Chapters Transcript Video Acute Aortic Syndrome and Evolving Management Paradigm Dr. Animesh Rathore discusses guidelines for the diagnosis and management of aortic disease. Thank you Dr Patel for the kind introduction. Good morning, everyone. Uh those who are online. Thank you for joining. Uh I have no relevant disclosures here. Uh Let's talk a little bit about what the acute aortic syndrome means. Essentially uh it's a constellation of life-threatening aortic disease associated with aortic wall disruption. Now, it can be of varying severity and we'll go into a little bit uh on the details for that. Most of these patients will present with acute onset pain involving the chest. Some uh most of the time I would say, radiating towards the back and depending on the extent of involvement of the aorta, it can be localized mostly in the upper back or chest area or all the way down to the abdomen, uh to the loins or the flank area as well. And then based on the the side branch involvement, you can see organ based symptoms. Uh For example, if there is a renal ischemia, you can uh see pain in the flank area or if there is a limb ischemia, then uh acutely ischemic leg and so forth. The spectrum of acute aortic syndrome includes aortic dissection which would be the most common type. Uh But we also see intramural hematoma, penetrating aortic ulcers, traumatic or a erogenic injuries are also on the spectrum. Now, there are a few other conditions that are uh are the some of the mimickers that we won't be going into too much of details on. That's probably a talk for the next time. Uh But uh let's move on. So, acute aortic dissection is a intimal uh layer separation in intimal separation of the media allowing for the flow uh to go through two channel or make it a double barrel tube. And that creates a true lumen and the false lumen. This is the most common form of acute aortic syndrome. The incidence is about three for every 100,000 person years. Majority of these patients are male. Uh The classification essentially is based on where the interval tear is and how extensive the the dissection is. So, there are two traditional ways of classifying uh acute acute aortic dissection. The debe type one and 212 and three, theey type one and has a entry tear in the ascending aorta. But it will involve the entire length of the aorta type two would be localized to the ascending aorta. And the type three which is Stanford type B uh which will have an entry tear in the descending thoracic aorta usually uh just past the origin of leola artery and then it will involve the, the remainder of the aorta. This is the new classification that was uh published in 2020. This is uh based on the consensus between the society for vascular surgery and the society for thoracic surgery reporting standards. Uh Now, it does say type A aortic dissection, but this is applicable to both type A and type B aortic dissections. So the classification, first of all, the aorta is d uh kind of defined in multiple zones going from zone zero, which is the ascending aorta to the AOM artery origin, uh down to zone 11, which is going to be the external iliac artery. The, the first nomenclature component is the location of entry tear. So if it's in the ascending aorta, it will be called a type A or a type B if it's in the descending aorta, and then they will also specify the proximal and distal extent of the dissection. So if, if, if a patient has a entry tear in zone zero and the dissection goes all the way to the zone nine, it will be called, is type A nine A type of dissection. If the entry tear is uh in zone four and it extends all the way to the zone 10, it will be called a type B uh 410 type of dissection. And that standardizes a little bit. Uh Now, frequently we will not be able to see any entry tear. And in those cases, we'll just call it in unidentified or indeterminate entry tear. And uh based on again the location of dissection, whether it goes from zone zero to zone 910, uh that will be classified in the same way. By the way, this is a uh open discussion, please feel free to interrupt me if you have any questions. Uh I'll be happy to talk more about any of these uh slides that we are going over. Uh looking at the cross section of the aorta. Uh just to describe what the acute aortic syndromes are or what they look like. Aortic dissection would have a clear intimal tear would have a blood flow in the subintimal medial layer. And uh there would be a flow there. Intramural hematoma would not have a clear intimal disruption, but there would be blood flow, which usually is a is a static uh blood within the layer of the aorta penetrating aortic ulcer will usually have a atherosclerotic plaque that has perforated uh past the confines of intima into the medial layer. Uh This is an another uh uh representation of how these syndromes present. And by the virtue of dissecting the layers of aorta uh which causes pain. And that's how these patients present. Uh some more definitions. Uh we talk about the chronicity. So the hyper acute dissection would be the ones that that is within the 24 hours of onset of pain. Acute would be 1 to 14 days, subacute 15 to 19 days and uh chronic would be greater than 90 days. And um on the imaging findings, we do have some of the high risk features that will go in more details later. But patients with refractory pain, hypertension, bloody effusion, uh aortic diameter, more than four centimeters radiographic malperfusion, often an organ readmission tear in the lesser curve and falsely more than 22 millimeters. All of these represent a high risk dissection and the complicated dissections are the ones that present with a rupture or malperfusion of and and organs. Doctor Kemp who's in the room, he can subscribe, he can attest to this when he does open surgeries. The intramural hematoma looks like a fresh blood clot within the subintimal layer but radiographically, it's very difficult or almost never. We we would see a clear intimal tear leading to communication between the true and the false human. It usually looks like a hyperdense crescent shaped hemorrhage between the aortic wall on the CT scan. There are a couple of different theories why intramural hematoma. Uh One of the theories, spontaneous rupture of vasa serum which will cause microscopic intimal the causing the bleeding and the hematoma. Uh And the other theory is there is a, I'm sorry. The first theory is the rupture of vasa ves or the second theory is microscopic intimal, the that may not be apparent on the CT scan and this can also progress to frank aortic dissection. When we are describing the CT scan finding, we always not only describe the proximal and distal extent of hematoma but also how thick the intramural hematoma because that will directly predict the outcomes uh for these patients penetrating aortic ulcer. Uh This is a atherosclerotic lesion which will penetrate the internal elastic lamina uh deeper. This ulcer is the risk of rupture goes higher. When describing these, uh we would typically describe how deep is the secular component is. What is the diameter of this as well as the diameter of the entire aorta because these will just like the aneurysm follow the rala principle as the diameter goes up. The risk of rupture goes up and often time penetrating ulcer, aortic ulcers can be associated with intramural hematoma uh by the virtue of extension of hemorrhage within the aortic wall. Uh The picture below shows contiguous uh pleural effusion of high density which uh may be a micro perforation or a reactive effusion, which uh can be determined by the houses field units. Typically let's go into the pathophysiology a little bit more. Uh the causes most of the patients in the Ira database. Uh had hypertension. Almost 80% of patients. There are fre uh several genetic underlying factors like marine syndrome associated with the fibrillin one gene Louis ST syndrome with the TGF beta receptor one and two Danlos syndrome collagen three, a one, familial thoracic aortic syndrome and dissection uh act A two mutation. Some of the congenital findings like bicuspid aortic valve cooptation of aorta Turner syndrome and cerro tulum are associated with higher risk of aortic dissection. Uh Some of these acute aortic syndromes are associated with trauma, uh blunt traumatic aortic injury, which we'll talk about in a little bit of detail later on, as well as AIC from the catheterization as well as penetrating aortic injuries. Frequently, patients will present with illicit drug use, uh like cocaine amphetamine. Uh and and others, there is a higher incidence of type B heretic dissection in African American patients than a type A while type A by far is the more common type of heretic dissection. Most of these patients will present with pain, chest pain radiating towards back, they frequently will describe the pain as a tearing type of pain. Uh And again, depending on the extent of dissection, some patients will have abdominal pain. Uh frequently patients will present with a syncopal attack. Uh more so in the type a dissections and when is present with syncopal attack, these patients are usually uh the ones that may not do as well. Uh Again, depending on different side branches, patients can have a pulse deficit between the two arms or uh or arm and the leg. Uh aortic dissection essentially is a great masquerader because it can mimic several uh cardiovascular as well as other differential diagnoses. Um and you know, not only in the, in the thoracic cavity but beyond it, because of the end organ involvement. So some of these patients will present with acute mesenteric ischemia, acute renal failure, acutely, ischemic leg or uh paraparesis, paraplegia, uh stroke, uh it can mimic a myocardial infarction or they can present with a, with a bad ST elevation M I just by involving the coronary. So the the index of suspicion should always be high in in the patients who present with this constellation of symptoms, uncomplicated dissection. So these are the patients who have dissection but no rupture, no mal perfusion or any of the high risk features. Patients who present with higher risk features. Uh They tend to have higher incidence of rupture and higher incidence of late aneurysmal degeneration. These are the patients who will have a refractory pain which would be very difficult to control or very difficult to control hypertension. Despite maximal medical therapy on the CT scans, frequently we'll see aortas with diameters greater than 40 millimeters. Uh primary tear which is larger than a centimeter wide. The tears located on the inner curve of the aorta in the arch tend to be the higher risk. Uh essentially uh with the with the flow jet of the aortic pulsation, which tends to make the tear and causes the higher risk of aneurysmal degeneration when the false lumen is larger than 22 millimeter, that means false lu has a significantly higher pressure. And that could uh that is also another radiographic feature for high risk patients presenting with bloody pleural effusion or the findings of radiographic malperfusion are also considered to be the higher risk dissections. Complicated dissections typically will present with a rupture which would be blood outside the aorta. Uh This can be a free rupture or a contained rupture. Uh patients who have a free rupture tend to be very unstable and uh would need to be in the operating room as soon as possible. Contained ruptures could be contained by the, the pleural space or retroperitoneum. And they also have a very high risk of evolving into a full blown com uh free rupture. When we talk about malperfusion, any of the target vessel from the aorta could be involved including the carotid visceral vessels, uh iliofemoral or spinal vessels. When we talk about malperfusion, there are two different mechanisms that we would say uh that that could cause the malperfusion. So there is a static malperfusion which may be a result of just fresh thrombus forming into the false limen which directly feeds the target vessel. And oftentime the intima will separate from the aortic intima to the intima of the side branch. And then that intima can intercept into the vessel causing a complete obstruction, dynamic obstructions are different because with the, with the aortic pulsation, they, they would be typically the false human is going to be going to have a higher pressure. And with the pulsation, the the false human can uh press against the origin of the uh of the vessel. And uh there could be a dynamic component that will just collapse into the origin of the side branch and cause a uh dynamic obstruction, which are quite tricky because when you see on the CT scan, we can see there is perfusion to the kidney for, for example, but these patients may present with acute renal failure. And uh and these uh again, we have to carefully look at the CT scan, uh gated CT scan or dynamic uh studies are the ones that are better studies at diagnosing diagnosing. These there are different diag diagnostic strategies. Nowadays, CT scan is is the investigation of choice. The sensitivity approach is 95% specificity approaching almost 100%. Uh All of these patients should get an EKG and potentially a chest X ray. Uh The additional imaging modalities like transesophageal echocardiogram, transthoracic MRI and, and geography while they all play some role, but they are of limited value in select patients uh to define the anatomy of dissection. These can play a big role. Uh One of the interesting things also is the biomarkers. So currently, none of the biomarkers have made it to the mainstream quite yet. However soluble elastin fragment, smooth muscle myosin heavy chain protein and different acute phase reactants have been study are, are being studied as uh biomarkers. Uh Again, the elastin and the smooth muscle myo could be released from a dissected aorta into the bloodstream and, and uh they can be elevated. Let's talk a little bit about the initial medical treatment for these patients. The main driving principle is the anti impulse therapy. So, gradient of blood pressure and time uh that is the central uh concept to the management of patients with dissection. What that means is you want to decrease the decrease the blood pressure, you also want to slow down the heart. So with the every impact of blood pressure, the the intimal tear does not get worse. And uh for this, uh we typically would say let's uh let's keep, this is solid goals in 100 to 120 range. Keep the heart rate less than 60 beta blockers are usually the first line of treatment. Uh uh because they directly align with the DP by DP or anti impulse therapy principle. Uh We prefer using short acting agents like Asmal all. Uh but if that does not work calcium channel blocker uh and then sodium nitro prey. Now, word of question here is you don't want to start with nitro prey because that's only going to uh increase the pulse pressure and that can actually make the dissection worse. So you have to make sure there is always some anti impulse component. Uh when you're um adding arterial dilators now and then there's going to be symptom control. So control the pain for the patients, always uh evaluate for any end organ malperfusion uh with the help of PV L testing, echocardiogram, additional CT scan. Now, one of the things uh when we were writing the EpiCor set for these patients, uh it it's very easy to give these patients very high volume of fluids. We can, you know, when we are not giving them maximum concentrated as MOL and cardine, these patients can very easily be receiving 200 to 250 ccs of fluid every hour. So we work with pharmacy to make sure we max concentrate these vessels. Almost all of these patients will receive a central line uh just to be able to administer these drugs. So, so we we try not to flood these patients with fluids. And the next component is especially if the patient presents at a outside hospital, initiate the alert. Uh The aortic alert process uh within Sentara, we have the type A and type B alert. Uh This picture is an example of type B alert and uh it just goes over who gets notified of the aortic alert. So it's going to be an emergency room, doctor, anesthesia team or our radiology technicians, blood bank, the trainees as well as the ICU attendings. The goal is, and it's evidence driven. Whenever there is a protocol based acute aortic emergency treatment, the outcomes are improved. The odds ratio of aortic alert system, especially in the ruptured aorta. We see there is um about 50% reduction in mortality in these patients. And uh and these protocols that we briefly talked about in terms of get early imaging, notify the involved team. And uh you know, some of these apply to the ruptured aorta as well. So they'll have a rupture kit and blood products available and so forth for ttic dissection for the medical management. Just to go over the, the protocol that we, we typically follow uh would be the same. So admit these patients in an IC U setting place, arterial and central venous line for in invasive monitoring, uh impulse control medical management that we talked about uh judicious use of IV fluids and then defining the dissection to plan for the treatment. Let's talk a little bit about acute type A aortic dissection. I am by no means the the expert we already have doctor camp in the room. So uh please uh add anything we have here. Uh But type a dissection is the more common type of aortic dissection uh amongst the type A and type B. Uh The, the, the famous line about the type a dissection is the mortality rate of 1 to 2% per hour after symptom onset. So this is a true emergency. These patients belong in the or as soon as they present and the diagnosis is made when these patients present with findings of complications. So, pericardial tamponade coronary involvement, cerebral malperfusion, advanced age, low blood pressure, renal failure. Uh these patients tend to tend to be the ones that do poorly and truly with, with surgery, the mortality can be significantly improved. So if the surgery is offered within 24 hours. The 24 hour, 24% mortality can be brought down to 10%. And as we move further down in two weeks, about half of the patients would die, uh, if they are not offered surgery. And, uh, while the outcomes are humbling, uh, even with surgery, but we, we can see almost 2.5 times mortality reduction with these patients. Talk a little bit about the surgical management of type A aortic dissection. All these patients will require some form of a sending aortic replacement. Some of these patients will require aortic root replacement, coronary reconstruction, aortic valve replacement as well. Um So this is uh just a uh this is a ascending aortic replacement with a with different renditions of it. So the first picture is isolated only to the ascending aorta. Uh Now, frequently we'll see a hemi arch which is going to also replace the lesser curvature with a total arch replacement and sometimes a complete de branching of the great vessels. One of the newer uh development to that is the frozen elephant trunk and we'll talk about it in our next slide. But um when and frequently these patients will have a multidisciplinary conversation in terms of what would be the best approach for these patients. And uh in vascular surgery and cardiac surgery, we are always using the, the the techniques that are essentially a fail forward of sorts. So plan for things not to work forever and uh have a plan for future and frozen elephant trunk is something on the same lines. Of course, it does talk about the way of um the aortic community in general has kind of gone from just doing the am er to to your point setting us up for success. And obviously, the goal with the type A is to have an alive patient at the end of the case, not for everybody. This is what we do. But for the 20% of patients after type A who need another operation or intervention, it's a lot easier to set ourselves up for a T bar than it is to set ourselves up for a new arch. So um this all kind of comes out of Penn and Joe Bear and his group, but essentially in the, in the younger patient and he's counting anybody who's expected to live 10 years and the relatively stable patient, um they advocate for zone two replacements, not necessarily frozen elephant trunks, but zone two replacements will be branching so that we can easily tar um plus minus frate and some cla in later. And that's, that's what we tend to do here. Um I'd say 1015 years ago, it was a lot of, you know, ascending hes, but nowadays, we're kind of setting ourselves up to be able to, to, you know, fix these things into vascular in the future. And I will put another plug in for our collaboration. I really appreciate it when you guys um sometimes are on the line with us, but oftentimes are urgently consulted because these truly are not diseases of the chest or CT surgery or the abdomen and vascular surgery. It's really of the aorta and that's where both of us uh work well together. Yeah, I cannot emphasize it anymore. Thank you, Doctor Kemp. Uh This is a representation of elephant trunk. So this one is a uh standard Dron graph that is sawn in uh alongside the aorta with the aortic replacement. This used to be the traditional elephant trunk technique which has now evolved into a frozen elephant trunk. But I guess before that I have this uh thorough flex device that uh that is increasingly being used. This is a device that is a true hybrid device for uh is sending aortic and the great vessel reconstruction as well as a stent graft that is deployed in the true lumen to Dr Camp's point that will allow for not only just a complete remodeling of the aorta, but if these patients need a future reintervention, this could be relatively easily extended as a tr uh and uh and protects these patients from uh future aneurysm degeneration as well as enhancement of true women. This is a picture representation of a frozen elephant trunk. Essentially in this patients. In this patient, corries were re implanted as sending aorta total arch replacement, but there is a antegrade deployment of a tr graph which eventually gets sewn into the Dacron aorta as well as the feld strip. So it ends up being a uh sandwich kind of repair and it's a, it's a very robust repair uh as well as sets us for success for down the line. So, surgical management again, what's new? So it's, this is the principle we live by open repair is the gold standard. However, we are seeing evolution of endovascular therapy for some of the high risk candidates. The principle of endovascular therapy are are similar whether it's a type A or a type B dissection uh which involves covering the entry tear. So that will allow us to depressurize the false lu try to get seal in the healthy aorta, which may not be available in a type A aortic dissection. And then the principles along along the lines of how to revascularize the carotids and the Suppan and the rest of the visceral vessel, prevention of retrograde dissection into the coronaries. And then true human pressurization, false human management, which is a very interesting field. We'll talk a little bit about different techniques for that in the, in the following slides uh over at Sara, we are currently enrolling in the Arise True trial, which is a stand for ascending aorta, which could be used as a isolated stent in the ascending aorta. Uh The goal again is to cover, cover the proximal entry tear, uh and deploy the stent in a healthy aorta or at least where the inter is intact and that can allow to pressurize the truly. Now, if the, if there is a coronary involvement or a valve involvement, obviously, this stent is not a, not a candidate for that. And this stent, this stent can be extended with a side branch stent which is a, this one is a thoracic branch and graft made by Gore medical uh which allows us to reconstruct one branch and the rest of the carotids can be Debra. These are the different strategies for de branching, the major vessels. So the first picture shows left of cla that has been transposed onto the carotid or a bypass, transposed left carotid and a bypass or right carotid to left subclavian and left carotid bypass. So these strategies will allow us to progress further into the aorta or having to reconstruct only one side branch as opposed to three or sometimes four. We often hear about laser inside to fenestration. This is one of the strategies for revascularizing the side branches. Uh Essentially what happens in this technique is we would intentionally cover side branch in this case, its Las Ofan and uh and then we'll come from a racial or a radial access, use a laser fiber to actually burn a hole within the stent. And then through that hole, we are able to place a covered stent, either I cast or a wire band balloon expendable stent which will Prevas this side branch. Now, this is a craft modification. This is of of off label at this time. But there's a lot of research and our institution has been one of the pioneers of this technology. There is another technique called the parallel stent graft where again, you would intentionally cover the side branches and then place parallel stent graft uh which could be described as chimney or periscope to maintain perfusion to these side branches. And by uh uh the, the space between the large aortic stent and the smaller stent, which is called the gutter. Um In acute dissection is usually not that big of a factor because these patients have not been generated into the aorta. So that's another strategy branch end. We briefly talked about the gore thoracic branch end with a single branch. This one is currently approved for zone two which means uh proximal to the left Sola but they still to the left common carotid artery next ascendo span uh which we are also involved in the trial for. It's a zone zero device with the ascending aortic component and a single side branch component which gets extended into the descending thoracic aorta. Some of the other investigational devices would be the cook arch branch device which comes in a two branch or a three branch uh rendition which um I did not include the picture for and Terumo has a dual two branch device as well. Some of the half the shell th abdominal, which is I think more relevant to the type B dissection cases where we have to reconstruct the visceral vessels, uh renal and so forth. Uh Gore medical and co both have their own uh devices. Uh cos T branch and Gore's TB device. These are both still investigational uh and not currently approved for FDA. One of the other interesting way of uh doing these cases is to modify the stent on the back table. Uh It's called physician modified end graft. Uh And this technique could be used for the ascending aorta hearts reconstruction as well as the thoro abdominal aorta. What this technique involves is uh getting your measurements and marking exactly where the target vessels are and making openings within the stent and reinforcing it with a typically with a radiographic marker and incorporating these fenestrations within the uh within the aortic stent graft and then reconstruct, reconstructing all these side branches from within the stent. Um while the stent is deployed, there is maintained perfusion to the renal and visceral vessel. So, so that gives you some luxury of time to reconstruct it again, this is off label uh has not made it to the mainstream yet. Let's talk a little bit about uh acute type B aortic dissection. Uh Medical management is on the same lines as we talked about. That is the sometimes the only treatment needed for several of the type B uncomplicated dissection. Uh We also know when the surgical management is offered in less than two weeks. These patients tend to do worse patients presenting, presenting with complicated dissections tend to have high mortality and morbidity. Open surgery is somewhat limited. Uh Typically when these patients present, their aorta is uh uh is very friable and uh they, it may or may not hold the sutures very well. Uh, but the different surgeries that have been described include open fest administration, replacement of the aorta. Sometimes these patients will need a femoral femoral bypass. But the main mainstay of treatment is tr there are a couple of different studies that have been done and are ongoing for uncomplicated type bic dissections uh instead trial uh instead Excel, which was the extended follow up and the VQY data. And um all of these trials have mixed results. I would say uh there is no survival benefit for routine tr over optimal medical therapy for an uncomplicated type aortic dissection over two years. However, patients who receive tr tend to have better aortic remodeling. Instead, Excel uh looked at these patients for up to five years and they still did not see a clear advantage with tr. However, another uh what's called a landmark analysis, which means when they looked at the patients who survived at least for two years and then they were following these patients, uh patients who received a tr tend to have significant mortality advantage uh if they had received a tr and less risk of aneurysmal degeneration and aorta specific mortality, high risk features. Again, we talked about it a little bit. So refractory pain hypertension, despite at least 12 hours of maximal medical therapy, different radiographic features. We've already gone over those. Uh If we are able to wait for about two weeks, these patients tend to do better, better complicated patients, complicated dissections need emergent T bar to help with the bow perfusion or rupture. The goals of therapy are very similar what we talked about. So cover the entry tear to exclude the false lumen and induce thrombosis in the false lumen. The goal is to always land in the healthy aorta. So for example, in this case, we don't want to land where the aorta is dissected. We want to land just past the left carotid and be ready with some strategy to revascularize the left sole, an artery attempt to cover all frustrations if possible. However, sometimes all we can achieve is get close to the celiac to reconstruct all the viscal vessels sometimes being too involved with an operation and a lot of coverage for thoracic aorta, increasing the risk of paraplegia. Uh do not oversize the stent, usually 1 to 1 sizing or 0 to 5% oversizing is all we would do for these patients. We don't like to do balloon angioplasty because that can put these patients at risk of retrograde propagation of dissection. Always use intravascular ultrasound. Uh That is a great tool. Uh we use IWS for confirming that we are in the true as well as to make sure we are measuring the diameter of aorta in the peak cysto, which may not be reflected in the CT scan. And often time we may not appropriately size our stent graft. And before and after always make sure the side branches are patent after the tr um I already went over some of this. Uh this is the configuration of aortic dissection before the tr and after the tr you see the trio were nicely expanded at different levels. So in the descending thoracic celiac artery level, uh S uh S ma level, abdominal aorta and iliac level. So always confirm with the IVIS and if there is any component of dynamic obstruction, be prepared to stand the target vessel as well. Other consideration uh spinal cord perfusion, uh we'll talk about the spinal cord strategies uh in the in the tail end of this talk. But uh if we have to put a covered stent that is longer than 20 centimeters, the risk of spinal cord ischemia goes up to about 3 to 5% sometimes even more. Uh The strategy is to protect as much of collateral perfusion to spinal cord as much as possible. One of the newer development over the last decade is the, is the, is the bear stent uh which is a zenith dissection stent. So there is no fabric but this bear stent will reinforce the intima from inside. And um and this is described as a petticoat technique, false human thrombosis is the goal to achieve. Uh and that will allow for a positive aortic remodeling and lower mortality and the principles of branch vessel management that we'll talk a little bit more about branch vessel perfusion. Uh Sometimes there is a dissection flap right against the origin of the branch vessel. And um you, you may have to make a hole in the intima to revascularize the renal or the side branch. Uh You have to make sure the stent actually projects into the lumen into the flow, lumen of the aorta, not flush with the ostium and also flare the stent to make sure there is good flow uh going into the target organ. Our preference is to use balloon, expendable covered stent for these. Uh because again, the vessels are very friable with high risk for rupture, false human management strategies. Um uh We talked about the petticoat, uh one of the change to or one of the modification to that is to use a balloon in the stent to allow it to take the the the native vessel diameter that will isolate the false human. Well, that's called a stabilized technique. The technical steps would be to place the proximal stent, place the distal bear stent and then use a compliant balloon which will cause intimal disruption and allow the stent to expand completely and completely isolate the false lumen knickerbocker technique which is essentially using a balloon to disrupt the intima within the somewhere in the middle of the stand which will isolate the false human in the proximal descending thoracic aorta candy plug. Uh is a, it's not available in our country. It's available in the, in the Europe and uh the rest of the world. However, uh this is a special stand which is uh shaped, looks like a candy uh wrapper. And um this can be deployed within the false lumen to shut down any flow into the false lumen. And then this narrow component of the stent can be shut down with help of a hemp pla plug. And that can allow for false human thrombosis, falsely coil embolization. Uh is another strategy used to induce false human thrombosis. Sometimes we do see despite the TV, the, the, the, the true lumen does not quite expand and the false lu still remains special pressurized. Uh Oftentimes we'll use a technique called laser sept me. In this technique, we will advance a wire through the true lumen all the way into the ascending and a second wire that goes through a fest administration into the false lumen. And then we'll activate a laser over both these wires which will essentially scissor through the, the intima and creating a single lumen which will allow for a stent to be deployed and seal in the in the aorta where the diameter is more conducive to getting a seal. Uh couple other ways of doing SEPT arty. So just using a stable sheet to make a uh make a septum within the intima or using a uh electrified wire to make a larger connection. And uh by, by doing the SEPT atomy, we tend to see significantly improved positive aortic remodeling. Let's talk a little bit about intramural hematoma. Uh We already know the hematoma is confined to the media but there is no clear connection between the aortic human and the media or intimal defect. These can evolve into a frank aortic dissection. This is one of the rare types of acute aortic emergencies usually affects patients who are older age. Uh These tend to be more in the zone three or zone four rather than more proximal. However, we have seen uh type a uh involvement with intramural hematoma as well. Uh The risk of malperfusion is relatively low with these. However, when these patients present with a aneurysmal aorta or a penetrating aortic ulcer or enhancement of the intramural hematoma. With contrast, those are predictors for poor outcomes and tend to require surgery sooner rather than later. Uh When the intramural hematoma is more than 12 millimeters of thickness. Uh that is a predictor for poor outcome, uh similar to dissection, intractable pain or complications would be the reasons to perform a tr early. Our approach typically is similar to dissection uh where we would do medical management and get a follow follow up CT scan in 24 to 48 hours. And if these patients either evolve into high risk features or fail medical management, uh we would often offer tr for these patients to take care of it. The other, other end of the spectrum is penetrating aortic ulcers. Uh again, uh always associated with the atherosclerotic plaque. Patients are older. When the ulcer is larger, there is a higher risk for rupture and we know tr is safe for these patients. Talk a little bit about blunt traumatic aortic injury as being a level one trauma center. There are four grades of blunt aortic injury. Um The first one is just a internal disruption. The grade two would be a focus focal intramural hematoma. Grade three would be a pseudoaneurysm and grade four would be a frank rupture. Most of these patients would not make it to the hospital because they would bleed out. These injuries almost always happen at the aortic is just past the left of Clavin artery origin and the mechanism of injury is the rapid deceleration. Grade 23 and four, are indicated for repair. However, there is increasing evidence for grade two just to monitor them at this time. Uh Grade three and four would typically need urgent and emergent repair. Majority of these patients will have other concomitant injury like intracranial bleed or liver laceration, spleen laceration. So it's always a multidisciplinary discussion whether these patients can receive heparin or can they receive just a procedural heparin. Um Our preference is to try to give at least a low dose since you're manipulating wires and catheters at the origin of the great vessels. But we have done tr without any heparin with good outcomes as well. The traditional open repair I I think has gone out of favor in favor for TV, because it's significantly less invasive for these patients. And uh another con controversy about these patients is the coverage of leola artery because we may not have enough landing zone. We sometimes will use strategies to revascularize leps, ovian. However, in the trauma database, as well as several as well as society for vascular surgery, it is acceptable to cover Leola with, with plans to revascularize if needed down the line. Let's talk a little bit about spinal cord ischemia. Uh different factors that affect spinal cord injury include the extent of repair if patients have renal dysfunction and the spinal cord perfusion, historic spinal cord ischemia rates and this is all comers including open thoraco tars and so forth. Traditionally, about 20%. But this could be brought down to 5% or less by using different strategies. These are the uh this is a nice diagram of all the collateral pathways to spinal cord, which include the vertebral artery, supple arteries, intercostal and number vessels, internal iliac, inferior mesenteric, inferior epigastric collaterals, as well as the paraspinal and sas muscle, uh collaterals. And this all becomes relevant when we start to cover thoracic aorta or replace it with a surgical graft and more of these collaterals are left, the risk of ischemia goes up. Um Different mechanisms for spinal cord injury include the ischemia, reperfusion, releasing neurotoxins and uh interruption of the uh the the blood supply. I'm not gonna go into great details about this today. Uh different uh different strategies for prevention, hypothermia. Uh some of the pharmacological agents which have been studied. Uh However, none of them have really proved to be definitive in when it comes to spinal cord protection. Uh Other strategies that we are typically using on the vascular side uh would be lumbar drain. Uh We are, we have gotten a lot more selective with the lumbar drainage nowadays, uh When we are, when the spinal cord is missing some of those collaterals we discussed or uh we are planning for extensive coverage only, then we'll do lumbar drain. Nowadays, uh strategies to re implant or revascularize spinal cord monitoring using lower profile devices, uh maintaining pelvic and lower extremity perfusion or staging these cases might be the different strategies to use. This is the protocol we use for our uh spinal cord ischemia prevention where we aim for a goal, intracranial pressure of 10 millimeters of mercury, aim for a slightly higher systolic pressure. Uh drain 10 CCS of CS F up to three times every hour. Uh try not to drain too much and management of heparin and antiplatelet therapy. And then if there's any uh neurological changes, different strategies that are used. Um This is available to all some of the other acute aortic emergencies that we did not talk about in this talk. Um would be the ruptured aorta, uh penetrating aortic injuries, acute aortic accusant uh symptomatic aortic mural thrombus that we doctor camp and I were just talking about before we talk, we started this presentation, mycotic aneurysms, aorto enteric fistula and aorto cable fistula. These I think these are topics for maybe next time. Um uh I would welcome you all to our uh mid Atlantic Conference uh which is happening in April. Uh We talk about some of these aortic uh conditions as well as the full spectrum of vascular disease. Uh With that note, I would be happy to take any questions. Published January 24, 2024 Created by Related Presenters Animesh Rathore, M.D. Sentara Vascular Specialists View full profile
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