TEG Interpretation Lecture

Good morning, my name is Jim Bradley. I'm a consultant anaesthetist here at NUH. I'm here to talk to you today about TEG interpretation. I've previously given this talk as a small groups workshop based thing, but that's increasingly difficult in a COVID environment. So this is intended to replace that. I usually give this to all of the trainees as they rotate through NUH, so in February and in August, and sometimes the haematologists rotate through so they get subjected to it as well. This year COVID's restricted that, so this is an opportunity to deliver that. In addition, we are shortly, hopefully, going to be expanding and using TAG in some other clinical areas. intensive care and obstetrics specifically and also this will be at both sites. So City Hospital hasn't had any Teg outside of cardiac before now and so now there's a new group of people who will need to have this kind of education. So I hope it's useful to you. We have a new Teg algorithm. Previously there was a trauma algorithm and a non-trauma algorithm and the trauma algorithm used to focus on the rapid Teg results. and the non-trauma on the standard Teg results. Well it's clear that both curves are useful for both scenarios and so this unifying algorithm is an attempt to consolidate those, crystallize it, and this be the final form. Now cardiac has its own arrangements and they use their own algorithms and that's absolutely fine. This is for everything else. The only caveat to that is that in obstetrics we're currently doing some research where we will establish the normal ranges for obstetric population. So there may be some minor tweaks, but that's in the future. For now, we use this algorithm for all of our bleeding patients. I'm going to focus on a trauma case and I'm going to use that as a focus, look at the curves that were generated by that patient and use those curves to showcase the algorithm. basically educating on how to interpret those curves. There are some limitations to the technology and I'll have to mention that too and I'll do that at the end. So this is our lady, she's a 31 year old lady who was an unrestrained rear seat passenger in a vehicle traveling about 70 miles an hour when they were hit by a truck or hit a truck, the specifics I can't remember, but they had a high speed RTC and were very sick. She was sick enough to have a cardiac arrest but got a return of circulation on scene when they did needle thoracocentesis and they'd given some blood. Queen's was pre-alerted and so a red trauma call was put out and the team were poised and waiting in Rhesus. And they were poised and waiting because the major haemorrhage had also been activated with trauma pack 1. So as soon as she arrived, trauma pack 1 was started. She ended up going to the CT scanner. and from there to theatre, but her teg when she came in looked like this. So for people who are not used to interpreting the teg curves, there's a lot of information. So I'm going to break this down into a more simpler format. There's basically four graphs or four curves superimposed on one graph in the top half, and then on the bottom half of the screen there's a graph. a table which becomes populated with results as they're known. So it starts off blank and it becomes populated as results are known. And the tech machine knows what our algorithm is and puts helpful red boxes when anything goes outside of the normal ranges. Now there are a few items on here which we don't need anymore. They're largely outdated. They have utility but they're not included in our algorithm. So I'm going to cover those up. This is something else which is mostly for future iterations of the algorithm. This may be of import in the future, but for now, I'm going to cover that up too. So we've got four curves. And as you'll see, all of these named curves start with a C. So we've got citrated kaolin, citrated rapid tag, citrated kaolin with heparinase and citrated functional fibrinogen. Now, the key thing there is that they're all citrated. So I don't mean to teach you to suck eggs, but on a citrate tube there is a collared line, an etched line in the tube, and the correct way to fill the tube is if the blood eventually comes to a rest as meniscus. between these two lines, so it's between the etched line and the collared cap. If it's between those lines the concentration of citrate will be correct for the machine and if you were to send a citrate tube like this to the lab and it didn't fall in that between those two lines, they would reject it. Now to a degree we have to self-regulate. This is a point of care test so it's important that you fill this tube correctly. What then happens? is you hand the tube to your assistant who may be an ODP or maybe an intensive care nurse and they will then take the sample, add it to a cartridge and then stick the cartridge in the machine. The machine will then spit out tech results which we can view on a tech manager program which is a browser-based system and can be viewed anywhere in the trust. The cartridges have four chambers you and the four chambers have got four different sets of reagents added into them which generate the curves. The top line was CK, which stands for citrated kaolin curve, and this is the standard Teg curve that you've been used to seeing beforehand. We're fortunate that the new version of the technology has these cartridges, so we can have all of the other reagents and all the other tests in real time as well. but previous iterations only had one chamber and you only got one curve and that's this one. If you can imagine the curves, if you imagine the older versions of technology used to consist of a cup in which your sample was put and a pin was suspended in the cup and in the liquid sample. The cup would move and because the clotting cascade hasn't happened yet, fibrin strands haven't yet formed. and so there'll be no displacement of the pin when the cut moves. As clotting factors cause fibrinogen to be converted into fibrin, those fibrin strands grip the pin and you see a deflection of the curve. So when we look at our teg trace, what we see is a flat line initially because this is liquid blood in which fibrinogen is present but there isn't enough fibrin yet to make the make that pin turn. At this point fibrin formation has begun to happen so depending on so the this is called the R time or reaction time and that's a clotting time, a clotting factor dependent process. If you have sufficient clotting factors then all of this will occur and fibrin strands will start to form in less than 9.1 minutes. So 9.1 minutes is the normal range for the curve. If you're deficient in clotting factors, this curve will be much much much much longer and this R time will be 10 minutes or greater. If your R time is greater than 9.1 minutes then you have insufficient clotting factors and the treatment for that is FFP. So we would give FFP in 15 mls per kilo. Once the R time has been populated in the table there, the curve will continue to run because the clot will proliferate and get stronger and stronger and stronger. Eventually, it will reach a plateau phase where the curve can't get any stronger. And so it will be at what we call its max amplitude. And it will be then populated in the table as a max amplitude. This is our trauma patient. And we can see our trauma patient had normal amount of clotting factors. They were receiving FFP and blood in a one to one ratio, but they were normal at the time the take was taken. And the max amplitude was low. So 52 is the threshold for max amplitude. And if the max amplitude, so the maximum clot strength is less than 52 millimetres on this graph, then there's a problem with clot strength. The graph will then continue to evolve and will continue to run and it will most likely, as in this patient, be a flat line because the clot strength will be the same because there's no significant fibrinolysis. The next thing we need to look at is the overall clot strength, which is called the CKMA. This is a situated K-Lin curve, which is the CK, and the MA is the max amplitude, which is the clot strength. We've already said that the... Clot initiation is a clotting factor dependent process so this R time is dependent on the concentration of clotting factors. The overall clot strength is dependent upon the fibrinogen concentration and the platelet function. The max amplitude of the CK curve, the limit that we say is a normal clot strength is 52 millimetres. So if the clot strength is less than 52 millimetres, we know that the clot strength is impaired. The clot strength is determined by the fibrinogen concentration and the platelet function. So the next thing we want to do is look at the fibrinogen concentration. We have this curve CFF which stands for citrated functional fibrinogen and this curve is our fibrinogen monitor. The number for our patients which represents a normal fibrinogen is over 17 millimetres. This curve is actually the reagents in the cup that make this curve. are the standard CK reagents but with added ReaPro which inactivate the platelets. So what you see is the fibrinogen participation in that max amplitude by itself and the CFFMA needs to be greater than 17 and if it's not we would give cryo. This is our trauma patient and we see that it was 7.5 which is way less than 17 so they did get some cryoprecipitate. Having established that the clot strength is low, we discovered on the previous curve the max amplitude was 47.6. So the clot strength is low and the fibrinogen is low, so we gave some fibrinogen. Later on, we've realised, we've done a tag after that treatment episode and this is now at 10 to 4 in the morning. Later on, the patient not having had any platelets, we found that the max amplitude has dropped. It's now below 47. Our threshold for giving platelets in our TEG algorithm is 47 millimetres. So if the clot strength is deteriorated to the point, the max amplitude is deteriorated to the point that it's less than 47, then we will give platelets. I want to look again at this platelets and cryo bit because it's just worth a bit of expanding on that. If the overall clot strength is less than 52, then that's too poor and represents coagulopathy. We will then look at what the fibrinogen number is. And if the CFFMA is over 17, we know that the fibrinogen concentration is OK. So if the clot strength is poor, but the fibrinogen concentration is OK, then we know we need to give platelets. If the clot strength has deteriorated to 47 or less, so if the CKMA is 47 or less, then that's too poor and we will give platelets to that as well. The final part of this CK curve is the LY30 and this is our marker of fibrinolysis. As I said previously, the max amplitude will be plotted on the curve at the point when the clot is getting no stronger. but the curve will continue to run for a further 30 minutes. What it will then do is it will compare the two, so it will compare the max amplitude scores at the point it was achieved and 30 minutes later. And if it's there's a significant difference this will be expressed as a percentage. Now it's highly unusual for there to be any difference in this number, it's usually 0.0. and the reason for that I think is because they get tranexamic acid either on the ambulance or as soon as they arrive in ED. However, if that LY30 number is greater than three percent that is significant and you would give additional tranexamic acid. So I've explained about the CK test because that's the most basic of the tests and it allows a more easy explanation. However, For both, however, we will spend most of our time looking at the citrated rapid tag curve. The CRT curve, citrated rapid tag, is the curve in purple. And as you can see, it practically overlaps the CK curve, but it's sucked to the left. What this curve is, is it's the same reagents, but with added tissue factor. That tissue factor being added into the mix causes everything to be activated much more quickly, which is important for a point of care test because it means that we get our results more quickly. So because of that addition of tissue factor, the R time is no use. OK, so on the CRT, we can't use the R time. We can use the R time from the CK curve because it's all the same sample. It's perfectly acceptable to use that CKR time as our trigger for do we need any FFP or not but We can't look at that R-time on the CRT because it's been shown in research to not be useful. However, we do have this TEG-ACT. TEG-ACT is an activated clotting time style test. This is a proprietary algorithm which takes elements of all of the other parts of the curve and converts it into a general marker of coagulopathy. and it measures it in seconds. The normal range is up to 120 seconds. The first test which will come back on your TEG curve is your TEG-ACT and if there's a red box around it and it's greater than 120 seconds then that means that there is some kind of coagulopathy going on. We used to use this as the marker for giving FFP but we don't do that anymore so please don't do that. However, in the context of a bleeding trauma patient who is a high shock index, we will use the fact that we know they're coagulopathic to activate the major haemorrhage and to commence giving blood and FFP as resuscitation in a one-to-one ratio. It's not a specific FFP monitor, but the response will be to give blood and FFP in a one-to-one ratio. that is of course only for patients coagulopathic. The CRTMA value is usually very similar to the CKMA value so we can use those two synonymously and because the CRTMA comes back more quickly round about 20 minutes rather than round about 35 to 40 minutes that is the one that we most usually use. The final test that we've not looked at already is the CKH. You can see CKH here is the final test. This is the same as the CK, the Kaolin-Tec test, but with added heparinase. Most of our trauma patients that come in aren't on heparin, so we don't usually need to look at the CKH in the trauma scenario. We don't put much emphasis on it. What the addition of heparin does to any sample is it inactivates the clotting cascade and prevents the fibrin being converted into fibrin. So what you tend to see on a TAG trace, this is a patient to whom I've given heparin in order that the surgeons can fix their aortic aneurysm. And what you see is a prolonged R time. The addition of the heparin has made this CK TAG curve. Much more that initial R time, the initial clot initiation is very prolonged. But our CKH has got heparinase in it, which cleaves that heparin and renders it inactive. So what you therefore see is a more normal R time. So if there's a big difference between the green and the red curves, if the R times are greater than two minutes difference, then we say that's because there is excess heparin in the sample. And that will, in a bleeding coagulopathic patient, prompt giving protamine to reverse that. I've taken the other two curves away and that just shows there's an obvious difference between those two. So heparin is present. We'd give protamine. On our trauma patient, this is the initial tag again, we see that these curves practically overlap. They practically overlap because there's no heparin in the sample, so there's very little effect of heparinase. Now you do sometimes get some endogenous heparin, so the things which can produce that are severe sepsis or severe trauma-induced coagulopathy. there may be a very very mild heparin-like effect. Most usually we'll do nothing about that but if the patient's extremis and you've tried everything else and the surgeons say that they're struggling it may be worthwhile considering a small dose of protamine. As we see after one patient no heparin effect. We're now on to the other considerations and limitations of the tests. So temperature in the machine all of the samples samples are heated to 37 degrees. 37 degrees is the operating temperature of the machine. So the TEC results that you see are the TEC results that you would get if your patient was at 37 degrees. Your patient when they come in off the street, when they've been scooped up by the ambulance crew, is most likely 34 degrees. So if you have the instance that you've got a patient with normal TEC results but very cold, and very runny blood that the surgeons are struggling with, the answer may be to warm the patient. There's a risk if you try and give extra clotting factors when the TEG is normal, that when the patient returns to their normal temperature they will be pro-thrombotic, which they won't thank you for when they get a PE later on in their treatment. So if they're normal, if the TEG parameters are normal, but your patient is hypothermic, warm the patient. you can believe what the TEG results tell you and you don't need to give any more clotting factors. Several drugs do not show up in the TEG curves which is a frustration and they're drugs which are commonly taken by our population. So clopidogrel, warfarin, all of these in this slide, all of the DOACs, basically any antiplatelet agents, they won't show up in the curves. So you may end up with a normal patient and again the same scenario that you've got a patient who won't clot but all the tag is normal. In this instance you might want to go back and get a further drug history and see if the patients are on any of these drugs and if necessary then ask the haematologist for help. I've put here time context. The other thing to bear in mind is that there's both a time context and a clinical context. What I mean by that is if you've got a Teg trace which is abnormal but your patient's stabilised and they don't need any further treatment and they're okay, you probably won't need to treat the results. If by contrast you've got a patient who's in theatre and is actively bleeding, then you very much would treat those Teg results. So it's just to bear that in mind. The other thing to bear in mind is that like any lab test results, the results only show you what was happening as the test was being drawn from the patient. It doesn't reflect an ongoing involving clinical situation. So it may be that your clinical experience sort of overrides the TEC results. What I mean by that is if the tap has not been turned off and the patient is still bleeding excessively, you may still feel it appropriate to give your major haemorrhage packs even though the tag shows you that the treatment you had already given has given you or produced a normal tag. Not giving that treatment may well have shown you an abnormal tag and it's just that to bear in mind. There's the treatment algorithm again and this algorithm is also present on the website, so when I say that on the anaesthesia home pages. The threshold for coagulopathy is an ACT of 120 seconds. If the R time is greater than 9.1, we're going to give more FFP. If the CKMA is less than 52, we know we've got a clot strength problem and so we will look at the CFFMA and that's the fibrinogen monitor. If the fibrinogen monitor shows that low fibrinogen was the cause of that low clot strength, then we'll treat it with giving cryo. If the fibrinogen results are normal but with poor clot strength, we'll give platelets. If the clot strength is so poor that it's less than 47, then we'll give platelets anyway. And finally, if you see fibrinolysis, you're going to treat with tranexamic acid. This is just an illustration of whereabouts you can find all of those on the results. and this PowerPoint presentation is going to be present on the anaesthesia homepage for you to refer to slow time if you prefer to do so. This is the URL for Tech Manager. Because it's a browser based system you can see these curves on any of the Trust browser systems. So any Trust iPhone, any Trust iPad, any desktop computer. That means that as the third encore with your phone you can pull up the browser in Safari and if you're the haematology registrar at home you can put the results on your Trust laptop and we can all be on the same page. Thank you for your attention. I know that the recording process made some of this maybe a little bit garbled so please send any feedback or anything which you didn't quite understand to me and my email address is there. As I've said the other information will be on the anaesthesia home page and Rob's going to put this the Trust YouTube channel and on the Anesthesia YouTube channel for further education. Thanks for your attention and I look forward to your questions.

Good morning, my name is Jim Bradley. I'm a consultant anaesthetist here at NUH. I'm here to talk to you today about TEG interpretation.

I've previously given this talk as a small groups workshop based thing, but that's increasingly difficult in a COVID environment. So this is intended to replace that. I usually give this to all of the trainees as they rotate through NUH, so in February and in August, and sometimes the haematologists rotate through so they get subjected to it as well.

This year COVID's restricted that, so this is an opportunity to deliver that. In addition, we are shortly, hopefully, going to be expanding and using TAG in some other clinical areas. intensive care and obstetrics specifically and also this will be at both sites. So City Hospital hasn't had any Teg outside of cardiac before now and so now there's a new group of people who will need to have this kind of education. So I hope it's useful to you.

We have a new Teg algorithm. Previously there was a trauma algorithm and a non-trauma algorithm and the trauma algorithm used to focus on the rapid Teg results. and the non-trauma on the standard Teg results.

Well it's clear that both curves are useful for both scenarios and so this unifying algorithm is an attempt to consolidate those, crystallize it, and this be the final form. Now cardiac has its own arrangements and they use their own algorithms and that's absolutely fine. This is for everything else. The only caveat to that is that in obstetrics we're currently doing some research where we will establish the normal ranges for obstetric population. So there may be some minor tweaks, but that's in the future.

For now, we use this algorithm for all of our bleeding patients. I'm going to focus on a trauma case and I'm going to use that as a focus, look at the curves that were generated by that patient and use those curves to showcase the algorithm. basically educating on how to interpret those curves. There are some limitations to the technology and I'll have to mention that too and I'll do that at the end. So this is our lady, she's a 31 year old lady who was an unrestrained rear seat passenger in a vehicle traveling about 70 miles an hour when they were hit by a truck or hit a truck, the specifics I can't remember, but they had a high speed RTC and were very sick.

She was sick enough to have a cardiac arrest but got a return of circulation on scene when they did needle thoracocentesis and they'd given some blood. Queen's was pre-alerted and so a red trauma call was put out and the team were poised and waiting in Rhesus. And they were poised and waiting because the major haemorrhage had also been activated with trauma pack 1. So as soon as she arrived, trauma pack 1 was started.

She ended up going to the CT scanner. and from there to theatre, but her teg when she came in looked like this. So for people who are not used to interpreting the teg curves, there's a lot of information. So I'm going to break this down into a more simpler format. There's basically four graphs or four curves superimposed on one graph in the top half, and then on the bottom half of the screen there's a graph.

a table which becomes populated with results as they're known. So it starts off blank and it becomes populated as results are known. And the tech machine knows what our algorithm is and puts helpful red boxes when anything goes outside of the normal ranges.

Now there are a few items on here which we don't need anymore. They're largely outdated. They have utility but they're not included in our algorithm. So I'm going to cover those up.

This is something else which is mostly for future iterations of the algorithm. This may be of import in the future, but for now, I'm going to cover that up too. So we've got four curves.

And as you'll see, all of these named curves start with a C. So we've got citrated kaolin, citrated rapid tag, citrated kaolin with heparinase and citrated functional fibrinogen. Now, the key thing there is that they're all citrated.

So I don't mean to teach you to suck eggs, but on a citrate tube there is a collared line, an etched line in the tube, and the correct way to fill the tube is if the blood eventually comes to a rest as meniscus. between these two lines, so it's between the etched line and the collared cap. If it's between those lines the concentration of citrate will be correct for the machine and if you were to send a citrate tube like this to the lab and it didn't fall in that between those two lines, they would reject it.

Now to a degree we have to self-regulate. This is a point of care test so it's important that you fill this tube correctly. What then happens?

is you hand the tube to your assistant who may be an ODP or maybe an intensive care nurse and they will then take the sample, add it to a cartridge and then stick the cartridge in the machine. The machine will then spit out tech results which we can view on a tech manager program which is a browser-based system and can be viewed anywhere in the trust. The cartridges have four chambers you and the four chambers have got four different sets of reagents added into them which generate the curves. The top line was CK, which stands for citrated kaolin curve, and this is the standard Teg curve that you've been used to seeing beforehand.

We're fortunate that the new version of the technology has these cartridges, so we can have all of the other reagents and all the other tests in real time as well. but previous iterations only had one chamber and you only got one curve and that's this one. If you can imagine the curves, if you imagine the older versions of technology used to consist of a cup in which your sample was put and a pin was suspended in the cup and in the liquid sample.

The cup would move and because the clotting cascade hasn't happened yet, fibrin strands haven't yet formed. and so there'll be no displacement of the pin when the cut moves. As clotting factors cause fibrinogen to be converted into fibrin, those fibrin strands grip the pin and you see a deflection of the curve.

So when we look at our teg trace, what we see is a flat line initially because this is liquid blood in which fibrinogen is present but there isn't enough fibrin yet to make the make that pin turn. At this point fibrin formation has begun to happen so depending on so the this is called the R time or reaction time and that's a clotting time, a clotting factor dependent process. If you have sufficient clotting factors then all of this will occur and fibrin strands will start to form in less than 9.1 minutes. So 9.1 minutes is the normal range for the curve.

If you're deficient in clotting factors, this curve will be much much much much longer and this R time will be 10 minutes or greater. If your R time is greater than 9.1 minutes then you have insufficient clotting factors and the treatment for that is FFP. So we would give FFP in 15 mls per kilo. Once the R time has been populated in the table there, the curve will continue to run because the clot will proliferate and get stronger and stronger and stronger.

Eventually, it will reach a plateau phase where the curve can't get any stronger. And so it will be at what we call its max amplitude. And it will be then populated in the table as a max amplitude.

This is our trauma patient. And we can see our trauma patient had normal amount of clotting factors. They were receiving FFP and blood in a one to one ratio, but they were normal at the time the take was taken.

And the max amplitude was low. So 52 is the threshold for max amplitude. And if the max amplitude, so the maximum clot strength is less than 52 millimetres on this graph, then there's a problem with clot strength. The graph will then continue to evolve and will continue to run and it will most likely, as in this patient, be a flat line because the clot strength will be the same because there's no significant fibrinolysis.

The next thing we need to look at is the overall clot strength, which is called the CKMA. This is a situated K-Lin curve, which is the CK, and the MA is the max amplitude, which is the clot strength. We've already said that the... Clot initiation is a clotting factor dependent process so this R time is dependent on the concentration of clotting factors. The overall clot strength is dependent upon the fibrinogen concentration and the platelet function.

The max amplitude of the CK curve, the limit that we say is a normal clot strength is 52 millimetres. So if the clot strength is less than 52 millimetres, we know that the clot strength is impaired. The clot strength is determined by the fibrinogen concentration and the platelet function. So the next thing we want to do is look at the fibrinogen concentration.

We have this curve CFF which stands for citrated functional fibrinogen and this curve is our fibrinogen monitor. The number for our patients which represents a normal fibrinogen is over 17 millimetres. This curve is actually the reagents in the cup that make this curve.

are the standard CK reagents but with added ReaPro which inactivate the platelets. So what you see is the fibrinogen participation in that max amplitude by itself and the CFFMA needs to be greater than 17 and if it's not we would give cryo. This is our trauma patient and we see that it was 7.5 which is way less than 17 so they did get some cryoprecipitate.

Having established that the clot strength is low, we discovered on the previous curve the max amplitude was 47.6. So the clot strength is low and the fibrinogen is low, so we gave some fibrinogen. Later on, we've realised, we've done a tag after that treatment episode and this is now at 10 to 4 in the morning.

Later on, the patient not having had any platelets, we found that the max amplitude has dropped. It's now below 47. Our threshold for giving platelets in our TEG algorithm is 47 millimetres. So if the clot strength is deteriorated to the point, the max amplitude is deteriorated to the point that it's less than 47, then we will give platelets. I want to look again at this platelets and cryo bit because it's just worth a bit of expanding on that. If the overall clot strength is less than 52, then that's too poor and represents coagulopathy.

We will then look at what the fibrinogen number is. And if the CFFMA is over 17, we know that the fibrinogen concentration is OK. So if the clot strength is poor, but the fibrinogen concentration is OK, then we know we need to give platelets. If the clot strength has deteriorated to 47 or less, so if the CKMA is 47 or less, then that's too poor and we will give platelets to that as well. The final part of this CK curve is the LY30 and this is our marker of fibrinolysis.

As I said previously, the max amplitude will be plotted on the curve at the point when the clot is getting no stronger. but the curve will continue to run for a further 30 minutes. What it will then do is it will compare the two, so it will compare the max amplitude scores at the point it was achieved and 30 minutes later.

And if it's there's a significant difference this will be expressed as a percentage. Now it's highly unusual for there to be any difference in this number, it's usually 0.0. and the reason for that I think is because they get tranexamic acid either on the ambulance or as soon as they arrive in ED.

However, if that LY30 number is greater than three percent that is significant and you would give additional tranexamic acid. So I've explained about the CK test because that's the most basic of the tests and it allows a more easy explanation. However, For both, however, we will spend most of our time looking at the citrated rapid tag curve.

The CRT curve, citrated rapid tag, is the curve in purple. And as you can see, it practically overlaps the CK curve, but it's sucked to the left. What this curve is, is it's the same reagents, but with added tissue factor. That tissue factor being added into the mix causes everything to be activated much more quickly, which is important for a point of care test because it means that we get our results more quickly. So because of that addition of tissue factor, the R time is no use.

OK, so on the CRT, we can't use the R time. We can use the R time from the CK curve because it's all the same sample. It's perfectly acceptable to use that CKR time as our trigger for do we need any FFP or not but We can't look at that R-time on the CRT because it's been shown in research to not be useful. However, we do have this TEG-ACT.

TEG-ACT is an activated clotting time style test. This is a proprietary algorithm which takes elements of all of the other parts of the curve and converts it into a general marker of coagulopathy. and it measures it in seconds.

The normal range is up to 120 seconds. The first test which will come back on your TEG curve is your TEG-ACT and if there's a red box around it and it's greater than 120 seconds then that means that there is some kind of coagulopathy going on. We used to use this as the marker for giving FFP but we don't do that anymore so please don't do that.

However, in the context of a bleeding trauma patient who is a high shock index, we will use the fact that we know they're coagulopathic to activate the major haemorrhage and to commence giving blood and FFP as resuscitation in a one-to-one ratio. It's not a specific FFP monitor, but the response will be to give blood and FFP in a one-to-one ratio. that is of course only for patients coagulopathic.

The CRTMA value is usually very similar to the CKMA value so we can use those two synonymously and because the CRTMA comes back more quickly round about 20 minutes rather than round about 35 to 40 minutes that is the one that we most usually use. The final test that we've not looked at already is the CKH. You can see CKH here is the final test.

This is the same as the CK, the Kaolin-Tec test, but with added heparinase. Most of our trauma patients that come in aren't on heparin, so we don't usually need to look at the CKH in the trauma scenario. We don't put much emphasis on it. What the addition of heparin does to any sample is it inactivates the clotting cascade and prevents the fibrin being converted into fibrin. So what you tend to see on a TAG trace, this is a patient to whom I've given heparin in order that the surgeons can fix their aortic aneurysm.

And what you see is a prolonged R time. The addition of the heparin has made this CK TAG curve. Much more that initial R time, the initial clot initiation is very prolonged.

But our CKH has got heparinase in it, which cleaves that heparin and renders it inactive. So what you therefore see is a more normal R time. So if there's a big difference between the green and the red curves, if the R times are greater than two minutes difference, then we say that's because there is excess heparin in the sample.

And that will, in a bleeding coagulopathic patient, prompt giving protamine to reverse that. I've taken the other two curves away and that just shows there's an obvious difference between those two. So heparin is present.

We'd give protamine. On our trauma patient, this is the initial tag again, we see that these curves practically overlap. They practically overlap because there's no heparin in the sample, so there's very little effect of heparinase.

Now you do sometimes get some endogenous heparin, so the things which can produce that are severe sepsis or severe trauma-induced coagulopathy. there may be a very very mild heparin-like effect. Most usually we'll do nothing about that but if the patient's extremis and you've tried everything else and the surgeons say that they're struggling it may be worthwhile considering a small dose of protamine. As we see after one patient no heparin effect. We're now on to the other considerations and limitations of the tests.

So temperature in the machine all of the samples samples are heated to 37 degrees. 37 degrees is the operating temperature of the machine. So the TEC results that you see are the TEC results that you would get if your patient was at 37 degrees. Your patient when they come in off the street, when they've been scooped up by the ambulance crew, is most likely 34 degrees. So if you have the instance that you've got a patient with normal TEC results but very cold, and very runny blood that the surgeons are struggling with, the answer may be to warm the patient.

There's a risk if you try and give extra clotting factors when the TEG is normal, that when the patient returns to their normal temperature they will be pro-thrombotic, which they won't thank you for when they get a PE later on in their treatment. So if they're normal, if the TEG parameters are normal, but your patient is hypothermic, warm the patient. you can believe what the TEG results tell you and you don't need to give any more clotting factors.

Several drugs do not show up in the TEG curves which is a frustration and they're drugs which are commonly taken by our population. So clopidogrel, warfarin, all of these in this slide, all of the DOACs, basically any antiplatelet agents, they won't show up in the curves. So you may end up with a normal patient and again the same scenario that you've got a patient who won't clot but all the tag is normal.

In this instance you might want to go back and get a further drug history and see if the patients are on any of these drugs and if necessary then ask the haematologist for help. I've put here time context. The other thing to bear in mind is that there's both a time context and a clinical context. What I mean by that is if you've got a Teg trace which is abnormal but your patient's stabilised and they don't need any further treatment and they're okay, you probably won't need to treat the results.

If by contrast you've got a patient who's in theatre and is actively bleeding, then you very much would treat those Teg results. So it's just to bear that in mind. The other thing to bear in mind is that like any lab test results, the results only show you what was happening as the test was being drawn from the patient. It doesn't reflect an ongoing involving clinical situation.

So it may be that your clinical experience sort of overrides the TEC results. What I mean by that is if the tap has not been turned off and the patient is still bleeding excessively, you may still feel it appropriate to give your major haemorrhage packs even though the tag shows you that the treatment you had already given has given you or produced a normal tag. Not giving that treatment may well have shown you an abnormal tag and it's just that to bear in mind.

There's the treatment algorithm again and this algorithm is also present on the website, so when I say that on the anaesthesia home pages. The threshold for coagulopathy is an ACT of 120 seconds. If the R time is greater than 9.1, we're going to give more FFP.

If the CKMA is less than 52, we know we've got a clot strength problem and so we will look at the CFFMA and that's the fibrinogen monitor. If the fibrinogen monitor shows that low fibrinogen was the cause of that low clot strength, then we'll treat it with giving cryo. If the fibrinogen results are normal but with poor clot strength, we'll give platelets.

If the clot strength is so poor that it's less than 47, then we'll give platelets anyway. And finally, if you see fibrinolysis, you're going to treat with tranexamic acid. This is just an illustration of whereabouts you can find all of those on the results. and this PowerPoint presentation is going to be present on the anaesthesia homepage for you to refer to slow time if you prefer to do so.

This is the URL for Tech Manager. Because it's a browser based system you can see these curves on any of the Trust browser systems. So any Trust iPhone, any Trust iPad, any desktop computer. That means that as the third encore with your phone you can pull up the browser in Safari and if you're the haematology registrar at home you can put the results on your Trust laptop and we can all be on the same page. Thank you for your attention.

I know that the recording process made some of this maybe a little bit garbled so please send any feedback or anything which you didn't quite understand to me and my email address is there. As I've said the other information will be on the anaesthesia home page and Rob's going to put this the Trust YouTube channel and on the Anesthesia YouTube channel for further education. Thanks for your attention and I look forward to your questions.

Transcript for:TEG Interpretation Lecture

Transcript for:
TEG Interpretation Lecture