Good morning. I'm Brett Christmas from Carolina's Medical Center, Charlotte, North Carolina, Vice Chief of Trauma there. Also currently the treasurer for EAST. And this year, whenever they were establishing Trauma University, basically these topics that came up were topics that the membership wanted to see. So knowing that, and geriatric trauma came kind of to the forefront, because let's face it, that's something every single trauma center's dealing with and the problem is not going away. When we looked at this, one of the biggest topics that came up was anticoagulation across the board. So whenever we look and say, well, management of geriatric trauma patients, at this point I can tell you from a national level there are entire task forces being created on how to manage the geriatric trauma patient. We don't have a good idea, you know, the days of putting swans and A-lines and every geriatric patient has gone away because, guess what, we didn't improve mortality with that. So we're trying to find the holy grail at this point, whereas anticoagulation is something that we see, you know, how many people, almost every patient that comes in is on some form of anticoagulant and the question is, what do we do with it? So as far as disclosures, I have nothing to disclose. Objectives are going to be to understand the mechanism and action of anticoagulants in these geriatric patients that we're all seeing, discuss the potential reversal strategies for these anticoagulants, and to discuss the utility and significance of several anticoagulation studies that we can use potentially to cater our reversal. So as the geriatric trauma patient and population continues to rise, our centers are being overloaded. We see them coming in and everybody's coming in on some form of anticoagulant. Well, we have particular challenges when they have traumatic brain injuries because if you don't reverse this, then of course it's going to blossom. Subdurals are bigger, contusions are bigger, or you run into massive hemorrhage. I get a geriatric patient that has a liver injury or spleen injury that may otherwise stop bleeding and a younger patient not on anticoagulants that turns into an absolute mess if they are on platelet inhibitors, TEN inhibitors, or what have you. And the fact is, the days of everybody sitting at home on their front porch in a rocking chair is gone. Our geriatric patients are out there and sometimes even more active than I am in a typical week. So it's not like they're on motorcycles. They are, you know, I don't want to say they're out there racing their little scooters, but sometimes you'd wonder whenever you see them coming through the store, right? So the one we've all known about forever is warfarin. This has been around for many years. This has been the mainstay of oral anticoagulation, approved for DVT, PE, AFib, mechanical valves, so clearly present out in the world everywhere for a long time. The good news is we have lots of experience with this drug. We've had about 60 years to get really good with managing it. It's inexpensive and it has reversal agents. Disadvantages are there's a narrow therapeutic index for these patients, difficult dosing and having to follow up, requires intense monitoring, and several food and drug interactions. And then the fact that we all know in the hospital you've got to bridge it to be able to get them therapeutic before you can get them home. And if you go back and look at the FDA history of your anticoagulants, heparin was first introduced in 1939 and then warfarin comes about in 1954. So as I said before, we've had over 60 years to get very good at managing this drug. Well, here's the problem and why it's really hitting us right now is as we've gotten more and more geriatric patients, we've almost got a new revolution of anticoagulants that are starting to hit the market with something new almost every single year coming out that we've got to figure out how to manage. So if you look at the coagulation cascade, when it started off we had basically the vitamin K dependent factors inhibited by Coumadin for many years, but then you go forward and you get the factor X inhibitors, you get thrombin inhibitors hit the market and you say, well, why does all this really matter? Because reversing every single one of these requires different agents. There is no strategy that is going to fix your entire coagulation cascade, so we have to know exactly what they're on, how long they've been on it, and what the mechanism is. And so if you go through each of these, enzyme inhibits the symptoms of your vitamin K dependent factors. It actually blocks an enzyme that converts the oxidized vitamin K to vitamin K, so factors 2, 7, 9, 10 vitamin K dependent factors. Your onset and duration is basically 24 hours after the dose it starts to kick in, but the peak effect usually isn't until 72, 96 hours after your dosing. And so the duration of action of a single dose is 2 to 5 days, so you have to take that into account with a patient that came in that they come in and if they're on a Monday, Wednesday, Friday regimen, you happen to catch them on a Thursday, then you may not be at their peak dose yet. Their peak dosing may not hit until Friday, so you look and say, well, do I need to reverse it now? Do I not need to reverse? And for us the knee jerk reaction is if it's high and I have an injury that I'm worried about, I'm going to reverse it. So this is our institutional guideline that we've developed for vitamin K dependent reversal and I'll kind of go through the different steps. Basically it's broken out based upon what your INR is. If you come in with an INR less than 1.5, you probably don't need to do much about it. Studies have shown that if you start giving FFP and try and reverse for an INR at 1.5, you're getting very low yield for the amount of volume and everything you're giving the patient. And then you fall into the next category, the 1.5 to 2 and then really the greater than 2.5. So if you look, a couple of things with vitamin K, it increases hepatic synthesis of all your vitamin K dependent coagulation factors when you give it. That's a nice, easy knee jerk reaction. Somebody comes in and they've been on Coumadin, I'm going to give them vitamin K just right off the bat. If I've got a real injury, that's easy. It's inexpensive and you've got multiple routes of administration that you can give it. So that's one. If you've got to reverse it, that's line one. Disadvantages is that it is slow in onset and it can take up to seven days to re-anticoagulate in a patient that's going to actually need anticoagulation once they're over their trauma. So once again, you've got to kind of weigh risk versus benefits of what I'm looking at in this patient for not only their traumatic injuries but their long-term anticoagulation needs. As far as cost, oral, it's $35. An IV dose is $25 for 10 mg and in healthcare today, that is a no-brainer. That's a very easy decision to make for the yield you're going to get from it. Now the time to INR normalization, if it's oral, 24 to 48 hours. At an onset, it doesn't even start until 6 to 10 hours. So if you've got to do something emergently, this isn't what you're going to do. You're more trying to get a steady state while you're giving them vitamin K plus FFP to correct them immediately. If you give an IV, then you're looking at 12 to 14 hours and that's if you're giving it alone. So if somebody comes in with an INR of one and a half and you want to correct them, you're not going to be giving them a bunch of FFP because it's going to be low yield but you can give them the vitamin K because you're already close enough to that one and a half with a decreased risk of bleeding and then you can give them the vitamin K at a slower onset. Now as far as FFP goes, now this is for, of course, emergent warfarin reversal. The advantages are that it contains all of your coagulation factors and it's available basically in all of our hospitals. Everybody here can get FFP now and if you can't, then we need to talk to your administration and somebody to make sure that that happens. Disadvantages are that it has to be thawed and can take time. Infusion of large volumes in a short amount of time, which in the geriatric population isn't necessarily what we want to do, right? COPD, CHF, multiple medical comorbidities and then I come in and I give them an extra liter of fluid and next thing you know they're in a beta pulmonary edema and we're going sideways from a critical care standpoint. So all of those things you have to take into account. Now the reversal of your coagulopathy is partial and inconsistent at best with your FFP. I mean the hard part is this has been our standard for years, right? But it's not all that great and not all that predictable. Variable onset of two to twelve hours and variable duration of eight to twelve hours to get your INR normalization. And your cost is about $135 a unit. So not tremendous but at the same time more than vitamin K, especially if you start having to throw several units at them. So then you get into the range of INR is greater than two, a patient that has a real bleed or needs something emergently done, what do you do? Well the newest thing to kind of hit the market for us has been the prothrombin complex concentrate. So four factor PCC and you're looking at factors two, seven, nine, ten, protein C and protein S. For this, it replaces all your vitamin K coagulation dependent factors and the indications are emergent reversal of coagulopathy on patients or patients that are on warfarin. Now contraindications, of course you don't want to use it if it's non-emergent. If the patient's in DIC, this isn't going to do you any good and no anaphylaxis to any of the products. Now the advantages of the four factor PCC are that there's no need to thaw, there's no need for cross-matching of your blood, it's a relatively low volume, 40 to 200 milliliters. So this is a big deal if I'm talking about a patient that I'm worried about getting volume overloaded that I've got to correct in a hurry. And once again, I'm looking at patients that have INRs of greater than two with significant hemorrhage that am I going to be better off to give them you know, four, eight units of FFP to try and correct them really quick and flood them or can I give them potentially 100, 200 milliliters of PCC, I can correct them within 15 minutes and then take them to the OR and not have to deal with all the critical care side effects. Now this has a long duration of action, about 24 hours, but the disadvantages are that it is expensive. You're looking at an average dose of about $3,800 whenever you give this. So it's $1.27 a unit and you also run some risk of thrombotic events. And just looking at your dosing you can see where INR of two to four you're going to give 25 units per kilogram, four to six, 35 and if it's greater than six you're going to give 50 units. So you look at it and say oh it's only about 27 a unit, well when you start adding all this up it turns into a real cost. You give it through a designated IV at room temperature and you give 500 units IV over three to five minutes and then give the rest. This is done with vitamin K to maintain your vitamin K dependent factors as I said before and the vitamin K cost is $25, that's the no brainer. Now the wild card in this is you don't re-dose the four factor PCC. You give it once and only once because that's all you need. It will correct within 15 minutes and you're off. And the great thing is whenever I was looking over this and thinking about all right geriatric problems, what am I going to talk about and I have a call night where every single case you're going to see here occurred within a single call night. And I was looking at it and going this couldn't have worked out any better. I got one patient in like each of the anticoagulation categories to show you. So this patient of course was on Coumadin and we get a call from the MICU at about midnight and they say hey this guy has been hypotensive all evening, he looks like crap, he's septic, can you come up and take a look at him, we just got a CT and he's got a bunch of free air. So we walk up and we get this CT scan and his INR is 3.9 on multiple pressers. They've already tanked him up with as much fluid as they can and I need to go to the OR and his lungs are going sideways because he's already headed toward ARDS. Well I'm certainly not going to pound him with FFP, his INR is 3.9 so I'd be giving him FFP all night long to try and correct him. He needs an operation, he needs an operation now so what did I give him? Pull the trigger on the four factor PCC. Take it, give it, correct it and this is the discussion with anesthesia too of I'm coming to the OR, I don't need to recheck coagulation factors, I'm giving him this, I'm coming now. If you want to hang FFP on top of it, you know great, you can send it whenever we're there but this is one of those emergent cases we have to do something about and that's where this comes into play. So if you kind of look at this, this is a good slide just showing you, comparing the three reversal agents all side to side. So really looking timed INR target, you can clearly see the fastest one is PCC and then you know vitamin K and FFP are 6-12 hours, 2-4 hours and then breaks down even the hospital costs. As you can see clearly the one that corrects the fastest is the most expensive but there are times when you're going to have to use it. So this then brings us to what happened in the last 7 years. The onset of what we all call the novel oral anticoagulants and if you look between 2010, 11, 12, 15 and I would wager about every single year there's going to be something else that keeps popping up in our current environment. It's what I like to kind of call the anticoagulation revolution and it seems like these companies are out here trying to turn their blood into Kool-Aid and I've got to figure out a way to correct it whenever I have to go to the OR. So what are these novel oral anticoagulants? Basically they target specific factors in the anticoagulation cascade whereas you had Coumadin, the vitamin K dependent factors, now you're getting down to specific targets in that coagulation cascade and the thing is all you've got to do is take out one. If you take out one, then that whole cascade stops functioning. So advantages for these anticoagulants are that they're equal or more effective than Coumadin is. They possibly have less bleeding and drug interactions although some of us that see these patients that are on these medications might argue that it's a heck of a lot harder to stop the bleeding which that's, you know, that's why we're here. They don't require routine monitoring or lab values or the risk of, you know, really overshooting like you do with Coumadin and getting a patient with an INR of 8 to 10. Most do require or do not require parental anticoagulant to start, meaning that with Coumadin we always have to start heparin to bridge them to then get them going. Well, with these medications, we don't. We just, boom, start the dose, they're there and they keep going, nothing to monitor and then they're off and running. Disadvantages are they are clearly more expensive, they have less indications at present although as we all know once new drugs hit the market you go and you keep testing them to see what indications you can ultimately get and so ultimately it spreads more and more with the usage. There is no reversal agent for most of these and that is the big one. As I said before, we had 60 years to get really good at managing Coumadin and now we've got all these that have hit within the last 10 years and we're trying to figure out what to do with them. And that's one of my favorite questions whenever somebody would come in and they go, hey, we've got this great new medicine that's now approved for DBT or for PE or whatever and what's my first question as a trauma surgeon? Okay, how do I reverse it? And what do we get? The blank stare, right? And so that's what we're all trying to figure out because from my standpoint it may work great for what I do on one side of my practice but as I'm seeing more and more people that are falling at home, hitting their head, coming in, rib fractures, hemothoracies and I'm saying, all right, what do I need to do to keep them from bleeding and getting worse once they come through my door and we don't have the answers to that. So if you look, one of these is Dabigatran. Dabigatran is a direct thrombin inhibitor and so this is one of those new ones that hit within the last 7 years. If you're looking at reversal strategies for it, you basically can say, consider giving them DDAVP. You can consider giving them FFP. Now do we really know if this really stops or slows down the bleeding associated with this drug? Not really but it's kind of what we've been doing up until now to do something to try and stop it. We clinically haven't been able to say that we improve it. We haven't been able to say that it makes it any worse. Now the thing about this drug to know is that there is a reversal agent and this has come out within the last 2 years. So I'm not even going to pronounce it every time I see it. I'm like it's the one that starts with an I and you can go and if you get a patient that comes in on Dabigatran, that should kind of set off something in your head and be like, all right, Dabigatran, that one's reversible. There is an agent and the hospital should have it somewhere in stock to be able to do it if you need to fix it. So remember that one out of all of them, you do have a reversal agent for it. Now these are the factor 10 inhibitors. So you get Rivaroxaban, Apixaban, Adoxaban, and the thing to remember, easy way to remember these, is they all contain an X in the middle of their word. So, if somebody comes in and they're listing it off and you hear something with an Oxaban or, you know, Adox in there, then if it's there in the middle and it's an X, X Roman numeral for 10, it's a factor 10 inhibitor. So, if you go and look at these, they will act specific agents to reverse the effect. There is nothing out there that anybody's come up with to directly inhibit them. And the problem is, they're highly protein bound and so they're not easily dialyzed out of the system. Some of these patients can go on dialysis in worst case scenarios, but these, it doesn't work because they're so highly protein bound. This is another patient that same night I was on call. She was at home, fell during the course of the day, hit the back of her leg, and she was on Apixaban. So, normally a little calf bruise, that in most people in this room, would just kind of amount to nothing because she was on a factor 10 inhibitor. This swelled up to the point that she got a hematoma and got so large, it caused her overlying skin to split and start decompressing and had to take her to the OR and evacuate it and put a back dressing and everything on it because she was on blood thinner. Couldn't be stopped, couldn't be slowed down. Well, then it brings us to the other group, antiplatelet agents. So, these agents permanently inactivate platelets, which means that it can take up to seven days from their last dose for the effect to go away. So, that's the big problem with this. And what's the other problem? How do, this is a list of all your antiplatelet agents that are currently out there. And what's the big problem with this? If it permanently inhibits platelets for seven days and you get a dose, the medication is still in the system when they come through the door. So, what am I gonna do to try and reverse it? Well, as I said before, we look at it and say, we're gonna try and do something because we don't really know. But in doing that something, what am I gonna do? Well, I'm gonna give them some platelets. Problem is, they just received the dose of their platelet inhibitor probably the same day. It's still in the system. So, I'm giving them platelets that permanently inactivates platelets. So, the platelets I'm giving are probably gonna end up getting inactivated. So, what do you do with that? And, but, coming in, if they're on these and I have a bad head injury or a large interabdominal bleed, something I'm worried about that's gonna keep bleeding, gotta try and do something. So, in general, what we do in our guideline and most other places is, we will give them an apheresis pack of platelets. Once again, that same night on call, this was another elderly patient, fell, hit head, and was on aspirin and Plavix at home. So, you come in and this is what I'm looking at. Once again, this is pretty bad contusion. It's gonna get bigger. I know they're on a blood thinner. What am I gonna do? Well, the best I've got is to give them platelets and or DDAVP. And, in this patient, I did both because I'm looking and going, if this gets bigger, it could very well kill them because of the location and contusions always tend to blossom out. So, if you look, this is kind of the guideline we have in our institution for reversal of our anti-platelet agents and the novel oral anticoagulants that we've established. I would say that over time, this'll change a little bit as new things hit the market and hopefully some things hit the market can help us reverse. And, the fact is, our guidelines are great, but what about active ongoing resuscitations and active hemorrhage and what am I gonna do with all this? So, what do I have to monitor? Well, I've got tests of the platelet phase. This'll show you bleeding time, although how often do we use bleeding time anymore? Almost never, right? This is kind of really falling by the wayside. So, basically, the measurement of bleeding time is a measurement of basic constriction, platelet plug formation to your clot matrix. Normal bleeding times in the range of seven to nine minutes and it can be prolonged if it's prolonged to show spontaneous bruising, the mucosal hemorrhage, and you'll see this with thrombocytopenia, platelet dysfunction, or if patients are on aspirin, NSAIDs, or bottom low brains disease. These are the classics that are gonna prolong your bleeding time. And then you look at your tests more specific for the coagulation cascade. So, PTT, it's time to generate fibrin from the intrinsic pathway. Factors seven, eight, nine, 10, 11, and 12, prothrombin and fibrinogen. It's prolonged if the activity is less than 30% of normal. And that's the scary thing. So, by the time you start seeing elevations in your PT and your PTT, basically 70% of the function has already been debilitated. So, it's not like you've taken out 20% or whatever. You don't even see movements in your PT, PTT until you're less than 30% of functionality. So, if you look at that, you're already behind the eight ball if you're in an active resuscitation. And then hemophilia A, B, vitamin K deficiency, liver function, these can all prolong your PTT. And then DIC and massive transfusion as well. So, for PTT, it is, there we go, PT, time to generate fibrin after activation of factor seven. This measures extrinsic and your common pathways and catches both, but it's factors five, seven, 10, prothrombin and fibrinogen. Now, the PT, what do we always use this to monitor, is warfarin. So, you can see where they are with their anticoagulation and that's the classic. But you see it prolonged in liver disease, severe bleeding, and massive transfusion is where we'll most often see it. And then thrombin time is time for fibrinogen to get to fibrin in the presence of thrombin. And then if you get deficient fibrinogen, that's only when you get to the point of less than 100 or abnormal, that's when you start to see changes as far as your thrombin time. And then if you get heparin or fibrin degradation products, those are the things to look at that are gonna tell you if I'm in DIC and I've got fibrin degradation products, that's gonna be the tip off to show me there and what I need to do. Or if I'm on heparin, that's gonna prolong my thrombin time and turn it off or reverse it with protamine. So, here's the thing. Are there any laboratory studies that are useful with our novel oral anticoagulants? And the short answer is going down that list, no. None of the traditional studies that we have do us any good whenever we're monitoring any of these and the coagulopathy in the patients that come in. And the fact is, this is what we're all dealing with at our trauma centers in this patient population and we're trying to avoid that death triad of coagulopathy, hypothermia, acidosis. I can correct the acidosis, I can correct the hypothermia and I've got numbers for that. And the question is, what do I do with coagulopathy? And half of these studies, whenever I go and get them, I'm measuring different points in the coagulation cascade and it's gonna take me a while to get all these labs back and when things are changing. So the question is, what do I have that can monitor every aspect of my coagulation cascade, especially in an ongoing resuscitation? And for us, and what we use is thromboelastography at our hospital and have become pretty adept at doing this. Everybody out there who uses TAGS at their institution. Okay, so really about a third of the room. And it's funny because whenever I give talks on anticoagulation and geriatric trauma and things, it's more and more people are kind of catching on and getting comfortable with it because we're trying to figure out what to do on our active resuscitations now. So what is thromboelastography? Basically, this is a test that can give you a whole picture of your entire coagulation cascade in an almost real-time assessment. And if you look, when this starts rolling off, a normal TAG tracing looks like this. So for those of you that have seen it, you know whenever you go, you start to form the clot and what this measures is kind of the clot formation, viscosity, and then even gets to the point that you start measuring fibrinolysis and clot breakdown as you go. So you can see where you are in real time and what all your factors are doing. So a lot of the rest of this talk is kind of going over when these patients come in and they are on anticoagulants and they're getting coagulopathic, what am I gonna do to fix it? And the best way for you to learn, I would say, is pay attention to the pictures. If you're there and you're a visual learner, then you'll do very well with this because as much as we try and make everything very complex, this is one of those tests that you can go and if you get good at recognizing the pictures, you can get good at correcting things in the coagulation cascade. So the first thing you're going to assess on this is the clot time. And if you look, the clot time is the time that it takes to basically form clot from going from, I guess, zero to two millimeters. And so whenever you go, that is basically your R time and this is an assessment of your clotting factors and what you have there. So the thing to look at is that's the very first little blip, how long it takes before you see my clot start to actually form. So you look at your R time. So if you get clot time irregularities and you see a long clot time that goes greater than eight minutes, possibly the allergies for that are factor deficiencies and then if a patient's on heparin. So where you would commonly see that is a patient that was getting, say, a vascular surgery or whatever and they gave them heparin and then they're going, they're still bleeding and they get the tag and look and it's prolonged. Well, that's easy, right? They were in the OR with vascular, they got heparin. You know, you give them protamine and you can fix that. But for the patient that is not in that circumstance, hasn't gotten any heparin, you've got a prolonged R time, then the way you're gonna fix that is to give them FFP. So that's the thing to look at with your R time. So if you get a short clot time, which is less than four minutes, you can actually get a state of hypercoagulability. In our discipline and what we do, this is almost never what we see and what we're gonna deal with. But the way you fix that is you give them an anticoagulant if you've got a patient that you're concerned about being hypercoagulable, if you will. So if you look at clot kinetics, this is K, is the number you're gonna look at here. And this is the time to go from two millimeters to 20 millimeters on your clot formation. And it's basically that time. And then you get an alpha angle that is the tangent of going from two millimeters to 20 millimeters. So these are the two numbers that you're gonna look as far as the rapidity of your clot formation, if you will. So if you get prolonged clot kinetics, you get a K greater than four, an alpha angle less than 47 degrees, you're looking at fibrinogen is low. So whenever you're going, remember I said it's looking at pictures and angles and getting good at that then whenever you see this and all of a sudden you go, okay, my K is way too long, my alpha angle's too low because it's basically not creeping up at the rate I want it to, I know as soon as I start to see that tracing come off that I need to go and I need to give them fibrinogen, give them cryo at that point basically. So as this is coming off in real time, you can see the pictures before you even have all your numbers together and you can realize I need to give this patient X, Y, and Z. And this test is done, you're watching it over about a 15 minute time frame so you can actually make assessments on what you need to do. Now if you get shortened kinetics, a K less than one or an alpha angle greater than 74, then once again you get into a state of being really kind of hypercoagulability and there's not much you can do about it. Once again, this is not gonna be the problem in our discipline of what we have to deal with. What we're going to see are the low angles and a longer time from K to get to two to 20 which tells you you need to give them cryo. The other thing you can assess is clot strength. And when you look at this, the clot strength is measured by the amplitude. So you're looking at MA and the thing to remember with your clot strength is that about 80% of your clot strength is dependent upon your platelets. So this is where you're measuring your platelet function. We've already seen one where you're looking and you know you need to give FFP. You saw the alpha and the K that's gonna tip you off as to whether or not you need to give cryo. Well, this is the one that's gonna tip you off as to whether or not your patient's gonna need platelets. So if you get a regular or a low MA, then basically the curve or the amplitude's gonna narrow out and that's gonna show you I need to give them platelets because you're trying to increase the clot strength and make that wider, if you will. So if you look, you get a high MA. As I said before, you get into that and that's platelet hypercoagulability. If you're gonna treat that, once again, not so much in our world, but you would give them antiplatelet agents of which I just gave you a whole list of them that you could use. So the low MA, these are the ones where you've got either poor platelet function, low platelet count, or you can have patients that are getting platelet inhibitors. So once again, this is gonna tip you off to the fact that I need to give them platelets and try and make that angle wider. The last thing you can look at is clot lysis. This is kind of known as the LY30. So what happens is you go, and as we know, you go, you form your clot, it strengthens up, and then all of a sudden it starts to kind of break back down a little bit, a little bit of clot lysis. So this is the LY30, and it basically looks at the change in amplitude once the MA is reached until the clot starts to break down. If you go and look here, you get primary fiber in a lysis, you can get an LY30 that is greater than 7.5%, and you see that curve where it goes, you form your clot, and then all of a sudden it starts to break right down. So things that can cause that are if a patient's gotten TPA, it's fiber analytic, right? So if you have TPA in the system, that can cause it. And if you start getting a curve like this and a massive resuscitation, which we've seen these before, the way you fix that, anybody know what you give? Well, it's an anti-fiber analytic that we put people on. It's out there in the literature everywhere, and everybody's debating it left and right. You can go with TXA. So this is where the TXA comes into play, and you're seeing that in massive transfusion protocols and initiating it's seen, and so the anti-fiber analytic is TXA, so if I see this curve, this tells me that the patient needs TXA. So then you get to the other curve where you see more of a slower clot breakdown, and what this is concerning for when you see these patients is for DIC, and this is the one that always gets me in the other part of what we do because most of us that are doing trauma are also doing the critical care part, and you see a patient with DIC, and these are the ones that you look and say, the treatment for that is to put them on an anticoagulant, on heparin, and that always looks, and it's so counterintuitive and scares you to death thinking, well, the patient's bleeding, and the way to fix it is to put them on heparin, but once again, this is a way to prove it that you're in DIC, and that's gonna be your treatment. So quick review, just kind of going over all of the things that we looked at. So clotting time is the first thing you're gonna look at. If it's prolonged, then you're looking at giving them FFP to try and correct. Clot kinetics, K in your alpha angle. If your K is high, alpha angle is low, that's gonna tip you off that you're probably gonna need to give the patient fibrinogen to correct. Clot strength, which is your MA, so you're looking at your amplitude. If your MA is too high, they're hypercoagulable, not a lot you're gonna do about it, and in our profession, in acute traumas, not much I care about doing about it, to be quite honest. If it's a narrow amplitude, that tells me I've got platelet dysfunction, I'm gonna give them platelets to try and widen that out to stop the bleeding from that standpoint. And then I get into the clot stability, the LY30. So if I go and I form a clot real quick and it breaks right back down real quick, that tells me that I need to give them an antifibrinolytic and that's gonna tip me off to TXA. So once again, we've been over all of the medications that everybody's on and there's no direct way to reverse these, so if I get patients that come in that are on these medicines and I'm trying to figure out how to reverse, this is at least something I've got that I can see where they're bleeding, what products aren't functioning, and where I can try and cater my resuscitation to that individual patient in front of me. So now's the time, since this is trauma university, where we get some audience participation and let people get some practice at reading. So if you look at this one, I was even nice enough to give you all the numbers up here for the normal in the upper left-hand corner. So example one, what does this show and what am I gonna give? FFP because I've got a prolonged what? Yeah, my R is too long. So if you look here, this shows that it's taking longer to get everything started, easy way to think about it. My R is too long, so what I'm gonna do to fix that is give them FFP. Now example two, what do I see here? What is it? So it's hypercoagulability, and so this is the one that I kind of look at and say, all right, it's a hypercoagulable state, it's a trauma surge, and I see this, and I get this rolling off, what am I going to do about it? I'm like, okay, great, maybe it'll stop the clot a little faster, because we're not doing anything about it right now. But, once again, so amplitude MA, farther apart, hypercoagulable state. So in this one, what do we see? Number of spots. So your angle is low, your K is high. So this is the one, lo-fi brenn engine. And what am I gonna give to fix this? Cryo. So once again, it's all about learning the pictures. So I see that, I can tell that. And then the other thing that you can look at with this one too is your K is high, your alpha is low, but then my amplitude kind of secondarily is also down. This is one of, I don't wanna say the worst, because I'll show you the worst that I've ever seen in a minute. But this is one of those that I consider pretty bad when I see this, because I've got a low amplitude, my K is off, my alpha is off, and I'm looking at this going, I'm giving platelets, and I'm giving cryo, and at least I'm not pounding them with FFP, because looking at this, you may go, and they're still bleeding. If I didn't know any better, I'd be pounding them with FFP, right? When what they really need are platelets and cryo at this point. So some more examples, and then this just gets down. We're gonna try and make it as simple as possible. So the first covered picture, what am I gonna give them there? What's going on? So the first one's a prolonged R. You can tell just by looking at it, and so I'm gonna correct that with FFP. So second picture. So second picture, you're looking at one. You've got a low MA, so you can give them platelets there, but then if you look at the alpha angle and the K angle, it actually shoots up okay, but your amplitude doesn't really get high enough, so that's gonna tip you off. That's more of just giving platelets. This is one that when it starts to form the clot, it actually goes from two to 20, pretty appropriately, but it's not gonna get high enough. It actually goes from two to 20, pretty appropriately, but what then happens is it stays narrow, so you need more strength of the clot, and you're gonna give them platelets. So what is this one, and what am I gonna give? So this is whenever we're getting into the fibrinolysis, and I'm gonna go after an antifibrinolytic. These are the patients that as soon as I see this rolling off, I'm gonna give them TXA in real time to try and start fixing it, and then the next one is hypercoagulability, so once again, hypercoagulability, great. We know the information, and we've got it, and then the last one is DIC, so if you look at that, that would be one that if you see a patient, they're in DIC, and you're gonna go and fix it. These are the ones that go on a heparin drip, but if I've got acute coagulopathy from trauma, that's not really in the same world. This is more in the critical care world for the patients we take care of, and then whenever you really get fulminant DIC and you're in stage two, that's what it looks like. Everything goes completely sideways, and all your clotting factors are pretty much done. So here's another good study. This is a 61-year-old guy that came in with hepatitis C, pulmonary stenosis, hypertension after a 20-foot fall from a ladder. His only injury was a left femur fracture, and when he came in, he had gotten a CT of the abdomen with a cirrhotic appearing liver, and re-canalyzed peri-umbilical vein, telling us that he is indeed a true cirrhotic, and came in, and otherwise, other than his femur fracture, no real injuries, and in the middle of the night, starts getting coagulopathic, bleeding from nose, mouth, everywhere. Gets transferred to the ICU, and one of my partners was on, no idea what was going on other than the patient's a cirrhotic. That was his first tag, and if you actually look at it, there is maybe a dot of displacement up and down, nothing else. So at that point, what are you gonna give him? And yes, the answer is you throw the kitchen sink at him, because he has nothing there to clot. I mean, this is the ultimate study in why patients die from cirrhosis right here. So he starts correcting, and throws FFP at him, cryo, platelets, and then gets his next tag, and this is what we look like. So okay, now we've got something to work with, so what am I gonna do with this one? He's building up clot, and it's tearing down, so next one, he threw TXA at him, started him on the TXA drip, and he managed to get him like this, granted, over a couple of hours. Now, did it ultimately salvage him? No, this patient, I mean, there are cirrhotics in the world, and then there are cirrhotics, and this one was unsalvageable to that extent, but as you can see, was able to look at the tracings in different time to see what he needed to give him to fix him, and ultimately got him to a coagulation cascade looking like this. So otherwise, we'd keep throwing everything at these patients and have no idea what kind of progress I'm making, where we're going, but you went from a patient that was that much displacement to somebody that looked like they can actually try and form a clot. I'd like to thank TCAA for the privilege of the podium today and being able to speak to you all, and if we have time, I'll be happy to entertain any questions. Yes? Sample to results, the big thing is how fast can you get it drawn and get it down to your lab and get it running? Once I get the tag on and it starts going, I can know most of my information and start recognizing the pictures within 15 minutes. No, you can keep sending these as the resuscitation goes on, and so the real question is, and the debate that's out there with a lot of trauma centers is when do you send the first one? So some centers will say we send it as soon as they arrive in the emergency department, and then we'll check our next one, even in the OR after the OR. I can tell you at our trauma center, we don't even send our first tag until after we get out of the OR, because the mindset and the debate is, if a patient comes in and I'm going ricocheting straight from emergency room to OR, and I've already got massive transfusion protocol going, that by the time that first tag comes off, I'm already six units of blood, six of FFP, and platelets into it, so those results from 20 minutes earlier in a massive hemorrhage are not where I'm at 15 minutes later. So our practice is to get them to the ICU once we've got what you would call the massive surgical bleeding stopped, or send it as we're coming out of the operating room so that it starts rolling off, and then I'm catering my transfusion, because if I'm in the OR with massive transfusion packs, I'm not really catering much. I'm just trying to give them all the product then. But as soon as you go and you start getting to the end of one, now what you wanna do is figure out from that tag what products I need, slam them in as soon as you've got those in, then send the next one and see what change you made and what it looks like. Yes? If you only had one tech machine, where would you put it? If you only had one tech machine, where would you put it, in your hospital? That's a very hard question when we're a 900-bed hospital. So for me, where I would want that would be outside my surgical trauma ICU, or in that area. I think for the ORs, for me, it doesn't really come into play as much, because if I'm in the OR with active hemorrhage, I'm giving them so much product at the time that things are changing so quick that I'm not gonna look and be telling anesthesia. Like I said, it's in the 20 minutes that I'm in there, things will change by the time it rolls off. If I'm up in the ICU, I should be out of the OR, where hopefully I'm slowing down in my resuscitation, but at least I'm starting to cater things. So that would be my preference, and that's where we tend to use it most. I think the advantage is in the new TAG system, in the S6, you can actually position it in the lab and get your results connected to your electronic medical record anywhere. So I think going from the 5000 to the 6S, there's pretty much a huge advantage. If you're limited in location. And I think that's the thing for us, it's all with ours, and it being real time, is that I can be anywhere in the hospital, and as long as I've got a computer screen that I can log onto, then I can pull it up. I can literally be sitting outside the patient's room, dictating my op note what I just did, and I'm watching it roll off on the computer screen in real time. Yes? Do you have a qualification for someone running it, like is it typical just a lab person, or is it something that many people can? No, ours all goes through the lab, and they run it down there, and as far as specific qualifications for that person, I'm, you know. No. Somebody that takes it, puts it in the machine, and kinda hits the button, let it run. Yep. All right, well thank you very much. If you have any other questions, I'll be around today and tomorrow. Thank you.

anticoagulation

geriatric trauma patients

challenges

reversal strategies

thromboelastography

coagulation cascade

treatment decisions

individualized treatment