Fresh frozen plasma

Historically, that was the instinct.

Practitioners would reach for fresh frozen plasma or FFP.

But relying on FFP alone to reverse severe warfarin bleeding is a major clinical mistake.

Wait, why? The factors are in there.

Why doesn't it work?

The issue is concentration and logistics.

FFP does contain coagulation factors, but they are very, very dilute.

Oh,

These patients need two large-bore IVs and continuous monitoring.

These patients often need blood transfusion, and we have a whole... series of episodes on blood transfusion and cryo and FFP and all that so check that out if you're interested but some of these patients need massive transfusion protocol as well so you need good vascular access you quite literally that's one of the smallest things you can do that can have the biggest impact and good vascular access is in the eye of the beholder a little bit most people would say at least to 18 gauge IVs.

Some would say, let's try to get even bigger ones, 16 gauge.

Other folks would say, you know, let's put in something like a cortis or a trauma line or a sheath.

And often any type of kind of balanced blood product resuscitation is important.

What that means is a much larger discussion.

But if you're given a couple units of blood, you should be thinking about if the patient should get FFP and platelets as well, you know, some degree of balanced transfusion.

And never forget the calcium.

Let's tackle the blood first.

The team orders transfusions of platelets to get his count up and fresh frozen plasma, or FFP, to provide immediate circulating clotting factors.

Both crucial.

But they also order intravenous vitamin K.

By administering vitamin K intravenously, we bypass the blocked gut entirely and deliver the raw materials directly to the liver.

Hoping that surviving hepatocytes can use it to build clotting factors.

While the FFP provides a bridge of pre-made factors.

Exactly.

This is the time from initiation of clotting at the point of separation of the resistance curves to a resistance level of 20 mm.

For prolonged kinetics, cryopercipitate and fibrinogen concentrate, and to a lesser degree FFP, can maintain or increase the circulating fibrinogen to increase the rate of polymerization.

And there is a trial that has compared fibrinogen concentrate versus cryopercipitate for this purpose.

Okay, next is MA or maximum amplitude for TEG and MCF or maximum clot firmness for Rotem.

Transfusion of packed red blood cells, transfusion of fresh frozen plasma, transfusion of platelets, cryoprecipitate, fibrinogen, and prothrombin complex concentrates.

need for additional interventions for hemostasis, whether interventional, endoscopic, or surgical, time to bleeding control, and mortality.

Transfusion of red blood cells, FFP, platelets, cryofibrinogen, and PCC was reported as the number of units and volume of the transfused product and the number of patients being transfused.

To simplify the reporting of the results.

Its factors two, seven, nine, and 10.

An alternative is fresh frozen plasma, which contains all of the clotting factors.

And these are usually combined with vitamin K.

All right, so that's Warfarin.

Protein C, with the help of protein S, breaks down factors 5 and 7.

What factors are in plasma or FFP? All of them.

What factors are in cryo or cryoprecipitate? Remember, cryo is most often given for low fibrinogen, so it contains 1, or fibrinogen, von Willebrand factor, 8, and 13.

Antithrombin 3 is another natural anticoagulant produced by the liver that inactivates thrombin or factor 2 and factors 9, 10, 11, and 12.

So the percentage of decrease in amplitude at 30 minutes after maximum amplitude.

So this is all fibrinolysis or clot breakdown.

In general, if you have a prolonged R time, you're going to transfuse FFP or plasma.

For a decreased alpha angle, you'd want to transfuse cryoprecipitate.

Because heparin depends on antithrombin, a patient with low antithrombin levels are not going to respond to heparin, and we call this heparin resistance.

So if you picture a cardiac surgery patient who's receiving that full heparin dose, but the ACT won't come up, one classic cause is antithrombin deficiency, and the treatment is usually to replace that antithrombin with antithrombin concentrate or FFP, which contains that antithrombin.

For a typical heparin infusion, you monitor the aPTT, usually aiming for about one and a half to two and a half times normal or an anti-Xa level.

For high doses like cardiac surgery, you're gonna use the ACT, 'cause the PTT is not going to be accurate for these high levels.

It works within minutes, and it's a small volume.

Always give vitamin K along with it because the PCC is gonna wear off, and then the vitamin K is gonna provide that sustained reversal.

Well, what about FFP? We've heard of this before, giving FFP.

It does work, but it requires a really large volume, so it's gonna take time to thaw.

You are lowering the interleukin-6, lowering the ammonia, and stripping out the excess von Willebrand factor that causes those microthrombi.

And at the same time, if you use donor fresh frozen plasma or FFP as your replacement fluid, you are immediately replenishing the patient's depleted coagulation cascade.

You're giving back all the good stuff.

Factor two, factor seven, factor nine and ten.

Yeah,

that's a recipe for disaster.

So by using two thirds FFP, they are actively replacing the coagulation cascade.

But they didn't use 100 percent FFP because massive FFP exposure brings its own severe toxicities, which I definitely want to talk about later.

Now, let me explain.

Well, if you're like, "What are we talking about here? Don't we do component therapy?" Yes, we do packed red blood cells and then platelets, and then we do, uh, FFP.

But the reason that during resuscitation or massive obstetrical hemorrhage we do a one-to-one-to-one ratio of those three is 'cause we're kind, trying to constitute what? Whole blood.

That was the original Parkland and UT Southwestern trauma and maternal resuscitation.

That leaves 15% of the population that's Rh-negative, and then you gotta get some donors.

There's the plug there for giving blood.

You've got to get some donors to actually donate their Rh-negative blood, so there's just not a lot, okay? The whole idea of component therapy, breaking up red blood cells, breaking up the platelets, and breaking up the FFP, is you try to get more bang for your buck per donor.

That, that, that's the main reason, okay? However, it is logistically easier to take donated whole blood and transfuse that into a patient, because what they are missing is all three components at one, plus you get the extra volume.