Virchow's Triad – Thrombotic Disorders

00:01 Okay, let's talk now on the flip side.

00:04 We've talked about bleeding disorders.

00:06 Let's turn to thrombotic disorders or hypercoagulability, also, called, “Thrombophilia,” meaning, “Loving tooth thrombose.” What leads to a thrombus? This is a very important concept, again, Virchow, our good German pathologist, who was kind of the father of pathology.

00:25 Identified kind of a triad, the things that will contribute to driving thrombosis.

00:32 And there are three components to it hence the triad.

00:35 Number one is probably going to be endothelial injury and that makes a lot of sense because endothelium is going to be really, really important, in terms of driving, both coagulation, but also, anticoagulation.

00:47 And if the endothelium is not happy, you're going to have a tendency to be more pro-thrombotic.

00:52 So, endothelium is one angle of the triangle of the Virchow’s triad.

01:00 Another one, is “Stasis” or “Turbulence,” so, basically, abnormal flow.

01:04 If you have blood sitting around for a period of time, you will get stochastic activation of coagulation factors and you'll form a clot.

01:11 If you have turbulence, that's actually on the backside of turbulence, you'll have eddy currents, so that you will have focal areas of stasis.

01:20 So, abnormal flow, non-laminar flow, is also going to be something that will lead into thrombosis.

01:27 And the final component of the triad is, “Hypercoagulability.” And this is much more than kind of a general concept, there are a number of things that we'll talk about shortly, that lead to a greater tendency to have thrombosis.

01:42 You make more coagulation factors, you make less anticoagulation factors, you activate coagulation inappropriately, all of these things will contribute to thrombosis.

01:55 Now, it's not just those three things in isolation, but they all crosstalk with one another.

02:00 So, endothelial injury, actually, because it's important for driving both, coagulation and anticoagulation, will lead to hypercoagulability.

02:08 An endothelial injury, clearly will lead to areas of stasis or turbulence.

02:13 And stasis or turbulence in turn will impact endothelial integrity, so, all these things crosstalk.

02:21 But in general, when we have a thrombus, one or more of Virchow’s triad has been in play.

02:29 So, endothelial injury, is going to be a major driver for arterial thrombi and it's mostly platelet-driven.

02:37 Keep in mind, as we talk about clotting that occurs anywhere in the vascular system, if there's a lot of flow, it's going to be very hard for coagulation factors alone to drive a thrombus, because they're going to be diluted, they're going to be driven downstream very quickly.

02:54 So, in the arterial circulation, if a thrombus occurs, it's usually because we've had endothelial injury and we've recruited platelets that can stick quite firmly, quite avidly to the underlying von Willebrand factor for example.

03:09 So, arterial thrombi, tend to be due to endothelial injury and are platelet-driven.

03:15 Conversely, where there's stasis, now we can have local activation of the coagulation factors and so, in venous thrombi, it's usually coagulation factor driven, not so much by platelets.

03:29 So, we don't have endothelial loss, we don't have exposure or underlying von Willebrand factor and so the venous thrombosis tends to be driven by coagulation factors.

03:44 Thromboembolism, let's just kind of look at a couple examples, three examples to be exact.

03:48 So, here we have a pulmonary embolus, the big inverted y-shaped white thing up top, is a pulmonary artery, that branches into the right and left pulmonary arteries and that defect in the whiteness, is a pulmonary embolization.

04:08 This occurred, almost certainly because of relative stasis, in the lower extremity veins and that could have been due to a variety of things, including just inactivity and then that thrombus that formed there, in the venous circulation, breaks free, goes through the heart and impacts in the pulmonary circulation.

04:31 So, that's a pulmonary embolism or a thromboembolism.

04:35 Now, we're on the arterial side.

04:37 So, that large circle near the top with the white defect.

04:42 That white defect is in fact the normal flow, we’ve put in a radio opaque dye, so that, we can see where the lumen is and there's a vast darker area around that.

04:53 That is an abdominal aortic aneurysm and the darker area, that is excluding the dye, is a big thrombus.

05:01 And it's occurring there, because we have abnormal flow, we have a dilated aorta, so, we can have relative areas of stasis and in that setting we are now getting a thrombus that forms.

05:15 We can also have, in the right ventricular chamber here, a thrombus indicated by the arrow that is forming, as a result of endothelial dysfunction.

05:24 So, we now have abnormal anticoagulation, regulatory effects occurring and we're getting a thrombus that's formed.

05:35 So, we have the three different components of Virchow’s triad.

05:39 On the pulmonary embolism, that's forming due to stasis.

05:42 We have abnormal flow in our aortic aneurysm.

05:46 And we've got abnormal endothelium and so all of these will be leading to thromboembolism.