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[00:00:00] Good morning everyone, and thank you for joining us for today's episode of Behind the Knife. I'm Luciano Del Bono and joined by my fellow residents, Andrew Wong, Carolyn Judge, and our faculty, Dr. Frank Davis, and our program director Dr. Robert eu. Today we'll be discussing the management of Type B aortic dissection with the focus on the increasing use of TVAR in uncomplicated dissections.
We'll spend about 10 minutes on a brief subject overview and then spend the remainder of our time discussing controversial and nuanced decision making. And we will end with quick hits to reinforce key concepts. So to begin, Carolyn, could you briefly describe what type B dissection is and how they're classified?
Absolutely. I'll first define an aortic dissection, which is the propagation of a potential space in the intimal medial layer of the arterial lumen caused by an intimal tear. Blood tracks into the space creating a false lumen which can expand approximately or distally. The Stanford classification system historically categorized [00:01:00] dissections as type A, if they involve the ascending aorta and type B if they were distal to the left subclavian artery.
More recently, the Lombardi classification system was developed, which divides the aortic iliac arteries into zones one through 11, and names dissections according to their proximal extent or entry, tear, and distal extent. The Lombardi classification system defines a type B dissection as one with an entry tear distal to the left subclavian.
Great. So moving more to the clinical realm, let's talk about how these patients will typically present. Andrew, do you mind taking this? Yeah. Classic symptoms of aortic dissections include tearing chest or back pain that is commonly with severe hypertension. Additional symptoms may reflect malperfusion of branches of the aorta, including the visceral.
The spine, lower extremities and renals, and it's apportioned to differentiate dissections that present with or without malperfusion as it determines a patient's course in the hospital. A dissection that presents without malperfusion [00:02:00] is called an uncomplicated dissection compared to those that present with malperfusion, which is called a complicated dissection.
Malperfusion occurs in about a third of, in a third of dissection patients with about half due to mesenteric ischemia and the other half due to lower extremity emia. The 30 day mortality with visceral ischemia is about a third of patients, despite surgical management that compared to one in 10 patients without visceral ischemia, these now perfusion events are about 80% dynamic and tend to occur in patients who are generally younger, but usually these present emergently.
Wait a second, Andrew, what do you mean by dynamic? What's the difference between dynamic and static? Yeah, so a dynamic outflow obstruction is generally. One that occurs at different parts of the cardiac cycle, obstructing the entry to a visceral vessel versus one that's static is one that's there and consistently pressing and obstructing the vessel.
Sir, are you just trying to come up with a fancy way of saying the flat moves when the he beats? Yes. [00:03:00] Awesome. Alright, go ahead. Back to your description of how we work these patients out. So, the physical exam is extremely important. You have to go through a pulse exam to assess for signs of distal malperfusion, acute limb ischemia, and abdominal exam.
Okay. These findings generally help correlate what you would expect to be seen on further steps, including imaging. Okay, great. So now you suspect somebody who has a type B dissection. How would you approach this person if they present to the ed? So, generally classically, you would start with evaluation with the chest x-ray.
But it should be noted that about a third of patients with or an ORIC dissection have a normal study and only about 43% of patients with a type B dissection. Have the classic blood and mediastinum. Cardiac gated CTA is generally the gold standard the to evaluate which vessels are patent and which ones are not.
And in the, or we can use something called intra intravascular ultrasound to allow for accurate device sizing for initial [00:04:00] measurements. Since many times the, the noninvasive imaging such as the CT can be confounded by hypotension. Also echocardiograms can be used to evaluate type A, but really in these type B, aortic dissections have pretty limited value when going through these modalities.
The most important aspect on deciding what to use during your workup is determine whether there is a type A component and whether further cardiac evaluation is required, and whether or not there's any radiographic evidence of malperfusion that corresponds to your physical exam. Great. So. Kind of bringing this back.
So how would you define if somebody has a complicated or an uncomplicated type B dissection? So, a complicated type B dissection is whether or not there's a presence of any comp features that define complications such as rupture, malperfusion or high risk features. High risk features will define as an initial aortic diameter that's greater than 40 millimeters radiographic evidence of malperfusion, such as malperfusion of a [00:05:00] renal.
Or asymmetric contrast enhancement of that kidney. An entry tear on the lesser curve, which is at higher risk for rupture and bloody, or a peral effusion or hemothorax refractory hypotension or hypertension for greater than 12 hours despite three medications or refractory pain, or if this is a readmission from a previous evaluation of a type BA aortic dissection.
An uncomplicated dissection is generally medically managed with impulse control. This is classically with either esmolol, different calcium channel blockers, such as nicardipine or vasodilators as needed to achieve a blood pressure with a goal, generally less than one, less than 120 over 60. To reduce the aortic wall stress and to prevent further dissection, it should be noted that complicated dissections, again, as stated before, is about a third of cases that are considered surgical emergencies.
In patients presenting with severe hypotension and shock, generally have a [00:06:00] 60% overall mortality with a 29.3% mortality for those who undergo surgical intervention. Awesome. And just to add one thing there is, if you are initiating them on anti-hypertensive medications, you typically wanna start a beta blocker first before a vasodilator to re to prevent reflexive tachycardia.
But let's go into a case now. So 6-year-old patient presents to the EZ with back pain and hypertension on imaging. They're found to have a type aortic dissection without signs of malperfusion or distal limb ischemia. What are your considerations for managing this patient, Frank? Yeah, th Thanks, Luciano. I mean, I think this kind of is really where the rubber meets the road, and we were talking about patient cases here and.
Take the data that Andrew has talked about and Carolyn's talked about how you manage these patients on their presentation. So the case that Luciano just talked about, 60-year-old patient presenting the ED with back pain imaging suggesting a type B dissection, but without, that's the key thing. Evidence of mal profusion or dis limb ischemia, that is by definition and uncomplicated [00:07:00] patient uncomplicated type B dissection.
Initially, it's appropriate to get pain control, to get that patient comfortable. Hypertension control, as Andrew appropriately pointed out with beta backer, beta blockers, calcium channel blockers, all that, get that blood pressure down to that goal of less than one 20, but addition beyond starting those medical managements of an uncomplicated type B dissection, I'd also wanna know if there's any other high risk features of this quote unquote uncomplicated type B dissection that would get me concerned that it might transition into a complicated.
Type B dissection. So before you go on there, do you mind kind of going into more detail about what you mean about these high risk imaging features? Yeah, yeah, of course. So even though patients might present initially as an uncomplicated type B dissection based upon imaging criteria, and you're trying to manage their blood pressure, things that get me concerned that they're gonna fail, that medical management are some of the imaging criteria, such as if they present with initial aortic diameter on the dissection of greater than four centimeters or 40 millimeters.
Those patients are at higher risk of failing medical [00:08:00] management and progressing onto a complicated version. In addition, I also look at the diameter of the false lumen, not necessarily the true and false lumen together, but solely the false lumen diameter. And if that diameter is greater than 22 millimeters, again, studies have shown that that predisposes patients to likely fail typical bread and butter medical management.
Other things you wanna look at is, is there a full thrombosis or a partial thrombosis of the false lumen? Partial thrombosis of the false limb has been associated with continued progression of the aortic size and progression of the dissection. So that's another one that I'd be on the lookout for that standpoint.
Yeah. Great. So back to your management strategy. Yeah. How would you continue sort of managing this patient that is uncomplicated? Yeah. Yeah. So what I do is there, you see them in the emergency department, you get your imaging findings. You start them on your pain control, you start them on your anti-hypertensive regimen, and then you're gonna wanna admit 'em to the ICU, right?
Because you need to have. Hourly and minutely monitoring of this blood pressure and make sure you're titrating those medications appropriately to keep them within that sweet spot. Less than one 20 for systolic blood pressure. [00:09:00] Then over then in the next 24 to 48 hours, like you're gonna wanna re-image that aorta to confirm the stability of that aortic dissection and confirm there's no further progression of the dissection.
If that's true, then I'd start to slowly titrate their IV medications that you have, monitor for, drips onto oral medications. Again, confirming that you can keep them in that. One 20 to less than one 20 range for systolic blood pressures while making that transition. If during that transition they continue to display absence of pain and keep appropriate blood pressure management, then you can work towards maybe a discharge to the uncomplicated type B dissection.
If at any point during that algorithm though their pain ratcheted up, they can't control their blood pressure, then you need to reset and you need to say, has this now transitioned from an uncomplicated to a complicated type B dissection? So you have to keep your. Sensors up at all times, and that's why they're in the ICU there.
So apart from pain, are there any other labs that you would look out for? Well, I mean, I think that's also when they came in the ed, you're gonna get your typical CB, C, you're gonna get your typical basic, you'll [00:10:00] start with an A, B, G, and you're looking at your creatine to make sure there's no change in renal function.
You're following your lactates to make sure there's no signs of visceral or end organ ischemia. From that standpoint, you'll get those labs daily, and again, if those change, then again, you have to reevaluate, has this made a transition over from an uncomplicated to a complicated type B dissection?
Awesome. So going back to our scenario, let's see if we, let's change this up a little bit. So now we have a 65-year-old patient who complains that they have significant abdominal pain as well as back pain. Now the imaging shows that there is a dissection flap that extends into the SMA. Bobby, do you mind kind of walking us through the management for this type of patient?
Yeah, absolutely. And I think the management has really changed based on what we found from the International Registry of Acute Aortic Dissections or the Irad database. Michigan was a big contributor to this database, but it's an international registry, so it's across the the globe, and essentially what it helped to do is move the paradigm from treating complicated patients [00:11:00] with aortic dissection from open.
To endovascular showing that TVAR or thoracic endovascular aortic repair has a better survival rate than open repair in these patients. And a lot of people kind of wonder how does that work? I mean, we're talking about malperfusion into a visceral segment now, and we're really only covering up a small area in the chest of this dissection with the graft and.
What we're essentially looking to do is identify what we call the initial entry tear or the area highest up on the chest, where that aorta demonstrates that intimal flap that is allowing blood to get into the dissection plane. And our goal is to extend a graft that covers that and it hopefully lands in healthy aorta up top.
With that, we're hoping that we can promote aortic remodeling. There may be some adjunctive procedures that you have to do in this case, so. We know Malperfusion is [00:12:00] likely gonna force us to the operating room, and what we do specifically after that depends on what the CT scan looks like. We want to try to cover the entry, tear and land in an area of relatively normal sized aorta, so that may involve covering the subclavian.
In emergent cases, you can proceed directly to the operating room with covering that subclavian, and that's an acceptable risk in cases where you may have a patient who's on the complicated uncomplicated. Threshold, you may have time to do something like a carotid subclavian bypass, which has generally receives a class one recommendation to do before a tbar in which you're considering covering the subclavian to both reduce the risk of spinal cord ischemia and posterior stroke.
Or you may be able to use an adjunctive endovascular procedure such as a thoracic branch device or even laser fenestration, something on the table. And all of those sort of extend out of. Where we need to cover that primary entry tear. Certainly when you're doing A-T-V-A-R, the goal is to allow for [00:13:00] aortic remodeling over time by pushing that dissection flap over.
And so we really have to also talk about the timing of doing things. As you stated earlier, acute malperfusion is a surgical emergency. We gotta get that patient in the operating room, otherwise they're gonna have gut mal profusion and they're gonna die. And I think a lot of what Frank talked about in terms of impulse control, pain control in a full set of labs, those tenants certainly hold true, but we're gonna generally get that patient into the operating room and perform a thoracic endovascular repair, and we're gonna do that with groin access.
Most typically, we use the intravascular ultrasound to confirm that we're in the true lumen. A little takeaway if you're getting pimped or anything on your rounds about what's the true lumen and what's the false lumen on a CT scan in general, the. True lumen is the smaller of the two lumen, and we usually pick which side we access based on which iliac has flowed from the true lumen.
'cause it just makes it much easier. But you do have to keep in mind there are fenestrations, maybe up and down this entire thing that could allow your wire to traverse true [00:14:00] lumen to fall, lumen back to true lumen and anything like that. And so having an IVUS is really important. Is there a classic trajectory that the Drew Lumen kind of dissects or like the aorta dissects formula, like the drew and false women?
Yeah. Yeah. Thank you for the leading question. You know, we typically think of the sort of spiral pattern of dissection and often the sort of term that the left renal is left out sort of helps you to visualize that spiral pattern. We'll often see that dissections that involve the visceral vessels.
Mostly the celiac, SMA and right renal will tend to come off the true lumen with the left renal coming off the false lumen. And that's all kind of like anecdotal, but it tends to kind of hold true. Once you get down to the iliac system a little bit more, all bets are off. You may have dissections that involve both iliacs that don't involve the iliacs that stop in the para visceral segment.
And so it's really important to personally review these CT scans before proceeding to the the operating room. But. In general, you're gonna want to get these patients back in [00:15:00] there quite, quite quickly. Mm-hmm. Alright. Awesome. I guess my other question is, even with just covering the entry tear, I know there's talk about sort of extending some of these graphs, trying to get better at position down closer to the visceral section.
Yeah, I mean, I think, I think we, I'm gonna let Frank take some of the adjunctive measures that we can do, but in general, answering your question about where we extend these graphs down to. We get worried about covering a lot of the thoracic aorta in normal aneurysmal disease because we don't want to cover lumbar arteries and increase your risk of spinal cord ischemia.
In general, when we're talking about treating patients with a type B dissection, we're often talking about taking your primary T-bar graft. So that covered graph down to about the celiac because it helps to promote aortic remodeling the best. You do want to try to keep the celiac. Intact if you can, and not cover across it though there are some cases where because of an aneurysmal [00:16:00] degeneration acutely in the setting of your dissection, you do have to extend that down.
But now we're sort of fighting if the fringe is about the, the teaching lessons here, and the most important part is you just want to try to get these tears covered so that you can allow the aorta to start going back to remodeling. But I won't take the cool stuff away. Frank, do you want to talk about any of the.
The PET code or aptly named techniques? Sure, sure. I think body prob pointed out like the most important thing is covering the proximal interrater with a covered tvar graph. But in addition to help long term for these patients to prevent ans degeneration to prevent chronic dissections progressing to persistent aneurysms, there's been a multitude of different studies and designs for different graphs that.
Have sought to promote positive aortic remodeling. So I guess the two primary strategies that help for to prevent treatment failure and help promote positive aortic remodeling. One is called the Petco technique and the other one is called the stabilized. So super fancy names from the super fancy trials, but let's go through each one, one by one.
So the pet coat technique [00:17:00] involves both a composite device, so what this composite device is, is the proximal, or the highest end portion of the device is actually a covered proximal tvar component. The second part of the composite device is a distal part that's a bare metal component that it actually extends through the visceral segment to continue to promote positive aortic remodeling expansion of the visceral segment of the aortic.
And it's important. As you can imagine, that's a bare metal stent because you can't have a covered stent covering all your visceral segments. You'll get massive ischemia. So the distal bare metal stent exerts a low radial force pressure while also allowing for future reinterventions. Say in the end, the patient eventually develops negative aortic mono aneurysm of degeneration.
You can still go in there from an endovascular standpoint, so it allows you to still have options. And the old mantra in, at least in vascular surgery and other surgical specialties, is you wanna fail forward. So if your primary option. Long-term inpatients doesn't necessarily work. How can you set yourself up for the secondary intervention that might need to happen?
And the two trials that really [00:18:00] sta actually founded the petticoat technique was the stable one and stable two trials that demonstrated that the petticoat deficiency was improving visceral profusion in the acute period in both uncomplicated and complicated dissections. And the second strategy for promote positive aortic remodeling is what's called the stabilized technique.
Or this also stands for stent assisted, balloon induced intimal disruption. So stabilize much cooler. And what it involves is it's a combination of both the petticoat technique but also the balloon rupture of the dissection flap itself. 'cause that dissection flap between the dis, the difference between the true lumen and the false lumen is actually what you wanna open up or expand to allow for full aortic remodeling.
Okay, so in this case, you actually put in the bare metal stent and use a balloon to assist in rupturing that dissection flap to allow the bare metal stent to fully expand to the overall aortic diameter. And again, this, the whole purpose of these two techniques is to allow for positive aortic or monitoring, preventing the [00:19:00] long-term aortic mortality for patients, whether it's anal degeneration or future aneurysmal, an aortic rupture from this dissection that we can eat itself.
Yeah, and I think the really important part that we haven't really talked about all that much just yet is the timing of all these things. Mm-hmm. You know, certainly our complicated dissections were taken immediately to the operating room or quickly to the operating room in the uncomplicated or managing medically, though we talked about some high risk features such as that initially aortic diameter, that's gonna prompt you to consider repair early.
But what does early mean? And we've traditionally divided this up into three different categories of timing. One is the acute phase. The second is the subacute phase, and the next is the chronic phase. And really what we're talking about with the acute phase is this one to 14 days, so one to two weeks where the aorta is incredibly fryable and at high risk.
The plaque, or excuse me, the wall itself, that flap is highly mobile and can make it very challenging and uncomplicated cases to get the [00:20:00] remodeling that you're looking for. Now. That being said, there are ongoing studies looking at how early we can intervene on these things to promote early remodeling, but a lot of that is where these Petco and stabilized techniques come into play.
Because if you can imagine at the distal end of your T-bar graph, so that one that's furthest down, if you've got hyper mobile flap that's going up against a rigid T-bar, you may create a distal tear or a stent induced. New entry, tear a sign, a DS sign. And so that may actually put you at a higher risk of having visceral malperfusion.
And so we really get a little bit nervous dealing with these acute phase. It seems like the subacute phase, the 14 to 90 days is where we may have a lot of room to to improve. You still have relative mobility of the dissection flap, but it's much more stable. And so you have the opportunity to perform an intervention that would not be at high risk for.
For that distal tear. And then beyond 90 days, [00:21:00] you kind of get in this point where this, the flap actually becomes thickened and more difficult to move to the side. That area of chronic remodeling and how you influence the dissection flap when you have that thickened realm, but a low radial force stent with that, that Petco technique that was talked about, that's another area that we're really exploring too.
So despite the relatively. Easy recommendations to say you surgically fix something that's complicated and you manage medically something that's uncomplicated. We've now introduced a lot of these considerations in which you have to take timing into account. You have to see how far you're gonna extend your graft, if you're gonna do so with an uncovered graft or a covered graft, and how that's gonna affect your long-term results.
Ultimately, what we care about is aortic related mortality and complication. Yes. So before we move on, or I guess to regress to the malperfusion, I just wanted to ask about the iliac malperfusion in particular and how you approach the management of that and when [00:22:00] you consider fasciotomies. Yeah, yeah.
So I guess that's important to, to think about, right? Because one aspect of malperfusion people get very concerned, or rightfully so about visceral malperfusion renal malperfusion, but also lower extremity ischemia is a, a significant portion of malperfusion that can present with patients with dissection.
So with patients who have lower extremity mal perfusion and after you put in your TVAR, they restore flow, patients can get profound ischemia reperfusion syndrome. So I think it's really important that when you're taking a patient to the OR to restore lower extremity ischemia, not worrying about the aorta and all that is great, but you also need to understand how long have they been a ski?
Ischemic for this, their lower extremities. If it's true that they've been ischemic for more than that six hour time period, and you restore blood flow to their lower extremities, as with any trauma based case, you should be doing bi bilateral lower extremity for compartment FAS osteotomies, because that's the only way to prevent significant muscle swelling and to prevent simple significant ischemia fusion injury.
Standpoint. [00:23:00] I feel like some of these patients are hard to tell because usually they come in either already sedated. So what do you do in that case where you don't really know what the initial timeframe is for limb ischemia? Yeah, great. I mean the great, great question. I think if you're ever thinking the answer is, if you're ever thinking about should I or should I not perform a fasciotomy?
The answer is you should always perform a fasciotomy. Fasciotomies have minimal morbidity. If you do 'em. But if you don't do 'em, it can have significant mortality risk for the patient. So if you're ever hemming and hawing back and forth, do the fasciotomy while you're in the or. I think it's the long term it's gonna be more beneficial for the patient.
And the other consideration is sometimes some of these patients are, you know what we say, kept down or intubated and sedated after the procedure too. So you may not get a reliable exam on them afterwards. It's not that you can't take 'em to the operating room, if you notice that you have some swelling in the lower extremities.
But these patients may get a significant resuscitative effort that can cloud that picture a little bit. And if you are [00:24:00] delaying that because you're not picking up on the early signs of compartment syndrome such as paraesthesia as a paralysis because they're the intubated, sedated, you may miss your window to really save that anterior compartment, which tends to be at the most risk.
You brought up renal malperfusion. At what point do we typically intervene? Well, so renal malperfusion is a tough one. Everybody likes to think that if you have malperfusion to the kidneys, that's an indication for repair. But what does that really mean? Does it mean if you go into acute renal failure?
Sure, that one's pretty easy. What about a creatinine that bumps from 0.9 to 1.3? Is that malperfusion? By the definition, it's probably malperfusion. But those are the patients that people tend to be a little bit more okay managing conservatively and making sure that their kidney function starts to rebound.
Some of these patients come in hypotensive. I mean, they're in screaming pain, they don't really eat or drink for the rest of the day, or they're in the hospital system not getting IV fluids, and so it may just be that you actually have an acutely [00:25:00] hypotensive patient who's got an acute kidney injury because of that.
So there's a lot of nuance when you're considering renal, isolated renal malperfusion. And I think it's one of those things that I wish I could give you a straightforward, normal answer to is what you do for everybody. But you have to consider probably the longitudinal view of creatinines over time. And I don't mean days but hours type thing.
Okay, y'all. So we're gonna, Frank and I are gonna turn the tables on you a little bit, and not to put you on the spot too much for. In front of your program director, but why don't we leave them with a couple quick hits that are gonna let us have some of these maybe ab site or V side questions that tend to show up a little bit in regards to this.
So, Carolyn, I'm gonna hit you first. What is the primary benefit of the Lombardi classification system you discussed earlier that would be localization of the entry tear? Yeah, super important. We talked about needing to cover that, so that's really good. Alright. Now Andrew, what's the biggest predictor of the failure of medical management in [00:26:00] acute un uncomplicated type B aortic dissection?
It'd generally be the in aortic diameter that's greater than four centimeters. Right? High risk feature seen on that initial CT scan with an aortic diameter greater than four centimeters. Great. And then Luciano, what about, what's the ideal timing to, to treat these endovascular with the tvar? Yeah, so kind of getting back to what you talked about earlier it's usually the subacute period from about 14 to 90 days while that septum is still relatively pliable.
Awesome. That's exactly right. Obviously if you, if you have to treat 'em because of Malperfusion syndrome before then get it done. But if you have the time to wait, that 14 to nine day window seems to be a really good time to intervene. Alright, Carolyn, last one to you. What's the most. Common familial syndrome associated with aortic dissection.
I believe that would be Marfans. That's correct. Yeah. Marfan syndrome. So that also leads away to just talk a couple other genetic aortopathy worth discussing. Both Louis Eats and vascular ER have the risk of dissection associated with it. [00:27:00] Those patients are a complicated group to manage. They tend to present younger in life with.
Vascular disease such as dissection or aneurysmal disease and other distributions. Certainly the aortas at risk for all of them. We usually like to do open repairs when we're talking about other visceral beds for these patients. But this may still be an area where you talk about getting patients acutely managed with a type B aortic dissection with an endovascular approach.
So a little bit of a departure from how you would normally do it. But I'd say anybody that you have that's young, that comes in, certainly under the age of 40, but you may have even in that 40 to 50 range, who has a type B aortic dissection that's not related to something like cocaine use or an obvious trigger such as a trauma.
These are patients you really strongly have to consider a genetic workup for. And I definitely have my eye on Marfan Syndrome as as one of the key predictors or risk factors. Awesome. Well, I think we've talked pretty in depth about [00:28:00] type B aortic dissection today, and I feel like I've learned a lot from some of our vascular specialists here at University of Michigan, so I wanted to thank everybody who participated.
I would also like to thank Behind the Knife for the opportunity to participate and go blue, dominate, dominate the day.
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