Thank you very much. I am getting accustomed to being the last formal presentation of the day. Unless the organizers are gonna tell me they're saving the best for last. I will try not to take offense. All right. So right off the app website like lots of others have done. You can see that the studies and interpretation for dialysis access actually represent a very small portion of this exam. More specifically, it's the interpretation of pre dialysis or pre access construction studies to determine the suitability for access as well as post construction evaluation for maturity and the presence of complications um As well as some emphasis on volume flow measurements. Um Truthfully the clinical information and the patient exam are such a huge part of evaluation of dialysis access that from an R. P. V. I standpoint, it's very difficult for us to actually interpret some of what we see. With the exception of a few things which I will point out that you need to mention most of this is largely reporting rather than interpreting and we allow the clinician or the examining physician to do the interpretation. So everybody knows that arteriovenous access basically represents a direct connection between an artery and a vein and it bypasses the capillary bed. So the hallmark of the flow in this type of a circuit is low resistance and high volume and that affects the appearance of the waveform, the velocities and what you will see flow is the driving force for this type of a circuit. So a minimum volume of flow for these types of circuits is somewhere between 306 100 ccs per minute. That's how it's measured and that may vary the minimum volume to keep an access patent, whether it's a fistula which can tolerate lower volumes and still stay open than a graft which requires higher volumes or at will thrombosis flow volumes somewhere between 713 100 are optimal for driving dialysis and then high flow volumes greater than two liters a minute may contribute to certain complications of dialysis access. And we'll review that in a little bit as well principle, you can't get flow that's adequate unless you have adequate arterial inflow and that's both pump function as well as not having any arterial inflow stenosis to the circuit and then having adequate venous outflow. So that means having no venus obstruction. Um And then again, just like any vascular circuit there's inflow, there's outflow and there's a conduit in between. An evaluation of the conduit is also done as part of dialysis access duplex. Also real quick. The differences between official and a graft most people are aware of official is autologous material of veins. So the diameter of that conduit maybe variable and it may be inconsistent and there's only one anastomosis and inflow anastomosis for a graph that's a bridge of prosthetic material between the arterial and venus circulations. So there are two anastomosis and arterial or inflow anastomosis and a venus or outflow anastomosis. Alright, so preoperative imaging is basically to assess the adequacy of arterial inflow and the adequacy of venus outflow. It also will identify the suitability and the location of any autologous material, meaning vein that is available for construction of a fistula. Most clinical practice guidelines that are available principally the ones from the national kidney foundation and the clinical practice guidelines recommend that duplex study is done on all patients who are being evaluated for dialysis access and in the minimum it's arterial and vein mapping and in our lab some additional studies as well. This provides an atomic and some physiologic information for the surgeon. So arterial duplex, the most commonly used extremities are the upper extremities and the most commonly used in flow vanes are the axial and radial. You want to see normal, try physic peripheral artery wave forms without evidence of stenosis, either at the level you're interrogating or inferred from the waveform. You're getting more approximately. Um We map the diameters of the arteries all throughout the putative inflow arteries. So again, actual breaking um and radio and do note any calcification, bulky plaque and atomic variations, other types of findings that might preclude the use of that artery for inflow. Now again we are not interpreting whether an artery is suitable for inflow, but these are the things you need to report, particularly if you see evidence of inflow stenosis or arterial disease that may steer the clinician away from using that artery for inflow venus mapping evaluates both the deep and the superficial veins for slightly different findings. The deep veins. We need to be sure that there's no evidence of current or prior DVt. You're looking for any an atomic information you can provide as well as for evidence of obstruction. So flow phases city and the presence of venus collaterals particularly in the more proximal or central deep veins is really important because this can give you clues where you actually can't see with duplex ultrasound and that's the veins of the chest you can see in the top image. This this is an axillary vein that has sort of normal restaurant physic venus flow, good wave form that you would expect in a different patient. The axillary vein waveform is very different and actually this was the case in all of the deep veins on this arm breaking axillary and subclavian. And this patient did have a known central venous obstruction. So this would be a warning sign to the clinician that well maybe this is not a good side to use or we need to investigate further with vina graham to figure out why the patient has these venus outflow wave forms. This may not either support access or it may result in huge arm swelling. If you put an a v circuit on this side, we look at the superficial veins again for evidence of current or prior S. V. T. And wall thickening and fibrosis is important to note in the superficial veins construction of official and then maturation official depend on that veins ability to dilate and arterial eyes and if you have wall thickening or fibrosis, scar scar tissue does not dilate. And so that is a segment of a superficial vein that is not going to mature into a very good fistula. And a surgeon is usually looking for evidence of that before deciding to use or not use that vein for a fistula. We're also interested in diameter because as we know the most important criteria for whether a vein will dilate appropriately and mature as official. Is it starting diameter? So we are looking on both arms? So phallic vein basilica vein for appropriate diameters. Again we're not interpreting whether a vein is usable or not usable and that may vary from surgeon to surgeon as to what's an appropriate diameter vein for many it's something above 2.5 to 3 millimeters. And so I've circled in red on this particular patient veins that I thought in the right arm that were suitable patient actually had a pacemaker on the opposite side. And we were staying away from that arm. Alright. And then the duplex is an important tool that's used for evaluation of access after construction both for evaluation of maturity of a fistula as to whether it can be used for dialysis and for complications. So this is the entire circuit is interrogated from inflow artery through the influence anastomosis. The conduit the outflow anastomosis. If there is one and then the outflow vein, an atomic characteristics that can be noted or things like what you see listed here and also flow characteristics, presence or absence. Is it patient Peyton or is it thrown boast? As well as some velocity criteria. Waveform morphology, volume, which we'll get to in a bit as well as diameter, depth branching, particularly in a fistula you're evaluating for maturity. Now, there are no strict or universally accepted criteria for what constitutes a hemo dynamically significant stenosis. In an A. V. Access circuit, you'll see velocities that are much higher than what you would expect in the peripheral circulation. Again, this is a high volume circuit and a high flow circuit. Um but that alone is not going to constitute an anastomosis. Any man as demotic area is going to demonstrate higher velocities because of the change in direction and the turbulence that's located at that spot, does that constitute a stenosis? Again, some other information is needed. Crystal is in particular are prone to Jax to an as demotic stenosis, but sometimes that can be hard to determine based on velocity criteria because you can't get a velocity immediately on the inflow side of that because you're at the anastomosis. So these can be very challenging things to interpret. Um the doubling that we usually use in the arterial circulation may not quite be enough to determine that you actually have a stenosis in this kind of a circuit. Many labs such as ours may call troubling of the velocity, a suggestion of stenosis in the circuit. But again, if you see a low PSV beyond dampening of the wave forms beyond if you see grayscale images that show you a thick and valve cusp, calcification lesion at the area of high PSV. Those are all suggestions that you have human dynamically significant stenosis in your circuit. So use all the information that's available to you and then again, what to do about that And whether this is something you have to report as a critical result or whether it's something that you need to let your referring know about. It depends on what the clinical situation is and it does not necessarily mean that it's dangerous to the patient or that an intervention will be undertaken. So that kind of interpretation is something we really can't do without knowing the clinical information for the patient. Uh Here we have on the upper left panel an example of what a usual flow pattern and wave form looks like in a navy circuit. You can tell it's high velocity, it's all almost all above the baseline with very strong diastolic flow. Um This is a low resistance circuit. You can also see the peak systolic velocities over 300 that seems high when you think about just regular peripheral artery duplex. But for an A. V. Circuit, this is actually not all that unusual. The characteristics of this, I left the scenes out just for size and for time. But there was a p peak systolic velocity of 350 centimeters upstream to this and 280 centimeters per second downstream of this. And the velocities were pretty consistent all the way through. So this pistol actually does not have a stenosis, not either at this point or anywhere else in the circuit. On the other hand, the patient on the right hand side, you see a really high velocity at this .600 cm/s. And you can see that waveform looks very different with a lot of spectral information there With a 250 upstream and a 108 downstream with dampening of the wave forms. And you can see on grayscale actually just around that color band, the fistula is clearly narrower where the stenosis is versus where the fish is upstream. So this this was a focal stenosis in this fistula and then other findings. Just this is an interesting finding, you could tell on duplex. This is a fistula. Um you see running along the top where the color is green and the patient had been back walled on cancelation, resulting in a large pseudo aneurysm off the underside of the fistula. Um that required surgical repair. So low volume. I got to spend a couple minutes on this because this comes up and it's in most protocols and is probably on the exam as well. There is a calculation that provides you with an estimate of how much volume is running through this fistula and that formula you see there it is dependent on a mean peak systolic velocity. So that measurement has to be accurate but you can tell it depends very much on the accurate radius or in our case diameter measurement of the vessel that is actually a squared value. So it's going to impact this calculation more so than the mean peak systolic velocity. If your if your diameter is off it will underestimate or overestimate this value by quite a bit clearly, a more uniform vessel will yield the most accurate measurement. This is typically why we use the artery um graphs are very uniform but if they're tapered, the diameter will change and then fiscally tend to be very inconsistent in their diameter. Throughout the access. Um the circuit flow volume is reported for clinical correlation and we'll talk a little bit about what you might be able to interpret from that. Again, we need clinical information to know how important this is to the patient and the patient's care. But what's known is that the volume flow may correlate with the maturation potential for a fistula. So a not yet established fistula, A maturing fistula should have a volume of flow somewhere between 509 100 CCs per minute by about four weeks post construction and that's what correlates with eventual maturity less than that or a failure to accommodate maybe represent official that is not going to mature very well. So that that's something that we can definitely say about it. Low low volumes may correlate with an access that's at risk for thrombosis in an established official or graph. So that is something that should be reported out because that may have demonstrated that there's something going on in that circuit that's about to spell disaster for that patient. And then again a high flow fistula so greater than two liters per minute. Really may be associated with some complications such as the development official, aneurysms, high flow ischemic steel or high output congestive heart failure. So that should be noted. And really what's normal for one patient may not be normal for another. So a change in the patient's baseline of more than 25% decrease can sometimes um signal that there's a stenosis or something impending in that fistula. So again, reporting is important. It's hard for us to make an interpretation in all cases just because we don't have the clinical information. So this is a patient on the top left that has a volume flow of almost 900 CCs per minute which would seem adequate over this fistula actually was one that was not maturing at all. It was still very small and was not getting anywhere. But this helps uh the clinician know that there is adequate volume in the circuit. Maybe we're looking at for some other reason this isn't maturing as it turns out this patient had a downstream stenosis, the patient on the bottom right, um this has a very high flow volume. You see more than three liters a minute. So very different. However, look at where the calipers are and you can see their place slightly outside the vessel walls. So again, this is going to overestimate the volume flow in this fistula. Still, by almost any definition, it's a high flow fiscal and this patient actually had ischemic steel. So high flow steel. This information is helpful. The last study that we do in the vascular lab for dialysis access is not a duplex. It's a PVR evaluation for distal hyper perfusion or steal syndrome. So this is a syndrome where there's an imbalance of perfusion pressure between the high volume low resistance circuit and the higher resistance distal extremity, peripheral circulation and it can result in signs or symptoms of distal limb ischemia. So truthfully, all patients who have a patent low resistance circuit in their arm will have some degree of decreased limb perfusion. Distal to that point doesn't always cause symptoms. And there's not always a problem that's more or less a physiologic finding. However, when you get those types of symptoms or problems that's where steel is a concern. And so really Steel is a clinical diagnosis based on these, We can't tell just looking at a study in the lab whether the patient has pathologic steel. So the noninvasive studies really support or not a diagnosis but really don't diagnose still and they really can't rule out steel as well. So this is the same. Everybody knows how this is done. It's digital pressures and wave forms taken at rest, which is the access open. And then with transient compression or occlusion of the access. That's the provocation. Radio side digits and ulnar side digits are looked at. And you report this as the percent increase or augmentation in the digit pressure with compression of the access. So you have here two patients, the one on the left has um Uh some augmentation anywhere in the 11-25% range. The patient on the right has augmentation in the 40% to 80% range. And we've seen some studies where patients actually have augmentation in the hundreds to 200% range. So who's got steel? How do you interpret this? That's that's the rub. So the patient on the left actually had significant steel and was having symptoms in the finger and early ischemic alterations. Her baseline was just that she could not tolerate that much taken away by her. Her access patient on the right side actually was completely asymptomatic and not having any symptoms at all. So again, You know, we don't we don't have a hard criteria because of this. Um but when you start getting augmentations above 50% to 100%. You may suggest that clinical correlation is advised. All right. And that's all I have. I'm sorry, that was so quick.