All right, so welcome back to the Internet Book of Critical Care podcast.

I'm here with Adam Thomas, and we're going to talk about disseminated intrabascular coagulation, or DIC.

Yay, death is coming.

Yay.

Oh, boy.

So Josh, we already set the groundwork for this with MTP and a lot of other prior post. You've

been building towards this with a little heparin resistance in COVID, some other coagalopathies,

but we're finally getting to one of the cornerstones of critical care, aren't we? Yeah, yeah.

So today we'll bend a lot of time around pathophys and a lot of time around labs and then we'll brush up on

our causes and our treatment so josh let's get straight into this general concepts of dIC we alluded to

some flavors on our last post around massive transfusion so what are we talking about here why does this

happen because it makes sense when I cut off my finger,

I clot. That's good. What is going on in DIC that causes multi-organ failure? Yeah, exactly.

So ideally, coagulation should always be focal. You know, we cut ourselves or there's some sort

of interim bleeding and we want to clot off as few capillaries or vessels as possible,

allow tissue healing, and then kind of lice out those clots and resume

being normal tissue. The problem with disseminate intravascular coagulation is dissemination of

coagulation activation. So basically, the coagulation cascade is activated in a non-focal

fashion throughout the body. And that can cause a lot of problems. So you can have

microvascular thrombosis throughout the body, which can cause tissue dysfunction, so you're not getting enough blood to the tissue, not necessarily because your cardiac output

is low, but because all the microvessels are kind of starting to become thrombosed.

You can develop macrombosis where you get dvets or pulmonary emboli or kind of like observable

...