Dialysis Associated Steal Syndrome 2 - 2_13_24, 10.29?AM

Hey, everyone. Welcome back to another episode of Behind the Knife. I'm Drew Brait here along with Bobby Beaulieu and David Sheckman, and we're here to talk about some more vascular surgery. So today we're going to dive into dialysis associated hand ischemia, or what many of you probably know as Steele syndrome.

And because we just love to make things complicated in vascular surgery, this has a lot of different names. You'll hear it called access related hand ischemia. Hemodialysis access induced distal ischemia or even dialysis associated Steele syndrome. So for simplicity's sake, we're just going to refer to this as Steele syndrome for the remainder of this episode.

And for any other trainees like myself, I know that ABSITE and VSITE are in the rear view mirror. But I think before we take a deep dive into the specifics of Steele syndrome, we should do a really brief review of some of the high yield basic principles in hemodialysis access. So patients should be referred for long term AV access when their GFR is less than 20 and

that corresponds to a CKD stage 4.

And when thinking of access, the autogenous AV fistula is going to be the gold standard and that's going to be preferred to prosthetic due to lower risk of infection and improved patency rates. You should always attempt your access first in the upper extremity before looking into the lower extremity.

And consideration should be given in making The fistula or access in the non-dominant arm first, and you should think about creating it as distally as possible in the arm. So the common fistula choices are gonna be the radio cephalic fistula or the snuff box fistula, a brachiocephalic fistula, or a brachial basilic fistula.

And when you're thinking about grafts, the common choices are gonna be a forearm loop graft, a brachial axillary graft, or an axillary axillary loop graft. All patients should have vein mapping performed prior to determine the size of their veins and arteries with a minimum artery size of 2. 5 millimeters and a

vein above three millimeters.

And I'm sure we've all heard of, know and love the rule of sixes, but just to quickly review a mature fistula that's ready to use has a flow of above 600 mils per minute, a vessel diameter of above six millimeters. Should be located less than six millimeters from the skin and have a cannulation segment.

That's above six millimeters as well So these concepts get tested frequently and if you miss them on this year's test, hopefully after this episode you can steal an answer On the test next year. No way. I'm gonna I'm gonna be done making some bad jokes here So Dave, why don't you kick us off and tell us what you know about Steele syndrome?

All right, Drew Moving away from the bad puns, Steele syndrome refers to a constellation of symptoms from having hand ischemia induced by hemodialysis fistula or graft. In other words, it refers to fistula or graft stealing or siphoning blood from the distal tissues, most commonly the hand. Unfortunately, in order to really understand dialysis

access and Steele syndrome, we do need to talk a little bit about physics.

When you create an AV fistula or AV graft, it substantially alters flow. The downstream effect of this is alterations to resistance and dynamics affecting flow going from one circuit initially, which is high resistant, to having a low resistance circuit competing with that high resistance circuit of the hand.

It's important to note that some amount of steel, what we refer to as physiologic steel, is a normal phenomenon after AV graft is creation. Physiologic steel is common and noted in up to 73 percent of autologous access and 91 percent of prosthetic access. Almost 90 percent of patients do have some kind of reduction in distal blood flow that we can measure but may not be clinically significant.

So only a small subset of these patients develop steel syndrome. And we have to remember when we're talking about a syndrome, we're talking about a constellation of symptoms. So no matter what your angiographic or duplex findings

are, what we're going to focus on today is what the patients are experiencing.

And this is often hand numbness, coldness, pain, weakness as well as significantly reduced blood pressure and changes to the tissue distally to the access. When we think about it from a physiologic standpoint, ischemia or Steele syndrome results from inadequate collateral circulation and inability to meet increased demand via increased cardiac output and vasodilation, leading to decreased distal perfusion.

When we think about this from a physiologic standpoint, ischemia or Steele syndrome results from inadequate collateral circulation. This can be an inability to meet increased demand in the hand when using it or maintain flow to the hand during dialysis sessions. This all leads to a decrease in distal perfusion and the patient experiencing symptoms.

So, Bobby, how common is Steele syndrome? Thanks, Dave. Well, the incidence of Steele syndrome is actually quite variable depending on the literature that you read, and it can be anywhere from 4 to

10%, but it's kind of all over the place. We do know that the incidence varies with the type and the location of dialysis access.

It seems that significant steel syndrome resulting in ischemia occurs in about 1 2 percent of autogenous access that's performed at the wrist, and between 4 8 percent of brachial based access. And some of this goes back to your Poiseuille's Law, in which you recall is the flow is proportional to the radius of the vessel raised to the fourth power.

So larger vessels, like the brachial artery, will have more flow going through them and can result in more steel. Now, that also may explain why AV grafts have higher rates of dialysis related steel syndrome than AV fistulas. Grafts, when you put them in, are just bigger, and they're in the 6 to 7 millimeter range, and can result in a higher steel rate than a blood vessel, such as a cephalic vein or bacillic vein, that would be smaller, typically.

Other factors that impact and that, excuse me,

other factors that impact the risk of SEAL syndrome include age over 60, diabetes, a history of peripheral artery disease or coronary artery disease, tobacco use, larger conduits or larger anastomosis performed at the time of initial conduit placement, female sex.

a history of Steele syndrome, not really surprising there, and then multiple previous dialysis access attempts, typically on that limb. Almost all of these have some intuitive physiologic explanation that you can use to base their association. For example, we know that vessel compliance decreases as we age, and this can lead to some decreased distal flow beyond a fistula.

In diabetic patients, hyperglycemia decreases, shear induced. vasodilatation beyond the site of a fistula, so you won't have as much vasodilatation of the vessels in the forearm leading down to the hand and therefore blood may want to go up the fistula instead. There's also decreased collateral recruitment, inflow, artery remodeling.

And then as you may imagine, atherosclerosis in the form of peripheral artery disease, of which coronary artery

disease is a risk factor as well, may increase the risk of a flow limiting lesion in either the inflow or an increased peripheral resistance due to atherosclerosis in the forearm vessels like the radial and ulnar vessels.

So Drew, how do we diagnose Yeah, sure. So, you know, steel center really can be somewhat of a clinical diagnosis. So obviously getting a good history and physical and exam on these patients is quite important. So when thinking about the symptoms, these really can depend and really are pretty variable in regards to the severity of the disease.

So typically symptoms are going to develop over the course of weeks to months after creation, but they can occur years after the official is created. And as we touched upon earlier, these symptoms include coolness, paresthesias, weakness, and pain. And these are typically often either during dialysis or worse with dialysis, but patients certainly can have some ischemic pain in some of these symptoms, even at rest.

And at its later stages, patients can even have tissue loss from this. So we'll talk a little bit more about this later when we

discuss the stages, but just to kind of touch on that now. And then when you examine these patients, you know, obviously it's gonna be quite variable, but you know, oftentimes they'll have a cool extremity with pallor, cyanosis, delayed capillary refill, and even some patients might have absent pulses or signals in their hand.

Some patients might have diminished sensation, a weak grip, or even ulceration and gangrene, like I mentioned. One thing that's really helpful is to do a compression of the fistula or graft when you're evaluating these patients and that can often lead to improvement in all of these symptoms that we just mentioned.

And as an aside, I think, you know, important to point out here that in a patient who presents with pain and profound muscle weakness immediately after creation of the fistula and they have normal pulses or signals in their hand. That's really concerning for ischemic monomyelic neuropathy and that must be considered at that point.

So prompt recognition and differentiation of IMN versus acute limb ischemia is important and ligation of the fistula is the

treatment in that case. I'm sure we've all taken some ab site and b site practice questions where that's been the stem. So let's say we have a patient with a six month old brachial basilic AV fistula and they come in with hand pain and paresthesias and it's only during dialysis, but their symptoms are pretty bothersome.

What diagnostic tests might be helpful to confirm the diagnosis of Steele syndrome? Thanks, Drew. So currently no clear guidelines exist for a testing definition of Steele syndrome. syndrome. Most of that is because we've had multiple studies that look at pressures, waveforms, angiographic data, and duplex in these patients.

And while patients on the extreme ends of the spectrum tend to have or not have Steele's syndrome, there's a really kind of heterogeneous group in the middle that may have relatively normal pressures and symptoms or relatively abnormal pressures and no symptoms. So,

my workup for this involves pressure measurements, pulse oximetry, sometimes photoplethomography, Doppler and duplex ultrasound, as well as transcutaneous oxygen pressure and even invasive angiography.

So there's lots of things in the toolbox to better understand what's causing the patient symptoms and what we can do about it. All these tests, when done, should be done both with the fistula open and fistula compressed to get an idea of the physiologic changes that happen when you compress the fistula.

I mentioned that there's heterogeneous data. One of the previous works published 2015 found that the digital brachial index, or DBI, of less than 0. 7 had 100 percent sensitivity but only a 73 percent specificity for Steele syndrome. This paper also found out that an oxygen saturation of Less than 95 percent was associated with Steele syndrome.

So once again, patients may have a higher drop in no symptoms, they don't have Steele syndrome, they do have an

abnormal pressure. Another paper in 2005 from Vascular Medicine, the co authors, measured digital artery pressures in patients with and without digital ischemia. They found that the mean digital pressure was significantly lower in patients with Steele syndrome, 30 versus 102 millimeters of mercury in the normal group, as well as a digital brachial index of 8.

Some authors have proposed using post operative systolic pressure index, which is the post operative forearm pressure divided by the contralateral forearm pressure. Using this, they found that 14 percent of mild to moderate ischemic symptoms occur in patients with an SPI or systolic pressure index at less than 0.

4. Finally, some authors have proposed that a digital pressure of less than 50 millimeters of mercury a digital brachial index of less than 0. 6, for a transcutaneous oxygen pressure less than 20 to 30 are most consistent with STIHL. I think the important thing to remember is that we have

lots of non invasive tests to look for this, and although there are no exact guidelines to diagnose STIHL, if you have a patient with the right symptoms and evidence of distal ischemia on non invasive testing, you probably have a patient with STIHL syndrome.

Yeah, Dave, and I think another point is it's probably helpful that when you get a duplex ultrasound you can get some sense of the flow that goes through that fistula, and the measurement of flow is not necessary, as you've pointed out. It doesn't really enter into the diagnostic criteria, but there's a couple numbers that are probably worth keeping in mind.

Fistulas that have a flow rate less than 600 mls per minute are unlikely to be useful for dialysis and probably low likelihood to have steel as well. Whereas a high output fistula is one that's over 1500 mls per minute, and these can get up into the several liters per minute category. And those are really the ones where you start entertaining the diagnosis of steel syndrome a little bit more.

I'd say angiography is a

staple of the workup in Steele syndrome. An angiogram allows for a clear assessment of other possible contributing factors such as an inflow stenosis, an outflow stenosis, and you get clear visualization of the Steele and the runoff to the hand. It's important to remember to repeat the angiography both with and without fistula compression.

You can often do this with metal instruments so you don't have your hand in the x ray beams. It's sort of Alara style right there. You may see a significant arterial lesion on the inflow and outflow that could be responsive to angioplasty and you can treat it at that time. These types of arterial lesions are present in about 14 percent of all patients with AV access and up to 80 percent of patients with symptomatic Steele syndrome.

Another little tip and trick is you should get an evaluation of the hand itself with and without fistula compression and sometimes it can be difficult to collimate your

If you put them with some water

below their hand or a wet towel, it'll change the rate of x ray generation and make it a little bit easier to see. So let's take the same patient who presents for follow up six months after creation of a brachiobacillic AV fistula. However, let's switch up the case a little bit and say this patient has no symptoms, but rather was found to have evidence of decreased digital pressure and evidence of steel on his duplex.

The patient says his hand feels great, and he has successfully used the fistula for dialysis without any issues whatsoever. Drew, do you need any other workup for this case? Yeah, I think what you're getting at here is grading Steele's Syndrome. So just to kind of go through that real quick. Steele's Syndrome is most often split into four grades, and it's usually 0 to 3.

I have seen some sources that say 1 to 4, but the kind of textbooks that we like to read. Generally say zero to three. So this patient is probably a grade zero steel. So that really refers to the fact that there's evidence of retrograde diastolic flow, but this patient is not having

any symptoms. So for patients with grade zero steel, we can really just observe them.

So I guess to answer your question, probably not. I think we could probably schedule him for a follow up appointment and counsel him on symptoms really to watch out for. On the other hand, grade one steel refers to mild symptoms. So this is hand claudication or coolness like we talked about. And these symptoms, or patients of grade one usually just have these symptoms during dialysis.

And in some cases they can be observed with routine surveillance and hand exercises. But if their symptoms are severe, meaning limiting their ability to get through dialysis, then you might need to do surgical intervention. Grade 2 steel refers to significant symptoms such as pain at rest or very severe claudication during dialysis.

And grade 3 refers to patients with tissue loss, so an ulceration, necrosis, or gangrene. And or motor and sensory deficits. And both grade 2 and grade 3 steel requires surgical intervention. Okay, so let's go back and pretend our patient has pain at rest and evidence of steel on non invasive

imaging.

Drew, what kinds of interventions can we offer for steel syndrome? Yeah. So in patients with steel syndrome, the main goals of treatment are really symptom resolution and access preservation. Obviously, if they have a working fish, so we want to save that at all costs. So patients with transient mild symptoms, like we kind of talked about, can be managed expectantly with reassessment, warming and blood pressure management.

However, in patients with grade two or three steel syndrome, surgical intervention is needed. So there's two basic strategies. There's access flow reduction and that's helpful in patients with high flow AB fistulas. So like we talked about those with the flow rate of above 1500 milliliters per minute and then augmentation of the distal arterial flow to alter hemodynamics and improve the digital perfusion in those patients with lower normal flow AB fistulas.

So the options that we have include banding. Revision using distal inflow, which we call Rudy, R U D I. Proximalization of arterial

inflow, also known as PI. And distal revascularization with interval ligation or DRIL. And then obviously there's a role for arterial angioplasty as well. And as a last resort, which just makes us all sad and nervous to even say out loud on this podcast, ligation can be used in those with limited life expectancies.

severe tissue loss or poor, poorly functioning access. So I think it's really helpful as we go through these options. We're kind of going to go through each independently. Really encourage you to check out the link in the show notes to this paper from 2016 in the Journal of Vascular Access. This article has great diagrams of each of these options.

So it's really helpful to kind of check on that as we kind of go through each of them and have like a little graphic to watch them. Awesome, so let's talk about banding first. So in general, banding refers to creating a stenosis near the arterial anastomosis of the AVF. Or, as Dave likes to call it, just

his anastomosis.

Decreasing the radius, and as you recall from your brief physics review that we just had, leading to an increased resistance in the fistula, and thus decreased flow through the fistula. There are many ways you can do this. You can let your fellow complete the anastomosis. It can also be done via suture plication.

a single tie, or wrapping a constrictive prosthetic cuff. However, determining the exact degree of stenosis needed is quite difficult, and is really more of an art than a science, because not enough stenosis and the steel won't be improved, too much stenosis, and you risk thrombosing off the fistula. Many of the early series of bandings based the degree of banding on intraoperative assessments of distal perfusion alone, and were limited by high rates of access loss.

So, precision banding is a technique that uses accurate measurements of the degree of flow reduction in conjunction with one of the aforementioned banding techniques. And on final analysis, access flow of 700 mils per minute is an important cutoff for

maintenance of AV access patency. And those that are above that have a 74 percent patency, versus those that are below it have a 38 percent patency.

Suggesting the reason for the earlier failures of banding may have been just tightening things too much and lowering the flow rates. However, banding is not commonly done in contemporary practice as it is still limited by variable outcomes and the inability to more accurately determine how tight you need to make the band.

Many surgeons now advocate for the Miller Technique, which stands for Minimally Invasive Limited Ligation Endoluminal Assisted Revision. The Miller technique uses a percutaneous 4 5mm endoluminal balloon placed as a sizing dowel with a suture placed around access with the balloon inflated via a small incision.

Series describing this technique demonstrated that significant clinical improvement occurred in 89 percent of patients with an early thrombosis rate of only 4. 4%. Although the role of

banding is still debated, it remains an option for the particularly useful for Seal Syndrome and high flow AV fistulas.

However, another technique has described banding between puncture sites in low flow AV fistulas to maintain a pressure gradient between the arterial and the venous puncture site. So Dave, how about Rudy, besides being an all time classic sports film and lead in to the character of Samwise Ganji in the Hobbit films, can you explain that to us?

Absolutely, Bobby. Okay, so Rudy, also known as revision using distal inflow. In this procedure, the AV fistula is ligated at its origin, or a vein or prosthetic conduit is used to establish inflow from a more distal arterial source, usually proximal to the mid radial artery. Again, if you aren't driving a car or riding your bike, take a second to pause and pull up the article with the pictures.

It will be helpful,

I promise. The way this works is using a smaller distal artery as your inflow, causes increased resistance, and the fistula is lengthened. By increasing the length, that also increases resistance. This reduces the flow in the AV fistula and can help relieve symptoms. One thing I want to say, though, is in practice, Rudy can be really hard to find a good patient for, because most of these patients have distal peripheral arterial disease, which is why the access is higher than a distal target to begin with.

So looking at studies evaluating Groody, they have good symptom resolution and good access patency. A review of 130 patients from 11 articles noted an 82 percent success rate, defined as resolution or improvement in symptoms at 12 months. However, 11 percent of fistulas did require ligation for continued symptoms, and another 7.

5 percent thrombosed. Other things to think about, recurrence was noted

in 50 percent of patients at 3 years. Another limitation is patient selection. As I talked about, patients with Distal Peripheral Arterial Disease and small arteries beyond where previous anastomosis was, would not be a candidate for RUDI.

They would need a new inflow procedure. Often times, patients won't be a candidate for RUDI because of this reason, and we have to talk about other options, such as PI. Yeah, Pi or Proximalization of Arterial Inflow is really all in the name. In this technique, the inflow for the AV axis is moved more proximally up in the arterial level.

Now, I know what you're probably thinking. This dude just talked all about physics and how a bigger vessel increases the flow and therefore could increase the risk of Steele Syndrome. So how does proximalization actually help with Steele Syndrome? Well, the first descriptions of pi, or by Zarnow et al, described ligation of the anastomosis in conversion to a more proximal inflow using just a 4 to 5 millimeter PTFE interposition.

In this

case, because PTFE is less compliant and it's a smaller diameter, and a longer length actually helps lead to an increased resistance and decreased flow through the graph. However, some groups have described the technique with vein and have similar results. In that case, The proximal arteries diameter in higher capacity creates lower pressure drop across the anastomosis at similar flow rates.

So our simple Poiseuille equation doesn't really explain everything in this scenario. The primary advantage of PI is preservation of the native arteries continuity. Symptom resolution occurred in 84 percent of patients, the remaining significantly improved. Access primary patency was 87 percent at 12 months.

67 percent at 3 years. Thurman et al. confirmed similar results, but found that patients with severe tissue loss did poorly. So last, but not least, what about the DRIL? Yeah, so DRIL stands for Discal Revascularization with

Interval Ligation. It always makes me cringe a little bit to ligate a normal artery.

This was originally described in the late 80s and is now considered the gold standard by many vascular surgeons. A drill consists of creating a vein bypass originating seven to ten centimeters proximal to the axis and asthmosis and terminating it distal to the ligated artery. Again, check out the pictures in the article to help you keep track of these different techniques.

I promise we don't get any royalties from this article. In the drill, retrograde flow is preserved and a new bypass creates a low resistance pathway to the peripheral vascular bed of note. Typically, when my practice prior to doing a drill procedure, I perform upper extremity angiography to confirm that the distal target for bypasses adequate diameter without significant calcifications.

Long term results are excellent for both symptom resolution and access patency with.

89 to 100 percent freedom of symptoms and 73 to 100 percent patency, depending on the series. Recent meta analysis found best results with saphenous vein conduit with resolution of symptoms in 81 percent of patients and patent fistulas at a mean of 22 months.

There are drawbacks to the drill. This includes perioperative mortality as high as 6. 8%. Just putting in context how sick these patients really are. There's also wound complications in the 10 to 20 percent range, as well as dependence of the hand on the bypass. So we're taking their native artery, replacing it with a bypass with two anastomoses that can stenose, and completely dependent flow to their hand is off this bypass.

Some flow may be maintained to lead to development of collaterals, which could also maintain distal perfusion if the bypass occludes. But I wouldn't tell a patient everything's going to be

okay if the bypass goes down. Wow, what a great review. Thanks guys. I don't know if I should be thanking you or crying about all those physics equations, but I guess they were somewhat helpful to hear how all this stuff works.

So, I mean, with all these options, how do we choose which treatment to offer our patients? Yeah, really, treatment should be individualized based on a combination of the severity of the patient's symptoms. The patient's life expectancy, access flow rates, meaning is it high, is it low, is the fistula even being used?

Are there other access options specifically in that limb or not? What are the current inflow options and what kind of conduit does the patient have? So Rudy, Drill, and Pi generally have similar outcomes. But they require a little bit bigger of a surgery with a higher morbidity and mortality. That's in comparison to ligation or banding, which is better suited for those with limited life expectancy.

But as we talked about with banding, it's hard to establish how much you need to limit the graft and that may both decrease your

effectiveness at treating steel and increase the risk that you thrombose off the excess. As well as it might require multiple interventions. So sometimes when you add up multiple interventions, you get a higher overall risk.

Most cases of Steele syndrome are high flow, meaning in autogenous grafts you have a flow higher than 800 mL per minute, and in prosthetic grafts you have a higher flow than 1, 200 mL per minute. And less than a third of patients that present with Steele syndrome have either low flow or normal flow. And in those, it's often due to poor collateral circulation or atherosclerosis.

Both Rudy and Drill traditionally require autogenous conduit, as described, whereas the Pi uses PTFE. Finally, patient's anatomy often plays the most important role. A Rudy cannot be performed if there is inadequate distal inflow, which is often the case. I think the best way to hammer this home is to go through a case or two, but before we cover that, I will mention a similar entity called Palmer Arch Steele

Syndrome, or PAS.

which occurs when retrograde flow through an intact palmar arch results in an adequate digital flow in those with radiocephalic AV access. You can think of it basically as blood being stolen only from the hand and blood going up in a retrograde fashion through the radial artery out of the palmar arch.

Treatment is ligation or coil embolization of the distal radial artery just beyond the fistula creation site. It is critical to evaluate the ulnar artery and pulmonary arch patency prior to this ligation, most typically with an angiogram. Okay, with that ROA, let's get into a few cases. Okay, great. First off, Drew, you can't answer peritoneal dialysis.

Okay. So, for our first case, you have a 60 year old woman with a history of tobacco use, hypertension, diabetes, endosadrenal disease. Who is on intermittent hemodialysis via left brachiocephalic AV fistula that was placed six months ago. The patient

has pain and paresthesias during her dialysis that are very bothersome and have resulted in her missing dialysis days on more than one occasion.

On exam, she has palpable but diminished pulses in the left arm and intact sensation to light touch. Doppler shows triphasic flow in her left subclavian with biphasic flow. And her brachial, radial, and ulnar arteries, all distal to the AV fistula anastomosis. Her left digit pressure and waveforms are low at rest, but increased with fistula compression.

Drew, how would you approach this patient? Well, I guess since I can't discuss peritoneal dialysis with her, I'll just discuss Steele syndrome. So, I think she probably has grade one Steele syndrome, at least that's what it sounds like. So, you know, this still does appear to be pretty severe to her, and I think this warrants further workup and intervention just based on her symptomatology.

Given that she has triphasic flow at her subclavian artery,

biphasic flow distal to that, I'm concerned that she might have a potential arterial inflow stenosis. So, given that concern, I think I'd book her for an angiogram, obviously after doing a full history and physical, and I certainly would counsel her on stopping smoking.

Alright, so the angiogram shows left axillary artery stenosis approximately 80%, Approximal left brachial artery stenosis about 90%, and evidence that steel does improve with fistula compression. You balloon angioplasty the stenosis with improvement to less than 30% Regi residual stenosis, and you repeat the angiogram of the fistula and the distal hand still shows evidence of steel that improves a fistula compression.

So you've improved the stenosis, but you still have angiographic evidence of steel syndrome. What do you do now? Well, I think that you first need to just see how she's doing. I mean, we've treated some inflow

stenosis, so her symptoms might have improved even though she still has radiographic steel.

So I guess I'd wake her up and chat with her about that and give her some time to see if she flies. And if she doesn't improve, then we can talk about doing an open revision. Yeah, exactly. In this case, the patient's steel is primarily from her inflow stenosis. She ended up doing well after her angioplasty.

Alright, Drew, you're still in the hot seat for this second one. So for our second case, we have a 54 year old male with a history of hypertension, hyperlipidemia, diabetes, a right nephrectomy for renal cell carcinoma, and end stage renal disease on hemodialysis through a left brachial placed about two years ago.

He reports symptoms of left hand coolness, numbness, and pain over the past two to three weeks, and more recently, decreased

fine motor function as well. He especially experiences coldness and pain during hemodialysis. On exam, he has a palpable but diminished pulse in his left arm and decreased sensation to light touch on the left compared to the right.

His left digit pressures and waveforms are low at rest, but increased with fistula compression. Duplex reveals a high flow AV fistula. How are you going to manage this one? Yeah, so I think this patient appears to have grade 2 steel. And really that seems to be that his symptoms are at rest. So this is, seems to be pretty severe for him.

It certainly sounds like this is probably a high flow AV fistula. Cause you told me that your powers of repetition are amazing. So I think I, you know, in this setting, I think I'd still just offer him an angiogram first. And certainly do fistula, you know, an angiogram with and without fistula compression to see where we're at.

Perfect. All right. So the fistula gram shows evidence of steel syndrome that does indeed

improve with fistula compression. His brachial artery and proximal radial artery appear healthy without evidence of stenosis. He has a patent owner artery. But a small caliber and calcified mid to distal radial artery with an intact palmar arch.

Is there an operation you would offer him and which one? Yeah, you know, I think I'd discuss a few options with him. I mean, he seems to meet criteria for a drill just based on the anatomy you've described for me. But I certainly think that other options could be a banding or a pie. And I suppose you could even try a Rudy.

As long as he's a Hobbit fan. But I'm pretty sure that the distal to mid radial artery disease would probably make Rudy not a good call here. So that would certainly make me skeptical of that. So I guess just kind of based on our discussion, I'd still lean towards a drill. Yeah, and that's what we ended up doing.

A drill using left great saphenous vein as the

conduit. The patient did fine post operatively and had an improvement in both the pain and numbness and had no more symptoms at rest. And I would say, you know, if you're looking at how to answer questions about Steele syndrome, in your mind, you should pretty much be considering a drill first after you've done your workup, provided the anatomy makes sense.

And then work through the rest of these after that it just tends to be the standard of care and a lot of patients do meet criteria for it. So great answer on that one. Cool. Well, well, thank you guys for a really comprehensive and nice overview of steel syndrome. And thanks for giving me the opportunity to answer some questions in front of a bunch of listeners.

So, so I look super smart. So as a quick recap, you know, we've reviewed some high yield pearls regarding the basics of dialysis access, the incidents and risk factors for steel syndrome. We've talked about kind of the general diagnostic approach and presentation. We did a deep dive of the non invasive studies and the surgical options including banding, drill, Rudy,

and pi.

And last but not least, we reviewed some physics concepts that I'm sure you were all hoping you could forget forever. We hope you enjoyed this episode and found something you could take away from this and apply to your practice even if you're not in vascular surgery. And as always, thanks for listening and until next time, dominate the day.

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