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ABSITE Review: Vascular Quick Hits (Podcast)
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ABSITE Review: Vascular Quick Hits (Podcast)
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>> Behind the Knife. The surgery podcast. Where we take a behind-the-scenes intimate look at surgery from leaders in the field. [ Music ] >> Alright. Welcome back to Behind the Knife. And, today we're going to focus on vascular for our ABSITE review. We're lucky enough to have Nathan Aranson, who is a staff surgeon at Virginia Mason University come down to the podcast headquarters of Behind the Knife in Tacoma.
So, thanks Nate, for joining us, and welcome. >> Absolutely. Thank you for having me. >> So, he's going to lead us through some vascular surgery ABSITE. He dominated the ABSITE while a resident at USC, and then went on to train in vascular surgery at MGH. And, is now moved out to Seattle to start his career-- what, about a year or two ago? >> Yes. Last August. >> Great, great.
So, ABSITE and Boards are still fresh on his mind. >> Very fresh. >> And, we're happy to have him, so. Let's dive right in. And, just a warning to listeners, none of this is intended to explain the breadth and depth of vascular surgery, but really just to highlight the important points that are testable on the ABSITE. So, here we go. >> Alright.
The beauty of vascular surgery is that it exists all over the body. It's a systemic disease. It comes in multiple forms, whether it's aneurysm, lesion generation, or bleeding, thrombosis, atherosclerotic disease, et cetera. So, I guess we'll start by talking about carotid disease, which is prevalent in the elderly Americans that we have. So, who are these people that we should be screening for carotid disease? >> So, for carotid disease, any patient over 70 years old with other atherosclerotic risk factors such as a cardiac history, smokers, peripheral vascular disease, any history of a stroke or TIA, would be the highest on my list.
And, of course, any patient that's had a bruit, kind of, on exam would be some of the people I'd be concerned about screening. >> Absolutely. Most studies would indicate that about 10 to 15% of patents that have a bruit actually have significant carotid disease, but anybody who has a bruit would definitely warrant a carotid duplex ultrasound. Otherwise, certainly anybody who's had TIAs or who's had a stroke should be screened with respect to their carotid disease, even though it's only about 20% of all strokes which are caused by carotid disease.
So, how do we screen these patients? >> So, generally it's a duplex ultrasound is the first step in screening patients. >> Absolutely. And, what are we looking for on these ultrasounds? >> So, the indications have been changing slightly throughout time. But, we're looking for high velocities, indicating stenosis. Generally above 60% for symptomatic disease, and above approximately 80% for asymptomatic disease, are some of the guidelines I've most recently read.
>> That's correct. And, most people go by the NASCET criteria, which was developed to provide a standardized assessment of people's carotid disease. And, we're looking at a peak systolic velocity in the ICA over 230, which is the most sensitive predictor of significant carotid disease. So, now let's say you have a patient. They're in clinic. They have a bruit. Now, they have a peak systolic velocity of 250.
And, they're smoking, they're not on an aspirin, not on a statin. What are you going to tell them? Are you going to tell them they didn't need an operation? >> So, with-- the medical management has gotten so much better in the past 20 years since these trials came out, that it's thought that patients on a statin and aspirin, and stop smoking, can manage a large amount of the carotid disease if they're asymptomatic beforehand. >> That's right. So, a lot of vascular disease-- or, the treatment of vascular disease is not interventional at first.
It's lifestyle modification. Smoking cessation. Walking programs. Initiation of statin, aspirin, beta-blocker, controlling your diabetes, et cetera. So, let's say the patient now comes back to you. They've taken care of all these things. And, they come back two months later, but now they're having transient monocular vision loss in their ipsilateral eye. >> Then, this patient has switched from the category of asymptomatic to symptomatic disease, which has a much more aggressive approach to treatment.
>> That's right. And so, if this patient's in your office, what would you recommend to them? >> You know, if they haven't had a history of radiation to the neck, previous neck dissections, and otherwise a good operative candidate, such as their ejection fraction, and their heart is OK. I would offer them a carotid endarterectomy. >> That's right. About 90% of all carotid endarterectomies are done in asymptomatic patients. And, about 90% of all carotid interventions are carotid endarterectomy.
This is a bit of tire country in the neck, to perform a carotid endarterectomy. What are the structures we're worried about injuring? Maybe we identify them beforehand? Or, do we just stay out of harm's way? >> Yes. So, there is numerous nerves. The ones that we talk about mainly in the carotid sheath, you have the vagus nerve that lies just in between the internal jugular and carotid, which is easily identified during the surgery.
More superiorly, you have-- and of great concern-- is the hypoglossal, just superior to the bifurcation, that you can injure and cause a defect in the ability to use their tongue. And then, you have your glossopharyngeal, and your ansa cervicalis, are some other important nerves. >> That's right. And, this is the type of question that's asked on the ABSITE. These anatomic questions. Also, what the deficit is with injury to these nerves, or what is the most common nerve that's injured?
And, the nerves that I usually tell my patients about are the vagus nerve, which injury to the vagus nerve can cause hoarseness. The marginal mandibular branch of the facial nerve, which extends along the angle of the mandible, and can be injured with a traction injury. It's a branch of the facial nerve, and it can cause some ipsilateral mouth drooping. And then, obviously, the glossopharyngeal nerve is one of the nerves that would be the most disastrous to injure, because it would lead to oropharyngeal dysfunction.
The patient may need a tracheostomy, PEG tube. And then, obviously, the hypoglossal nerve, which would call ipsilateral tongue paralysis. >> In your experience, have you seen transient hypoglossal, kind of, stunning of the nerve that resolves within a week of follow-up, or something? >> Absolutely. Probably the most common nerve that gets injured transiently is the marginal mandibular branch of the facial nerve. And, it's the one that we hear about a lot, because in the PACU, the nurse will call you and say the patient's mouth is asymmetric, or their smile's asymmetric.
We think they're having a stroke. And, obviously that raises the blood pressure of the surgeon, and they run down, and they see the patient. They're oftentimes quite relieved to see it's only a, you know, marginal mandibular nerve traction palsy. And most of this, about 90% will resolve in a month, even upwards of a year. And, that's what I tell any patients that have this. Certainly the same goes true for the hypoglossal nerve. Oftentimes, traction stunning or injury, and it does resolve.
>> And, the thought on the marginal mandibular is, you know, if I'm right, it's like a higher lesion that you're having the intern retract the Army-Navy or whatnot to expose it, and that's kind of what causes-- I've seen a question like this, either in my question banks, or something. So, is that the thought? >> That's absolutely true. So, it exists on kind of the angle of the mandible, and the teaching-- or at least the teaching I had in fellowship-- was that you should not be retracting on the angle of the mandible, but the soft tissues above or retracting on the digastric muscle up in the neck instead.
>> Great. >> So, let me ask you this. Say you were in the middle of this carotid endarterectomy. We're dissecting out the bulb and all of a sudden the anesthesiologist tells you, now the patient's heart rate is in the 40s, now the 30s, now their blood pressure's dropping. What do you think's going on, and what do you think we can do for that? >> At the carotid bulb, you have the carotid body which actually has parasympathetic tone, which can be activated by operating in that area. And, which will cause bradycardia.
And, this is not infrequent phenomena. Like a lot of the phenomenas we talk on ABSITE. This one happens quite frequently. And so, generally, you want to have 1% lidocaine up on the table, and you can inject the carotid body to help resolve this bradycardia. >> That's exactly correct, and it's pretty amazing when it resolves itself with the lidocaine. OK. Now, we're ready to clamp. We've got a blood pressure ready for clamping.
How do we know if the patient has enough flow from their vertebral circulation, or their contralateral carotid circulation? Is there something we should be doing ahead of time? Or, at the time of planning to clamp? >> In my experience, it's largely surgeon preference of whether to shunt or not to shunt. If you decide not to shunt, there's a few ways that you can assure that you're not causing ischemia to the brain. Some people would do the operation awake, and have the patient respond with a local block to the neck.
Others would use stump pressures to make sure-- I think it's some pressure greater than 40, which is-- will help you feel confident you're not going to cause ischemia. And, there's different neuromonitors, or ultrasounds-- I'm not exactly sure-- that you can use to monitor blood flow during the case. >> And, this is a question that's asked on the ABSITE. They'll usually say what's the most sensitive indicator of cerebral perfusion during carotid endarterectomy? And, the answer is, do it awake. Because then the patient's squeezing a squeaky toy, or talking to you.
That's difficult to do, both because of patient anxiety and pain control, but it's done commonly. Otherwise, follow the patient with an EEG, stump pressures. Some people just clamp and go. And, I've written papers of the success of that. >> What do you choose to do? >> EEG monitoring, with selective shunting. >> Oh. Really? Selective shunting.
OK. >> So, it's only about 10 or so percent of patients will have basically incomplete perfusion, or will have an EEG change, and will need to be shunted. >> Do you have to have a neurologist there to read the EEG's? Or, how does that work? >> No, there's an EEG tech, and they're in communication directly with a neurologist who probably sits in a room with multiple different computer screens of EEG's that they're following, and they'll communicate directly to say there's a transient change or not.
>> So, to wrap up carotid disease, I've seen a few questions about the differences in flow on the Dopplers of the internal carotid versus the external carotid. How do you keep this straight, Nate? >> The external carotid flows into a high-resistance arterial bed in the face, and so it will be more of a peripheral artery, or similar to a peripheral artery, with a triphasic flow. So, that's what you listen for with the Doppler. Whereas the internal carotid artery has to have continual flow to the brain, because the brain obviously needs this continual flow to keep you from passing out with every heartbeat.
And, it's a low resistance bed, so you have a continuous diastolic flow, and it's biphasic. >> Great. And, that wraps up carotid disease. We just want to cover a few quick points on aortic dissections for the ABSITE. You really just need to know the Stanford Classification which has Class A, which is any ascending aortic involvement. And then, there's Class B, which is descending aortic involvement only. So, distal to subclavian. The patients you want to look for this in are these patients that are severely hypertensive.
And, a lot of times, these patients can be drug users, specifically cocaine abusers have a much higher risk for this. Traditionally, Marfan's are also at high risk for this. Legit generally have kind of a crushing chest pain similar to a heart attack that radiates to the back. So, any Type A dissection requires CT surgery, reconstruction of their aortic arch, and replacement of it. For Type B, aortic dissection, many of them can be managed medically, and if there is no complication such as end organ ischemia, whether the end organ is the kidneys or the bowel, or the lower extremities.
If there is none of this, many of them can be managed with just medical management. >> So, John [assumed spelling], one thing that they commonly ask on the ABSITE is, you have a Type B dissection, what medications do you want to have these patients on to help prevent propagation of that dissection? >> So, you want to control the blood pressure, mostly with IV beta-blockers, esmolol drip is most common, and then, also nipride as well. >> Nipride reduces the afterload, and the beta blockers help with the impulse production to help prevent propagation.
And, the other thing that could happen, kind of on the basic science side, is that the dissections happen in the medial layer of the blood vessel wall. And then, John, one last question, aortic dissections, when you repair these with a thoracic endograft, if you're repairing these, what is your most common complications going to be? Or, the most feared complication, I should say, of a thoracic endograft. >> So, the most feared complication is paraplegia. But, you can also have minor myocardial infarction as well as renal failure, the result from that.
>> What do we do to minimize the risk of paraplegia? >> So, you can place a lumbar drain. Keep their blood pressure above a certain level are the two most common ways. Generally keep them in the ICU, and then, keep a close eye on the lumbar pressures. >> That's right. What's the most dangerous, I guess, real estate territory in the aorta to cover, I guess on a spinal level? >> The artery of Adamkiewicz, because that it what supplies the blood from the aorta to the spine.
And, our favorite, artery of Adamkiewicz. >> That's right. It usually exists in , kind of, the TA to TL-1 level, so any coverage in that realm is considered high real estate, and should have a spinal drain. >> Alright. And, we'll move on to the next commonly tested topic, aneurysms. >> So, what's the risk factor for aneurysm formation? Abdominal aortic aneurysm we're talking about. >> Thankfully, in vascular, there's a common theme of patients with hyperepidemia, smokers, hypertension, and old age would be the most common indications.
Not indications, but risk factors. >> Yes, the most important risk factor is actually family history of abdominal aortic aneurysm. >> Now, when these are usually identified incidentally, who are we recommending repair for? >> So, we recommend for repair-- the first question should probably be is it asymptomatic, or is it symptomatic? For asymptomatic patients, generally we're looking at patients who-- larger than 5.5 centimeters for males.
A little bit smaller for females at about 5. And then, we look at the growth. So, during surveillance, if it grows generally somewhere over a period of a centimeter per year growth rate, those are people who should be referred for elective repair. >> That's right. And, this is a disease of the media. So, let's say you have a 75-year-old gentleman who's got a 6 centimeter infrarenal abdominal aortic aneurysm, how are you going to fix him?
>> His aneurysm met the criteria for an EVAR. I would offer him an EVAR as a first-line repair. As, it's been shown to be superior, in the short-term at least. So, the kind of anatomic criteria that are kind of important to know, to make a patient qualify for an endovascular repair, is they have to have an adequate neck length, both below the renal, and kind of before or after the hypogastric. So, you'll need at least 15 millimeters of a landing zone, both proximally and distally. The neck diameter has to be-- at the infrarenal-- has to be less than 30 millimeters, otherwise you won't be able to seal the graft, and you'll get an endoleak like we'll talk about in a second.
And, you can't have too much of an angulation, generally 60 degrees is the cutoff for that. And then, your iliac arteries, they can't be too small, and they can't be too big. So, they can't be under 8 millimeters, otherwise you're not going to be able to get your devices up, and they can't be greater than 18 millimeters, because then you're dealing with aneurysmal iliacs, and there's ways to deal with that, but for the ABSITE, they do not qualify for an endovascular repair. >> OK. So, let's say you put in an off-the-shelf, standard EVAR, and at the end of the case you have an endoleak.
Jason, what are the types of endoleak, and which ones do we have to fix before we leave the operating room? >> So, there's five types of endoleak. So, Type 1 endoleak is broken up into Type 1-A and 1-B. So, these are leaking at either the proximal or the distal landing zones, respectively. A Type 2 endoleak is a retrograde flow from lumbar or intercostal branches of the aorta into the aneurysmal sac. Type 3 involves structural failure of the graft, or leakage between components of the graft.
And then, a Type 4 is leakage through the graft, due to graft porosity. And then, there's a Type 5, which is kind of mysterious, endotension. Which, if anybody can explain to me, to where I can understand it, I would much appreciate it. As far as the ones you have to fix, specifically, you know, right before you leave the operating room, certainly any type of graft structural failure. So, the Type 3 endoleaks, where there's leakage between components.
And, a Type 1 where there's a leakage either at the proximal or distal landing zone. Those need to be addressed with either ballooning up the graft, or placing further components, proximally or distally. The Type, you know, small Type 2 endoleaks can be observed. >> That's right. And, one of the actual things that the ABSITE loves to ask is, post-operative complications of aneurysm repair. So, they'll ask what's the most common reason these patients die in the hospital? >> Yes, and this both applies to carotid disease also.
I've seen-- and, the answer's the same for both of them, after carotid endarterectomy. But, the reasons these patients die in the hospital, is a heart attack. They have a myocardial infarction. And, you can remember these patients are generally high-risk, and you put them under a large operation, there's a lot of stress. They're at high risk for a heart attack. >> That's right. And, one of the other topics regarding aneurysm that they like to ask, it's usually a patient, post-op Day 1, in the ICU passes blood per rectum.
>> Yes, this is a, you know, the feared situation of all aortic repairs, of colonic ischemia. And, the thing you really have to differentiate in the question is whether they're telling you that you have a sick, septic patient with concerns for frank ischemia versus-- so you generally want to get a sigmoidoscopy on these patients. You want to start them on fluid resuscitation, antibiotics. And then, you want to get a sigmoidoscopy to determine the-- if it's frank necrosis versus just some mild ischemia that might be able to be improved with resuscitation.
So, if the patient isn't, you know, crashing in front of you, or peritoneal, you can likely treat this with fluid resuscitation, and antibiotics. But, if they downtrend, or they get worse, you're going to have to do a colectomy on these patients. >> That's right. Now, evaluating a patient with abdominal aortic aneurysm, is there anywhere else we should be looking to see if they have an aneurysm? >> Yes. So, as we, kind of, hinted at, you know, these things run in families, so people who are at risk for abdominal aortic aneurysms are at risk for aneurysms at other places, but specifically peripheral aneurysms, so popliteal aneurysm, I think has a 50% associated rate-- lower than that?
>> It's vice versa. So, if the patient has a popliteal aneurysm-- >> That's what it is. >> -- they have a 50% chance they'd-- >> -- have a triple A. I knew 50% was in there somewhere. OK. >> And, who are you fixing with respect to popliteal artery aneurysm? >> So, with popliteal aneurysms, they have kind of a different nature of disease. They're not as high risk for rupture, but they do cause problems with thrombosis and emboli to the distal extremity.
So, generally the indications are if either of those things happen, would be an indication of repair. And, also if it's greater than 2 centimeters. >> Yes, or with thrombus inside of it. >> Or, with thrombus. OK. And then, what is your, kind of, criteria for iliac aneurysms, size-wise, that you consider treating. Or, would you consider treating on the ABSITE? >> Well, I think at the time of repair for an abdominal aortic aneurysm, anybody that's with an iliac aneurysm greater than 3 centimeters warrants repair.
But, overall, people can say 3 1/2 or 4 for just standard, isolated iliac aneurysms. They have a much higher lethality when they do rupture, mostly because the operative exposure's much more difficult. You can imagine, down in a male pelvis, trying to get control of a ruptured iliac artery is no fun. >> So, just return quickly to the popliteal aneurysms, I know I see on the ABSITE in the past, they'll ask you how you're going to repair it, if you're going to repair it. And, there'll be a number of things listed. Either interposition graft, or exclusion bypass, or stenting in a vascular lane.
So, historically the answer's never been to stent, because of the-- it'll get kinked behind the knee, and it's not really amenable to stenting and excluding an aneurysm that way. But, I understand there's some new ways of treating this, and I was just wondering-- you're not under oath or anything, or nobody's-- I promise nobody's going to sue you, but how would you answer this question on the ABSITE if you got it? >> You're right, it is a bit of a moving target with respect to endovascular therapy, the popliteal artery aneurysms. I would say if it's a small aneurysm with no mass effect, I would approach it medially with exclusion and bypass, using a saphenous vein.
If it's a large aneurysm which is causing mass effect, I'd approach it posteriorly in order to get the aneurysm to basically shrink down, or help it shrink down. Treatment with a stent grafts, mainly the GORE VIABAHN, is a stent graft that people are using in the popliteal space, because of its flexibility. And, there are papers out there that show that it has good success. Although, the feared complication is that you get thrombosis and limb loss secondary to your procedure. >> Yes, that might still be a little-- controversial.
So, I think on the ABSITEs I would probably be hesitant to put any endovascular repair for those popliteal aneurysms. >> Exclusion and bypass. >> So, just a few quick highlight points that I've seen also for aortic questions. Jason, you have a guy that's had an open aortic aneurysm previ. Even seen this asked on a question bank, not the ABSITE, but for even after an EVAR repair, but, comes in and has a hematemesis six months after an EVAR. But, you know, that resolved in the ER, and he looks great now.
Are you concerned about anything in this guy, or is it just a little gastric bleed that he had? >> Yes, I think this is the most described, rarely seen aortoenteric fistula, so that would be the herald bleed that would be presenting with that hematemesis. >> That's right, and it's more often seen with open repair, along the suture line. We do close the sac over the aneurysm, but what intestinal structure lies right over this anastomotic line? >> That's when I'd be in communication with the duodenum. >> That's right.
And, these patients present in one of two ways. You mentioned one, with the herald bleed. How else can they present? >> They can actually just become septic from this breakdown of their duodenum into their aorta. >> That's right. And, that's actually a question that was asked of me on my general surgery oral boards. Basically, a scenario of a patient who had aortoenteric fistula. You know, how are we going to fix this?
>> One thing to just keep in mind, any infected aortic graft of any sort, on the ABSITE, you're going to do, generally, an axillary to femoral bypass. And, yes, so you're going to cut out the graft, get source control. And, you're going to-- so, a long PTFE from their axilla to their femoral, then you do a femoral-femoral bypass, would be, kind of, the go-to repair. >> That's right. Then you debride the aorta, remove the graft, stuff some momentum into the dead space, close the duodenum if you need to, and hope for the best in these patients who have a high mortality rate.
>> And then, what are the two-- Jason-- bugs that you see in infected aneurysms? >> So, are you speaking about mycotic aneurysms, or are you talking about infected grafts? >> Just cover both. >> OK. So, for mycotic aneurysms, you know, the, I think the most popular, most famous one is salmonella, but it's actually become not the most common that's found. So, it's still staph that's most common in mycotic aneurysms. But, your top two are staphylococcus and salmonella.
And then, for infected aortic grafts, so any type of, you know, infected material, infected graph, that's-- you know, staph epi is the most common because of its excretion with that biofilm. And then, e. coli is also very common for infected aortic grafts. >> Well, that's perfect, because I generally choose staph for almost every answer anyways. >> Another prevalent vascular disease is peripheral arterial disease. So, this comes in ranges of severity. Let's say another 75-year-old smoking gentleman comes in saying, Doc, I can only walk two blocks before I get this terrible pain in my calf.
What do you think's going on with him? >> Right. So, the concern would be, you know, in this patient of high risk factors that he has claudication from peripheral arterial disease. And, if it's reproducible pain at a specific distance like that, and isolated to the back of his calves, it's high likelihood that it is claudication, and in these patients, there's also the ABSITE question that I've seen in the question banks at least, is that if you want to start them off-- a lot of these people can get better with medical management, so you, you know, they stop smoking, get on a statin.
If they're not on aspirin already, they'd probably require an aspirin. And then, an exercise program where they kind of walk to their point of where it hurts, and walk a few steps past that, and keep pushing on a daily or every other day basis, to help. And, a lot of these patients will improve. And then, the other question I'm kind of seeing involving this, is what percent of these patients that present with claudication, end up needing amputation? And, you know, at least, it's a very small number.
A lot of these patients, with medical management, it's as low as 5%, will end up-- >> Five percent at 5 years, that's what I tell my patients. A lot of them come in, and they are nervous that they're going to develop gangrene, or they're going to need an amputation, but I assure them that that won't happen, but in order for them to improve their walking distance, they're going to have to work at it. Either weight loss, smoking cessation, medical optimization in a walking program. >> And so, generally we get ABIs in these patients, but Jason, when are ABIs not as reliable?
>> So, anything that affects the compliance of the vasculature, so classically diabetic patients, the bad diabetics, the ABIs are less reliable. >> Why is that? >> It's because of the calcification, hardening of the arteries. And, they just-- makes the compression of the vessel-- they lose compliance, so it makes the compression during the ABI inaccurate. >> That's right. Usually patients who have diabetes, chronic kidney disease, obese folks, and people with a lot of leg edema are very difficult to obtain reliable ABIs.
>> And so, these patients, you'll generally get toe pressures on-- And so, when you are getting this ABIs in these patients that do not have diabetes, you'll generally start to be concerned for intervention. It's patients that have critical limb ischemia. And, critical limb ischemia constitutes a patient that has rest pain. A patient that has tissue loss or gangrene. So, when they're less than .4 is when you're going to start getting patients that you'd be concerned about critical limb ischemia, or their toe pressure's less than 30.
So, those are the patients that require intervention in a peripheral arterial disease. >> These patients are very sick. These patients are-- half of them will be dead in 5 years. About 30% of them will lose a limb within about a year. So, it's a very challenging patient population to take care of. What about the anatomic distribution of disease based on patients' comorbidities? Are there differences between people who smoke, or have diabetes, et cetera?
>> Yes, you see a little bit of variation in the distribution of disease between, you know, classically smokers or the diabetic. You know, smokers will sometimes have-- or, classically have more proximal disease, so, you know, iliofemoral disease, and calcifications, atherosclerosis. Whereas your diabetics-- kind of makes sense-- diabetes is a microvascular disease, so they tend to have more distal, you know, kind of below knee-type of disease patterns. And, that leads into the next classic question that you hear in vascular rounds, is how to determine the level of disease that patients have?
And, what-- just based on their symptomology, so generally what they say is that it's one level above where they have pain or problems. So, if they have calf pains generally, that's a [inaudible] disease. If they have thigh pain, you're looking more to the common femorals, or external iliacs. And then, if they're having buttock claudication, you'll look towards the common iliacs, or aortic disease. So, Jason, what is Leriche syndrome?
>> So, Leriche syndrome is a constellation of findings where patients have, essentially no femoral pulses. They have buttock/thigh claudication. They frequently have-- or, they do have impotence from decreased flow to the internal iliac arteries. And, this is associated with, you know, lesions at the aortic bifurcation or above. Typically, these patients will require, a bypass. Aortal, bifemoral bypass graft.
>> I saw one of the score questions yesterday regarding these aorta bifem grafts, and I definitely missed this question. It was asking at what part of the common femoral artery do you want to sew in your bypass graft? And, to spare every one the pain, I'll just answer it. So, they recommend-- so, it's like do you want to sew it in to the proximal common femoral, the mid-common femoral, or where the profunda and SFA take off? And, you want to sew, according to this question at least, to the, where the SFA and the profunda take off, because you have the least chance of having stenosis at the level, sewing in kind of at the common distal femoral.
>> That's right. And, it's actually the profunda which tends to stay open in these patients, long-term. And, that provides the perfusion for the limbs going forward. OK. So, let's say you've done a femoral to tibial bypass in a patient, and your surveilling this bypass, but the bypass goes down, in say, a week after surgery. What usually caused that? >> So, the easiest way to remember it, is if it's less than 30 days, it's usually due to a technical error in the graft itself.
>> Yes. Either the anastomosis technically wasn't put together correctly, or the vein was no good to begin with. Let's say it looks good at a month, but at six months, it's now got high velocities in the graft, or it's thrombosed completely. >> So, this would fall in the category of intermediate bypass graft failure, which usually runs from greater than 30 days, anywhere up to two years. And, that's usually due to intimal hyperplasia at the anastomotic site, or valve sites within the graft. >> What about patient goes back five years after bypass with recurrent claudication?
>> So, this would be considered a late bypass graft failure, since it's greater than 1 to 2 years, and this is always due to progression of atherosclerotic disease, within the inflow or outflow vessels. >> Alright. The next patient's a 65-year-old gentleman with diabetes, now chronic kidney disease, stage 5. Nephrologist refers him to you to discuss a fistula or dialysis options. What are his options? >> So, you have-- the preferred is the fistula placement. Or, you have a peritoneal dialysis options that you can offer them.
We won't really get into peritoneal dialysis in this discussion, but for fistula access, you generally get a vein mapping of their arm. And, you want to find-- I think the kind of target number is 3 millimeters is the size of vein that you need to make a autologous graft that has a high chance of maturing. And so, you generally want to start distally. So, I think they say radiocephalic. Some people would do the snuff box type of things, but more practically, the radius to phallic, and then, like a brachiocephalic are your, kind of, go-to for fistulas, if you have adequate vein size, which like we said is 3 millimeters.
So, that's what I would talk to them about, and I'd get a vein mapping, and hopefully plan for a fistula placement. >> What's something you can do to assess them on exam to, you know, ensure that they don't have steal, or not at risk for steal post-operatively? >> So, classically, we do the Allen's test. And, it's where we, you know, evacuate their hand of any blood, and then release the ulnar artery to see if it has perfusion of the hand-- adequate perfusion. And then, release the radial artery. >> And, what's usually the dominant blood flow to the hand?
>> Generally, it should be the ulnar artery. >> Yes, about 85% of people are perfused through their ulnar dominantly to their hand. So, they shouldn't have problems with a radiocephalic fistula, but some people do. >> OK. So, let's say you go ahead, and their cephalic vein at the wrist is not of size, so you have to do a brachiocephalic fistula in the arm. You create a nice fistula. You're real pleased with the result. You get to the PACU, and the patient wakes up and they've got terrible pain in their forearm and hand.
What do you think's going on? >> So, this is the syndrome that's like IMN. Essentially a severe steal syndrome. Requires take back to the operating room to take down the graft, because their hand is at risk. >> That's right. It's real disappointing. They think that this is steal to the nerves, specifically. But, they can develop a Volkmann's contracture, if left like this, and also would be quite unhappy.
So, let's say, a different story. They come out of the oR, and they've got a little tingling in their hand, but nothing that's that bad. But, six weeks later, they start dialysis, and now they're having a lot of cramping in their hand when they're on dialysis. What do you think's going on? >> This is a concern for true steal syndrome. That they're having arterial inadequacy to their hand. And so, you can compress the fistula to see if that improves their symptoms, and if it does, that can kind of confirm your suspicion of steal syndrome.
And then, if you do have steal syndrome, sometimes they do need to get their fistula ligated, but you can first attempt to improve arterial end flow with endovascular methods of balloon dilation of the artery, and improve inflow. >> That's right. And, is there a surgical procedure that you can do in these patients? >> You can do-- there's a few fancy ways of re-vascularizing the hand. So, DRIL procedure is one of them. Distal revascularization with interval ligation.
There's a few other, kind of-- where you can actually stenose the outflow of-- that way more blood goes to the hand, and not to the fistula. And, hopefully improve the steal syndrome. So, the main thought of all these is too much blood is going into the fistula, and too little blood is going to the hand. So, all the procedures are attempting to redirect the blood flow down to the hand. >> That's right. The venous circuit is of lower resistance than the arterial circuit. Have you ever heard of the rule of sixes, as in how to ensure that the fistula is ready for primetime?
>> Yes. So, you want it to be within 6 millimeters of the skin. You want flows of 600 centimeters per second. You want it at least dilated up to 6 millimeters, the actual fistula itself. And, I'm sure there's some others. Or, is that all? Just three? >> Usually six weeks post-op. >> Six weeks post-op. >> [inaudible] >> And, that should cover dialysis access questions.
Quickly, we just wanted to cover venous insufficiency. This is a, you know-- generally the issue is a medial malleolus ulcer in a patient. Lot of times they'll have edema, and they'll maybe have some evidence of veins. Their foot will have lots of small blue veins throughout it. And, this kind of gives you a clue that it's likely venous insufficiency. So, for these patients, the mainstay of treatment, if they ask you on the test, is compression therapy to help reduce the venous insufficiency.
And then, you can evaluate them with a duplex ultrasound, and see if they have a saphenous vein reflux. Because if they do, they could be a candidate for an ablation of their saphenous vein, which would improve their venous insufficiency. As long as they have adequate deep venous return, and no DVTs. So, that's just a quick point to remember. >> Yes, and the way I've seen that pop up a lot of times, this is very amenable to a picture question. So, if everybody out there hasn't seen, you know, what venous stasis ulcers look like, or you haven't treated a lot of it, just Google it, because changes are, the first Google image that you see is going to be the one that's on the test.
So, look at that image, and just know the treatment for that. >> OK, now we're going to introduce some quick hitters on the common weird vasculitis-type diseases that we see from Step 1, Step 2, all the way to ABSITE. And, they will never leave us alone. So, Jason, you have a young male smoker that has ischemia to his fingers. What are you concerned about, and how do you treat it, and what do you see on angiogram?
>> So, this is Buerger's disease. So, again, this is classical. Young smokers, they get necrosis of their fingers. The treatment for it is they need to stop smoking, absolutely. And, what you'll see on angiogram, is you'll see these little corkscrew collaterals. >> Are they allowed to dip? I'm just kidding. I don't know. [laughs] Alright-- >> Only vaping.
Only vaping. >> OK. Vaping only for Buerger's. That's from Doctor Bingham. So, John, how about the female who has renal artery hypertension? And, she has, kind of, beaded vessels. They can be both in the renal arteries and in the carotid arteries. What is this called, and how do you treat it? >> So, this is fibromuscular dysplasia, and you usually treat this with angioplasty in these patients.
That is commonly in the renal arteries. >> And then, the last two things we just wanted to cover are Marfan's disease. The question, you got to know, just hopefully you remember this back in the day, but it's a defect in the fibrillin gene, and you'll-- a lot of times, these patients as far as vascular disease will go-- they'll have aortic root dilation, and will need a CT surgeon to replace the aortic root. And then, for Ehlers-Danlos, they're at risk for dissections, and aneurysms.
And, it's generally-- it can be multiple different collagen defects. There's at least 10 types that have been identified, so just know that it's an overall collagen defect, and that they have dissections and aneurysms, whereas Marfan's is fibrillin defect. And then, you'll be able to get those answers right. >> The two other ones that you might commonly see on the ABSITE is Kawasaki disease, which is [inaudible] in children. You get an aneurysm in the coronary arteries. And then, temporal arteritis.
This is most commonly found in women who get headaches and fevers, and will also present with blurred vision. And then, they also have the giant cell arteritis upon biopsy. You can usually treat this with steroids. >> Yes, steroids. So, this past year, I've been sent 13 patients for temporal artery biopsy, and zero have come back positive. >> Well, that wraps up our, kind of, highlights of vascular surgery on the ABSITE. And, we really appreciate Doctor Nathan Aranson for joining us today down in Tacoma, to help us cover this topic.
A broad topic. And, there's obviously much more you need to study than what we told you. And, I recommend just knocking out the question banks, and really seeing the questions on your own. I think that'll be the best bang for your buck. But, hopefully, this will get you a little closer there on your drive in to work or something. So, thanks, Nate for joining us today. >> My pleasure.
Thank you. >> Until next time, dominate the day. [ Music ]