[SOUND] [BLANK_AUDIO] The Direct-Thrombin inhibitors work on clot-bound thrombin, and that is the holy grail. To actually get the clot to stop growing and to allow the body to break it down. It prevents the activation of both free thrombin in the blood as well as the clot-bound from thrombin. And it also prevents the activation of platelets by thrombin.
Remember one of the main platelet activators is thrombin. So if you have an anti-thrombin, then that helps prevent more platelets from clumping together, and therefore helps with the clot situation. If you have a new clot forming on a tool in the brain or anywhere else that you're using intravascularly, such as coiling an aneurysm, or a catheter, or a guidewire, that's almost always going to be platelets. You want
to stop thrombin from from activating platelets and you want to use an antiplatelet agent such as Reopro to get rid of that. Heparin does not treat those very well. The antiplatelets work like magic. So here is the situation with all our antiplatelets, and heparins, and how they work, and what dose we use. This is very confusing. It's hard to understand.
You need to spend some time studying this because this is a very important subject, and it really can make a difference in your patient and clinical outcomes. This is an important concept. Also, how do you reverse heparin that you've given? At the end of the case, they have gotten 10,000 units over a period of a couple of hours. How much protamine do you give them? We know that protamine is a
drug that can reverse heparin, but how much of it do you give? You don't wanna give too much. Protamine itself can have side effects. You can be allergic to protamine because protamine is used in insulin. So you have to be aware of that, but you also don't wanna give too much of it and change the coagulation cascade. So how do you calculate how much protamine to
give? Well, the first thing you need to realize is that heparin has a half-life of about one hour, maybe 50 minutes, maybe 70 minutes, something like that. But let's focus on the one hour cause that allows us to calculate how much heparin is on-board, and that's the key. You need to know how much you're treating not how much you gave. You need to know how much heparin is actually still in your body.
So you have to calculate how much is on-board, and this is how to do it. Let's say you gave 5000 units of heparin at 9 AM. Well that means at 10 AM there's 2500 units left, at 11 AM, there's 1250, and at noon there's only 625 left. Let's say you gave another 3000 bolus at 10 AM, so that means at 11 AM you got 1500 units,
at noon you have 750, you gave another 3000 at 11 AM. So the total of all this is 625 + 750 + 1500 from the last bolus, which means you've got about 2900 units of heparin that's still on-board. You wanna reverse that. Remember that 10 milligrams versus 1000 units of heparin. So in this particular case if you reverse with 20 milligrams of
protamine that'd get rid of about 2000 units of heparin leaving 900 units of heparin. 900 units of heparin is homeopathic, doesn't do anything. So I would give about 20 milligrams of protamine in this situation to get the dose down to where you're not gonna have bleeding, you're not gonna have trouble with any sheath that you pull, and you're not gonna have any problem with bleeding in
your brain, for instance, and you've reversed all the effects of heparin down to a normal level. Another practical point is, how do you stop oozing around a puncture site? This happens to us
and Plavix on-board for their whatever disease state they've got. And at the end of the case there'll be a little
oozing around the puncture site even if I've used a closure device. How do you stop that? Some people know about the lidocaine with epinephrine trick, but the key thing to remember about this is it's not really the epinephrine as a vasoconstrictor that's helping the problem. Remember, epinephrine is a direct platelet activator, and therefore, when you use it the platelets clump and that plugs
the hole. So just use about 10cc of lidocaine with epinephrine, saturate the area that you're working on, and hold pressure there just for a second. The platelets will be activated and all the oozing's gonna stop. This is the difference between the regular heparin and low molecular-weight heparin. They're all heparins. It's
reaction. It is prothrombotic. It's not thrombocytopenia just because your platelets go away, what happens is your platelets begin to stick to each other, and they turn into microemboli. So it's a multi-embolic thrombotic situation where everything is clotting in your body, and paradoxically, it looks like you have no platelets.
Well you do. It's just that the platelets are all sticking to each other. They clog up all the various arteries and arterials, and you get thrombocytopenia secondarily. It's essentially a severe drug reaction. We miss it all the time. We have patients that seem to be clotting, we give them more heparin, it doesn't work, we give them more heparin, it doesn't work, and then we're in a mess,
because we've made their allergic reaction even worse cause we keep giving this to them. We cannot treat this with more heparin. We cannot treat this with more Lovenox. What we have to do is give them a direct thrombin inhibitor such as the bivalirudin, lepirudin, hirudin, dabigatran. On the table during a case, the bivalirudin is very good to use, it's
quick, it's to the point, it actually acts as an antithrombotic with these things. And lepirudin has a much longer half life, but it'll get the job done too because these patients are in big trouble, frequently. So good luck with all of the treatment of the patients who we we're talking about here. This is a difficult subject, there's
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