7 TAAA
Authors: Rachael Forsythe, Mohamed Barkat, Nicholas Greaves, and Michael Jenkins
Contributors: Sharif Ellozy, Leanna Erete
This episode was developed as a collaboration between Audible Bleeding and The Rouleaux Club in the United Kingdom.
Treatment for thoracoabdominal aneurysms has become a bit of sub-specialization within vascular surgery, with the best outcomes achieved at high-volume centers with close partnerships with cardiothoracic surgery.(Cowan et al. 2003) While the majority of vascular surgeons may not manage these patients in their day to day practice, and many trainees have limited exposure, this topic is still fair game for examinations and should be reviewed. However, endovascular techniques are still evolving and practice varies widely between centers and so covering this topic may not be particularly high yield.
Take a Listen
Check out our conversation with Dr. Tom Forbes where we discuss some challenges and opportunities in specialized aortic training and centralization of services.
This chapter was developed by surgeons in the United Kingdom, where manufactured custom devices have broader regulatory approval and are more widely available. The availability of these devices in the United States is more limited and so management decisions are different depending on what devices are available. However, the basic principles of open management and overall clinical decision making are shared no matter what side of the Atlantic ocean you practice.
7.1 Demographics
7.1.1 Anatomy
Can you take us through the Crawford classification to start off?
The Crawford classification is relatively recent (1986) and is a very practical classification, depending on body cavity and how to get to an aneurysm.(Crawford et al. 1986) This classification doesn’t follow an expected pattern as getting either more extensive or less extensive.
Type I - These extend from the left subclavian down to just below the diaphragm, which distinguishes it from an isolated thoracic aneurysm, which you can get to just from the chest. Going into a second body cavity is a very important differentiating marker.
Type II - These are the biggies, they extend from the left subclavian all the way down to your bifurcation. So both abdominal and thoracic exposure, all the visceral, renal arteries and a lot of intercostal and lumbers–so big impact for cord supply, et cetera.
Type III - These extend from the mid chest down to and involving the viscera, renals, and bifurcation. These differentiate from Type 2 because you may not need to utilize full support and may risk a clamp and go approach.
Type IV - These are characterized by being accessible from the abdomen, in most patients, although it often does require division of the crus. In most patients, because there are some anatomical situations with body habitus, which means that going into the left chest is useful even for type four aneurysm.
Type V - This was an additional classification that was added by Dr. Hazim Safi’s group later, which is a bit like a type III at the top of the type I at the bottom effectively.(Safi and Miller 1999)
Take a Listen
Check out our conversation with Dr. Hazim Safi where he discusses the history of TAAA repair and much, much more.
There appears to have been an increase in the incidence of thoracoabdominal aneurysms. Do you think it’s a true increase or does this relate to having scans for other reasons picked up by accident and then going on from that? What sort of many referrals do you get in a year and what’s your turn down?
The overall incidence of infrarenal atherosclerotic abdominal aneurysms is going down every year in the national UK vascular registry, likely related to smoking reduction for a big group of patients. I think thoracoabdominal aneurysms are going up partly because we are now imaging more and more people and therefore we are imaging the chest and seeing them.
So that’s an artificial increase in incidence, but also the rate of aortic dissection is on the rise and chronic post dissection aneurysms are increasing. In addition, I think it’s a small group, but there is more knowledge about connective tissue disease, genetic studies and family screening, which perhaps is also a small part of annual increase. So over the next 10-20 years, aneurysms are not going to go away, and there is a huge number now within the national UK screening program under surveillance for small aneurysms.
7.1.2 Etiology
Are there major differences in presentation and etiology between thoracoabdominal aneurysms and abdominal aortic aneurysms from your experience?
On presentation, the majority of aneurysms are asymptomatic so they are most often found incidentally. Rarely, they get symptomatic and can get tender as they approach a time when the wall is going to breach pre-rupture. I think thoracoabdominal aneurysms tend to be a bit more symptomatic than infrarenal but may have some atypical symptomatic presentations.
Some that extend into the arch may present with hoarseness from recurrent laryngeal tension or bronchial compression.
There is a group that cause dilatation of the crus. The crus of the diaphragm acts like an extrinsic wrap and can be extremely tight. These patients present with excruciating pain, radiating around their costal margin, which is a presentation not often thought of as a sign of an aneurysm.
The larger extent and more chronic aneurysms may even present with things like weight loss and general poor health.
The other group that is a little different than infrarenal aneurysms, is the post dissection aneurysms. The majority of these are known and followed closely, however there was a time when patients with a type A dissections that extended all the way down were only followed with with echo of the ascending and the rest was forgotten about. Many of them got lost from cardiothoracic follow up. That group is a different group because we already know they’ve got an aneurysm. So there are subtle differences.
And then the connective tissue group, I suppose, is a bit different because they tend to have more extensive aneurysms rather than just confined to the infrarenal segment, which is by far and way, the most common for abdominal aneurysms.
Do you think patients with thoracic aneurysms as a result of dissection or connective tissue disease have a different threshold for intervention compared to the non-connective tissue disorder patients?
I think we need to be aware that the connective tissue disorders we talk about—Marfans, Loeys Dietz, vascular Ehlers Danlos—are probably the tip of the iceberg. There are likely a number of other cases that we don’t have genetic sequencing for, but behave differently than classic atherosclerotic aneurysms. The data from a dimension point of view is not quite as robust as one would hope, but the threshold that most people would agree for non connective tissue disorders would be about six centimeters. That takes into account the increased risks of operating both in the chest and the abdominal segment.
I think most people would agree that five centimeters is a better cutoff for connective tissue patients. Some cardiac surgeons would repair a young Marfan ascending aneurysm at four and a half centimeters. It does vary a little bit geographically, a bit like the threshold for infrarenal aneurysms, which varies between Europe, the States and the UK. So you’ve got to look at the patient in front of you and make a decision. I would certainly increase the threshold for someone who was not so fit and perhaps lower it a bit for a younger patient.
For more about connective tissue related aortopathies, see Chapter 8
Also, be aware if it’s something odd anatomically—a saccular bulge, an eccentric penetrating aortic ulcer (PAU), or something where you think there could be a mycotic element—those are all very different. You can’t be reassured by a dimension in an axial plane that is safe. These findings up the ante, in terms of whether you would repair at an earlier threshold because they do not behave like a conventional fusiform aneurysm.
Can you talk us through the Ishimaru zones of the aorta?
Ishimaru is a useful classifications. There are a lot classifications in medicine, but it’s nice to find one that’s actually useful. This classification made sure that everyone was on the same page when reporting proximal seals zones for thoracic devices. That is important for two reasons:
The extent of coverage
The complications increased, the more proximally you go. The main complication for that is stroke.
So historically, Ishimaru decided to classify these zones as(Ishimaru 2004):
Zone 0, the first most proximal zone, is the ascending aorta up to and including the brachiocephalic trunk
Zone 1 is between the brachiocephalic trunk and including the left common carotid artery
Zone 2 is between the left common carotid artery and including the left subclavian artery
Zone 3 is the aortic segment just distal to the left subclavian artery.
Zone 4, added by some people, is distal to the T4 level, which is much lower down the thoracic aorta
Most thoracic stenting will go really to zone three or perhaps into zone two. The more proximal you go, the more work needs to be done in terms of either extra anatomical debranching or using some form of fenestrated or branched arch device with an increase in stroke risk. What this allowed people to do is compare different series. You’re not just saying these were a group of TEVAR patients, but you could define exactly how proximally they go.
And the same applies for the Crawford classification. It allows comparison within thoracoabdominal groups, and that’s important with both survival and complication rates. Because if your series is mainly type II thoracoabdominal aneurysms, you’re going to have a very different outcomes from someone who’s got mainly type IV aneurysms. Both classifications allow you to look at and compare data between groups.
For a discussion of the new SVS/STS classification system for aortic dissections, please see Chapter 6
7.2 Management
7.2.1 Ascending aorta and arch
The cardiac surgeons use many different techniques for managing an ascending aortic aneurysm or dissections, which is beyond the scope of this review. However, in preparation for management of aneurysms or dissections that extend beyond the arch, they often utilize an elephant trunk down the descending aorta. Can you briefly summarize the difference between a conventional elephant trunk and a frozen elephant trunk, and when to use one over the other?
This is particularly pertinent to aortic dissection. The the main purpose of repair in Type A dissection is to protect the heart. People die of either rupture into pericardium causing tamponade or stripping the coronary ostia off and getting myocardial ischemia. So the priority of repair in acute ascending aortic dissection is primarily to protect the heart and to some extent to ensure a true lumen flow distally. Therefore, it was very popular because it was the least invasive to do a short interposition ascending repair, but that left problems for later.
As people became more adept with cardiac and cerebral protection, it became more popular to do a more extensive repair in the first sitting. This involves an arch repair and an acceptance that eventually the descending thoracic aorta will still need to be repaired, but at a later stage. The ascending and arch is done from a median sternotomy, and it’s really difficult to get beyond the left subclavian from that position.
So when the arch was done, the elephant trunk came from leaving an extra piece of Dacron within the descending thoracic aorta in the true lumen of a dissection or in the main lumen of an aneurysm by a double sewing technique on the distal anastomosis and then inverting it down the descending thoracic aorta. The benefit of that was when returning to repair descending thoracic segment via left thoracotomy, you couldquickly open the aorta and clamp that Dacron for a ready, made proximal anastomosis. This was much easier, because it meant you didn’t have to dissect all the way up to the left subclavian with scar tissue and a previous anastomosis.
Now, what industry realized is that they could help with this procedure by developing a Dacron device sized to be an arch replacement which had three or four ready-sewn 10 millimeter branches with an extra pipe for rewarming. These branches are used as bypasses to the innominate, carotid and subclavian and attached to that piece of Dacron was a stent graft, which could be placed distally in lieu of what was previously a floppy piece of Dacron.
And two manufacturers, JOTEC and Terumo Aortic, have made these devices, which facilitate and make things much easier. Therefore, so-called FET or frozen elephant trunk, has now become quite popular. I don’t quite know why it’s called frozen, but I think it perhaps means that the thoracic segment is stiff with a supported stent graft rather than just a floppy Dacron segment.
7.2.2 Isolated Thoracic Aneurysms
For isolated thoracic aneurysm treated with TEVAR, what is the optimal landing zone?
So I think the isolated, thoracic aneurysm is a perfect application for TEVAR because if you can get a good seal zone, proximally and distally, it provides an an endoluminal approach and saves a thoracotomy, which is a massive difference for these patients. Unfortunately I suppose those cartoons you see on the industry advertisements are vanishingly rare, when you’ve got a perfect proximal and distal landing zone and a really straight thoracic aorta.
I think for the majority of cases, you need a 2cm seal zone proximally and distally. However, if you have a torturous aorta, you likely need a longer seal zone. You want to land in an area where there is a good parallel walled walled segment. You have to be careful of so-called “bird-beaking” when a stiff, less conformable device lands perfectly on the outer curve, but holds off on the inner curve. This results in a lip, which protrudes and allows blood to get under that and cause stent graft crushing.(Marrocco-Trischitta et al. 2019)
Modern day outcomes are very good, because I think modern devices have become much more conformable. We’ve learned many lessons to avoid too much oversizing and how to taper stent grafts when there’s mismatch between proximal and distal landing zones.
These have all significantly improved things, but there’s still no getting away from the fact that some anatomy is not well adjusted to the currently available stent grafts. Gothic arches, torturous and large sacks, are a problem and can allow a stent graft to move away from the center line to the outer curve.(Iwakoshi et al. 2019) If that sac doesn’t shrink, you can imagine that draws on both the proximal and distal seals zone, and reduces them.
I think you can sometimes get away with a shorter landing zone. If, for example, you’re doing a post traumatic aneurysm where it’s only on one segment of the outer wall where there’s a problem. But for the vast majority of true aneurysms, you need that seal zone and you do need to oversize to achieve that.
For more on the endovascular management of traumatic aneurysms, see Chapter 9
Do you utilize rapid ventricular pacing when deploying these stents?
I think the majority of aneurysms at the left subclavian area, you can just drop the blood pressure to a systolic of 70 or 80 pharmacologically. Once you go more proximal to that, especially if you’ve got a custom device, with a scallop or branched device where you need an absolutely critical landing zone, you then really need to achieve a short transient period of circulatory arrest, either with adenosine, which is perhaps sometimes a bit unreliable, or rapid pacing.
Rapid Pacing can be difficult and does come with complications though, such as ventricular puncture. There are some newer techniques in terms of caval occlusion balloons, which basically stop venous blood returning to the heart with a reduction in output. Those are gaining popularity certainly in Germany and they can be quite effective for that. I think having tip capture on devices and better, more accurate deployment and better imaging does allow you to be more accurate in deployment, but there are still problems.
These devices have been inserted to very torturous iliac systems sometimes and they retain some energy. When you deliver them by removing that sheath, sometimes that energy is still there and they can jump forward as well as back. This can cause problems because you end up covering a vessel that you didn’t intend to.
As we have described TEVAR is a great option for the majority of isolated, thoracic aneurysms, but is there still a place for open repair?
I’m not so sure in isolated, thoracic aneurysms, unless for some reason they’re not suitable for TEVAR. I think if you’ve got problems with a mycotic aneurysm or a fistula into the bronchus or esophagus, these are our big problems with high mortality and your duty bound to go for open repair.
Patients with hemoptysis and a previous aortic repair should carry a high suspicion for an aortobronchial fistula. TEVAR is considered preferred repair, due to high morbidity and mortality with open repair. Bronchoscopy should be avoided due to high risk of rebleeding.(Bailey et al. 2011; Léobon et al. 2002; Quintana et al. 2006)
Certainly with connective tissue patients, open has advantages. In some unique situations it is possible to bridge between repairs. I think in some of the younger connective tissue patients, they will end up having certain segments repaired at different stages of their life. Although it’s probably now accepted that “all endovascular” is not a good option for these patients, if you’ve got Dacron proximally and distally already, bridging those segments with an endovascular device might work well. Although the Dacron will slowly dilate, it won’t dilate as much as aortic tissue in these patients. So there are options, but I think in reality, isolated, thoracic aneurysms on reasonable rare and TEVAR can be used for the majority of them.
7.2.3 Thoracoabdominal Aneurysms
Moving on to thoracoabdominal aneurysms. Earlier we used the Crawford classification to describe the anatomical extent of the thoracoabdominal aneurysm. So let’s talk firstly, about type 1, 2, 3, and 5, which involved the thoracic of water to a greater or lesser extent as well as the abdominal aorta. We’ll come back to type IV later on in this podcast.
So type II open thoracoabdominal aneurysm is arguably the most invasive operation a patient can undergo and carries 30 day mortality in excess of 10 to 15%. What is the size threshold for type II that you currently use in your practice and what is the evidence for this?
So, as I suggested earlier, the evidence is that it’s a bit historical, and most people would actually say about six centimeters. I think that can be brought down a little bit for connective tissue patients and can go up a little bit for atheromatous patients. But in general, you’re talking about a younger segment of patients. This is not an operation for people in their eighties. Outcomes stratified by age greater than 50 found a higher rate of death, paraplegia, renal failure, cardiac complications and length of stay.(Coselli et al. 2017) These patients need to be in very good shape because it is a big onslaught physiologically on them. It’s not just getting them off the table, it’s getting them out of intensive care and out of hospital and to recover back to their baseline.
I think that’s one of the things that can be really difficult about this disease. You are taking patients who are effectively functioning quite well, and they’re often relatively asymptomatic and you’re putting them through a prophylactic operation to try and prevent rupture, which no one quite knows if or when it’ll happen.
So to that end, can you talk us through the decision making process when you’re assessing a patient with a thoracoabdominal aneurysm types 1, 2, 3, or 5?
I think it is really dependent on anatomy, physiology, and the patient in front of you. Unfortunately, it is a bit of a bespoke assessment for an individual patient. So firstly, I think you have got to look at what are the options for that patient, which goes from conservative to endovascular, to open surgery.
The endovascular domain has changed hugely now with the increasing availability of branched devices. When I started, there weren’t custom devices. There were some FEVAR devices just coming out, and we did use long covered stents going through devices with TEVAR above. However, there wasn’t the option for what we’ve now got from an endovascular perspective.
Take a Listen
The availability of fenestrated and branched devices is very different between the United Kingdom, Europe and the United States. In the UK, custom fenestrated and branched devices have received CE mark approval, which is similar to FDA approval in the United States. These devices do not have FDA approval in the United States, so access to them is far more limited.
Check out our conversation with Dr. Gustavo Oderich where we discuss the advances in endovascular techniques for branched and fenestrated devices in the United States.
Check out our conversation with Dr. Benjamin Starnes where we discuss the process of an investigation device exemption (IDE), which is how the majority of custom devices are performed in the United States.
So I think you’ve got to choose the patients that are either unsuitable for endovascular, or are we really going to benefit from a durability of an open approach. Those are the two big differences, and they are differences. One, you’re going for gold standard approach because you think they’re life expectancy warrants that. The other one is much higher risk, because they haven’t got another endovascular option. These range from people with very tortuous anatomy, to difficult renal arteries, such as early divisions, that make them unsuitable as target vessels. Another reason is complex dissections, which are not suitable for an endovascular approach. Therefore, it is quite variable, but the first thing you must consider is whether this patient is going to get through this and get out of hospital. And that really is looking at them in the eye and considering what’s their quality of life or what’s their family support, and are they up for this?
The second one then is anatomical difficulties— Is there a shaggy aorta, atheromatous disease, or calcification of a target vessel, etc. Severe aortic wall thrombus is associated with solid organ infarction (24%), acute kidney injury, without dialysis (21%) and delayed oral intake by 3.4d, however rarely resulted in mortality (0.5%).(Ribeiro et al. 2017) Rarely is this a hundred percent or 0% decision, but it’s about building up relative contraindications. Some of them are pretty simple, like access problems for endovascular, and it’s a combination of those which then will sway you in one way or the other. And if anything, that decision-making is probably more pertinent for type III and type IV, where there really is a different option and these patients are n their sixties and seventies with classic atheromatous disease. The really, young fit non-connective tissue patient with a type II TAAA is a rare beast.
For connective tissue disease, many textbooks prefer an open approach over an endovascular approach do you still agree with this?
Yes, I do. I think certainly, what were you know about patients who’ve had total endovascular approaches for connective tissue diseases is that they don’t last. They may last five years or so and then you get progressive aortic dilatation and loss of those of seal zones. Whether that is the natural history of the native disease or whether it is regional force hooks, barbs or whatever is related to the device is unclear.
But when you sew these pensions and just touching the back end of a needle on the anterior wall can create a massive problem or just being a little bit clumsy and you get a radial tear. It’s very clear that a stiff device sitting in those aortas for many years with 60-70 beats per minute going through it and often hypertension, isn’t going last.
However there are some caveats, as I mentioned earlier, bridging between previous prosthetic open repairs is a possibility. And sometimes in a lifesaving situation, such as when someone has presented with a rupture, you may have to use an endovascular approach. However, be prepared then to treat that as a bridge and go back to do a definitive repair when things have calmed down and in the cold light of day.
So we don’t really have the scope to dive into complex endovascular repair in this episode, but can you describe the broad principles of your operative approach to open thoracoabdominal aneurysm repair?
In terms of the patient, for anything juxtarenal or type IV, I tend to have a patient supine on their back, but with a break in the table at the level between the costal margin and the anterior superior iliac spine. By breaking the table at that level, you can increase the exposure to that segment of the aorta.
However, there are some patients even with a type IV repair that demand a left thoracoabdominal incision. For a type four, if you’re doing a left thoracoabdominal approach, it’s usually for someone with a very narrow acute angle of the costal margin, such as a more petite frame female patient or a crus that is very high on the aorta. And if you look at CT scans, which is something I’ve realized over many years, that not everyone is the same. So where the celiac and SMA are can be in a different proportion, depending on where the costal margin and and skeleton is, which can make them easier or harder to get to. And certainly in a situation, if there is a rupture within the left side of the abdomen, you wouldn’t really want to go into that without getting proximal control. Because as you do the visceral rotation, you could have catastrophic bleeding.
So under those circumstances, I’d also go into the left chest with a reasonably low segment so that you can place a clamp ready before doing the visceral rotation. So for type IV the one above then, the higher you go, the higher your thoracotomy and the more tipped over you need the patient. So for a type II, you’re going probably fifth intercostal space and the shoulders are at 90 degrees and the pelvis is 60 degrees. For type three, you’re slightly further over, so you’re down to about 60 degrees and you’re perhaps in the seventh intercostal space. So the lower you go, then right up to being pretty much supine.
The left arm is put over top. You mark the scapular and you go into the chest and abdomen. I tend to go intraperitonealy into the abdomen, so I can see the bowel, although there are people who do a retroperitoneal approach. I tend to divide the diaphragm down to the central ligament and mark that. Then effectively you are looking at your clamp zone. You dissect around your clamp zone, both proximally and distally. We don’t tend to expose the celiac and SMA in particular, or the right renal. It’s important to find the left renal artery. For the visceral rotation, you effectively extend the left colon up, find the white line and get under that and get right onto psoas. The key is to get right down on the psoas early on, and then it is a relatively bloodless field. Everything has taken medially to leave the ureters out of the way. I always take for left kidney up. You will see in the textbooks and some advocate to keep the left kidney down. I that’s utter madness to be honest and I can’t see any point in it.
So for me, everything rotates up then out of the way. And it it looks a bit strange, like a postmortem. It looks very odd to see the whole left side abdominal cavity when all you’ve got is diaphragm muscle, psoas muscle and nothing else left. It does give you a very safe exposure then to the aorta. I don’t tend to go round the aorta with slings, I think that can cause problems. I go around with my fingers and be very aware of the right sided lumbers or intercostals because you really don’t want to cause a problem there because you can’t easily get into the right chest from that exposure. So you have to be a bit careful so you can see exactly where you’re getting round.
So in specifically with a type II TAAA, many people establish a left heart bypass. Do you always operate in that way and do you use a cardiac surgeon and the setting?
I think type II you are mandated to have some sort of adjunct to keep the rest of the body perfused while you’re doing the proximal anastomosis. I think in an elective setting left heart bypass is the right way forward, because it does give you more flexibility and it allows you then to sequentially clamp and keep the legs, the viscera or the kidneys perfused. There are some negative aspects to left heart bypass, though, in terms of needing a much higher ACT and bleeding is the enemy here. The more you anti-coagulate, the more problems you’ve got. It’s also not pulsatile flow and you’re putting all your cells through a pump and you’ve got to be aware of increased problems around stroke and everything else that goes with that. I think it is very convenient for that set up, because you can get to the inferior pulmonary vein quite easily and femoral cannulation is quite easy for you to return and then you’ve got the option then of individually cannulating celiac and SMA for perfusion, whereas usually renals are cooled down.
If you’ve got a perfusionist there as well, you can get cold perfusate for the renal arteries. So it gives you more flexibility, and if things go wrong, you’ve then got an option to switch to conventional bypass if needed or even drain out and go to circulatory arrest and cool-down.
However, in a more emergency setting, an approach that tends to work quite well for us is to do an ax-fem approach. You use an ax-fem graft onto the right subclavian artery, not tunneled but on the outside of a body onto the right femoral and use the other limb as a single cannula, usually for the SMA, because the SMA is the king vessel with all of this. Most of the other things can go, but if you lose the SMA, you’ve got a dead patient. And that allows you to do an emergency procedure, a mid type III approach, without some of the problems associated with left heart bypass. It allows you to have a lower ACT; it gives you pulsatile flow; you’re not smashing your cells up all the time; and it’s relatively quick and straightforward to do. You don’t have to mobilize a perfusionist and everything else that goes with that. It’s worked well for us in emergency settings. It’s better than a clamp and go approach because with a clamp and go approach, for the type III repair, you need to complete in 15 minutes, your inlay anastomosis at the top, the clock is already on. If you get down to the visceral segment and you’ve got to do some removal of thrombus to get your Carrel patch on or you’ve got to reimplant the left kidney separately, it’s a lot of time pressure and there’s no opportunity for something to go wrong there. That’s where this gives you a bit more breathing space that you’ve got the lower body perfused while you’re doing your proximal anastomosis.
7.2.3.1 Complications
As you’ve mentioned, open repair is a high tariff, high risk operation, but apart from death, what are the specific complications to the open approach?
The big problems are bleeding and clamp times. Those are the things that cause problems for those patients who survive. So problems with large transfusion which cause problems with ventilation afterwards. The most common complications after a TAAA are pulmonary with 8.5% of one cohort requiring a tracheostomy.(Coselli et al. 2016) Renal ischemia is an issue of people will quote a 40 to 50 minute renal warm ischemic time, you increase your risk of renal failure. They may need to go on the hemofilter for temporary support, but these patients have already lost a lot of nephrons, so they haven’t got a huge amount of capacity to lose more. That’s why eGFR or high creatinine is a really important prognostic marker of outcome in this patients. I think it’s like a barometer on their micro-circulation.
The big one and the Achilles heel of these approaches, whether it’s endovascular or open is spinal cord ischemia and that is because of the segmental of blood supply to the cord comes from all the intercostals and lumbers. If you’ve got that aneurysm extending both proximally and distally involving the internal iliacs the left subclavian, then you’re taking out your crucial collateral supply. Important aspects to reduce ischemia include:
Getting the legs back in circuit early, whether that’s removing the large sheaths, during a endovascular repair or getting the leg supply earlier in an open approach.
Keeping the left subclavian in circuit.
Maintain the mean arterial pressure in theater
Place a spinal drain and ensure it is working.
Post TEVAR leg weakness needs to undergo urgent evaluation. Differential diagnosis includes spinal ischemia due to subclavian or intercostal artery coverage, distal embolization or stenosis of the TEVAR graft. Stenosis should be treated with angioplasty and extension.(Buth et al. 2007)
So the major issue is the spinal cord ischemia, can you explain in more detail the blood supply for the spinal cord and how this plays into the occurrence of spinal cord ischemia?
So it’s complicated actually. There are anterior and posterior spinal arteries, but I think depending on what level you are in the cord, they get a blood supply from a more dominant approach. So higher up in the cord—cervical and higher thoracic—vertebral arteries are important, so hence the importance of a left subclavian bypass.
The lower you go, then they become a bit less important and the actual segmental arteries, intercostals, become dominant. Much is talked about the artery of Adamkiewicz. I think, yes, there may be a dominant vessel at about the level of the 9th-12th intercostal, but it’s rarely one, absolutely single one that if you preserve that one, then the rest don’t matter. I think they all matter.
And then the more distally you go, collateral supply from internal iliacs, median sacral, all those contribute to a collateral circulation that should be seen in some ways all connected. And that is why, more recently in endovascular approaches, staging repair is really useful because you can allow the surviving arteries then to remodel and increase flow. It’s why, during a type II repair, when you get the whole aorta open, it’s very important to block the intercostals early—either by sewing them off or putting a little Pruitt balloon in and to stop losing blood from that collateral supply. It keeps the pressure in the spinal cord. Also the differential position of that blood supply is why patients then get a particularly prominant motor problems and sometimes preservation of sensation.
So purely for exam purposes and a bit of physiology. Can you remind us how to calculate the spinal cord perfusion?
All that is really is MAP minus the CSF pressure. So it’s your mean arterial pressure, take out the CSF pressure and that’s what you’ve got perfusing the spinal cord. It is a useful equation to remember because it allows you to decide what’s the way to enhance spinal perfusion as much as possible, which is to increase MAP and decrease your CSF pressure. We do that by enhancing the mean arterial pressure as much as possible, and draining off CSF with a spinal drain to reduce your CSF pressure and allow more blood into the cord.
I think people perhaps get a bit hung up on spinal drainage and it’s importance. It is just as important to maintain oxygenation and hemoglobin over 100 (which is equal to 10 g/dL in the USA), reduce blood loss and all those other things are as crucial. Spinal drainage is an adjunct, but it shouldn’t be seen in isolation. It’s one of many adjuncts to try and help prevent spinal ischemia.
So in regards to the mechanism for spinal cord ischemia during open thoracoabdominal aneurysm repair, do you think it’s related the blood loss, clamp time or or implantation of the intercostals?
I think it’s multifactorial. So I think the majority is due to ischemia scheme in terms of a watershed situation. Segments of a cord just not getting enough blood. And the very reason the more typical area around T7, 8, 9, to 10, is because it is in the middle between the vertebral artery and internal iliac artery supply. This is probably a kin to a splenic flexure of the colon, it’s between two territories.
However, there is also potentially problems with microemboli or trashing of a spinal arteries, which can occur in some patients. It’s a slightly confusing situation, but I think in terms of intraoperatively—blood loss, dumps in blood pressure, with hypotensive episodes really don’t help.
When do you remiplant intercostal arteries?
Again, that is a bit confusing. Some people would argue if there’s massive back bleeding, you don’t need to be reimplant because they’re getting collateral supply from somewhere.
I think it will depend on how the case is going. We do use motor evoked potentials (MEPs) but that’s quite a specialist situation and you’re very reliant on the readings you get. They can be confused by leg ischemia, cooling down or edema. But if you have already got the legs back in circuits and got the MAP up and things weren’t improving and there was a sizable intercostals that could be reimplanted, well, then that’s worth doing. And that’s why the technique of using Pruitt balloon occlusion methods in pairs rather than ligating is good because you can then just reimplant those. If you don’t need to implant them, you can just ligate and remove them. Whereas if you’ve already ligated them, you’ve got a problem because you’ve already destroyed the ostia.
We tend to leave a branch already attached in the mid thoracic aorta to save an anastomosis. You can, if you’ve got really good intercostals, fillet the branch to open it up and sew it on like a long patch longitudinally along the paired intercostals and then plumb it back on the other end so it’s a circuit in series with your main aortic graft. That probably decreases the resistance to flow and that might remain patent for a bit longer, rather than having a big 10mm graft going into a single pair of intercostals with what are likely to have quite a high resistance, and they probably don’t last as long.
Several spinal protection protocols have been described to reduce risk of spinal ischemia or mitigate the impact of spinal ischemia in patients who develop weakness.(Estrera et al. 2009; Yanase et al. 2012) An easy way to remember the important components are COPS:
C - Cerebral spine drain status - keep for 7 days, pressure less than 5
O - Oxygen delivery - supplemental oxygen, increase hgb, increase cardiac index
PS - Patient Status - Keep BP greater than a MAP of 90mmHg
So do you think we’re good at predicting preoperatively who may get spinal cord ischemia? You mentioned a few risk factors already that can predict who will or won’t post-operatively.
I think we’re utterly hopeless at it actually. I really don’t think that there’s a good method. You can see people having an infrarenal repair getting paralysis and you can completely replace the whole aorta from the arch down to the iliacs with prosthetic and have people walking around without a problem at all. So I don’t really understand it and I think that comes into the business about whether it is about emboli, flow, or collaterals. I think it’s a combination of things. When people started embolizing intercostals preoperatively prior to endo repairs, people thought this is a mad thing—you want to keep them perfused surely. But I think it does show the importance of maximizing the collateral supply, and I think some people have a better collateral supply than others. And of course, what we don’t know is when you get down to the more microscopic level of actual arterial supply at cord level, what that is like in an individual patient that you can’t see on imaging. If that is already compromised, I suspect those patients are more at risk than whether they have a macro vascular problem when things go wrong terms of hypotension or blood loss.
Many reports state that the highest risk factor for spinal cord ischemia includes length of aortic coverage or repair, followed by whether they have had a prior repair, preop hemoglobin, and intraoperative hypotension.(Bisdas et al. 2015)
We haven’t really touched on complex endovascular repairs yet, but can you explain when you might choose a hybrid approach to this thoracoabdominal aneurysm repair?
So visceral hybrid operation came in really as a bridge between open surgery and endovascular. This is a bit dated now, because it is before custom devices and we only had thoracic stents at this time, the era of the Talent stent, which was a very early thoracic device made by Medtronic. Perhaps not the perfect name because it wasn’t a particularly talented, it was a difficult thing to deploy, but it actually got us into the thoracic aorta. What we realized was that if you could operate in one cavity, such as the abdomen, but still excluding any aneurysm in the chest without cross camping and without rendering that patient ischemic over a large part of their body—they could withstand that hit much better than open cavity surgery with cross clamp and massive reperfusion.
So the concept of a visceral hybrid was to do an extra-anatomical bypass of the celiac, SMA and both renals from either the distal aorta or the iliac vessels. So patients would only get sequential ischemia of one organ at a time, say the right kidney or the celiac territory, and during that 10 minute anastomosis, the remainder of the body and organs were refused. And finally, at the end that, you could then put in a thoracic device as a freebie, because you’d already perfused the organs from distally. You’d ligated those target vessels and then you would just excluding the aneurysm so that you were transferring blood from above the repair to below the repair and perfusing the vital organs retrograde.
So it was very attractive and we started doing it quite early at St. Mary’s and initially we had some very good results in the first 30 or so patients.(Jenkins et al. 2011) And as always, then it allowed you to consider older, sicker patients but it wasn’t easy surgery. And actually I think because it was doable in terms of just an abdominal approach and relatively familiar territory for anyone who’s done occlusive disease for the viscerals or renals, I think a number of centers started doing small numbers and not getting so good results. And then when better, custom made devices came in, I think it’s purpose became less and less because why would you do that if you had an opportunity to do something which was even less invasive.
So what we’ve been left with now to consider a hybrid type approach effectively are those patients who are physiologically not fit enough for an open approach and those patients who are anatomically not suitable for a total endovascular approach. In some ways, they are the worst of both worlds in that outcome group. And so I don’t think you’ll ever be able to compare outcomes legitimately with the fitter group having a fully open approach and the anatomically suitable patients having a total endovascular.
But I must say we still see quite a lot in our multidisciplinary reviews coming back. What surprises me is the durability of those grafts. The visceral grafts remain patent for many years, some of them are 15 years now. Occasionally there will be an accessory or small diseased renal artery, and the renal graft will go down, but the others have been extremely durable. And even though we’ve had to re-line the stenting portion or extend it, the grafts have maintained really well.
A unique situation that uses a similar technique is with mycotic aneurysms of the visceral segment of the aorta. The mainstay of treatment is a debranching of the aorta and debridement of the infected aorta with in situ revascularization or ax fem-fem bypass. There is an evolving role for FEVAR, such as with most aneurysmal disease.(Sörelius et al. 2016; Sule and Dharmaraj 2016)
So moving on to Type IV thoracoabdominal aneurysm repair. These can be repaired using endovascular or open techniques. Can you talk us through your approach to open Type IV repair in terms of exposure and any tips such as how to minimize the visceral ischemia?
So I think an open Type IV from a subcostal approach is a doable and durable procedure. And what I mean by that is that the hit to the patient is not enormous, and a reasonably fit patient can get through that reasonably well. You have to be a little bit selective, but not super selective. For example, in my first hundred, I had one 30 day death and one in hospital death, which was someone at about three months who just didn’t get better, so that puts it into perspective that actually it’s an operation with a very good outcome, if you get it right at the beginning.
The approach I mentioned earlier, nothing too special. This is a supine patient. Getting the break on the table in the right position to allow you to extend the abdomen. You lower both ends of a table to open up that segment of the abdomen and get better exposure. I tend to do the vast majority via a subcostal approach, some people would call it rooftop, then extending on the left side down below the costal margin a bit. And it gives you really good exposure even if you have to go down to the iliacs. It does cause a bit more of a problem getting to the right iliac bifurcation. The left is easy, because it’s right there next to you. So that’s an added complication.
The visceral rotation needs to be done carefully because what you do not want is to create blood loss right at beginning. And as I mentioned earlier, it’s getting under the left colon along the white line onto psoas and then getting up under psoas and I always tell the registrars when they’re doing it, you’ve got to go as far as possible on psoas from below. And when you think you’ve gone as far as possible, you’ve got to go another five centimeters. So you get right up to the diaphragm from below. And then you can get into the supra-colic compartment around the splenic flexure and get your fingers either side of the lienorenal ligament and take that off the lateral and the posterior abdominal wall. The more and more you do, the more you are freeing and the whole of the viscera comes up towards the right side of a patient and eventually they will rotate up and you’ve exposed the whole left wall of the aorta.
The first thing I then do is ensure that I’ve got a clamp zone, and I do that by dividing the crus which sometimes can be really tense at that level. The crus can act as an extrinsic wrap around the dilated aorta, to an extent that the distal end of the crus is almost ligamentous, causing a tight band on the aorta. I tend to get my finger underneath that before it with a diathermy and opening it, and then very carefully choosing the clamp zone and getting my fingers right round that area, so I know I’ve got a healthy clamp zone.
The next thing I then do is look for the left renal artery. I’ve already tended to make a decision about what I’m going to do with the left renal artery, which depends on the number of things. So it depends on, to some extent, the age of a patient, where the left renal is in terms of a clock face. So if you’re looking at an axial cut to the CT, the more the left renal is around before three o’clock, up to two o’clock, the easier it is to incorporate because you’ve got less aortic tissue there. If the left renal is beyond 3:30 and posterior on the sidewall of the aorta or if the left renal is more distal compared to the right renal, then it’s a long way away from the right renal artery and you’re going be leaving a larger patch of aorta. This is usually bad news, unless you have a more elderly patient.
You’re making this decision about whether you’re going to try and incorporate the left renal artery into a big patch or whether you’re going to reimplant it separately or perform a jump graft. So you’ve already thought about that, but it’s crucial to find the left renal because when you’ve clamped and you’ve done your left aortotomy, you’ve got to get that aortotomy underneath and posterior to the left renal artery so that the orifice goes up with that segment of the aorta.
Then I tend to get the iliacs out. The left is easy, it’s there. I have no qualms on the right by going back over through the peritoneum to find the right iliac artery to expose that. I don’t go around any of them. I just find a very discrete camp zone. You don’t need much, just enough to put a clamp on.
And then I tend to take the fat and lymphatic tissue off the left side of aorta. So when you open the aorta, you’ve not got a lot of immediate bleeding. If you’ve got a retro-aortic left renal vein, you’ve got a line gate that cause otherwise you’d be going through it. And surprisingly, on CT, the main left renal vein is anterior, but there is often a vein there which has stretched across, either a lumbar or phrenic vein, which you should deal with prior to your aortotomy.
It’s about getting everything set up before you cross clamp, because once you cross clamp, the clock is on. So it’s getting the whole team ready for that moment and making your anatomy as perfect as possible before you do that. Obviously it goes without saying that you have cell salvage and we use a Belmont with the big bucket on the top of it, so that you can rapidly give blood back when you need it.
Can you talk a little bit more about a Carrel patch and when would you choose to do a jump graft to the left renal rather than encompass all the vessel vessels onto that patch?
I tend to think of a Carrel patch more in a way with a type III repair, because with a type III repair, you’ve done your proximal anastomosis and then what you’re doing is you’re putting on a patch of aorta to include the celiac, SMA, and right renal, which tend to be together, whereas sometimes the left renal is a bit away. The more tissue you leave there, the more chance that aortic tissue will dilate to over time, hence the patch aneurysm. If your patient has got some form of connective tissue disease, we reimplant directly.(De Rango et al. 2011; Afifi et al. 2017) There is a very nice graft available with four side bunches already put on and you can go straight onto the ostia. So you’re basically leaving no aortic tissue at all.
For type IV, you are doing an oblique anastomosis and you have to be aware that the right side of the aorta is really left there. It’s a compromise, these patients with atherosclerotic type IV aneurysms, they may be in their sixties, seventies or even into their eighties. Even the good candidates, they’re not going to live 25-30 years, and therefore over time that segment may begin to dilate a bit. I think that is acceptable. Half of that segment is Dacron and the other bit may dilate.
I think if you’ve got a Carrel patch, which really balloons out, that’s something which is different. We don’t have good data as to when those will give away and rupture. I think what is clear is that if you’ve got dehiscence between your suture line and your graft, that is a dangerous situation, akin to a false aneurysm. And although it may look similar on CT, that’s a different beast and they’re at risk at any stage. True aneurysmal dilation of a segment that is left behind is a bit different and I think that’s a bit safer. In essence, what you’re trying to do is a compromise between leaving as little aortic tissue as possible, but also getting the patient alive through their first repair safely.
If I know I’m not going to incorporate a left renal, then I will sew on a six or eight millimeter side branch onto the tube golf before I cross clamp, because that saves you one anastomosis. And then now my favorite technique is just to amputate the left renal artery and sew that directly onto your branch and leave that in a bit of a lazy C configuration in the paracolic gutter, so as the rotation comes back, it’s not under tension. The other technique is to have very short graft, right from your aortic prosthetic, but you’ve got to really judge how that will sit when the kidney is back in its anatomic position. So it can’t come off the anterior aspect of the tube graft. It needs to be further down and that’s awkward to judge and I think we’re probably not good at that so the lazy C is a better approach.
I much prefer that to trying to either reimplant the native artery directly onto the Dacron, as they tend to restenose or try to bring the aortic sidewall down on to the Dacron. I think that’s fraught with difficulty. You’ve often got calcification at the ostium, and it’s also very difficult because you’ve got the rest of your anastomosis really close and sometimes not enough room to bring your clamp down, which is exactly what you want to do. The left kidney will take a bit of an extra ischemic hit, but you want to be perfuse the right renal and viscera. You’ve got to have to bring your camp down below your proximal anastomosis.
When it comes to late complications from TAAA repair, 8% are from progression of aortic disease and 3% are related to the graft repair. Risk factors associated with late events include female sex, partial aneurysm resection, expansion of remaining native aorta or initial aneurysm rupture.(Clouse et al. 2003)
Have you ever had to treat the Carrel patch aneurysm in your career?
We have a number from previous Type III repairs and I think these are very suitable for fenestrated or branched devices. You’ve got a beautiful lending zone, proximally and distally. Why not? These tend to be well-suited to that and it’s a much easier approach mixing endo and open, changing from one to the other, I think that’s fine. It’s just at a different stage of a patient’s life and repair
Any final summary or closing words about aortic surgery?
We have a bit of a tipping point with open aortic surgery at the moment, certainly in the UK. Looking at registry data, many are tipping back to open now. Whether that was as a result of NICE guidelines, I suspect not, perhaps that just put it more into focus. I think many people are seeing more problems with patients surviving after what was very good endovascular surgery at the time, but they’ve outlived the repair. Now we’ve got problems with patients where you got to wonder whether that wasn’t perfect anatomy and should they have had open surgery?
Now the difficulty we’ve got at the moment is the patients that perhaps weren’t that suited for endovascular repair, did well initially from it and they are paying the price later on. But those very patients are the ones that are also more difficult from an open approach. They are patients with shorter, more tortuous necks or more calcification. There is a concern that there is an era of surgeons now that haven’t done as much open aortic surgery, who may not be as confident with adverse anatomy.
That lack of confidence influences your decision-making, so patients don’t get a full appraisal of what options are available. The default then may be to go with a less than perfect endovascular option. I agree, this may be less easy to kill a patient upfront with an endo option but you perhaps pay for that later on. This is a very difficult thing to get around and we’ve got to get to a compromise of finding the patients with the likely better life expectancy and sending them to groups with a larger open practice and get them through a big operation safely and capitalize on those benefits.
The really lucky ones are the ones that are anatomically really suited for endovascular repair and their sack really shrinks and their seal zones remain good. They are the best of both worlds as they tend to also be fitter with less extensive disease and get the benefits from a less invasive approach. Not all patients are the same and we’ve got to now accept that we’ve gone down the line of working with industry, which they didn’t necessarily focus on durability. What they wanted to do is to extend the applicability, to treat more patients and get better, lower profile devices to go for these percutaneous cardiology market in the United States. And we’re now paying the price of some of those decisions, so we’ve got to reboot and take a stance on which patients are going to actually benefit from which approach and have a better evaluation of that going forward.