7.4 Aortic Dissection and Aneurysm

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Next section is aortic dissection and aneurysm.

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We're going to start with dissection and then work our way to aneurysm.

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So in an aortic dissection,

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the idea is that you've got this blood vessel wall,

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which contains an intima,

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a media,

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and an adventitia.

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And of course,

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the blood would be flowing up through this wall.

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Now as the blood flows through the wall,

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there's a tear in the intima.

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The blood then goes through the intima,

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which is of course super thin,

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and then gets access to the media and begins to rip across the media.

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dissecting the wall of the blood vessel,

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and so that's an aortic dissection.

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Here's a picture of the aortic dissection,

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and again the same notion,

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blood is sort of running along this vascular channel,

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and for some reason there's a little tear in the intima,

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that then allows blood access to the media,

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it rips through the media and begins to go through the wall.

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So this is an example here of blood ripping through the media

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of the blood vessel wall.

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Now, it's important to know that you don't get a dissection unless you have two

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things.

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So an aortic dissection requires two things,

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and this is really the summary of the entire disease.

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First of all,

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you need a ton of stress.

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You're not gonna be able to normally rip through the media of

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the wall unless you have a lot of stress present within that bloodstream.

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And so it usually occurs within the proximal 10 centimeters of the aorta.

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That's right off the origin of the heart.

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So it's coming directly from the heart.

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It's got a ton of pressure associated with it.

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And it's at that point,

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within that first 10 centimeters of the aorta,

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that you're going to find an aortic dissection.

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So that's principle number one.

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Principle number two is that you're not going to get a dissection,

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even within the first proximal 10 centimeters,

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unless you have preexisting weakness of the media.

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This is very important.

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You must have preexisting weakness of the media.

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So then the discussion arises.

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how could you get pre -existing weakness of the media?

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And if you understand this,

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then you understand the causes of aortic dissection.

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The most common way by which we can get pre -existing weakness of the media would

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be hypertension.

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Now what's the idea here?

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Let's take a blood vessel and remind ourselves that we have an intima,

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a media,

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and an adventitia.

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Now, it so happens that the intima,

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media, and adventitia all contain cells that are living,

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and therefore,

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these cells of the intima,

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media, and adventitia also require oxygen.

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Now, they happen to be lucky enough to be carrying blood,

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so the oxygen that's sort of running through the blood will also be able to

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diffuse and will be able to feed the intima,

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the media,

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and the adventitia.

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And that's the normal way by which the blood vessels remain alive and healthy.

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However,

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in the proximal first 10 centimeters of the aorta,

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you know that the wall is super thick.

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So very early on in the aorta,

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in the very proximal part of the aorta,

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as it comes off the heart,

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the wall is very thick,

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and the diffusion of oxygen across that wall is not sufficient

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to be able to feed the entire wall.

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And so in the adventitia here,

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if you go back to normal histology,

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in the very thick -walled blood vessels,

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we've got

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something called vasovasorum.

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So vasovasorum are these tiny blood vessels that provide blood to

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the outer aspect or the outer half of the blood vessel wall.

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Now what happens in a patient with hypertension is that they're going to get hypertension and

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hypertension results in highline arteriolosclerosis.

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Remember that discussion?

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And so that high blood pressure will result in highline arteriolosclerosis

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of these vasovasorum.

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That would decrease the caliber of the lumen.

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which would decrease the amount of blood flow going through them,

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and so now you're gonna get decreased blood flow to the outer half of this

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blood vessel wall.

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That's then going to result in atrophy of the smooth muscle out here,

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which will result in weakening of the media so that

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a dissection can occur.

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So that's a very high yield association,

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and that's the easiest way to understand why hypertension is

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the most common cause of an aortic dissection.

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The other way by which you can get weakness of the media would be to have an inherited defect

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of connective tissue.

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Remember that the media contains a lot of elastic tissue,

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especially in that initial portion of the aorta that comes off the heart.

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And so if a patient has a defect of fibrillin,

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which is also called Marfan syndrome,

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remember that fibrillin is the molecule upon which elastic fibers

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are laid down.

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And so if there's disruption of elastic,

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then there would be weakening of the media.

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In addition, a disorder called Ehlers -Danlos Syndrome,

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in which patients have defective formation of collagen,

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can also result in weakening of the media.

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So again,

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you need to have weakening of the media before this dissection will occur.

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When patients get a dissection,

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they present with sharp tearing chest pain that radiates to the back.

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The major complication of aortic dissection is pericardial tamponade.

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This is the most common cause of death,

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but you can also get rupture with fatal hemorrhage,

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and you can also get obstruction of arteries that are branching off the aorta.

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For example,

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let's say that this is the heart,

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okay, and we've got this proximal 10 centimeters coming off

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the heart, and then let's say that blood is flowing through here,

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and all of a sudden we get a dissection.

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Now when we get a dissection,

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blood's gonna go into the media,

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and then it's gonna dissect through the media.

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So there's a couple possibilities.

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It can dissect through the media,

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and then it can go down.

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And as it goes down,

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imagine if eventually we've got the renal arteries coming off here,

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it can compress and push down on the renal artery,

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which would then,

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of course,

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create obstruction,

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and then end organ ischemia to the kidney,

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as one example.

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Another possibility would be that

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we get this dissection,

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and then the dissection goes backward,

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and when it goes backward,

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it can get access to the pericardium,

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and so we can get filling of blood in the pericardium,

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which would be called pericardial tamponade,

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and that's the most common cause of death,

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and the third possibility would be to simply rupture out into the mediastinum,

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and if we blew through the entire blood vessel and then ruptured

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out into the mediastinum,

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that would result in fatal hemorrhage.

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So these are the complications of aortic dissection.

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The next discussion that we want to have concerns aneurysms,

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and before we even get to aneurysm,

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You just need to know a couple basic principles and everything is downhill.

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So first of all,

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the first principle is what is an aneurysm?

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An aneurysm is a balloon -like dilatation of a blood vessel wall.

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So here's a normal blood vessel and we've got this balloon -like dilatation of the

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blood vessel wall.

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So that is an aneurysm.

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That's point number one.

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Now aneurysms can occur in classically two places.

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You can get it in the thorax and you can get it in the abdomen.

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So you can have a thoracic aneurysm or you can have an abdominal aortic

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aneurysm.

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Those are the two.

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two classic locations in the large blood vessels.

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Now what you need to know in order to understand how these might occur is

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that the only way you're going to get an aneurysm is you need weakness in the aorta

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wall.

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You must have weakness in the wall.

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It's the weakness in the wall that allows this balloon -like dilatation to

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form.

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In the case of the thorax,

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so in the thoracic aneurysm,

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the way by which you're going to get weakness in the wall is classically seen,

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or the classic example is tertiary syphilis.

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Now what's the idea here?

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The patient's got tertiary syphilis,

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and remember that syphilis is an end arteritis.

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You get inflammation of the small blood vessels.

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So imagine if this is the intima,

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this is the media,

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and this is the adventitia in the thorax,

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you know that within the thorax,

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the adventitia contains

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these vasovasorum,

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which are important for feeding and keeping this blood vessel wall healthy.

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Well, if the patient gets an end arteritis of these vasovasorum,

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that's gonna decrease the blood flow going through the vasovasorum,

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and that's gonna then result in atrophy of the wall of

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the blood vessel,

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just like we kind of talked about previously.

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And so when you get atrophy of the wall of the blood vessel,

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that would make this vessel wall weak,

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and the weakening of the blood vessel wall would then result in an increased risk.

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of getting this balloon -like dilatation,

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which again would be a thoracic aneurysm.

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And so in the thoracic aneurysm,

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the key mechanism by which we weaken the wall is classically tertiary

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syphilis.

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That's a classic one.

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There are others,

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but that's really the classic high -yield one to be familiar with.

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Now, when you have tertiary syphilis,

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one of the classic findings is tree bark appearance of the aorta,

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and that's because you're getting all of this scarring and fibrosis

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due to the end arteritis that's occurring due to that tertiary syphilis.

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And so this is a picture of tree bark appearance,

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and what I'm trying to highlight,

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this is the surface of the aorta here,

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and you can see that there's fibrosis,

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which is then subsequently giving it a tree bark -like appearance.

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So what are the complications of a thoracic aneurysm?

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Well, the most important,

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perhaps the highest yield,

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is that you can get dilatation of the aortic valve root.

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Now here's the idea.

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If this is the heart,

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and you've got this aorta coming off of it,

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if you get a balloon -like dilatation of the thoracic

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aorta, that's going to pull on this root of the aortic valve.

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And as it pulls on the root of the aortic valve,

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that's going to result in aortic insufficiency,

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and that's the highest yield complication.

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of a thoracic aneurysm.

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You can also get compression of mediastinal structures.

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As this thing balloons out,

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it can compress upon other structures within the mediastinum,

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and then the third complication would be to get thrombosis or embolism.

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When you've got a balloon -like dilatation in any

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blood vessel,

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remember that normally blood flow is laminar,

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so you've normally got this laminar blood flow,

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but when patients get an aneurysm,

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that results in some disruption of that blood flow,

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and as you lose the laminar

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flow of blood,

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you increase the risk for activation of the coag cascade.

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So it's not uncommon to get thrombosis along the wall

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of the aneurysm.

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Now, of course,

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if you get thrombosis,

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the next thing that can happen is this thrombus can eventually embolize,

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and so that would be the complication of thrombosis.

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So that's why I say that you can either get thrombosis or embolism.

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Now,

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when you think about the abdominal aortic aneurysm,

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it's very similar.

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You're going to get a balloon -like dilatation,

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but instead, this time,

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we're in the abdominal aorta.

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Super high yield to know that this is going to occur below the renal arteries,

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but above the aortic bifurcation.

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And so here's a picture highlighting that we are above the aortic bifurcation,

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but below the renal arteries.

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And this blood vessel should have normally been like this.

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However, we've got this balloon -like dilatation to make the blood vessel aneurysmal.

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All right,

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so this is a key picture which highlights an abdominal aortic

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aneurysm.

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Now the question would be,

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what makes this wall

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become weak such that the aneurysm forms.

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And it occurs due to atherosclerosis.

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That's the key way by which this wall becomes weak.

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Let's remind ourselves that you've got an intima,

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you've got a media,

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and you've got an adventitia.

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And when you're way down in the abdominal aorta,

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remember that their oxygen that's coming from the blood basically

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feeds the entire thickness of the wall to keep the entire thickness of the wall

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healthy and alive.

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Now let's assume that the patient's got atherosclerosis,

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so they've got thickening of the intima.

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Now they've thickened that diffusion barrier for oxygen to be able to feed the wall.

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That's going to result in less oxygen getting to the wall,

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and so you're going to get atrophy.

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of the wall,

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and when you get atrophy of the wall,

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that's going to create weakness within the wall,

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which will then allow for that balloon -like dilatation to occur.

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So that's why I say here in your text that it's predominantly due to atherosclerosis.

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Now, when you think about the classic patient,

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it's going to be the patient that's got all of the risk factors for atherosclerosis.

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For example,

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higher incidence in males,

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higher incidence in smokers,

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higher incidence in patients greater than the age of 60,

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and high association with hypertension.

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So these are all risk factors of patients who develop atherosclerosis.

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And in fact,

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one of the most common locations of atherosclerosis in the human body is the

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abdominal aorta.

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How do these patients present?

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They present with a pulsatile abdominal mass that grows with time.

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As you get an aneurysm,

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one of the complications of aneurysms is that you've increased the wall stress as you get the aneurysm,

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and so these aneurysms can over time expand.

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And as they expand,

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then the feared complication becomes rupture.

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So the patients will present with a pulsatile abdominal mass that will grow with

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time.

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The major complication,

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of course, is rupture,

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especially when it's greater than 5 centimeters.

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This number is key.

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Greater than 5 centimeters,

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there's a very high risk of rupture,

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and when it ruptures,

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it will present with a triad of hypotension because they're bleeding,

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a pulsatile abdominal mass because you'll be able to put your hand on the abdomen and feel

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that aneurysm,

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and it'll be pulsatile because blood is flowing through it,

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and then there'll be flank pain.

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And so these are some of the classic signs and symptoms of a

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ruptured abdominal aortic aneurysm,

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which of course is a medical emergency.

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So that completes this section on aortic dissection and aneurysm.

7.4 Aortic Dissection and Aneurysm

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