or blood parasites, hematrophic mycoplasma, babezia in anaemic patient you're likely dealing with hemolysis, and then some animals that have hemolytic disease that occurs at a rate rapid enough to overwhelm the liver's ability to conjugate bilirubin, you might see icaris, so haemoglobin, it serum, you might see, . You know, elevated bilirubin and all that matters basically these days when it comes to determining whether you're, you know, icicate is the total bilirubin. You have to do the breakdown, unconjugated, conjugated.
It doesn't help you determine what you're dealing with. Intravascular hemolysis, extravascular hemolysis, something else, because basically, both forms of bilirubin are increased with everything that increases bilirubin, so just look at the total. So this may be a way to help you determine what your regenerative anaemic patient, whether you're dealing with haemorrhage or hemolysis.
Now, like we talked about, you know, regenerative anemias are more severe. The diseases that cause them, well, let's put it this way, they're more acute. These are the patients that you might have to actually give blood products to because their anemias can be more profound.
Luckily there, that's a less common presentation than nonin regenerative anemias, by far more common. These by nature tend to be milder anemias, so the hematorate isn't as low. The haemoglobin is not as low.
These guys rarely would need a transfusion, right? You just need to find out what is causing what disease this patient has. Is it chronic kidney disease?
Is it some inflammatory process, is it neoplasia? What is it? Correct that and the anaemia resolves, OK?
And the classic picture of these anemias, they're non regenerate, so the reticulocyte count will not be increased. There will be some reticulocytes, there are always some reticular cys replacing those senescent red cells that die off and get cleared by the, you know, the macrophages in the spleen, primarily some in the liver. And then this anaemia is typified by having normal indices, so normocytic normochromic anaemia, so the MCV and the MCHC are normal.
OK, we're kind of taught that 100% you got to have her ticks when you've got an anaemia so that you can classify it. But now we know it's great to have her ticks on every CBC because even in non-annemic patients, at times, you will find a higher tick count and that can be a clue to significant underlying disease. In fact, In a study of over a million CBCs done at all the IDEX labs worldwide by Dr.
Diaola, in 37% of those CBCs, reticulocytes, and their their numbers and their properties were clinically useful. So certainly in helping us deal with anaemic patients and classifying them, but also in non-annemic patients. So what's the deal there?
So let's just take an example of 10 year old spayed female dog that comes in with vague clinical signs, and we are doing kind of the routine CBC that most labs do and that I did up until maybe 10 years ago now, where you just look at the CBC and you don't, the red cell parameters and you don't see an anaemia. So in that case, you don't need a ret count. But if you had a retic count?
Now we have an increased reticulocyte count, right? This makes no sense in our old way of thinking when it only matters that you get a retic count when you have an anaemia. This patient now is a whole different ball of lax for us.
This is a sign that she has some underlying neoplastic or inflammatory disease that is causing an increase in the reticulocyte count. Remember, reticulocytes are born in the bon bone marrow and they mature in the spleen. All right.
So when you have high retics without anaemia. You wanna think about disease in the organs where reticulocytes go, right? So in an older dog, what am I gonna be thinking about splenic disease when I see this picture, OK.
So try to get your chicks on all your CBC's, you're gonna find. In up to about 10% of dogs, depending on how critical, what kind of acuity you see in your patients, sort of clinics that seem mostly healthy animals, the incidence of this high reticulocyte count without anaemia, 2 to 4%, up to 10% if you see emergencies. Now you might be looking at this and thinking, well, the machines can't be right.
Why would there be re ticks if there's no anaemia? How can you verify this result? You can look at graphics.
We're not gonna spend much time on this, but one way to verify the lab result is to look at the graphics that you get with your CBCs from your analyzers. And this is a normal dot plot for red cell picture in a normal dog. Here's our dog.
OK? These purple dots are reticulocytes. Our dog, whose report said she had high reticulocytes, well, there's a lot, there's more dots.
We can believe that. Also, if you look carefully, we can see that the red cells should be kind of clumped altogether without much happening. In this area here, our dog has lots of cells here.
Every dot is basically a cell, and she's got the sizes on the Y axis, so she's got red cells of differing sizes. This is the average size. She's got smaller red cells.
Well, how can you determine what they are? Are they fragmented cells? Are they errocytes?
What are they? Look at a blood film. So the CBC basically.
You get the lab report, but the other components of a complete CBC would be the graphics to verify the lab report and give you a clue as to, oh, there's something here I have to take a look at, and then finally, looking at a peripheral blood film. So with our patient who's got those. Cells that are kind of smaller than normal red cells, we want to look for changes that could help us diagnose her.
So she's could have smaller cells, could be anthocytes or schistocytes, which are kind of signs of liver or splenic disease. Oversimplifying, but those are the two things that you should keep in mind, or spherocytes, which we would see in dogs with hemolytic anaemia. So you can kind of get more information following all those three steps in interpreting a CBC.
Bottom line, you get an older dog in that has higher ticks anaemia, image the abdomen. Find the splenic mass before it ruptures, where you have a stable patient that you could schedule surgery instead of an unstable patient with a belly full of blood that you now have to do an emergency surgery. So this is the advantage of having ticks on all CBCs.
When you see a hybrid t count without anaemia, there's two basic reasons for that. So one is, you know, where do reocytes mature in the spleen. So, An excited dog whose epine or cat whose epinephrine levels are up because they're excited did.
Would have splenic contraction, and that alone can squeeze those maturing, those reticular sites in the blood cir into the circulation, raising the retic count. It could just be physiologic excitement. But in an older animal, especially if in one that's not quite right, a higher ret count without anaemia, I'm gonna be imaging the belly because the organs, primarily spleen also liver, where the ticks might go, could be damaged, and I wanna find that mass.
You could also have, you know, bleeding. Intestinal tumours, bladder tumours, other things that can, if the bone marrow can keep up with the mild or early loss, so there's no anaemia, by producing reticulocytes, high reticulocyte count, in those scenarios, the balance is maintained. The anaemia doesn't occur because the bone marrow can keep up by higher tick by producing more reticular sites.
So higher tic count without anaemia, physiologic, just excitement. Pay attention to your patient, make sure there's nothing that could be causing mild blood loss where the bone marrow can keep up by producing more tics. Older patient, look at the spleen, look at the liver, and consider sort of a cult things that could be dropping the red cell count.
Estimated that in sort of busy practises a few times a year, maybe even once a month or so in a really busy practise that sees acute patients, you might find that splenic mass before it ruptures. OK. All right.
So we've talked about the reticulocyte, the importance of having the count, whether the patient's anaemic or not anaemic, but there's also an aspect of the quality of the reticulocytes that's important, and this is called the reticulocyte haemoglobin concentration. This is kind of a new parameter that kind of became available a few years ago and it shows up on your CBC. And on the bottom.
And the abnormality we're looking for here is a decrease in the reject haemoglobin. And what that tells us is there's a decrease in iron availability at the bone marrow level for haemoglobin production. And why is that helpful?
Just a brief review. You gotta have iron in order to make haemoglobin, OK? And it's the macrophages in the bone marrow that sort of deliver the iron to developing red blood cells.
Here's sort of a graphic of that, and here's actually a bone marrow aspirate showing that central macrophages with encircling immature red cells getting iron for the haemoglobin production. If You have a decrease in retic haemoglobin, that can be for one of two reasons, right? So you just have less iron.
And how does that occur? Most iron in the body is in the blood. So external blood loss will not only will you lose blood, but the iron in the blood.
So you'll develop a true iron deficiency. So that would be seen with things like gastrointestinal tumours, ulcers, erosion. Bladder tumours that are bleeding, severe endo or ectoparasites think puppy with severe hookworm infestation or kitten with massive flea infestation.
All that stuff causes blood to leave the body, iron goes with it. It decreases the availability of Reticulocyte production, haemoglobin production in the reticulocytes in the bone marrow, so retic haemoglobin goes down. In the instance of that being due to external bleeding, they have an absolute iron deficiency, so you give them iron in the form of ferro sulphate, the most bioavailable form, to get that hematocrit up quicker.
If you don't have external bleeding, then you've got inflammation causing the decrease in retic haemoglobin concentration. Now, It with inflammation, it's not that there is an absolute lack of iron. There's plenty of iron in those macrophages in the bone marrow.
It's just not available. It's sequestered there. So, with inflammation, we now know that inflammation in the body, you know, you have those inflammatory mediators like interleukin 6 and 1 and tumour necrosis factor alpha.
Well those. Cause the liver to produce something called hepsidin, which goes to the bone marrow macrophages and it causes them to hang on to the iron. It's not available for the maturing red cells, so the retic haemoglobin goes down.
So what do you do when you see a decrease retic haemoglobin on your CBC? First, rule out external blood loss because that's more severe. Luckily, that's less common as a cause of decreased decreased retic haemoglobin than inflammation.
But you have to rule it out first because it's, you know, you gotta fix that. That's more severe. If you have no external blood loss by default, you have inflammation, you don't know what kind or where, but you got to go looking for it.
And in these patients, this is not an absolute iron deficiency like external blood loss causes. This is a relative one. There's plenty of iron in there.
It's just not available, so we don't give these guys iron. So, to drive that point home, the importance of external blood loss, decrease in the retic haemoglobin, if this splenic mass ruptures, is this dog gonna have a decreased retic haemoglobin? No, right?
Because the iron that's in the blood, it's gonna be in the free blood in the abdomen, reabsorbed, utilised at the bone marrow for haemoglobin production. And why are we concerned about the the haemoglobin concentration in reticulocytes. Anything attached to reticulocytes gives you an early indication of a change at the bone marrow level.
So with iron deficient anaemia as we know, back from vet school again, that we would expect to see changes in the red blood cell indices. So a drop in the MCV and a drop in the MCHC, the microcytic hypochromic anaemia, which is Seen with iron deficient anaemia, if it's been happening long enough. Again, those are means sizes mean haemoglobin concentrations, takes weeks for months to the average to change, but anything attached to haemoglobin is going to be noticeable.
The change is going to be noticeable within a couple of days. It's never been possible to detect a decrease in iron availability. This quickly.
So it's a very useful tool to get an early jump on the identification of iron issue in terms of red cell production. So pretty cool. OK, so with that review of anaemia, diagnosing it, classifying it, dealing with higher tick counts even in non-nanemic patients as a warning sign for like splenic masses or other inflammatory neoplastic diseases, and then Understanding how useful retic haemoglobin can be when it's decreased, that's the abnormality in letting us know our patient has something that's impairing iron availability at the bone marrow for haemoglobin production.
Having all that out of the way, let's just talk about dealing with our patients who are anaemic. Common causes, how to treat. So bottom line.
These are the common causes of anaemia that we deal with. Again, the anaemia of chronic disease that mild normocytic, normochromic, non regenerative anaemia, that's the most common. So chronic kidney disease, any, any disease, basically, so the PCD is not the problem here, the diseases, so figure that out.
Then, immune mediated hemolytic anaemia, this is an important one, and we've got news on how to diagnose and treat that. We'll cover chronic kidney disease, especially in cats, because that's, you know, we see more CKD in cats than in dogs, you know, they last longer with the disease, they get it more frequently, and then bleeding. So these are the things we're gonna focus on.
There are lots and lots and lots and lots of other causes of anaemia. You can see some of them listed down. On the bottom of the slide, but we're gonna focus on the ones that we encounter most frequently.
Now, I would like to point out useful resources for practitioners and here's two that both have to deal with immune hemolytic anaemia. These are ACVIM consensus statements and there's a whole slew of these on many diseases in terms of sort of state of the art, how do you diagnose and treat what we see in practise, whether it's heart disease or Cushing's disease or leptospirosis or you name it, right? Blood pressure.
Changes. Do we use gastroprotectants, how it's rationally use there, pancreatitis and cats list goes on and on. It's open source, so you just Google it and you'll see the whole menu of what's there and I highly, highly recommend doing that and and.
It's been at least 1 to 2 new consensus statements per year, so it's a good thing to, you know, check that resource, that website periodically. Anyway, we're gonna kind of summarise the consensus statements on diagnosing and treating IMHA. All right, because there's some news here, and I think it's can be a little confusing and we're gonna straighten that out.
So bottom line is immune mediated hemolytic anaemia can be a primary autoimmune disease or it can be triggered by something else, secondary IMHA. And there's a whole list of things that we kind of think about when we are looking at like. Well, could my dog with, you know, tick-borne disease develop immune hemolytic anaemia?
How often does do drugs, do vaccines? How often does this really happen? Dogs and cats?
Well, the members who wrote this consensus statement actually looked at the literature and came up with evidence-based recommendations or, or, or, or on causality versus just correlation, right? So this like, dispel the myths about. Things that could trigger a secondary IMHA.
Bottom line is, the higher up you go on this IME scale, this is a metric of evidence, the more valid causality becomes, right? So it looks like, you know, the, the lines are, this is like, you know, negligible, low level, moderate, and good evidence, basically. So when it comes to secondary, I mentioned, the bottom line here is that infection, OK, is kind of the main thing in dogs and cats that Trigger secondary IMHA and these infections are pathogens, usually.
And again, with pathogens, there's a whole list of things. Well, do I have to screen every dog that has Leishmania or I don't know, Ehrlichia with a Coons test for IMHA? Well, maybe not because looking at the evidence, Babezia, OK, is basically the only one.
In several species that reaches a high grade of evidence for causality, OK, in dogs and in cats, it's basically the hemotropic mycoplasmas. OK, so don't draw on, we don't wanna dwell on this too much. I'm just saying it's all in those documents and it's really helpful kind of kind of.
To come up with a rational plan when we have a patient who's got, we suspect, immune hemolytic anaemia. How far do we go in searching for an infectious cause? Maybe not that far.
OK. All right. So now on to the diagnosis.
What was really interesting is they broke it down. It's not easy to make it, in all patients, a firm diagnosis of IMHA. So they have three categories and we're gonna cover each briefly.
There's diagnostic, there's . Supportive, well, I forget what, what are they? We'll get to that.
There's diagnostic here, if you, in order to be diagnostic for IMHA not supportive or suggestive, you have to fulfil certain diagnostic criteria. They spell those out for us, so that is. Anaemia with two or more signs of immune mediated red cell destruction and the options for that two or more of serocytes, only dogs have these cats red cells don't have much central power, so it's hard to really identify when they're smaller and lack that anyway.
Positive saving agglutination test, positive coon's test, or a positive saving glutination test that persists after washing and we're gonna go over this in a little bit more detail because it's practical and, and useful, OK. So So anaemia with 2 or more signs of immune mediated red cell destruction and 1 or more sign of at least 1 sign of hemolysis. Hyperbilirubinemia, hyperbilirubinuria icterus hemoglobinemia, hemoglobinuria.
Now, this is, this is kind of another way to differentiate where your hemolysis is coming from. If you have hemoglobinemia and hemoglobinuria, you've got intravascular hemolysis, OK? If you have, you know, hyperbilirubinemia, hyperbilirubinuria icterus, you could have either.
Most of it's extravascular hemolysis, but if you have hemoglobinemia and haemoglobin pink serum, pink urine, you've got intravascular hemolysis, that's usually more serious and your patient, you know, kind of needs more aggressive therapy. And then RBC ghost cells. What these are, and we'll, I'll show you some.
These are RBC red blood cells that have had that have broken open and have their the hemoglobin's gone. So they just look really pale. Like this.
So we have serocytes, those small round cells that lack central pallor, and we have ghost cells, those sort of ring cells that have nothing in the middle because the cells have been broken open, a big chunk has been taken out and they've sealed over without that with that gap of with less haemoglobin. OK. All right.
Now, agglutination is a big, big diagnostic criteria. One of the criteria for diag diagnosing INHA. It's to be differentiated from luo, which is just an artefact of the cells just sort of clumping together when they sit in the tube.
So basically think about those like grape clusters versus like rolls of pennies as a way to kind of in your visualise the difference between a blue nation and roule, all right? But the, as mentioned, To be diagnostic for MHA, you have to have a glutination that persists after cell washing, because with that, maybe, maybe these are just like all that have wrapped around each other, right? So, persisting after washing is really important and we'll we'll talk about how to identify that.
OK. So then we had diagnostic for IMHA. The statement also has supportive for IMHA, so not a slam dunk, and the criteria you can see there, anaemia with one of either having a seocytes if you're a dog, positive slight utination test or positive direct coons, and only one sign of at least one sign of a red cell destruction, OK?
Suspicious for MHA is anaemia with one of either spherocytes, positive slimination test or positive direct. So you can see how, you know, in order to be kind of convincing, in order to be convinced your patient has IMHA, you have to fulfil more of the same criteria is the bottom line. OK, now, how do you do a slide agglutination test?
OK. You need one drop of EDGA whole blood, anticoagulants, you know, purple top 2 whole blood diluted with 4 drops of saline. OK.
Sometimes we were kind of taught maybe 1 to 1 dilution. You have a much higher specificity, well near 100% specificity in identifying a glutination if you do a more dilute sample, OK, because that would just make low and and less strict clumping. Separate.
All right. So if they still persist in these great clusters with a 1 to 4 delusion, or 1 to 5 delusion, but then you with certainty can diagnose that as a mutation, not low formation. OK.
And you can see here, you can get some false positives, if you have marked hyperglobu anaemia, the globulins can sort of cause agglutination, in which case you might need to do more than one a red cell rinsing, etc. Right? You want to perform these tests right off the bat before things get cold, and, you know, again, it's looking for those great clusters.
Now, I'm not sure this is gonna work, we're gonna give it a shot. So, Doing the 1 to 4 delusion, one part blood, 1 drop blood 4 drops saline is great. That's how you do a saline ination test.
Unless you're Doctor Dicole, who's super smart, who has his own method, which is you put a drop of EDJ blood on the slide, cover it with, cover it with the cover slip, and then you put some saline on the edge of the slide, and you wash, you watch as that saline gets whipped across the slide. Acting, acting like a rinse cycle to see if these clumps persist or dissolve, and what's happening here, they're not dissolving. So one drop of EDJ whole blood on a slide cover slip, some saline, one edge of the mic on the cover slip, and it'll by capillary action, just get whipped across underneath the slide, the cover slip, and you'll be able to see whether these clumps persist or not.
OK. So this is persist after rinsing, one way to do that. That that worked.
That's how you're diagnosed. We went through it kind of quickly. I just wanted to show it to you.
It's all in those consensus statements. Now let's talk about treatment. And looking through the evidence, they came up with recommendations and classified or characterised recommendations either as strong or weak evidence based on the literature.
So strong evidence weak evidence W. So strong evidence, prednisone or prednisolone. If you can't give oral medication, you know, you can give dexamethasone at 10% of the dose cause it's 10 times as potent, right?
And that's, there's strong evidence that that is an effective therapy for IMHA. We tend to hit these guys with other drugs. And there's weak evidence that that helps.
Now, sometimes we do reach for a second immunosuppressive to minimise the side effects of prednisone or allow us maybe to taper off the prednisone quicker if the animal, like particularly the dog is having severe side effects, but Rely on prednisone. If you're not getting anywhere, then there is strong evidence for like a salvage drug for human intravenous immunoglobulin. Now this works.
It's not maybe always possible to obtain it. I used to get it from human. Hospital pharmacies, they got a little strict with that, but if you can get this stuff and your patient is not responding to your immunosuppressive therapy, this is the strong evidence that this will work.
I just wanted to point that out. OK. The part you get them on your immunosuppressives at those doses.
Oh, by the way, one thing. OK. Some of us were trained, like, you know, yours truly, to get these guys started on 2 mixs per kg of prednisone twice a day.
There's no real advantage to going over 2 mixs per kg per day. That's another thing. So the dose is as effective, if not more, well, it's as effective at 2 to 3 weeks per cake per day as 2 makes per cake twice a day, so 4 makes per cake per day.
Basically you don't have to go above 2s per cake per day is what I'm saying here. OK, so when it comes to tapering, the the the goal here is to go slow. The consensus statement has these recommendations for when to taper.
After 2 weeks, if you're happy. OK, strong evidence to wait at least 2 weeks, OK? All right.
And then we want to decrease the prednisone dose by only 25% every 3 weeks if you're happy with your hematocrit, basically. Strong evidence for that. Amount of dose reduction.
And we want to follow the hematocrit, ideally before each dose reduction and at the midway point between, you know, as we go along, one of my mentors likes getting the hematocrit checked a week after dose reduction to see if it was already dropping rather than wait 3 more weeks or 3 weeks and then have a lower hematocrit, so. But the statement says PCV before each dose reduction, ideally every 1 to 3 weeks. Strong evidence that that's a useful way to monitor your tapering.
There's not really much of a consensus on, if you have them on more than one drug, whether you just stop the second drug without a taper, about a month or two after stopping the prednisone, if you get out that far, or following the same schedules for tapering that you use for the Pred with the second. So that's clinicians preference. Most of these guys are on these drugs for months, some way longer than 3 to 6 months.
If you have severe ones that are auto glutinating, you know, think cocker spaniel that comes in if it vomiting and you somehow managed to get them controlled, well, that dog may be on immunosuppressors forever, right? But this tapering schedule will let you know at what dose you should maintain that dog on. Now, here's where it gets a little bit trickier.
If you've got a relapse, so you had them controlled, and now you've tapered them down, things are looking great, they come in and they've had a relapse or anaemic. The disease is active again, they're out of remission, let's put it that way. Strong evidence says start over.
Is that really what you had? You know, do you have IMHA? Is there a secondary thing that's entered into it now?
Maybe you have immunosuppression, so you have an infectious disease that's triggering secondary IMHA. Maybe on your immunosuppressor if you've got some GI haemorrhage and again, where would you look on your CBC for evidence of that at that retic haemoglobin? And you know, make sure that there's not anything else.
Maybe there's some chronic disease now that's contributing to the anaemia, OK? And then there's weaker evidence on what to do about it. If you never relapse, right?
Other than revisit the diagnosis, but if it's mild, so clinically the patient's stable and thematic it's not scary little, it's above 20 let's say. Then last effective dose regimen. If you've got, you're starting from scratch, your hematocrits below 20 patients unstable, then just go way back up to your initial high dosages of immunosuppressors and and start that slow taper.
Here is where I, if I was writing this consensus statement as a criticalist, you know, after you get them under control a second time. Weak evidence for tapering more slowly. Like, does it matter if you go slower?
Well, maybe it's no different than tapering at the same rate as you did the first time in terms of preventing subsequent relapses, but I don't even like tapering until I'm 2, at least 2 months. On the high initial dose and happy, because to me, it's way easier than keep, to keep them in remission, than to get them back in remission if I taper quick and we lose control. So, the statement says, you know, PC above 30 for 2 weeks, strong evidence for that.
I like, I don't taper that quickly, to be frank. I, I, if the patient can tolerate, and the owner can tolerate the high dosages of prednisone. I'm 2 months before I drop that dose, if, if possible, to minimise.
Now this drive is there strong evidence that that's gonna make relapsing more less likely? No, but anecdotally in my experience, that's, that's worked. And then splenectomy is a whole other discussion.
It's not uncommonly done in people. There's weak evidence that it will help, you know. A dog or cat who's got multiple recurrences of INHA, but the point here is, you take the spleen out, well, you better be sure there's not any vector-borne disease.
In that dog, you know, because then often they're sequestered in the spleen and when the spleen is gone, they become fullin and so do your vector borne disease PCR panel before considering splenectomy, but in some of these patients without the spleen gone, the liver takes over destroying the red cells. So. You might get some temporary relief, but it, it's not, that's that's why it's not a strong recommendation to go with splenectomy.
OK, but there is a strong recommendation to give antithrombotic drugs to all these dogs and cats because this, along with, you know, the disease by itself, along with the treatments that you may give all predisposed to making this a thromboembolic potential here. So everybody gets thrombo prophylaxis, unless you also happen to have so-called Evans syndrome where you have IMHA and immune thrombocytopenia. But if your platelet counts OK, get him on, some form of thromborophylaxis.
OK. What do you use? Well, this is, this is venous, not arterial thrombosis that we're worried about here.
And so this is where anticoagulants come in, like basically heparin in all of its various forms, and then newer drugs like factor 10A inhibitors, these are gonna probably become the drugs cause they're been shown to be quite effective in people and we're having more experience with them in dogs, right? So basically, in these guys, when they're in the hospital, if they're critical, we want to get them on. On fractionated heparin.
What you have in your vial in your clinic right now, OK? Fine. That can be given IV, that can be given some Q to get these patients home if they need to be on ongoing and thromboprophylaxis, then they can be on subcutaneous low molecular weight heparin formulations, OK?
And then these guys should be monitored if you can, we want to monitor their anti 10A. Levels with the targets that you can see here based on whether you're using unfractionated heparin or low molecular weight heparin. Got to admit this is not that commonly done outside of universities.
What we would do in practise is just look at our old good old. You know, partial thromboplastin time or PTT or activated clotting time or ACT, getting a baseline and then shooting for, 1.5 times the baseline to indicate that we have these guys on adequate dosages of their heparin formulations, whatever that is, whichever ones we choose.
OK, now, again, antiplatelet drugs, they're easy, they're oral, they're better than nothing, all right? They're good for arterial thromborophylaxis. Think a cardiomyopathy cat that could throw a saddle thrombus, that aortic thromboembolism, you know, that cat that has a big left atrium with atrial smoke, you want them on.
Antiplatelet drug, right? But, and, and clopidogrel turns out to be the drug that you would use in that cat as well. So our two options for antiplatelet drugs for basically any condition that is potentially prothrombotic.
These days is clopidogrel works better than aspirin. And may be safer in terms of less GI side effects. So there's your dosages there.
Big concern among a lot of practitioners for treating severe anaemia that's immuniated with transfusions, like fueling the fire, right? Don't worry about that, OK? If your animal, if your patient is anaemic to the point where it's clinical, meaning usually less than 20.
Sometimes though, if it's a slow onset of red cell destruction, you know, they can compensate maybe down to 15 or 12 or something like that. But at some point, these animals need transfusions when their hematocrits get below 2015 or so. They just need Because we talked about earlier, it's all about the haemoglobin to carry oxygen, deliver oxygen to the tissues.
You can't give them oxygen, that's not gonna do it cause there's only like a fraction of the arterial oxygen content is dissolved in the blood, which is what you They're trying to change by giving supplemental oxygen, but over 98% of it's bound to haemoglobin. So just gotta give him. Haemoglobin and the blood product to reach for is packed red blood cells because There's just less antigen there than getting whole blood.
It's the bottom line. So, keep it simple. You have a severely anaemic patient, no matter what the cause is, IMHA or anything else, pack red blood cells.
Try to use component therapy if you can, because it makes each unit of blood, you know, able to help more patients, right? OK. When do you get them transfusions, clinic, basically the the the the answer is when they're clinical for the anaemia.
Or, meaning if they have a a sudden drop in hematocrit, they may be clinical, tachycardic, hypnick, weak at a PCD of 25, if they're normally 45, and it's dropped in 12 or 24 hours, right? If it's been a more gradual thing, they can be stable at 20 or 15, but don't let them go below 12. This is the bottom line.
Use, by the way, strong evidence for using packed red blood cells, but that are no older than a week or so because Things go wonky if the in these patients when the blood has been stored for longer than that. Remember too that the endpoint for blood typing and cross matching is looking for a glutination. So if your patient's auto agglutinating already.
You know, in the patient, so that that cocker spaniel again, that has severe autoglutinating alytic anaemia, that's gonna cause false positives. So it's kind of hard to accurately cross match your blood type, auto glutinating patients. So to con you know, read the package insert, contact the test manufacturer about the effect of autogluttonation on their specific product or strong evidence that that's important, .
And again, to minimise giving these guys more antigens, fresh rolls and plasma is not recommended. Just stick with packed red blood cells. OK, that's IMHA.
It's kind of an overview. I think you get the picture that it's probably a really good idea to, when you get a minute to read those consensus statements cause I just gave you like the overview. So for all the detail and the dosages, if you didn't have time to jot them down, they're all directly taken from that consensus statement.
So that's a common cause of anaemia we deal with. We also deal with anaemia. In animals that have CKD again, mostly cats, per the iris guidelines, you know, you, there's staging guidelines for CKD and there's treatment guidelines per stage.
It's usually not until a cat or dog gets into stage 3 or 4 CKD that they develop anaemia to the point where you're gonna need to treat it. All right? So it's recommended in stage 3 or 4 to assess for the need, you know, you'll be looking at this all along, but certainly by that point.
Again, erythropoietin comes from the kidneys. By this late stage of CKD, chances are there's less of that, so less stimulus for red cell production. Or the treatment, the use, the treatment trigger for the anaemia CKD is a hematocrit of less than 20.
And the drug we want to reach for here is Darbopoietin, less antigenic. You need to give it less often than er erythropoietin. If you're using this in cats, you want to make sure they have enough iron because this is going to stimulate red cell production, so you need more iron and they might not have as much from having decreased appetites and GI issues as well, etc.
So when I start them off with iron Dexran at 150 migs per cat, I have. That should just be 150 Ms per cat, and then repeat that monthly. So they have, they can respond to the DAAuin that you're giving them.
OK, now we're gonna finish up on a review of what to do with bleeding patients because then that's, that's another common cause of anaemia we see, right? Haemorrhage in our patients. Now, coagulopathies, you know, can be the result of either a problem with Blood clotting factors or platelets.
So, primary hemostasis is the domain of platelets. OK, first line of defence for haemorrhage. Platelets and platelet function is necessary to plug.
You know, holes in blood vessels. After that, then secondary hemostasis, the domain of clotting factors come in and they form a stable firi clot on that platelet plug. So platelets first, then clotting factors.
So when it comes to assessing for a bleeding patient, we have to consider both primary and secondary hemostasis. So, primary hemostasis, you're having Usually, well, the hallmark is superficial haemorrhage. Atechia ecchymotic haemorrhages of mucosal surfaces, the skin, epitaxis, mucosal bleeding, hematuria, OK?
That's what primary hemostasis problems show up as that kind of bleeding and also immediate bleeding after the puncture, all right? So you look at the platelet count, and if the platelet counts normal, then you have to think about platelet function, and we'll talk about how to deal with that in a minute. Secondary hemostasis, but the domain of clotting factors, that's different type of haemorrhage.
That's deeper tissue haemorrhage, so plural. So hemothorax, hemo peritoneum, bleeding into the joints, bleeding into tissue, lung tissue, that's what secondary hemostatic problems look like and that's where we have to evaluate our clotting times looking at our PTTs and PTs. Prothalinine PT and partial thromboplastinine PTT.
So that's the overview. Bleeding patient, is it a primary hemostatic problem, platelet issue or a secondary hemostatic problem, clotting factor issue. You can look at the type of haemorrhage to get you started there.
Then you look at your CBC to assess the platelet count. If that's not the issue, then it's either platelet function problem or a clotting factor problem. And let's just play with a couple of examples.
So, we just kind of covered this platelets circulate in the resting form. It's just little discs. When they hit exposed.
Collagen from a vessel injury, then they send off these pseudopods, they activate, they aggregate, they form that plug. And that's great when they do that in the patient. That's less great when they do it in the blood tube, which is sadly all too common.
And so, platelet clumps can affect automated platelet counts. They lower automated platelet counts to unpredictable degree. So the bottom line is when you get a machine count that's low, you have to verify that.
Look at a blood film, look at a dot plot, the lab does, you have to do that as well to see if the platelet count is low because of clumps or not. We most often see mild to moderate drops in the platelets, and that is most often in over half of patients with thrombocytopenia. It's that mild decrease where you've got an infection, underlying infectious or neoplastic disease.
And in these patients, the platelet count is not low enough to cause bleeding. It's a warning sign that you've got some disease to investigate and then treat the disease and the platelet count resolves. When you have platelet counts below the bleeding threshold, which is about 3000 to 50,000, then the only disease that causes that drop in platelets is, you know, immune mediated thrombocytopenia.
So when you have a platelet count of 10,000, that dog or that cat has, you know, ITP and that could be secondary to an infectious disease or neoplasia or could be primary just like IMHA but here the platelet count is the problem. And so you gotta get the platelet count up above the bleeding threshold with prednisone, primarily, right, to in order to then investigate for something that might have triggered the thrombocytopenia. If you have a platelet count that's low enough that your animal is bleeding and anaemic, then yes, you want to hit them with the same dose of prednisone that you would use for IMHA that we talked about, but also it's been shown that giving one injection of vincristine IV at the cancer dose.
And or that same human intra intravenous immunoglobulin, those in addition to prednisone, get the platelet count above the bleeding threshold faster than using prednisone alone, OK? . And again, if your patient with ITP is bleeding and anaemic, it needs haemoglobin.
Just get a pack red cells. Pack red cells, pack red cells, pack red cells until you stop the bleeding by getting that platelet count up. OK, so that's the platelet count issue.
OK, we'll talk about platelet function here in a minute. We're kind of taking these in the order, the most common order. We most often see bleeding in our patients due to thrombocytopenia.
Then we can see bleeding due to the secondary hemostatic problems with clotting factors. So here is a report on a dog of the PT and PTT that are both prolonged, they reach no endpoint. When you see this pattern, if we look at our sort of simplified scheme of The clotting cascade that we're all taught with the intrinsic pathway with factors 1211, 9, and 8, and the extrinsic factor 7.
When both the PT and PT are elevated, both arms of the clotting cascade are affected, and the two things that cause these dramatic increases, anticoagulant adenocy toxicity. And severe liver disease. Super easy to differentiate, right, you look at your patient, you know, it's like you can tell this is like acute hepatic necrosis.
So you've got sky high liver enzymes, a super sick patient, probably icteric, right? Or you have a dog or usually a dog that's got some potential exposure to an anticoagulrodenoide, OK? If the patient's bleeding actively, you gotta stop the bleeding.
Vitamin K is gonna be your anecdote antidote, but Antidote, but that won't stop bleeding fast enough to keep the hematocrit potentially from getting to the point of where it's critical. So you got to give them clotting factors. They don't have clotting factors.
So they do, but they're inactive by the vitamin K antagonists and that's like warfarin, or both of the Com, right? So you got to give them clotting factors. Where are clotting factors?
Which blood products have clotting factors? Whole blood, the plasma component, or fresh frozen plasma. So if you have A bleeding patient with anticoagaldeocide.
That has a hematocrit low enough that you're concerned, give either fresh whole blood or fresh frozen plasma and pack red cells if you're using component therapy. And then get them on vitamin K1 as quickly as possible and oral vitamin K1 as quickly as possible because it works faster given orally. Because there's such a high first pass metabolism in the liver and that's where the clotting factors are.
So that there's like a direct local action of vitamin K1 at the site. And if you give vitamin K1 with a fatty meal, then that just enhances its absorption. So get them on orals as quickly as possible.
Here we have the results of a patient who's got a platelet count of 8000 and hemato of 28, totals of 42. What does this dog have? We mentioned when you got a platelet count below 20, 30,000, it's ITP, right?
That's what this dog has. It's also got a quite a low hematorate. And so we would look at the dog and we would go, OK, well, he's or she is stable, not tachycardic, not tippnik, not weak, so it's been a gradual drop, so.
We're just gonna start prednisone. Fine. If though this dog is bleeding, so we see GI bleeding or epitaxis, or we've noticed that the hematocrit is trending down if the dog's been with us, then in order to get that platelet count up above the bleeding threshold where it will stop the bleeding, again, we want to give.
Than Christine at that anti-cancer dose once. It's very, very, very bad to give it, you know, outside the vein. So super careful so you don't have any of that vasculitis occur tissue sloughing that can occur if you extravasate and crystine, or you can give that intravenous immunoglobulin if you can find it.
And then get on in addition to the prednisone. So this is what ITP looks like and here's how you treat it, stop the bleeding if it's bleeding. If the animal's hematocrit was 12, then we would give pack red cells, pack red cells, pack red cells until the bleeding stopped.
There's no way to really transfuse. Platelets in these dogs, we don't really have the products. You can, there, there are opalized platelets and other formulations of platelet concentrates, but what's gonna happen to any transfused platelets in a dog who's or cat is actively destroying platelets by their immune with their immune system, they're gonna destroy the transfused platelets as well.
So we don't focus on giving them platelets, we just give them what haemoglobin pack red cells. OK, so now we have this young dog who comes in and bleeding, and it looks like secondary hemostasis because it's got a swollen joint. Or it's got a big hematoma.
It got hit playing baseball in the yard. The kids are playing baseball, baseball hit the dog by mistake, and now it's got a big subcu hematoma. That's what secondary hemostasis looks like.
And these are what our clotting times come back as, prolonged PTT normal PT. So where is this dog's problem in the intrinsic pathway. So this is what, what would you do next?
What you have to figure out what factors are low. So you would send off Sitated plasma for factor analysis and see which one of those is a 1211, you know, 9 or 8. So this is what basically haemophilia would look like in a young dog, right?
So there's haemophilia A factor 8 deficiency or 9 factor or B factor 9 deficiency. This is what that looks like when you test these dogs. If this guy is bleeding.
What it needs is clotting factors, and the blood products that have clotting factors again are whole blood, if that's all you have. The plastic component of the whole blood will provide the clotting factors. Fresh frozen plasma will as well.
If it's factor 8, that's the problem, giving DDAVP, which is what we would give for von Willebrand's disease bleeding, it also increases factor 8 levels and improves platelet function in general. So another option to enhance the stopping of this dog's bleeding. OK.
Now, the question here though is, this is a young dog and it's like rooting around outside and stuff, and, and you know, it's bleeding, it's like got that scu hematoma, so it's secondary hemostasis, could it be rodeoide? Well, could it? If the PT is normal, when the PTT is elevated, it cannot.
So this is important, I think. With anti-be or genocide, the factors that are affected are 279, and 10. 7 has the shortest half-life of all of those.
So what's gonna increase first after exposure to antiro adenoside? The PT because factor 7 is in the extrinsic pathway, which is what PT assesses. So early in rodenoide toxicity, you could have a PT that's increased with a normal PTT.
But by the time the PTT is increased from anti-coagrodenocide, the PT is already increased. So this is not consistent with anti-genocide. So if you ask the owner, you know, did could your dog possibly have gotten into anticoagulgenocide, and they say no, sometimes, you know, we go, well, all right, well, you don't watch, you know, you can't see the dog all the time and they just don't know.
Well, in this case, they're correct. The dog did not get in the codenoci toxicity. If this dog is bleeding, what does it need?
It needs clotting factors like, you know, it just needs clotting factors, . Like our dogs that, you know, we just saw in a couple of slides ago. So we, if we are using whole blood, give it whole blood.
If we're using component therapy, then break it down. Give it the component therapy that we're talking about. Thresholds and plasma and DVABP to get those platelets activated and get those factor levels up, factor A levels up.
OK. Last one I think. So now we have a dog that comes in with what looks like primary hemostatic haemorrhage, OK?
It's got epistaxis, let's say. And we look at its platelet count, and it's clotting times, and it's normal. That's what we would do first.
We go, well, platelet count, CBC that's normal. So now, since it's bleeding, we better get a PT and PTT even though maybe with epitaxis, that wouldn't be quite what you'd see from the secondary hemostasis. We're gonna get those anyway cause it could be more than one, you know, the same animal could have both primary and secondary hemostatic abnormality like say DIC for example.
But the PT and PTT are normal. So now we think, OK, now we have a platelet function issue to assess because with that sort of superficial surface bleeding, primary hemostasis, that's a platelet number issue, not in this case cause platelet count is normal, or a platelet function issue. What's the pet side test for a platelet function problem?
The buccal mucosal bleeding time, and I just wanted to show you what that looks like. So use that simple plate device and it makes these razor sharp nicks in the mucosa, and then you take a coffee philtre, you know, and you dab below, not touching the incisions, and then you time it from when you Activate the device to when you get a clot. And over 4 minutes is abnormal.
OK? Now, this is a platelet function abnormality, and this is usually von Willebrand's disease. And here, we need to give them von Willebrand's factor.
So what has that? Well, threshold blood, right, for sure. Thresholds and plasma.
Has voran's factor as well as other clotting factors. Cryoprecipitate if we're getting down to like specific targeted component therapy, cryoprecipitate would be the one to reach for because it has the highest concentration of von der Lebra's factor in it, and then DVP again because it just improves platelet function in general. OK?
So this is what how you would assess a dog for platelet function. Let's say you have a Doin pinser. Puppy that's coming in for like a neuter or a spay and you want to screen for Balibrand's disease, this is what you would do.
If this test is normal, then you can anaesthetize and do surgery on that dog. If this test is prolonged, then you want to send in sturated plasma for von Willebrand's factor analysis to determine whether you have a level low enough to be concerned about and that you can then decide if you want to have blood products on hand or pre-treat with DDAVP 30 minutes prior to get any bolos factor that's in the endothelium into circulation, you know, that sort of thing. So that's where you would use this test most commonly.
And that's it. So I cannot wait till we can be together, so we can have a discussion more than a lecture, but until then, stay safe and be well. Thank you very much.
