Hello, I'm Lizzy. I'm one of the ICU nurses at Langford Veterinary Services. So I'm going to do a lecture on anaemia and coagulopathy, which I know is quite a big topic.
So I'm gonna try and sort of cover everything very briefly and then sort of go into a bit more detail with the things that I see quite often. So the reason I called it quick, they've got no blood is because essentially, people can panic in these situations where something's really anaemic. And also, when something's obviously rapidly bleeding as well.
And actually, it's, you sometimes just need to take a step back and just work through the process like you would with any case. And also, there's always a bit of a rush to maybe give a blood transfusion, and actually, that patient doesn't necessarily need it. I'll go into that further in the lecture.
So anaemia, the 3 main causes. So hemolysis, haemorrhage, and reduced production. Hemolysis and haemorrhage are the main two that I'm gonna really focus on.
I'll have like one side and reduced production, but it's not really my area of expertise at all. Although we do have some patients, obviously, that have bone marrow disease. So the picture's here.
So we have this little cat who was very, very anaemic. So had a PCV of, I think it was 4 when he was really, really bad. He had a transfusion when his PCV was 4.
But I think actually, at this point, his PCV was 8, and actually, he was just waking up from an anaesthetic. And he was very bright with his PCV of 8. So this is like, An indication that maybe you don't need to give blood.
Always go by what the patient looks like. And this is just a dog that had a minor coagulopathy, sort of, you can see all it's bruising around its wound, etc. From its surgery.
But this one, again, didn't need any intervention. So, immediate treatment is sort of similar to any case that you would see in that was a critical case. So place a catheter and then take blood from your catheter.
It's always preferable to do it that way, really, especially if you've got a patient that you think has a coagulopathy, cause you're not gonna be sticking them twice. And you're gonna want that catheter for other things anyway. So the main things I want to take from that catheter is PCV and to solids, your blood gas, if you have a blood gas machine, if not, hopefully some of you have sort of in-house lactate metres and you'll want to get a glucometer as well and just get a little glucose on there.
And then an EDTA is all you need. Your baseline things are getting a blood smear, cause then you can look at all your cells. You can do your cell counts, etc.
Etc. Blood typing. There are quite a couple of sort of in-house kits that you can get.
So there's the Alvidia kit, and there's also the Rapid H kit. We use the Alvidia ones. We just find they're much easier, they're less likely to sort of have Any subjective view on it, essentially, when you run them.
And saline agglutination, so if you suspect there's IMHA, you can do a saline agglutination test as well. And then potentially you'll get fluid therapy if the patient is hypovolemic. Some of your anemics won't be.
They will be euvolemic, especially if they've sort of had hemolysis or have got some sort of chronic thing going on that's causing their anaemia. So they might have compensated for it and actually be evollimic. So it's important to check.
That your patient is hypovolemic before you give fluid therapy, but often you'll have patients that do really well, from just being given a fluid bolus rather than actually just going straight into giving them a blood transfusion. You don't need to worry really about, hemodilution. I think that's often something people can worry about in first opinion practise that you're gonna dilute the circulating PCV.
And actually that doesn't really happen. You're actually gonna make all those cells get to where they need to go. You're actually gonna just improve their .
Perfusion, and that's really what you need to achieve if the hypophalemic. Great. So then you want to move on to your history and exam unless your patient is really crashing, in which case you might want to either send someone else to do this if you can, with the history, obviously not the exam, or.
Ideally, just, or wait till later if the patient really needs absolutely immediate treatment. So vaccines, especially in cats, you want to be checking for FIV, FELV and mycoplasma, and lepto in dogs. Lepto, you tend to get obviously all the other signs associated with lepto.
So you're not probably gonna get a dog that's just presented with anaemia or a coagulopathy. You're gonna get a dog that's presented with hepatic failure or kidney failure. But it's just important to consider that these all tie into one.
Medications, any current medications that the patient is on. So, obviously, if they're on anticoagulants, or if they're on clopidogrel for something else, or, rivaroxaban, which is the newer one that we use, if they're having chemo cause then they're more likely to be immunosuppressed and have bone marrow suppression, and also flimazole. Diets.
So if there's any presence of any potential for any toxins. So, I think a long time ago, but I, when I was learning as a nurse anyway, some people fed their animals baby food, which actually has a high concentration of onion and garlic. I've never actually seen an onion or garlic toxicity.
I don't think they're as common, but may I work in referrals, so maybe actually first opinions do you see them. Also, if their diet is something like raw food diet or an unusual diet where they could have iron deficiency, that's also important to consider. Then we go into potential diseases, alongside.
The medications, but I sort of left that out. So any renal or hepatic disease or diabetes mellitus, that can also be associated with anaemia or coagulopathies. I'll get more into, obviously all this later on.
Any potential toxins that are around, so zinc, lead, or rodenticide. Again, I've never seen a zinc or a lead toxicity. They're quite unusual.
Redenticides, I've seen quite a few. And it's all about. Obviously, being aware of the animals are scavenger, but especially your farm dogs, so Jack Russells, seen a couple of Labradors with it as well, because obviously, they eat everything.
Those, travel, you have to consider things like Bbezia, Elia, mycoplasma, again. Babezia is actually in this country now, so it's quite useful just to test. They've got sort of in-house tests you can do now called a 4DX.
And you can do a blood smear as well to check for Babezia. Any previous history of bleeding? So if they had a spa or castrate and there was any bleeding after that, or if they've had any other, procedures, or if they've never been spayed or castrated, that's another important thing to consider that actually, this might be the first time they've had an insult and then that's caused them to bleed.
If they're in a multi house household, again, increased risk of HIV, FALV transmission. You want to examine the patient completely for bleeding. Sometimes it's not always as obvious as you'd expect.
So, examine all the mouth, the sclera. You, obviously, you won't see joint bleeding. That's quite difficult because that's sort of just joint pain.
But look for signs of melena, hematuria. Those are all sort of the major places to look in the ears as well and the nose, to staxis. And then, yeah, also looking for Iru, so that could be an indicator of a hemolytic process going on.
And then palpate the abdomen, feel the spleen, so if you can feel for potentially any splenic masses. And then if they're pyorexic, then you've got an indicator if there's an inflammatory or infectious process going on. And that's quite a good sort of thing to sort of round everything together and get some idea of what's going on potentially.
So then we move on to the lab bit. So I've already said about PCV and total solids. So that's in the top left corner.
Underneath, you've got your saline agglutination test. So essentially you put one drop of EDTA blood onto a slide and then mix 3 drops of saline with, and you should see sort of macroscopically, these sort of specs form if you've got a positive agglutination test. So that's where all the red blood cells are sticking to each other.
You also can look at it under a slide, under a microscope, sorry, it's on a slide. In order to see it microscopically, but quite often they'll just show up the minute you put it on the slide like that, and it's quite obvious. And then you want to look at your blood smear.
I'm not an expert on blood smears, but, these are some of the sort of obvious things to be looking for. So, and your So start from the top. So the very top one, that's just to show you platelets.
So the little purple blobs are platelets. So when you do your platelet count, you want to be looking for those. I'm gonna go into what your platelet count should normally be, but if you have less than 2 or 3 high power fields, then you're very, very thrombocytopenic, and you're likely to spontaneously bleed.
Then if you go to the next one on the right, if you work your way around, . Those are reticulocytes, so there's sort of indicators of regeneration. So you can get punctuate and aggregate.
Reticulocytes in cats. We only actually count the aggregate reticulocytes. And those, nucleated red blood cells aren't actually very useful because they can be produced by other diseases.
So you can't really go by them for regeneration. You have to look for reticular cys. If you don't have any reticular cys, then you've got a non-regenerative anaemia.
However, this could be because actually it hasn't had time to regenerate. So actually, if it's been an acute bleed of sort of 2 to 4 days, or hemolysis every 2 to 4 days, then just take this into account. Otherwise, it could be something like Renal failure, or something causing reduced erythroin production.
Then, next one down to the right, those are schistocytes. So those occur basically, they're fragmented red blood cells. But they've had to go through a very sort of.
Small vessel. So essentially the red blood cells have been subjected to a shearing injury. And this can be indicator of DIC, so death is coming, as we sometimes call it, or disseminated intravascular coagulopathy, hemangiosarcoma, or splenic torsion.
And then if you work way down to the next one, you've got sort of your hypochromic cells. So those are indicators of iron deficiencies. So they're pale, and they're slightly smaller than normal red blood cells.
So there's a, that's, yeah, iron deficiency. Then go to the next one. So the bottom left now we're on.
Those are spherocytes. So essentially, those occur when in IMHA when essentially a macrophages come and taken a chunk out of the red blood cells. And then the red blood cell, hasn't been completely destroyed and basically it's reformed a smaller and darker staining cell.
And those are spherocytes. They're a really good indicator of. IHA.
And then if you come up to the next one, the last one in the ring, you've got your Hein's body anaemia. So that can occur basically from, Mm, sort of haemoglobin formation. So that's damage to your haemoglobin.
So it especially happens in cats. They have actually really weak red blood cells. So this can happen with paracetamol toxicity most commonly in cats, especially because they're so susceptible to it.
It could happen on dogs as well. And then your onion and garlic also will causes Heinz body anaemia. Great.
And then hemolysis. So hemolysis has lots of different causes. So immune-mediated is probably the one I see most commonly, infectious.
Toxic congenital and microangiopathy. I'm gonna go into each of these sort of individually, so I'm not gonna sort of discuss what each of these are gonna be now. So essentially you can have extravascular intravascular hemolysis.
It's much more common to have extravascular. And so this is destruction within the liver or by the spleen. Yeah, that is spleen.
I know it looks a bit like a kidney. And then that causes hyperbilirubinemia. So that causes your icterus.
And quite often, IMHAs are incredibly yellow, like really sunshine yellow, quite amazing. Intravascular hemolysis is less common, so that's your haemoglobin anaemia and haemoglobin urea. So that's quite darker urine that you're gonna get, rather than sort of just the yellow, orangey urine from bilirubin.
But again, it causes also bilirubin because you're gonna get. For the breakdown as well. So your IMHA, so it's very breed related.
I'm sure you've probably seen IMHA cases, mainly spaniels is what we see. I actually very rarely, I realised since actually researching for this, that I very, very rarely see it in other large breeds. It seems to be spaniels or really small patients.
We've seen it in things like pugs and dachshunds and Sort of other small dogs. But yeah, I've never seen it in anything giant and I've never really seen it in anything sort of Labrador or above. So your diagnosis, it can be primary or secondary.
So, main secondary causes are neoplastic, but it could also be an infectious cause. And sometimes they can have ITP or systemic lupus. Erythrotosis, on top of it, but I've, we've, I've never had lupus as far as I'm be diagnosed.
ITP we see quite commonly alongside it, and that gets called Evans syndrome. So the main things you're looking out for, so your spherocytosis, which I showed you in the last couple of slides. So at the bottom here, these cells, which are smaller and darker staining, where the macrophages come along and taking a chunk out, and then the cells reformed.
You're also looking for your auto agglutination, so in the top left, picture, that's your sign of your agglutination. So all those red blood cells are sticking to each other. And then you can do a test at the lab called the Coombs test.
So that tests for the actual antibodies, . That are being produced against the red blood cells. So sort of you'd want to do all three of those tests to really confirm IMHA, but you can definitely start treatment with your suspicion from your stocytosis and your agglutination.
Other potential secondary causes, you could have drugs, vaccines, or tick tick-related disease, so mycoplasma or Babezia. And then you want to move, so your treatment for it is pre corticoids. You should be seeing a response within 5 to 7 days, with your Preds.
We sort of vary. Some patients seem to respond really, really well. We only need to give one blood transfusion and then they're doing really well and sort of they're regenerating and they're not hemolyzing anywhere near as much.
We've had some patients that literally after a week in, we've sort of added in every single. Immunosuppressive going and they're still hemolyzing. I don't really know why this occurs in some cases and then not in others.
So the, the other ones you could potentially add in are cyclosporin, azathioprine and mycophenolate, and then give a pack for blood cell transfusion if it's indicated. Like I said before, these patients might be quite used to actually having a low PCV and sometimes they might be hypovolemic because they've hemolyzed so suddenly. So it was always worth trying, providing they show signs of hypovolemia, try a 10 mL kilo flu bolus and see how they respond before rushing into the blood transfusion.
I have seen reactions to blood transfusions, not, not huge hemolytic reactions, but anaphylaxis, and we've seen a couple of plasma reactions, and I think it's something that's quite easy to rush into giving when actually it might not be the best thing for the patient. Your main risk to the IMHA is PTE, and we've actually had a couple of these happen recently. So pulmonary thromboembolism.
So, the IMHA means they're in a procoagulable state. So we quite often start these patients on clopidogrell, . And or rivaroxaban now to try and prevent this occurring.
Cause we often have patients that respond really well to the actual treatment for the IMHA and then they throw a PT in, and that's really hard. And I think there's a whole lot of different risk factors that go into it. So they have platelet activation and increased tissue factor.
They also have vascular stasis, and, they're not moving as much either, because obviously they're very anaemic, so they don't want to get up and move around. And also the fact you place an IV catheter in them, and then you give them a blood transfusion on top, which is also another huge PTE risk. So it's not a huge surprise that they get these.
But that's another important thing to consider, and it's always important to watch their respirating effort, throughout the time they're in. So infectious causes, I'm not really a pro at these, so these sort of tick-borne diseases, I don't see them very much. And I think it's because the anemias they cause are quite mild, so they don't actually come into ICU.
So it's basically just research for, for this, webinar. So essentially you can have infectious causes. So, cats, you've got EFIV, FALV, and mycoplasma, and dogs, you get perbezia.
So it can, Babei is an odd disease, so it can be quite acute, disease that it cause, it can cause like did I see respiratory distress and SERS signs. But then other times it can be very chronic, and sort of have a mild, moderate anaemia. Quite often these patients not only have Barbezia, but they have a lick here as well, because, because of where they're from, essentially all sort of tick-borne diseases will be in that area.
So it's not really a surprise they get infected with multiples if they haven't had any tick cover. So on the top left picture, at the very top, those little things that look like little teardrops in the blood cell. Those are be, yeah, they're quite pretty, really.
And then at the bottom, I was told this weird black thing is a lichia, but, Other people have said it does look somewhat like a lia, but also could potentially be other, another thing wrong with that cell, so don't take my word, that's definitely what it looks like, but I think that's very similar. And then on the, in the middle slide, you've got mycoplasma, so you've got that little, little lesions all in those red blood cells that you can see. And then I've put a picture of the 4DX on the bottom right.
So those are our in-house tests that you can get. So they test all sorts. They do plasma, Elichia, Dirifilaria, a heartworm.
I think they do a 4th 1, which I can't remember the name of right now. But, yeah, they must do a 4th because of 4DX. But those are really easy to run, so you can literally run them on whole blood.
You just need to warm up out the fridge for half an hour, same as any snap test. And they'll give you just a dot for whichever one they've got, or if they've got multiple. I've had one positive one that I've seen since I've, we've had them for anaplasma.
And then top right is your FIV FVRV comb test. I'm sure all of you know pretty well. So I think that's all sort of tick-borne diseases.
So treatment, yeah, those drugs that I've written on there, like I said, they're not really something I see very often, and I think if we do see them, they quite often end up not in ICU because they're not actually got the acute Babesia signs. The other thing that I thought was quite interesting about Pirbezia is the parasitized blood cells, tend to sort of like sludge together in small capillary. So sometimes if you do an ear sample, you're, you'll get a better.
You're more likely to basically see the Babezia cause they're sludge in those capillaries in the ear, so just to consider that. And then toxic causes. So, toxic causes, I'm looking mainly at the oxidative injury ones.
So that causes those Heinz bodies that I showed you on that first lab slide. So it causes methemoglobinemia, some damage to the haemoglobin. And then, after ingestion, you'll form Heinz bodies within 24 hours, and then hemolyze all of those cells 5 days after that.
Cats, like I said, have much weaker sort of haemoglobin. So they are much more susceptible to these things. So they can get it from also lymphoma propofol.
So if you have a cat that's on propofol CRIs, having repeated GAs, you need to really be considerate of the fact they might get high anaemia, so you might need to switch to alfaxolone. Hyperthyroidism and diabetes mellitus. And then also, obviously, your onions and garlic that I put on the top there.
I don't know, I don't need to tell you which picture it is. So, so, but again, like I said, I've never seen actually an onion or garlic toxicity. Paracetamol toxicity in the middle.
I have seen that, I've seen it in a cat and a dog, actually. So, yeah. So that's basically like biding your time.
You can treat with like positive sort of liver-friendly drugs, essentially. So Denamarin, and things like that, but that's sort of to do the best you can. Otherwise, sort of need to ride it out, and you might need to give them a transfusion if they form that many Heinze bodies and hemoly that badly.
And then I think, like I said, I haven't really seen many z toxicities. So, zinc, essentially is contained in US pennies, apparently UK pounds and 2 pounds, and obviously nuts, bolts, and screws. And essentially, the acidic environment in the stomach, turns them into soluble zinc salts, and then they get absorbed.
And then that causes, and then the higher zinc, concentration causes, intravascular hemolysis. So you get the haemoglobin anaemia and haemoglobin urea. And you also get GI signs with them.
Most of the time when they present the owners, hopefully will know that they've swallowed the coins, that makes it easier, but otherwise, you can do an X-ray and obviously that will give you a clear sign. Main treatment is to remove the object itself, so by scope is ideal or . Gas gastrectomy, if you have to.
And then give fluids and pack of blood cell transfusion if you need to. Omeprazole, just to reduce the, acidity of the stomach, and that can really help reduce the absorption. And apparently, you can also give calcium, disodium, UDTA.
I think, what is it for zinc? Congenital disorders, so there's two main ones. They're very, very rare.
So, phosphory fructokinase deficiency, which is present in, American coccus, like on the right, and also apparently English springer spaniels, so it causes sort of chronic mild to moderate anaemia. And essentially, you get an intravascular hemolysis due to alkalosis. So, the dog runs around and gives itself a respiratory alkalosis, then it's at risk of getting intravascular hemolysis.
I've seen one dog that has this. It was actually a collie. And the owners were very, very good at, sort of managing him, but he managed to sort of sip his lead and go for a run around, and then he was struggling a bit.
You can do an enzyme assay to confirm at the lab, and, there's no real treatment for it other than managing it from a reducing their exercise point of view, or giving them very slow, gentle exercise. They are regenerative though, so most of the time they won't need a blood transfusion or anything like that. Then you've got pyriva kinase deficiency, which I've never seen.
So that's in Basenji and beagles. And that causes chronic severe hemolysis. So, so they sort of, they don't do very well with this.
So they have moderate to severe anaemia for sort of 3 to 6 months. And then they have a slow decline over sort of 1 to 3 years of their life. And then, although it is very regenerative, eventually it will quite often leads to minor fibrosis.
So damage essentially to the bone marrow, it becomes fibrotic and then you don't get any regeneration. So then we want to reduce erythroparesis. So this is basically issues with the bone marrow, that means that your, Not producing your red blood cells, white blood cells, platelets, for whatever reason.
So you can have extra marrow. So that's your sort of systemic disease. So that's things like renal or endocrine diseases or FELV, although you'll sort of get a milder signs with FELV.
Or you can have drugs, so quite often we've seen it a couple of times bone mass suppression with things like phenobarb, we've seen a couple of times and also actually we had one case of fenbendazole, . Well, that was what was suspected anyway, and then you can have infectious causes or nutrition such as sign deficiency again, . And then inmari, I find these different terms really difficult, so I sort of on your.
Handout thing that I gave you, I sort of tried to break it down to make it clear what all the different things were. So you've got your my, I'll try and do it in order actually. Aplastic anaemia.
So essentially, your bone marrow turns to fat. And then that'll cause a pancytopenia. So you've got reduced, cells across the board.
You've got your myelodysplasia. So, sort of infected hemastoparesis, so it causes a non-regenerative anaemia. Myloroliferative.
So you make sort of too many cells, so you're actually, Rather than being panic or, what's the word? Producing too many. And then myelofibrosis, so your bone marrow actually becomes scar tissue.
So like I said, with that horrible disorder, the placentas in the beagles, they form horrible scar tissue in the bone marrow and that's why they don't remain regenerative. And it can be acute or chronic. So if it's an acute case, you tend to get thrombocytopenia and sort of a very mild, such no anaemia and, and a granulocytopenia.
So your granulocytes are your neutrophils, enophils, and basophils. The one that's going to be most obvious is your neutrophils. So your neutrophils have the shortest.
Lifespan. So that's gonna be the first thing that's actually obvious the neutropenia. You don't have that many basophils or is inopils so that might not be so obvious or harder to find at least.
. And obviously your your thrombocytopenia as well, you'll find. And then if you've got more of a chronic thing going on, you have sort of a moderate sphere anaemia, . And your white blood cells actually might be sort of variable amounts and you also have a thrombocytopenia.
So the main way to diagnose this is bone marrow biopsy. Like I said, this isn't something I'm an expert on at all. There's, we have quite a few cases that do have bone marrow disease of some form.
But I just find it quite difficult sometimes to put my head around all the different actual. Things that go on, . So we move on to haemorrhage.
So haemorrhage, main causes, trauma, coagulopathies, and a parasites, GI, or neoplasia. I'm gonna mainly go into coagulopathies. With this.
So, primary and secondary, we all know this lovely picture. I'm sure we all know off by heart. Yeah, it is very confusing.
So basically, I'm gonna make you just focus on the most common ones and not make it about really this picture at all. So your primary gragopathies, so primary, you get sort of TA, so you get your sort of very small areas of bleeding. You get, you're more like to get GI bleeding, so you need to look out for Melina or, Hematemesis, you tend to get like multiple locations.
They tend to get and they're like out to men in their mouth. That's why it's really important to look sort of all around them, and they tend to have repeatable bleeding signs. Secondary coagulopathies tend to have hematomas or they beat into their body cavities or joints.
So you have to think about, that's why your, pos comes in really important. So scanning their abdomen for any signs of, free fluid, and also scanning. The thorax for any signs of free fluid.
You won't actually get abdominal distention for a very long time with bleeding, so it's really important to actually scan them because it won't be very obvious if there is any blood in there. They also get localised bleeding and it tends to be. Sort of delayed.
So after, so they will have had the trauma seemed OK and then they will have bled. So then we move on to primary. Great.
So then we've got our platelet counts. So they normally should be 10 to 25 high power field. If there's less than 2 to 3, then you're at real risk of spontaneous bleeding.
And you also want to look for macro platelets. The platelet count on your, haematology machine is just not very accurate, unfortunately, especially in cats. So it's really important you actually do a platelet count, do a smear and check it yourself.
And even if your machine actually says It's fine. You should still double check it. Micro plate that's especially common in cavaliing to our spaniels and greyhounds, so they tend to have fewer larger platelets, instead.
And then you do your BMBT. So that's, I don't know if I had a picture. I thought I did have a picture of it.
No. So BMBT, so in the top picture, you use one of these little stick, things, so these lancets. So essentially you want to pull the lift up and then tie it up with a bit of, You can use just wow bandage.
And then essentially you just put the lances in and then you want to make two separate incisions. And then you just want to hold, like a swab or, blotting paper underneath, but you don't want to touch the actual clot itself, and then you just wanna time how long it takes for the clot to form. So in dogs, it should be between 1.7 to 4.2 minutes.
In cats, it should be much quicker, so 1.4 to 2.4.
I don't think I've ever actually done a BMBT on a cat, if I'm honest. But I've done a couple on dogs. 4.2 minutes seems very, very long.
I've definitely always had them caught much before that. But apparently it can be that long. And then another set of primary coagulopathy is a tag, so a thromboelastograph, but I'll get onto that in a bit.
And the bottom picture is just a picture of your platelets again. And then your secondary crayopathies, your PT, so your prothrombin time, so that tests your extrinsic and common pathway. I'm gonna ask what was that.
So factors 257, and 10. So this is really useful for identified. I'll go into that in a bit more detail later.
So it's, it should be very quick, your PT. So between 12 to 17 seconds in a dog, 12 to 23 in a cat. And we've got this sort of thing on the top right, that's our in-house coag machine.
We can also send it to the lab and they'll run coags for us. Down there. But in-house coding machine is really useful if it's out of hours or if you need it tested really quickly, or if you don't get enough blood, actually, because our lab needs quite a bit to run it.
Essentially, you've got these cartridges that you put in, you just need to warm them up again for half an hour to room temperature. And then you just add the blood and it should press start. It's really, really easy to use.
In the bottom right is the cartridges that we put in. So your PT and your APTT, and you do always do both. So your APTT is your activated partial thromboplast in time.
So that's more useful for testing for your intrinsic and common pathway. So that's better indicator of things like DIC or if you've got, some kind of hepatic issue going on. So it should be between 71 to 102 seconds in a dog or 70 to 129 in a cat, so it's a bit of a longer test.
Other potential tests you can do, you activate the clotting time. So these sort of these tubes that are full of diomatous earth at the bottom. And essentially you fill with blood up to the line, and then you keep them warm, so you tend to put them in your armpit.
And then you sort of invert them every 5 seconds and then just time how long it takes for it to clot. So 160,110 in dogs, 50 to 75 in cats. It's not the most accurate test.
So essentially, if you don't have access to APTT and PT. It's better than nothing. But it also is affected by other things.
It's affected by Fabrinogen, if you're, got reduced platelet counts, that's why it's really important to check the platelets as well. And if you've got also thrombocytopathia, so again, your BMBT is really important to check that. And then if you're still getting a prolonged result when you know your platelets are both working and There's enough of them, then you know that you probably do have the clotting disorder, secondary coagulopathy, so.
But yeah, it's reduced sensitivity and specificity compared to your PT and ABTT. Great. And then D dimers, so this is one we do at the lab.
We don't have any way of testing this in-house. So essentially your D dimers, if they're over 250, then they're abnormal. That's right, .
So essentially, it's Quite a complicated thing, but there's quite a good indicator for DIC. It's not a definite test. It doesn't confirm that it's DIC, but it will make you strongly suspicious of it.
And again, I put the tag on there. Again, I'll get more into what the TEG does. There are a couple of other tests that I didn't add to there because we don't ever do them.
So platelet aggrogrommetry, God, I really can't speak tonight. And platelet function analyzer. So, they test the function of your platelets.
I'm not. I mean, I, we don't use them. That doesn't mean they're not useful, but it's just not something we use in clinical setting.
Our BMBT does test our our platelet function to a degree. It probably isn't as accurate as those tests, but. It's much easier and we don't have the equipment.
Primary hemostasis. So, thrombocytopenia. So you've got your three main causes is reduced production, destruction, or consumption, or slash sequestration.
I'm only gonna focus on destruction, but I will go into the other causes briefly. And then thrombocytopathia, your von Willebrand, so we'll go into that, and you're acquired, which is your drugs. So, Where do we start?
So I'll briefly go into consumption, so the top left, so if you've got severe acute bleeding, that'll be kind of obvious, . And you also, everything will be affected. So obviously, you're going to be hugely anaemic.
You're gonna be thromyophonic, you're gonna have reduced crossing factors, etc. There's all these things to consider. So you'd have to supplement absolutely everything.
So you want to try and get some platelets and plasma and plasma and give them pa red blood cells. Your panic torsions, we've actually seen two of these in the last month, which is bizarre. They're not very common at all.
I think I've only seen one before the last month's random to, in the 5 years that I've worked in ICU. And then DAIC, so, disseminated intravascular coagulopathy, like it, I'll get mentioned a lot. .
Those are really your main three, but you'll probably have quite a good idea that that consumption is happening. So I'm not gonna go into a huge amount of detail on that. Then you've got your.
Reduce production, I'll do that first. So essentially. You have your drugs, so chlorophenacol apparently is one that causes this, and obviously your cytotoxics, that'll be the main one that will cause, your thrombocytopenia, .
You can also have megaaryocystic hyperplasia. So that's actually a bone marrow, disease, that you diagnose just by exclusion and then see how they respond to immunosuppressives. .
And then, yeah, neoplastic causes as well. And then on destruction, so IMTP, that's the main thing that I'm gonna focus on the next slide is about IMTP as well. So it can be primary, so it's got no, no obvious, like actual cause, or it can be secondary.
So, again, neoplastic or infectious. So very similar to IMH today, again. So, IMTP, main treatment is, again, similar IMHA.
So you can give glucocorticoids, and then you'd add an omeprazole as well. And then you can give zinc that will stimulate the, platelets release from the bone marrow. You can expect to wait 2 to 7 days for a response, and you wait for the platelet count to go over 50, for discharge.
You can then reduce the glucocorticoids for 25% and taper them over 3 to 6 months. There is a fairly high rate of relapse, so sort of 10% relapse. So my pictures have got rapid exo, which obviously glucocorticoids, which we'd give that first and then we researched into Prad, and then maprazole in the top corner.
That's actually our cat blood. So we accidentally ordered in whole blood or they accidentally sent us whole blood. We'd normally only ever order impact our blood cells.
This went to a little cat called Alfie, who didn't actually have IMTP at all, but he, had a RTA and he had horrible jaw fractures and things, but that's just to show you the blood, . That we get, so we get it from somewhere in Portugal, and I can't remember the top of my head right now, . But that's just to show it.
So then thrombocytopathia, So, The main one that I care about on this page is von Willebrands, and that's the one that I'm going, going to a more, a lot more. I realise there's actually a a lot of different causes of thrombocytopathia, . So essentially, you're required, so you've got your drugs.
So that tends to be NSAIDs or colloids being given also antibiotics, pancreatitis, minor proliferative disease. So that's when the bone marrow is producing too many cells, but probably the platelets that are being produced aren't so great. Hypothermia, so you can reverse that.
So essentially, when you get to a certain temperature, your platelets just don't function as well. And that's why it's really important to Actually realise the importance of body temperature on your patients that are recovering from surgery, and try and keep them as warm as possible and get them back to being as warm as possible. And the thrombocytopathy will be completely reversed just by them getting back to the appropriate temperature.
Hepatic disease and uremia, and then you're inherited, the top two are very Unusual and I haven't ever seen them as far as I'm aware, and then Von Witerbrandts, which we have seen a few cases of. We've one of brands, so there's 3 different types, so type 1 to 3, and they're sort of. Get worse as you go along them.
So, type 1, you've got a deficiency in the total amount of vulnerable brands, but you still have some. So that's what most breeds have, including Dobermans. Number 2, you have sort of deficiency of, the big.
Molecules of, von Weddebrand's factor. So those, so they have reduced clotting. So they're worse than type one.
And then type 3, you've got absolutely no von Wennerbrand's factor at all. So that tends to be Chesapeake Bay retrievers and Scotties. You can make the diagnosis by doing a BMBT, and then you probably also want to check your Platelet count to obviously make sure it's not a thrombocytopenia that's causing the issue.
And you can also do a specific assay at a lab. But if you obviously have a dog that you want to take to surgery and it's, got a prolonged BMBT, but it's not normal platelet count, then you want, you might just want to treat the suspected von re brands rather than waiting for the lab samples to come back. So treatment for it, you can give, cryoprecipitate or fresh frozen plasma.
We prefer cryo because it's just smaller volume and it's gonna have the same effect. But if a lot of places don't keep cryo because obviously, it's only really for this and, the haemophiliacs. So if you've only got fresh plasma, that's absolutely fine.
So give that, you can also give whole blood if the patient's already been bleeding, and you need to give red blood cells at the same time, just cause the whole blood, will contain the von Brown's factor. And then you can also give DDAVP so Desmopressin acetate, which my cat's actually on, cause she's got diabetes and scis. So that will reduce your BMBT 4 hours, so it doesn't last very long.
So you might need to repeat doses. And it's only really for type one. It doesn't, it, it might have a minimal effect on type 2.
It's got absolutely no effect on type 3, because it stimulates release of, more von Wennerman's factor from the bone marrow and obviously, if you haven't got any, then you haven't got any to release, . And you want to give It 20 to 30 minutes prior to the surgery to ensure it has the maximum effect, and then repeat the BMBT at 30 to 60 minutes to see. Oh, sorry.
So in the pictures you've got a DV DDOVP as I'm sure you can see on the left, and then your right, this is the the cryo and plasma that we get from the pet blood bank. So The one on the left is our plasma, and one on the right's our cryo cryos obviously, as you can see, it's much smaller, much thinner bag. And we also get our patch of blood cells from there.
So, secondary hemostasis, I realise I should have talked about the tag in the last one, but I'll talk to you about, talk to you about it now, cause it's on the slide. So essentially, this is a tag machine in the middle. So a thromboelastograph.
So essentially, it's really good for showing. What the clot's doing. It shows sort of every phase of the, both like, how quickly the clot forms, how stable the clot is, the strength of the clots, etc.
So it tests all different things, . So, we actually mainly use it for patients that we think are hypercoagulable, because there's no really other test for hypercoagulability, whereas there are tests for hypo. But it's quite interesting to do it on your patients that are hypocoagulable as well.
So you've got different things to test. So you are, so if you look on the bottom of both of the tags, you can see that they're quite different. So, the bottom tag, you can see is hypocoagulable, because it's got, it's formed a very thin sausage.
That's what we call it. Whereas the top one's a bit wider. And looks a bit more like what you'd expect a normal tag to look at, look like, although I think some of its things are still out of range.
Maybe it's a bit too wide. So you've got an hour, it's your reaction time. Which tests your intrinsic pathway, then it's like you've got your K, which is the speed of your crop formation, which is an indicator of your factor 8, thrombin, fibrine, your platelets and your hematocritte.
And then you've got Your angle that also is another indicator of your speed of clot, and then your MA, which is your platelets, fibrinogen and hematocrit as well. . So it just really shows sort of like.
And in vivo. Sign of what your clot will. What your clock will actually be like, it's quite interesting, we've taken on a new machine now which This machine is a bit, the one that we, on the picture here, is a bit complicated and quite difficult to run, and it doesn't really like me and seems to just run them wrong all the time.
Whereas we've taken on a new machine that runs them much quicker and we can just use whole blood. Whereas this one, we need, saturated blood. And so we need to take a bit more.
I forgot to actually go through all the different causes second hemostasis. So second hemostasis, you get your, you've got your identified. And so we see a few cases of that.
Andrew Stronglu, which have so we're not seeing as many cases of this. I don't know if they're going to first opinion and not doing very well, or if maybe. People are more clued up that long worm, and actually they are preventing it, which I hope is the reason.
Hepatic disease, haemophilia, I've had a couple of those cases, they're not very common at all. Dilutional coagulopathy, DIC and I put sort of a little bit about slight hands and that sort of weird coagulopathy in there. So denticide, essentially.
You've got, in this picture here, you've got Warfarin, there's obviously different types of written side and I know there's all different levels of it, . And the newer ones are a bit harder to treat and need longer doses of vitamin K. But I thought it was interesting, sort of the process of where rodenticide stops.
The process for vitamin K dependent factors. It's sort of the recycling, so if you can see, so on the left you've got your VIK one, which then gets converted to quinol, so quinone to quinol, . And then it goes down, and that's when your factors 279, and 10 will go from inactive to active.
And then you form your epoxide, and then you basically like, Return the cycle. And where I put the big cross sign, is where the reddenticide has its effect. So essentially, it's just not theIK is not getting recycled.
So that's why giving them VIK works. It's it's kind of obvious, but equally, it's something I didn't act, wasn't aware of actually the process. So the first factor that really gets affected is factor 7.
So that's sort of, it's got a half-life of only 4 to 6 hours. So that's why your PT is really useful for that, because that will become prolonged first of the two. And you normally get signs 2 to 5 days after consumption.
Some owners might be aware that the animals just eaten their identified, and then you obviously go to actually decontamination. So you want to use, Upomorphine and activated charcoal, to try and reduce the absorption. But the majority of them, I think, probably aren't aware of the dog's eating it.
And sometimes their dog will have eaten it over quite a long period of time, if it's just written inside that's been left out on a farm and it's Jack Russell or Labrador. It's just takes a nibble every day. So you're treating.
Is that OK, as we all know, so you give that subcut, and then you want to treat the actual coagulopathy with plasma. You might need to also add in whole blood, and packed red blood cells, depending on how much they bled. So if they've bled to the point where actually they're thrombocytopenic, And also, you want to give them the plasma anyway, then you want to probably give them whole blood.
Otherwise, you can get the pack red blood cells and plasma. It's really what you've got available. There's no sort of right or wrong.
So it, you want to give, subcut, and then you want to continue it orally after 24 hours, and then continue that for a whole 3 to 4 weeks. It's quite a long treatment, and then recheck the PT, after 48 to 72 hours after starting the treatment, prior to discharge. What is written side.
Yes, we've had lovely Labrador with it quite recently. So he came in and he had . A hemothorax, actually.
And he ended up having 2 units of plasma and, I think 1 unit of parod blood cells over the course of the day. And they, touch wood, I haven't had one do see one that's gone really badly. They are very treatable.
Haemophilia A and B, so I've seen. 12 cases of this. So A is factor 8, so that's more common.
And the main test for this is a prolonged APTT. B is number 9, it's Christmas disease. I don't know why.
So this you can treat with cryoprecipitates, and you can also give them tranexamic acid. Tronic examic acid wasn't, Present the last time I actually treated one of these, which shows how often I see them. Apastic failure, so coagulation and abnormalities happen in 50 to 7% of plastic failure cases.
It's not really a surprise, your liver is responsible for producing all your crossing factors. So your deficiencies can vary loads and you can get obviously variable, . Things from your PT or your APTT.
So you want to really go by other signs rather than just jump into the factpatic failure. So if they've got any signs of GI bleeding, and then obviously look at your liver enzymes and your biochemistry. I've sort of added Xylitol in there just to be aware of toxic potential causes for hepatic failure, but you will obviously, if the patient's ingested Xylitol, you're likely to get the hypoglycemia signs, and then you'll get the hepatic failure.
So it's unlikely that you'll just get them come in with hepatic failure. Andrew Stronglus, so that was really interesting to actually learn about the life cycle. I'm sure all of you guys know about the life cycle much better than I do.
But, so essentially, it starts off in your. I'll start it at the slug. It starts off in a slug, where it turns from an L1 to an L3 larvae.
I don't know, it has so many stages. And then it goes, it gets eaten by a fox. And it penetrates into the right heart and pulmonary arteries, .
Essentially the larvae, this is, and then it produces over, which is then turned into L1 larvae, which then moves to alveoli. And then it coughs, coughs the larvae out, and then re-swallows them, and then defecates them, and then it goes back into the slug. Amazing.
But anyway, so essentially, no one really knows why ang caused this horrible coagulopathy. We think it's sort of a chronic low grade DIC that occurs. They present all all different signs.
They can be thrombocytopenic. They can have acquired from other brands, and they have a prolonged, PT and APTT. So it can be quite unclear what's wrong with them.
So the main test you need to do for this is, the Angiosynap test, the IDEX angiotect test, and also do a faecal smear as well to look for the larvae themselves. Treatment is, advocate, or you can give famundazole over sort of, I think it's a week, course. And then you just want to treat the signs.
So if they, They might potentially need plasma, they might potentially need, patch of blood cells. They quite often are dysic from the, worm burden in their lungs, so they quite often need quite vigorous oxygen therapy. We haven't, like I said before, we haven't really actually seen a case of this for a while.
So I'm hoping people are just preventing it more. I'm hoping it's not that they're going to first opinion, and we're just never getting the referrals, but I will, won't ever know. .
But yeah, we're still not 100% sure what. The system is for why it causes the coagulopathy. Dilutional coagulopathy, isn't actually something I've seen very much at all.
So you actually have to have quite significant hemo deletion of 40 to 60%. So it's quite a lot of fluid that you'd have to give. It's definitely much worse if colloids to use, so, hydroxyetyl starch, because the colloids stay in the vascular space.
So, with crystalloids, they move out of the vascular vascular space, so you're not gonna actually dilute your, clotting factors. Normally, actually, your platelets aren't affected. So, it's normally a PT and APTT that will be prolonged.
And in, after two blood transfusions. It's quite uncommon that we actually give two blood transfusions side by side, but in people, that's much more common. So they quite often have issues actually with dilution or coagulopathy, .
And yeah, the treatment is as you would with most coagulopathy, give them plasma. So this is the sort of system that occurs. So you have your loss of blood, you have reducing intravascular volume, then your interstitial fluid moves into the plasma.
So actually you've already got a Dilution that's occurred and then you further dilute it with your IV fluid resuscitation, so your crystalloids, aren't so bad, but your colloids and your patro blood cells will have a, have a significant effect, . And then you get depleted fibrinogen, so you get reduced speed, strength and ability of your clot, and then it's sort of a vicious circle because you're getting, you've got less clotting factors to make your clot, . So, yeah, it's something I've not really ever seen it, but possibly actually without some of our patients that have been in theatre and things this has occurred.
DIC, I found it really difficult to actually put this into a little picture, cause it's quite a complicated disease, so. Essentially with DIC you need some. Horrible insults.
So sepsis, heat stroke, SARS, or neoplasia. We, there's a couple of our neoplastic cases actually are weird. So, they have DIC, but they have sort of like, almost a chronic DIC, quite similar to angio.
So most animals with DIC are actively dying. They look awful. Whereas we've had a couple of cases of neoplastic DIC where they actually, they've been like, up and about.
And obviously, they haven't been great. But they haven't been so affected by it, but most of the time the cases we see with DIC are sepsis, and they are very end stage and it's very difficult to get on top of it, so. With sepsis, it's really important to treat everything before it gets to this point.
So essentially what occurs, you have activation of all of your different coagulation pathways, your extrinsic and your intrinsic through different methods, and you also have activation of recoagulation factors. Then you become pro to thrombotic, so you form all these microthrombi in all of your organs, so your liver, kidneys, etc. And then do fibrinolysis of these clots, so they do break down.
However, they do cause, ischemic injuries to these organs. The by making the microthrombo and continuously breaking them down, you're also using up all your platelets and coagulation factors. So then you have poor hemostasis and you just bleed everywhere, .
And Then essentially you're bleeding because you've consumed. All of those things, essentially, and then you go into multi-organ dysfunction because you've got a double whammy now, you've got basically the microst, of course, ischemic injury, so there's been lack of fusion to these organs, but also you've got lack of fusion through, Hypervolemia, . And That then you go into multi-organs dysfunction, essentially.
It can be made worse by acidosis and hypoxia. So it's important to be aware of this in the cases if you're looking at your blood gases and treating any acidosis you can, and also leads to vascularstosis. It's just a horrible, horrible thing, and The cases that get it that have sepsis, none, I haven't seen any that we've managed to make do well.
And the same with heat stroke. It's only really a neoplastic ones, but we haven't really been treating the DIC. They've sort of had a chronic version themselves, and it's, then neoplasia has got to an end point as well.
So I've sort of put this in here. This is Viha Triad, . Of What's it called?
Hypercoagulable, clot formation, essentially. Why, why can't I think of the word? Thromboembolism?
There you go. So you have hypercoagulability, vascular damage, and stasis. So like I was saying with our IMHAs, I guess they don't have vascular damage, but they have our stasis, hypercoagulability, plastic foot and IV and plastic foot part of cells.
So it's just to make you aware of, like, what makes this prothrombotic state happen, So your diagnosis for DAC, it's quite quite difficult to diagnose. You've diagnosed it basically based on the signs, but D dimers, are your main things, but they're not very specific. And then you can also do your TEG.
So you should, so if you get it at the start of DIC, you should be getting hypercoagulable. If you get it towards the end of DIC, then you'll get it hypercoagulable, but it'll be in incredibly hypercoagulable. So you treat them, fluid therapy, Ideally you want to essentially remove the activated cutting and fibrinolytic factors, .
Cos otherwise you're gonna, the process is just gonna continue on, it's very hard to get them out of it, so you almost want to just remove their blood and give them whole new blood. That's not really achievable, maybe it is in people. But you want to maintain adequate tissue profusion, .
And correct any acid-base balances and electrolyte imbalances, the oxygen supplementation, and then plasma and, fresh whole blood, if necessary, and antithrombotic meds, if they're in the hypercoagulable phase. So things like fidogram, riveroxaban. But like I said, it's really, really hard to get on top of.
So I thought I'd add a little bit about sighthounds. So we've had a couple of sighthounds that are bleed quite badly, post-op, and we now give tronicsamic acid to, all the sort of greyhounds and lurches, during surgeries and post. So greyhounds essentially have a much higher post-op bleeding rates.
So their bleeding rates are 26%, after a spa or castrate. In normal other breeds of dogs, not normal breeds of dogs, they're sort of 0 to 2%. So, quite Quite a lot lower.
So it normally happens 36, 72 hours after surgery trauma. That's not really what we've found. We do find they bruise quite before we used tryingicamic acid, we did find they bruised quite badly, .
But actually, we're finding the bleeding sort of during the surgery and immediately post, if they don't, receive cymic acid. They'll actually perform normally in the coagulation test. So if you do your PT or APTT, they've got normal platelets, etc.
They do have the macro platelets, so, like I said. And then, what they, all they found is that they actually have lower antiplasma and antithrombin. So, essentially, they, Have increased fibrinolysis.
They're just breaking down their clots sooner than they really should. And that's why it's sort of a delayed bleeding that occurs. So we treat with tranexamic acid.
So you give it 10 mg 3 times a day prior during and post-surgery. It's a drug, you so, I don't know if any of you have given tranexamic acid, but basically, you just need to dilute it, And give it over half an hour because it's quite potent emetic, so if you give it as a bolus, then it'll make them sick.
