My name is Nicole Siparsky. I'm a surgeon intensivist here in Chicago at Rush. It's a pleasure to be here with you today. I forgot to put a disclosure slide on. I apologize. I'm an up-to-date author on post-op fluids, post-op electrolytes, and post-op TPN, which is all evidence-based and not really a true conflict. I'd like to thank the Society for the opportunity to be here. I'd also like to thank Janice Zimmerman, who prepared this slide deck. I have lightly revised it for my talk today. So today we have a very clear mission. Number one, bleeding. Number two, clotting. And number three, thrombocytopenia. And that is what we're gonna talk about. So all successful outcomes start with a good history and physical. Why? Why not just go right to where the bleeding is? Well, if you take the time to get a good history and physical, you will probably find out things that you could miss that will make your job harder and potentially impact the outcome. So it's all as important to get all of the information that you can possibly get about a recent event. Was it a surgery? Was it a procedure? Was it an accident? Was it a chemo treatment? All of these things are relevant. You'll ask the patient about history of bleeding issues with dental work, pregnancies, things like that, that might suggest an underlying hypocoagulable state. It is helpful to know what the pattern of bleeding is, if the patient had a trauma and then an immediate large-volume bleed, or did they have a seemingly benign procedure like an endoscopy and then have, suddenly, hours later, a massive bleed. You're gonna look for conditions that are associated with bleeding, whether it's thrombocytopenia, coagulopathy, those are the things that are gonna impact the patient's outcome that you have to address. So if the patient endorses drinking, you'd be thinking maybe this patient is a decompensated cirrhotic and is thrombocytopenic and coagulopathic. That kind of person is a very different person from a healthy person in terms of bleeding. When you do your exam, of course, you're looking for any obvious evidence of bleeding, something that is externally bleeding, always a good one to identify and control quickly. You might be looking for something tiny like petechia, which are little tiny bruisey spots all over the body, or when they come together into little patches, we call them purpura. When the patches are really big and there's bleeding in the subcutaneous tissue, we'll call that echemosis, and when there's a volume of blood that creates a mass, we call that a hematoma. So that hematoma could occur in the soft tissues. You might see a giant thigh hematoma in the soft tissue or in the deep space of the thigh, but there's also a lot of potential places in the body for large hematomas to form, in the pleural space, in the abdomen, in the pelvis. These are all things to think about. You're also looking for signs of other medical problems that would explain or help you to understand if the patient does not respond appropriately. For example, let's say you have a young, healthy person, but that patient has joint laxity. Does that person have Ehlers-Danlos syndrome and a collagen production disorder that might render them at risk for, let's say, an aneurysm that might be bleeding? These are all things that are gonna help you figure out where the bleeding is and what you need to do to correct it. Typically, you start with a battery of tests. You are all familiar with all of these tests. A couple of things to keep in mind. Number one, when you're taking your test, your board exam and such, they love to ask about the clotting cascade. It gives me PTSD to look at it. I don't really think about it too much in my day-to-day practice. I include it here for completeness, but what's not on this clotting cascade is one of the most important things, which is calcium. Remember, calcium is necessary for platelets to be activated. You can't do that, you can't clot. People often forget to check an ionized calcium to make sure the patient has enough to clot properly, so always check that early. Check it often. Aggressively replace it when people are bleeding because it's often forgotten. In terms of CBCs, I often see providers check hemoglobins after they start resuscitation, and they miss checking the full CBC, which will give them an idea of how much dilution is occurring, how much thrombocytopenia is occurring, so whenever you're checking sequential labs, don't be chintzy, get the whole CBC. When it comes to COAGs, we all check them. It is informative when we're looking for things like the effect of Warfarin on the INR or the effect of heparin on a PTT, but there are some more modern ways to evaluate someone's clotting ability, which we will discuss in a moment. Oftentimes, people forget to check a fibrinogen, and the reason this is important, in addition to the fact that it's part of clotting, is that we do have a much better way of replacing this with cryoprecipitate, where the concentration of fibrinogen is very high, and the volume you need to give is much smaller than if you were to give FFP to replace that portion of the clotting cascade, so it's a good thing to check frequently. I'm a surgeon. Everyone I take care of is bleeding and clotting. D-dimers don't help me at all. I don't check them. I've never ordered one in my entire career, but I'm sure if there are people in here who see patients before they start bleeding, or if they are just clotting and you're trying to figure it out, it might be helpful to you. There are a lot of tests that I consider fancy medical tests. They are not helpful to you in this moment when your patient is bleeding, but let's say you have someone that's insidiously bleeding for a while. You can't figure it out. You're putting on your medicine hat. You might wanna do a platelet function analysis. You might want to look at a mixing study to see if there's an inhibitor or something promoting hemolysis. You could even do a von Willebrand factor antigen quantity and activity study. These are super fancy. I've never ordered one in my whole career. Clotting factor assays are interesting as well. We sometimes will do them in liver failure patients who are getting worked up for a transplant. Those patients typically are floridly coagulopathic, and I'm not really sure it's helpful to me as an intensivist, but everyone else thinks it's interesting. In terms of the patterns of the labs, these traditional labs, there is a traditional pattern for different kinds of problems. I include this table for reference. I think it's pretty straightforward. If you have von Willebrand's disease, then your PTT will be prolonged, for example. Each one of these types of problems has a characteristic pattern. It's a very popular test topic. More modern way to assess coagulation is with a viscoelastic study. Raise your hand if you have TEG or Rotem in your institution, and you actually use it. Amazing. You guys are all experts because you have seen this before. Just in review, for those of you who are not familiar with this, I'll describe the TEG, which is the test that I'm more familiar with. They would take a sample of blood, put it into a little cup with a needle, put it on the jiggler, and then the jiggler will shake the cup back and forth. As the blood clots, it kind of drags the needle with it, and as the needle moves more and more with the clot, the machine will trace it out, and it will look something like what appears in the top left corner of the slide, or your right, sorry, your top right. As the clot forms, the machine will measure how long does it take to form, how long does it take to reach its maximal strength, how long does it take, or how much of it starts to fibrinolyze by 30 minutes. And these are all standard measurements that it will report to you, or you can look at the tracing itself and get a sense of whether you think there's something abnormal. If there's a deficit in the component of clotting that is occurring in that moment, you can then replace it in a focused fashion and limit your transfusional support to only what you need, and usually less of it to achieve hemostasis. This is a very popular topic for the exam, and so you should expect to see one of those cartoon depictions on the left. Maybe you'll have a real life one, like we had in the question session a moment ago, and they'll ask you, here's the tag, this person is bleeding, what do you give? Let's say, for example, the patient is having thrombolysis, excuse me, fibrinolysis, and the patient's lysis time at 30 minutes is abnormal. In that situation, you would wanna give an antifibrinolytic drug, like tranexamic acid, or aminocoproic acid, rather than a whole bunch more products, and that would be very effective. So, when we're talking about thrombocytopenia in the ICU, in my world, we see sepsis, sepsis, sepsis, bleeding, and occasionally some drug-induced thrombocytopenia. If you work in the medical world, I think you come across more immune thrombocytopenia, or TTP, and I think we all see a little bit of DIC. So, we'll start off with drug-induced thrombocytopenia. There's two kinds, there's the immune kind, and the non-immune kind. The non-immune kind is very straightforward. Those are things like chemo, that suppresses your bone marrow, and then you don't make platelets, pretty straightforward. The immune kind is a little bit more complex, and then you're talking about antibodies that promote thrombocytopenia, due to a drug that you're administering. There isn't a really good test for this. You're gonna see the platelet count go down, within a few weeks of giving the drug, and then once you stop it, you should see the platelet count recover quickly. The caveat to that is, if it's a long-acting drug, it won't recover quickly. It'll take as long as it takes for the drug to wear out of the system. So, if you gave someone chemo that's gonna work for a few weeks, you're gonna have to be very sad for a while. Typically, we see the platelet count go down really low, in this condition, and when we see that, we should be thinking about common things, like iodinated contrast, a lot of popular antibiotics, and of course, drugs that are given for chemotherapy. I hate those drugs, which is a huge problem for everyone. Typically, we do not treat the number, we treat the patient, and the patient is not at risk for a spontaneous hemorrhage, until the platelet count goes really, really low, typically in the 10,000 range. So, the only time you wanna be thinking about platelets is if the patient is actively bleeding, or if you have to mitigate the risk for the patient who's gonna have a procedure. Depending on the procedure, the risk may be very low. Let's say, for example, you've got a vented patient, you need to do a bronc to get a BAL, they're sedated, there's an atraumatic procedure, that's a low-risk procedure, you don't need much, maybe 20K, very little, if any. But, that converse would be, someone going for a craniotomy, you cannot have any bleeding after that procedure, that patient will not tolerate any bleeding, so you need to have a really respectable six-figure platelet count. Keep in mind that platelets may come single unit, or they may come pooled. Where I work, we get a pooled unit of five or six donor packs of platelets. When it comes to immune thrombocytopenia, we're typically thinking about a primary problem, antibodies focused on the platelets, or a secondary problem, most commonly, a viral infection. In a viral infection, your immune system makes a response to the infection, but oops, it also picks up platelets in its tracks. So, typically, there's not a lot of really good testing for this. You can do a very exhaustive medical workup, looking for a cause, but in the end, you call the hematologists, and they do some more testing. In the meantime, you're sad. If the patient has to be treated, because it's a really advanced problem, then you're typically talking about suppressing the immune system, and you're either gonna carpet bomb it with a bunch of steroids, or if someone's going to surgery and can't have that degree of immunosuppression indefinitely, you can consider using IVIG. If you wanna go hardcore, you can do an antibody therapy that will target antibody production, so rituximab will shut all that down as well. Very rarely do we do splenectomy anymore, and I've never administered a thrombopoietin receptor agonist, but it's an option. When it comes to TTP, it's a different game. The thing you wanna remember with TTP is ADAMTS-13. That is the enzyme that modifies von Willebrand factor for it to be working in its normal way, and when that enzyme is not working properly, or it's in very small concentrations, von Willebrand factor rolls around in the body larger than normal, causing clotting in the microvasculature. When you have a patient with that, they will typically have the, quote, Pentad, unquote, of thrombocytopenia, hemolytic anemia, fever, and renal and central nervous system dysfunction, so you're gonna look for the Pentad, and when you see it, you're gonna do lots of labs like you normally would, but the real test to do is the ADAMTS-13 activity level, and when that is less than 10%, it's diagnostic, and you can do an antibody test to confirm that. So, how do you treat immune problems in general? When you wanna go really aggressive, you basically remove all of the patient's plasma from their body, and you do that with plasma exchange. If you've never done it, it just looks like dialysis. You put in a giant dialysis catheter, they hook up to a giant machine, they pull all the blood out of the body, and they replace it with a bunch of FFP, so all these patients get transiently coagulopathic, which is something you should keep in mind. I personally do not do any non-lifesaving procedures on a person who gets plasma exchange. They are always coagulopathic. It's not always something you're gonna pick up with spot coags, and if you do a seemingly well-intentioned procedure after plasma exchange, it could go very badly, so I don't recommend that. You typically wait till the next day. In terms of other things to do, the plasma exchange is gonna pull out all the antibodies right now, but it's not gonna prevent future production. That's where you wanna shut the immune system down. You're gonna give steroids. Again, you might use an antibody therapy that will modulate the immune system production of these antibodies. Again, you're not giving platelets if the platelets are not really, really low, like less than 10,000, and only should be thinking about platelets when there is severe bleeding. Hemolytic uremic syndrome. We're very lucky. We live in the United States. I don't really see much of this. We do, however, see a lot of food poisoning. We still see that, and E. coli 0157 is notoriously the most common food poisoning that produces hemolytic uremic syndrome. The way it does it is it creates this shigella-like toxin, or shigatoxin, and shigatoxin's pretty nasty. It basically incites cell death through a very complex response that is impressive, and the production of a massive inflammatory response and cytokine response, and so with that, it makes people really sick. I met one person who had this. It was very impressive. It was the sister of a colleague of mine who went to Greece with the whole family. They did some hike. They hike up to the top. There's a barbecue the locals put on. Nobody wanted to eat the local lamb, but she tried it. She was very adventurous. Then they came home, and by the time she got home, she was on the verge of death. She had the worst colon I've ever seen on a CAT scan in my life. She was a healthy 20-year-old woman, and she had E. coli 0157. It was very impressive, so I don't think it's subtle. When it's happening, it's very impressive. Typically, the treatment here is the same. Again, when the toxin is the problem, you gotta get rid of it very quickly. Then you're just gonna draw all the plasma out of the body to get rid of the toxin, and then you're going to do supportive care, let's say dialysis for renal failure, and then there are some fancy antibody therapies you may consider if the infection doesn't go away on its own. So, moving on to heparin-induced thrombocytopenia. Most of you are very familiar with this condition. Just remember that there's two kinds. There's the non-immune kind, and there's the immune kind. We do not care about the non-immune kind. If it happens within the first couple days of treatment, it is probably the non-immune kind. You do not need to stop heparin. You can treat right through it. It goes away on its own, no problem. The one you want to worry about is the one that usually sets in about five to 10 days after starting heparin. It can be very insidious. It might be a heparin flush of a dialysis catheter or a heparin lock of an IV five days ago. One dose is all it takes. So, within five to 10 days of starting heparin, you're gonna see the platelet count drop, and you wanna pick this up before the patient has a complication, i.e. a thrombosis. So, how do you make the diagnosis? Well, first, you have to think about it. Second, you wanna stop your heparin. Third, you're gonna check the ELISA to look for the anti-platelet factor four antibody. If you find a positive ELISA, you're gonna do a confirmatory serotonin release assay. What do you do with it? Let's have a practice question. So, a patient with a previous MI and ESRD comes in for a pulmonary embolism, and you treat with a heparin drip. On day five, the patient's left foot is cold. No pulse is present in the leg. The platelet count has dropped from 250 to 100K. You stop the heparin. What do you start? Your options are Fonda Paranox, Bivalarudin, Argotraban, and Warfarin. Everybody loves Argotraban, because that is the answer. You guys are smart. So, why, actually, why not the other things? You could do Fonda Paranox. You could do Bivalarudin. They're just a little bit more complicated in terms of dosing and whatnot. Warfarin's a no. You don't wanna give the Warfarin until the platelet count has reasonably recovered and the patient has a bridging anti-coagulated state in place, or you could induce what? Thrombosis, right? Or Warfarin, skin necrosis, all things we don't want. So, management of HIT, again, direct thrombin inhibitors are the drug of choice, Argotraban being the most popular. You could do any of the ones we talked about, and even if the patient has no thrombosis, you're going to treat to prevent that complication. So, again, you're not giving platelets unless the patient is exsanguinating and it's a really serious problem. In very unusual cases, you might think about IVIG and plasma exchange, again, to get rid of that antibody. Okay, diffuse intravascular coagulation, DIC. I think of this as bleeding, clotting, and fibrinolysis all wrapped up together, like all the problems in one. Typically, you're gonna have a patient who has some kind of event that's causing it, whether it's a bleeding event from trauma or sepsis, or they have an underlying medical issue like malignancy. You can do typical labs, all of your typical labs, and you're gonna see a mixed picture with coags that are abnormal, a low platelet count, a low fibrinogen, because you're consuming all of it when you're making clots, and then some split products that are gonna pop up as well if you check them. Again, we don't treat numbers, we treat patients. So if there's no bleeding, do not treat the patient's abnormal lab values. All right, here's a practice question. 30-year-old woman comes in with altered mental status, fever, and purpura. There is no bleeding. Her blood pressure is 110 on 58, heart rate is 110, respiratory rate is 18. You get some labs, and the platelet count is 25, PTT 20, PTT 58, hemoglobin nine, white count is 18, and creatinine is two. Which of the following treatments are appropriate after you start antibiotics for suspected sepsis? Do you give platelets, FFP, factor VII, blood, or nothing? Do you wanna give some platelets? Why not? They're 25K, and she's not bleeding. Okay, she does not wanna give platelets because the patient is not bleeding, is that correct? Correct, very good. We don't give platelets to people who aren't bleeding, so just be sad. All right, guys, sometimes you just have to be sad. It's okay. All right, we're gonna switch gears very quickly to hepatic failure. This is one of my favorite types of bleeding problems because it's so dramatic, right? You have a patient that comes in, imagine you're decompensated, cirrhotic, with portal hypertension, variceal bleed, right, like the worst candidate to clot ever. No platelets, no clotting factors, not a lot of hope. So this is a patient who's gonna have all kinds of problems. They're gonna have platelet sequestration in their enlarged spleen from portal hypertension. They're gonna have deficiencies in a variety of clotting factors because their liver doesn't make proteins. So they're gonna have a lot of abnormal tests as you would typically expect. How do you treat it? Well, don't forget to give vitamin K. Many of these patients do not have good nutritional intake, and this is an easy fix. Where I work, we do 10 milligrams of IV vitamin K each day for three days, and we do that. There's really no risk, right? These are really not clot-worthy people. Just give it to them. Don't even think twice. When there is active bleeding, then you have to think about balanced transfusion versus something that's a one-shot fix like prothrombin complex concentrate. That's a small volume. Giving a bunch of blood products is a large volume. You have to decide, do I want a small volume or a large volume? If your patient has been hemorrhagic shock and they need volume, then you might give those blood products. But if they don't, then you may be better off with PCC. You have to put it into context. Again, don't forget about checking fibrinogen. Most of these patients also have a low fibrinogen level. And when it comes to planning a procedure, a lot of times people will request, this is a very common thing, how often does your IR specialist request a platelet count of 100,000 in a person with advanced cirrhosis? I feel like it's all the time. And they say, start transfusing the platelets at least 12 hours ahead. That doesn't work. They just disappear. So the platelets need to go in right as the procedure's happening. That's it, one or two units of platelets. It's not gonna really do a whole lot, but it makes them feel better. You could also do DDAVP to increase the von Willebrand factor and factor VIII in circulation a little. It's not amazing, but everything helps. So what do you do? We're switching gears to, let's say, a trauma patient or someone who needs a massive transfusion, like a GI bleed. These patients are always hovering within the triangle of death. Have you heard of the triangle of death? In trauma, in our surgical world, the triangle of death is very reproducible. If you have a patient bleeding and you just let them keep bleeding or you can't control the bleeding, they enter the triangle of death. And that starts with bleeding. And as they bleed and they clot and they bleed and they clot and they bleed, they consume all their clotting factors. And they become coagulopathic. So they keep bleeding. And as they keep bleeding, they become hypothermic. And now they're hypothermic and they're hypovolemic and they've lost a lot of blood and they get cold and they get acidemic. And basically, it's just a triangle until they just die. If you don't interrupt the triangle, if you don't interrupt that process by controlling the bleeding, controlling the acidosis, and correcting their deficits and clotting, then they're not gonna survive. And so really, these massive transfusion plans, these heroic support efforts in the ICU always should include some kind of source control for bleeding, for sepsis, whatever is causing the problem. So when it comes to blood transfusions, there are a couple really good studies. Most of you are probably familiar with the PROPER trial. When it came out, it was a landmark paper. They recommended one to one to one or one to one to two, meaning a unit of platelets, a unit of FFP, and a unit of red cells to essentially create a whole blood transfusion, balanced transfusion. And in this way, you avoid some of the dilutional components of ongoing bleeding that you would have if, let's say, you just gave four units of red cells up front. Typically, any major hospital have some kind of massive transfusion protocol, which will include usually four to six units of red cells and FFP, but it takes a little while for them to get the platelets to you. So oftentimes, they will send the platelets later. So it's very common for people to initiate an MTP, and then they get behind, and they have dilutional thrombocytopenia. So always remember, when they send the stuff, you also need to ask for platelets if they don't automatically send them. So with one to one to one, there's no difference in mortality, but you get earlier hemostasis and decreased death by exsanguination in the short term. Also, the CRASH-2 trial came out, which showed that there's a benefit from the early administration of tranexamic acid to patients who have had a trauma with bleeding. So if you give it within three hours of the trauma, it shows decreased death and all-cause mortality. If you give it more than three hours after the trauma, it is dangerous, it increases the complication rate, so you have a very narrow window to make the intervention. All right, we've got a 20-year-old who is shot all up. He comes in somnolent, hypotensive, tachycardic. You start MTP, the nurses get it going, red cells, three units, FFP2 units, and a liter of saline are given. What do you give next? Red cells, FFP, platelets, or a liter of normal saline? Do we like to give lots of fluids to people who are bleeding? No, we don't. We do not like to do that, right? We always want to be giving balanced transfusion. So what do we give? Platelets, very good. All right, very quickly, von Willebrand disease. Patients with this condition will have an elevated PTT on screening. You can give DDAVP, which will promote the release of von Willebrand factor from cells, along with factor VIII, but you could also just give recombinant von Willebrand factor, which was much more effective. For patients who have hemophilia, we now have good factor VIII concentrate and factor IX concentrate availability, but let's say you don't want to think about this, you just want to get the job done, you can always just give factor VII or prothrombin complex concentrate, the most miraculous drug ever. All of you are familiar with Warfarin. It's been around for decades. In the past, we used to reverse it with FFP, but it takes so much volume. So if your patient needs a lot of volume and you want to give them massive amounts of FFP, go for it, but usually four-factor PCC is so much better. Also, don't forget to give the vitamin K. It doesn't hurt, it takes a while to work, but it will be helpful tomorrow. When it comes to antiplatelet agents, you just have to be sad. There is no good reversal agent yet, so you have to be sad. There are a number of trials which we've talked about in the last day and a half that show that giving platelets in the setting of an antiplatelet agent does not help. In fact, it increases the risk, so don't do that. You can wait for bentrasamib to come out. That's in FDA trials, but it's not available yet. You could also hook your patient up to ECMO, which is pretty hardcore, but if you wanted to get that stuff out, apparently that works, too. Now, dabigatran is the oral drug that has its own reversal agent. I know we're not supposed to use brand names, but the drug is Pradaxa, and the reversal agent is Praxbind, which is pretty clever naming, I think. Unfortunately, most studies for any problem don't include dabigatran, so I've never had a patient actually on it so that I could use the reversal agent, which is a bit of a downer. Bleeding with 10A inhibitors, again, you can give andexanet alpha, which is a reversal agent that is FDA approved for rivaroxaban and apixaban. Seroparentag is still in study, hopefully will be approved in the near future. And that is all I have. Thank you. Sure, the question is, can I talk about vitamin K, PO versus IV? I only see life-threatening bleeding. So I don't even think about PO, vitamin K. Remember, it's still going to take time for your liver to make new clotting factors with the new dose of vitamin K that gets into immediate circulation by IV form. So the last thing you want is to throw in the factor of will it be absorbed by the gut? Will this patient be able to swallow it? Are they having diarrhea from their lactulose? Oh, forget about it. Just give it IV. So it's immediately 100% bioavailable, 10 milligrams IV every day for three days would be what I would do. Yes, question? Did you talk about one-to-one-to-one versus whole blood? I did not talk about one-to-one-to-one versus whole blood. Dr. Kaplan's wondering what I have to say about whole blood. I think it depends on the patient population that you're taking care of. In an ideal world, we would just give whole blood. Decades ago, we separated it out. We thought that was very clever. Then we realized that you can't just give red cells. You also need FFP. Then we realized you can't just give FFP. We also need platelets. And here we are. We're ready to go back to whole blood. But I don't think it's the standard of care everywhere yet. It's certainly not widely available to do that everywhere. I will say that in the trauma population, we've really pulled back on fluids. We recognize how pathologic it is to give a lot of fluids to a bleeding patient. So there are trauma systems that carry blood in the field. With the paramedics, start the blood on the scene. The standards for traumatic bleeding are one liter of fluid, and then you go to blood transfusions. We used to do two. Now one is the standard. Pretty sure once we get it worked out, we're going to just go back to whole blood altogether. But it's not yet the standard widely. So don't be sad about that. Mechanical mitral valve and bleeding. Mechanical mitral valve and bleeding. Oh. Well, when people are bleeding to death, I don't really worry about anything else. I forget altogether that they have a mitral valve at all. I have to think, try before you buy. That's the slogan. And I really have to think about it. Where's the mitral valve? Don't care. I'm joking. I care. I'm joking. I care. I care a lot. I care globally. When people are bleeding to death, those are the only kinds of people I see, then yes, you need to fix the bleeding, and then you've got to fix the problems from fixing the bleeding. And that's how it goes. If it's a problem that you can externally compress, let's say someone ruptures their AV fistula, they've lost two liters of blood in the emergency room, and all you need to do is compress the fistula and you can control the bleeding. They don't need to have their anticoagulation reversed. They need a surgeon to come and put a stitch in it. That's a person who I might just hold pressure on until the surgeon gets there for 30 to 60 minutes and the OR gets a room ready. I think there are unusual circumstances where you can externally control something with a manual compression, a blood pressure cuff, a clamp, and outside of that, where there's a quick fix that doesn't involve a major cavity invasive surgery, yeah, maybe I'd wait to reverse it, but outside of that, yeah, save a life. Worry about it later. The cardiologist will yell at you later. What? I'll say no more. That was great. Thank you. You're welcome.

bleeding management

thrombocytopenia

coagulopathy

viscoelastic studies

massive transfusion

anticoagulants

trauma care