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Physics of MRI 5: Relaxation and Image Contrast - Part 2b
Physics of MRI 5: Relaxation and Image Contrast - Part 2b
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The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
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PAD/CLI Diagnosis | CLI: Cause and Diagnosis
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More Effective Techniques Of Thrombolysis With Microbubbles And Ultrasound: Feasibility, Safety And Effectiveness In A Clinical Study (The MUST Trial)
More Effective Techniques Of Thrombolysis With Microbubbles And Ultrasound: Feasibility, Safety And Effectiveness In A Clinical Study (The MUST Trial)
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Case 2: Upper GI Bleed | Emoblization: Bleeding and Trauma
Case 2: Upper GI Bleed | Emoblization: Bleeding and Trauma
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PET/MRI Case Study #2 | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
PET/MRI Case Study #2 | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
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Stent Graft Deployment | TIPS & DIPS: State of the Art
Stent Graft Deployment | TIPS & DIPS: State of the Art
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New Developments In Radioactive Sodium Fluoride (18F-FBG) Imaging On PET CT To Predict AAA And TAAA Growth And Rupture
New Developments In Radioactive Sodium Fluoride (18F-FBG) Imaging On PET CT To Predict AAA And TAAA Growth And Rupture
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The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
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Lymphatic Intervention: Thoracic Duct Embolization, Pulmonary Lymphatic Perfusion Syndrome, And Hepatic Lymphatic Disorders
Lymphatic Intervention: Thoracic Duct Embolization, Pulmonary Lymphatic Perfusion Syndrome, And Hepatic Lymphatic Disorders
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Complications & Pitfalls | TIPS & DIPS: State of the Art
Complications & Pitfalls | TIPS & DIPS: State of the Art
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Why Open Surgery Is Still The Best Treatment For Juxta- And Pararenal AAAs In Good Risk Patients: Technical Tips
Why Open Surgery Is Still The Best Treatment For Juxta- And Pararenal AAAs In Good Risk Patients: Technical Tips
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Treatment Of Recurrent NTOS: Role Of The Pectoralis Minor: Tips And Tricks In Diagnosis And Treatment
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Work-up for PAE | Nursing Management in Prostate Artery Embolization
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Benign Biliary Strictures | Biliary Intervention
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The Disease Process | TIPS & DIPS: State of the Art
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TIPS Case | Extreme IR
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Post-intervention Non-invasive Tests | Determining the Endpoints of CLI Interventions
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Transcript

So now we're going tomove on to discussing some of the contrast mechanisms underlying spin echo. So just a brief review of the spin echo pulse sequence, so again it's actually very similar to the gradient echo. So here we have our initial RF pulse, and our gradients to read out the data. So the only two differences are first of all, we almost always use a 90 degree pulse in spin echo scan. And the major adddition is we add this 180 degree refocusing pulse, which

as we saw in previous lectures, purposes to refocus the magnetization. So let's just show what's going on here. So initially we play out our 90 degree RF pulse that tips the magnetization down, and we know that begins the signal. Now, we then do our 180 that tips the magnetization around by 180 degrees, and then we do our turn on our gradients, and that reads out the case based data. So again

we put on a negative X gradient that means it's out to the left hand side of case base then we turn on a positive polarity gradient that allows us to sweep out a line of case base and acquire a line of case base data. So that's the basic mechanism underlying spin echo pulse sequence. So now we are going to show in the next couple of slides how we can generate contrast, what sorts of contrast we can generate

with this pulse sequence. So now let's examine what sort of contrast we can generate with the spin echo pulse sequence. So in this slide I'm going to consider the case again where we have three different water molecules which you see a slightly different magnetic field. So initially we play out RF pulse or initial 90 degree RF pulse that tips the magnetization down into the translation/g plane. So now let's

see what occurs a period of time after we've tipped our magnetization down. So we call again that each of the water molecule sees a slightly different magnetic field, because it sees a slightly different magnetic field we're going torotate at slightly different frequencies and therefore over time they are going to be begin to deface relative to each other. So for example let's say

the white one is going tobe rotating in the counter clockwise relative to the others. The orange one is going tobe stationary relative to the others and the black one is going tobe rotating in the clockwise direction relative to the others. Now we saw from earlier, from the T2* decay that when you have this dephasing that causes a signal loss. And this as I mentioned is the T2* decay because now

the magnetization adds up destructively because now they're incoherent relative to each other. So now the next thing we do, we play out our 180 degree RF pulse. So this seems like a relatively simple thing to do but as you see it has a profound effect so when we do a 180 pulse that rotates the magnetization around by 180 degrees. Now the key to note that occurs here is the white one that's still

rotating at the same speed. We've flipped it around but it's still rotating at the same speed relative to the others. So in particular it's still rotating in the counter clockwise direction, similarly the black one is also rotating at the same speed it's rotating in the clockwise direction. So after a period of time this individual the magnetizaion associated

with these individual water molecules will begin to re-phase relative to each other at this time point here. So the analogy that people often use to explain this concept is runners in a race. Let's say, runners at a race start off in a race, and after a 100 meters, the faster runners will be further ahead than the slower runners. If at a 100 meters they all turn around and run back

to the starting line, and by the time they get back to the starting line they'll all be again in phase with each other. Each other because the faster runners will still be running faster, the slow runners will still be running slower but the faster runners now have further to go. And this concept of turning around after 100 meters is exactly the same as the 180 degree pulse so it essentially

causes the magnetization to reverse what it had previously done. So because the magnetization is now back in phase signal will then re-grow, sort of re-grow and we'll get back the signal. And in fact this is called an echo or a spin echo because it is essentially an echo of the original signal we have, so we re-grow signal. Now one important feature to note about the way I

have drawn this is if you notice the echo is actually the lower intensity than the initial signal intensity. And the reason for that is because well we've been able to correct for the decay caused by inhomogeneities, we are not able to correct for the decay caused by T2 decay. So simultaneous with this, all this 180 degrees rephasing and dephasing that's occurring, we're getting an overall T2 decay

of the tissue. So, this signal is decaying away with T2. So, our echo is never quite the same intensity as our initial value. And, the echo time, the TE, controls when that rephasing occurs. So, the rephasing occurs exactly at the echo time TE. So that's the parameter that we're going to control in a spin echo sequences, the echo time. So, if you're called from, what I mentioned earlier

in my first talk, signal loss caused by inhomogeneities is often described as e^-t/T2*. And the overall signal loss is then going to be the sum of the T2 signal loss and the T2 prime signal loss. And that's reflected in a T2* value, e^-t/T2*. So, the

effect of spin echo, is essentially to remove this T2 prime component. So remove any decay caused by inhomogeneities so the spin echo produces a decay that's purely due to T2. So there's no T2* in this case it's equal to T2 cause there's no T2 prime component. So, here we have an example of a T2 weighted image produced by spin echo. So, these are two images of the knee acquired in an

echo time of 7 milliseconds and an echo time of 33 milliseconds. I'm going to highlight three different tissues here we have muscle with a T2 value of about 50 milliseconds, fluid with a T2 value of about a 1,000 milliseconds and cartilage with a T2 value somewhere between 30 and 70 milliseconds. So in our initial, here we have our initial

echo time of 7 milliseconds and if we compare that to an image a part of the later echo time 33 milliseconds, you can see that the cartilage and the muscle have decayed away substantially relative to the signal from the fluid. Because again the fluid has a much longer T2 value so its signal has not decayed away to a great extent in comparison with the cartilage and the muscle. So I want to make

a final comment on contrast we generate with fast spin echo imaging. Because as I have mentioned in previous lectures fast spin echo has virtually replaced spin echo in routine clinical MR scans. So, here we have the basic fast spin echo pulse sequence which we'll just briefly review here, so we start out with our initial

90 degree RF pulse followed by the 180 degree RF pulse which we now know the purpose is to revoke its magnetization. We then play out our initial Y gradient which again we are starting in the center of case space this moves us down to a particular line in case space and we then play out the negative lobe of our X gradient which moves us to the left hand

side of case space followed by the positive lobe of the X gradient which allows us to read out a line of case space. Now up to this point, this is the same as fast spin echo. So if this is spin echo we would stop here. But in the case of fast spin echo we then repeat that procedure, following another 180. So we play another 180 that again refocuses the magnetization and then we acquire

another line of case space. So we essentially play out another Y gradient that moves up, on the vertical direction, moves to another line of case space and we read out the second line in case space. We can repeat that procedure as many times as we want in some cases, you can do what is called a single shot fast spin echo imaging when you essentially acquire the full extentive case space following the initial 93 RF pulse. So one question that arises

here is what is the echo time in this case? Because in this case we're actually going through multiple lines of case space. It's not just one single line. Well the echo time in this case is defined as the time between the initial RF pulse and the time where we go through the very central portion of case space. So whichever line in here corresponds to when we go through the very central portion

of case space, that is defined as the echo time or the TE value of a fast spin echo pulse sequence. And let's just look what goes on with the signal in a fast spin echo pulse sequence. So here we have our initial spin echo pulse sequence, so again we have our decay and the refocusing so we have the echo here. If we add in another 180 then again we're going to refocus the magnetization a second time

following this 180. And again recall that during this period of time we have consistent T2 decay occurring. So the echo time TE again just corresponds to time at which we acquire the central line of case space and that T2 waiting will correspond to how much decay has occurred during that period time. So let's just summarize the concepts for contrast in spin echo or equivalently fast spin echo. So in this

case we just had really a single parameter that we can vary which is the echo time or the TE and again defined as a time between the RF pulse and a time when we acquire the center of case space, which in case the spin echo follows 180 degree pulse. Generally speaking the longer the TE the heavier the T2 weighting because this allows more time for T2 decay and therefore allows for more signal discrepancy

with tissues with different T2 values. So that's the end of the relaxation and contrast lecture thank you.

I like to talk about brain infarc after Castro its of its year very symbolic a shoe and my name is first name is a shorter and probably you cannot remember my first name but probably you can remember my email address and join ovation very easy 40 years old man presenting with hematemesis and those coffee shows is aphasia verax and gastric barracks and how can i use arrow arrow on the monitor no point around yes so so you can see the red that red that just a beside the endoscopy image recent bleeding at the gastric barracks

so the breathing focus is gastric paddocks and that is a page you're very X and it is can shows it's a page of Eric's gastric barracks and chronic poor vein thrombosis with heaviness transformation of poor vein there is a spline or inertia but there is no gas drawer in urgent I'm sorry tough fast fast playing anyway bleeding focus is gastric barracks but in our hospital we don't have expert endoscopist

for endoscopy crew injections or endoscopic reinjection is not an option in our Hospital and I thought tips may be very very difficult because of chronic Peruvian thrombosis professors carucha tri-tips in this patient oh he is very busy and there is a no gas Torino Shanta so PRT o is not an option so we decided to do percutaneous there is your embolization under under I mean there are many ways to approach it

but under urgent settings you do what you can do best quickly oh no that's right yes and and this patience main program is not patent cameras transformation so percutaneous transit party approach may have some problem and we also do transit planning approach and this kind of patient has a splenomegaly and splenic pain is big enough to be punctured by ultrasonography and i'm a tips beginner so I don't like tips in this difficult

case so transplanting punch was performed by ultrasound guidance and you can see Carolus transformation of main pervane and splenorenal shunt and gastric varices left gastric we know officios Castries bezier varices micro catheter was advanced and in geography was performed you can see a Terrell ID the vascular structure so we commonly use glue from be brown company and amputee cyanoacrylate MBC is mixed with Italy

powder at a time I mixed 1 to 8 ratio so it's a very thin very thin below 11% igloo so after injection of a 1cc of glue mixture you can see some glue in the barracks but some glue in the promontory Audrey from Maneri embolism and angiography shows already draw barracks and you can also see a subtraction artifact white why did you want to be that distal

why did you go all the way up to do the glue instead of starting lower i usually in in these procedures i want to advance the microcatheter into the paddocks itself and there are multiple collateral channels so if i in inject glue at the proximal portion some channels can be occluded about some channels can be patent so complete embolization of verax cannot be achieved and so there are multiple paths first structures so multiple injection of glue is needed

anyway at this image you can see rigid your barracks and subtraction artifacting in the promenade already and probably renal artery or pyramid entry already so it means from one area but it demands is to Mogambo region patient began to complain of headache but american ir most american IRS care the patient but Korean IR care the procedure serve so we continue we kept the procedure what's a little headache right to keep you from completing your

procedure and I performed Lippitt eight below embolization again and again so I used 3 micro catheters final angel officio is a complete embolization of case repair ax patients kept complaining of headache so after the procedure we sent at a patient to the city room and CT scan shows multiple tiny high attenuated and others in the brain those are not calcification rapado so it means systemic um embolization Oh bleep I adore mixtures

of primitive brain in park and patient just started to complain of blindness one day after diffusion-weighted images shows multiple car brain in park so how come this happen unfortunately I didn't know that Porter from Manila penis anastomosis at the time one article said gastric barracks is a connectivity read from an airy being by a bronchial venous system and it's prevalence is up to 30 percent so normally blood flow blood in the barracks drains into the edge a

ghost vein or other systemic collateral veins and then drain into SVC right heart and promontory artery so from what embolism may have fun and but in most cases in there it seldom cause significant cranker problem but in this case barracks is a connectivity the promontory being fired a bronchial vein and then glue mixture can drain into the rapture heart so glue training to aorta and system already causing brain in fog or systemic embolism so let respectively

they travel together so that's what leads to the increased pain and sensitivity so in the knee there have been studies like 2015 we published that study on 13 patients with 24 month follow-up for knee embolization for

bleeding which you may have seen very commonly in your institution but dr. Okun Oh in 2015 published that article on the bottom left 14 patients where he did embolization in the knee for people with arthritis he actually used an

antibiotic not imposing EMBO sphere and any other particle he did use embolus for in a couple patients sorry EMBO zine in a couple of patients but mainly used in antibiotic so many of you know if antibiotics are like crystalline

substances they're like salt so you can't inject them in arteries that's why I have to go into IVs so they use this in Japan to inject and then dissolve so they go into the artery they dissolve and they're resorbable so they cause a

like a light and Baalak effect and then they go away he found that these patients had a decrease in pain after doing knee embolization subsequently he published a paper on 72 patients 95 needs in which he had an

excellent clinical success clinical success was defined as a greater than 50% reduction in knee pain so they had more than 50% reduction in knee pain in 86 percent of the patients at two years 79 percent of these patients still had

knee pain relief that's very impressive results for a procedure which basically takes in about 45 minutes to an hour so we designed a u.s. clinical study we got an investigational device exemption actually Julie's our clinical research

coordinator for this study and these are the inclusion exclusion criteria we basically excluded patients who have rheumatoid arthritis previous surgery and you had to have moderate or severe pain so greater than 50 means basically

greater than five out of ten on a pain scale we use a pain scale of 0 to 100 because it allows you to delineate pain a little bit better and you had to be refractory to something so you had to fail medications injections

radiofrequency ablation you had to fail some other treatment we followed these patients for six months and we got x-rays and MRIs before and then we got MRIs at one month to assess for if there was any non-target embolization likes a

bone infarct after this procedure these are the clinical scales we use to assess they're not really so important as much as it is we're trying to track pain and we're trying to check disability so one is the VA s or visual analog score and

on right is the Womack scale so patients fill this out and you can assess how disabled they are from their knee pain it assesses their function their stiffness and their pain it's a little

bit limiting because of course most patients have bilateral knee pain so we try and assess someone's function and you've improved one knee sometimes them walking up a flight of stairs may not improve significantly but their pain may

improve significantly in that knee when we did our patients these were the baseline demographics and our patients the average age was 65 and you see here the average BMI in our patients is 35 so this is on board or class 1 class 2

obesity if you look at the Japanese study the BMI in that patient that doctor okano had published the average BMI and their patient population was 25 so it gives you a big difference in the patient population we're treating and

that may impact their results how do we actually do the procedure so we palpate the knee and we feel for where the pain is so that's why we have these blue circles on there so we basically palpate the knee and figure

out is the pain medial lateral superior inferior and then we target those two Nicollet arteries and as depicted on this image there are basically 6 to Nicollet arteries that we look for 3 on the medial side 3 on the lateral side

once we know where they have pain we only go there so we're not going to treat the whole knee so people come in and say my whole knee hurts they're not really going to be a good candidate for this procedure you want focal synovitis

or inflammation which is what we're looking for and most people have medial and Lee pain but there are a small subset of patients of lateral pain so this is an example patient from our study says patient had an MRI beforehand

of critical of ischemia well a lot of times it starts in our office with a physical examination so we do a risk

factor assessment and this is what happens before they get on our table with with everyone in this room and us seeing the patient assessment of intermittent claudication and it can be subtle many patients don't come in and

say oh yeah I have pain when I walk for a short time and then it I rest and it goes away a lot of times it's yeah you know my leg gives out or now it doesn't hurt it's kind of this weird feeling when I walk and it these atypical

symptoms and then obviously if they have a wound you have to a wound evaluation on physical examination things we're looking for feeling a pulse you'll be surprised how many primary care providers never feel a pulse and if we

say if you feel a pulse you may save a life because you may be the first one to say hey this patient doesn't have a pulse maybe they have got peripheral artery disease and if they prefer order these maybe have coronary artery disease

and maybe they should we start on aspirin or statin and save them from a heart attack and stroke and so you really can save a life abnormal capillary refill so in other words you've got such bad blood flow

that if you smush on their foot it takes a long time for that blood to come back because they have such poor perfusion there's something a Peugeot stess TWEN that if you lift their leg gravity alone pushes their blood isn't it overcomes

the force of blood and so there are foot becomes power becomes losing some color and then when you put them down it dilates and you get sort of this ruborous red color so that's a burger sign I just had a good example in clinic

about a week or two ago so what do we ask for patients do of any pain or discomfort in the leg thigh or butt with walking your exercise I will sell you tell you I often don't use the word pain because everyone thinks pain is

different so so some people say well it's not paying it's a key lake ease pain to me I'm a guy everything's pain to me right low low threshold but discomfort is a good way of asking it foot or toe pain

that disturbs your sleep do you have any skin ulcers or sores on your ankles feet or toes I think it's very important to know what kind of patient you're talking to in terms of Education level or in terms of just language so some patients

don't know what it all sir is and they use the term sore some people don't know what a sore is they used term wound and so just sort of you ask things different ways I think is really important when we all talk to our patients and again a lot

of classic history will miss a large majority of PAE because patients don't read the textbook the one thing I'll say is I hear this all the time well the patient had pulses and so they don't have P ad that is hashtag false and the

reason is pulse exam is insensitive so in other words even if you feel pulses they can still have peripheral artery disease okay now if you don't feel pulses they certainly have peripheral artery disease or you're just terrible

at it PID classification the way we talk about patients with PA D we use a classification scale called Rutherford it may come up so in other words patient who has PA D but asymptomatic is

Rutherford zero a patient who has got major tissue loss and is basically 1 for amputation is Rutherford 6 and then everything in between is sort of a gradation we cut off 3 to 4 so 3 is claudication pain only 4 is critical in

ischemia rest pain alright so rather for classification when we talk about wounds you may see this you don't need to go in details but there's a Wi-Fi classification that sort of Germans how bad is the ulcer and how likely are you

to to lose your leg it's sort of a prognostic I will remind you that in medicine there's differentials for everything in other words the patient comes to you with pain or you talk to your friend or whatever with pain

there's a lot of things in cause pain it could be back pain arthritis infection DVT so there's things we have to think about when I was in medical school I sort of loved this my OB GaN professor said when he sees a patient the first

thing he does is say what do I think this patient have if this were a man because you get so pigeon-holed in your specialty every patient we see as well must be vas here must be vas care but you've got to take a step back and say

okay well am I missing something maybe it's arthritis may something else so don't get pigeonholed by your own prejudices which is a good life lesson in general there's also a differential for wounds so obviously

when we see a wound we could have arterial arterial tends to be sort of the toes and distal foot it can be severe pain if you see an ulcer around the ankle that tends to be more venous so vein related which again we

can treat and then a common cause is neuropathic so if you see I'm sort of at the pressure points where people walk a lot of times patient diabetes will step on something and where you and I would be like oh man that hurts

I better oh my god I have a wound there I better check that out they'll never know because they don't feel their feet and so they could have this monster ulcer and finally someone inspects their feet and says you know you have like a

golf ball sized hole in your foot and that's the first time they ever notice it so how do we test ever for peripheral artery disease well a lot of it is non-invasive now we do a B is a b is is a measure of blood pressure in the foot

or leg we can do some ultrasound to actually look at the artery and obviously we can do CT and MRI when we look at ultrasound you may look at this every once a while this is a normal ultrasound Doppler waveform where we've

got good blood flow up down and back three now the reason that's important is that correlates the sounds so if you listen to a artery i'ma do my best Doppler impression out okay a normal artery goes once you start getting

peripheral artery disease you lose that triphasic waveform it becomes biphasic when you get severe peripheral artery disease you lose that biphasic waveform it becomes monophasic and when you have nothing it becomes

okay so here's want to be alert to that so ankle brachial index is important and it's helpful again some patients who have calcific us a-- fication it's not helpful for I will tell you a B eyes alone actually not only do they predict

PA D they predict death that's how important PA D is link to mortality CT and MRI is very useful you can see here we can see a good anatomic description of the arteries unfortunately patients with calcium

sometimes we can't see as well because the calcium is so bright on CT scan that it obscures the lumen so we have other problems in patients with diabetes and heavy calcification and a lot of those patients just need to go to angiogram

and as you know my techs and nurses know sometimes rarely but sometimes we do an angiogram and it's normal and we say or there's mild disease we say okay perfect we've taken that off the table we need to move on when some of these

non-invasive testings aren't as clear so alright so in summary critical of ischemia is a morbid disease and can be the first presentation of PA d clinical suspicion and accurate diagnosis is essential for early diagnosis and

treatment and a multidisciplinary team that includes vascular venture loss who know critical limb ischemia not just the SFA and iliac artery jockeys and wound care specialists do decrease amputation rates I like this quote it's not mine

but I'm going to steal it with impunity amputation is not a treatment option it is a treatment failure okay so we have to keep that in mind I appreciate everyone's attention because we can save questions to the end or you do it now if

there's pressing I think we may need new batteries or my thumb's weak which is also a possibility any questions

for it's very it at centers where CTA protocols are very good it's basically equivalent to a angiography has been shown in multiple papers to be so newer studies show that

CTA and Emory are equivalent so I don't know it depends on your institution there are a lot of places that still practice with the MRA is kind of the gold standard but CTA is just so much more available that CTA is becoming kind

of the new gold standard for for quick vascular assessment often like to use it to help us plan our intervention so if we don't know what's going on above the level of the groin CTA could be helpful to see whether or

not we could even go from right to left how calcified the vessels are or whether or not there's concomitant aneurysms things that we don't like to discover at the time of the procedure because we might not have the equipment we need to

treat it one of the strengths is that it's quick and that it's cheap but of course it uses contrast and just like you know we like to minimize the amount of contrast that we're using at knee and rogram this can use anywhere from 75 to

150 cc's of contrast or not a small amount and if you're gonna do an intervention the same or the next day that's a lot of dough that's a lot iodine in a couple days these are examples of what we can see at the time

of the procedure there's a 3d reconstruction and a BU these are kerf planer reformatted images what basically they draw a line down the image and you can lay the entire vessel out even if it's very squiggly and then this isn't

this an angiogram and that same patient you can see that they correlate exactly another example a patient with aortic calcification you can see that it can be potentially challenging this patient with diabetes to determine whether or

not these vessels in below the level of the knee are paetynn or not because I can tell you that the one that's closest to the small bone there is actually occluded it's just all calcified you can't really tell what's going on and

the one that's behind that is actually Payton so it could be difficult to tell whether it's calcium or contrast that you're seeing this is where MRA can be

want to go over is we're gonna kind of fast forward but this is kind of like our record holder in terms of prostate

volume so this guy's six seven year old history of BPH for a long time obstruction he's been fully dependent for several months and so we can't he can't even fill up that IPS or Christa doesn't pertain to him is she's fully

dependent but his call it life is obviously very bad it's at six he has a lot of core abilities like diabetes hypertension he is on chronic pain medications due to some sciatica and he also has some unknown contrast allergic

reactions that we don't even know about and he's allergic to bactrim and his MRI showed at 306 grand process so this is so far he's our holder so this is just the idea of how biggest prostatitis

again tear white is to the frontal view of the process it looks like is basically compressing most of his bladder right there so who knows how much bladder or how much urine he's able to retain in that bladder and to that to

your left is the shuttle of you and you could see that fully basic line there and the base of his bladder so with this guy since he has some unknown conscious allergy he had had undergone eye referral to our allergist team it was

confirmed that he wasn't learning to contrast after also the several weeks for us to get that confirm the first time he went to our clinic he actually had getting he had the episode of UTI so when our nurses checked him he was I

believe he was taken some subtract zone injection because he couldn't get sipper because it was allergic to it so he's getting home health subtracts from an injection and so since he showed up to our pre-op with a current or of he's

getting treated for Kearny ty we had to postpone and rescheduled him so this guy was obviously because of his prostate volume was a grade 150 we had to be the stretch with a Foley we had to make sure that this patient gets followed up with

our urologist and because his allergic to cipro which is the medication said we would typically give a patient and we have to set up home health to make sure that he gets his four seven injections at least one week post procedure and all

the patients that are sent home with a Foley since they tend to have more symptoms of bladder spasms we would get on some oxybutynin so he's gone oxybutynin and some narco ibuprofen and the pp is and some colace as all the

other set orders prescriptions that we would typically prescribed for patients so with this guy upon a follow up when I call them a day or two later his main complaint was bladder spasm and again this is related to probably from the

from the inducing press inflammation or prostate are probably having the the catheter in place but so at once I call him when I have to reassure him that make sure he takes the oxybutynin to see if that'll help him

which he did and he was basically taking ibuprofen every eight hours for the first two days which helped most of his symptoms so a lot of its patience you just have to really reassure them and make sure they're compliant with the

medications and if they are having symptoms of post elbow station syndrome then he had to reassure them that those things should get better so when we see this guy on page so this patient we saw him in clinic he was seen by the

urologist two weeks after and he was able to have his Foley remove so he was totally happy he was actually able to fill up that IPSS car which is 15 however more importantly his koala life went from 6 to now - so just to kind of

wrap things up in conclusion you know PAE is safe and efficacious excuse me and effective I did at least based on short term follow-up it does how yield a high patient satisfaction I would say like more 80% or so patients are fairly

satisfied when we see my month or two later it is tecnique technically challenging is not performing a lot of IRS are programs and I think more importantly for our nurses is vital for us to be

knowledge of this procedure that way we can educate our patient better and also minimize any arrests and complications that are associated with with this PAE so just the close things up this is probably my favorite nursery code this

by mother Teresa it is not how much you do but how much love you put in the doing thank you

- So thank you ladies and gentleman, thank you Doctor Veith for inviting me again this year. These are my disclosures. So more effective thrombolysis by microbubbles and ultrasound has been proven actually effective in earlier studies, treating a myocardial infarction or acute ischemic stroke.

But what are these microbubbles? These are 1 to 10 micrometers, gas-filled bubbles with a lipid shell. It oscillate when subjected to low intensity ultrasound, and can cavitate when subjected to high intensity ultrasound. Initially they were designed for diagnostic use

as intravascular contrast enhancers. However, they have many advantages, non-specifical mechanical effects, to induce thrombus breakdown due to mechanical force of microbubbles if they are subjected to ultrasound. So we conducted the first human trial

in peripheral arterial diseases in Microbubbles and UltraSound-accelerated Thrombolysis, the MUST study for peripheral arterial occlusions. Which is a single phase two trial for actually safety and feasibility study. The MUST-TRIAl consist out of 20 patients

for safety and feasibility, which in 10 patients will be treated with Urokinase, and 10 with Alteplase. And then added, for the first hour, microbubbles and we evaluated the VAS pain scores, duplex echography for circulation or revascularization, microcirculation and daily angiography as usual.

Included were men and women 18 to 85 years. A maximum of two weeks of symptoms of lower limb ischaemia due to thrombosed or occluded lower limb peripheral native arteries or venous or prosthetic bypass grafts. And Rutherford class 1 or 2A. They have to understand the nature of the procedure

and written informed consent. And excluded were all known factors that exclude standard thrombolysis therapy, hypersensitivity to contrast enhanced agents, a recent acute coronary syndrome. Endpoints, again, it's a safety

and then a technical feasibility trial. Also we looked at the organisation, and the treatment duration for technical, angiographic, and clinical success. We looked at the severe adverse event and mortality rates, VAS-pain scores and microcirculation.

If the patients came in, we inform them about the MUST trail, we performed an ECG analysis and informed consent. They fill out some questionnaires and when they come in to the angio-room, we started a thrombolysis with a catheter, the Mc Nemara.

And the first group, the Urokinase 10 patients, we treated with 500 units of bolus and then continued with a 50,000 units of Urokinase per hour. The Alteplase group had started with a 5 milligram bolus and then they continued with 1 milligram per hour

for the first 24 hours. And then, the ultrasound room, they got a bubble infusion for the first hour of treatment. Then we would continue with thrombolysis on a surgical ward, every sixth hour we'd look at if there was revascularization at the duplex ultrasound.

And if signs of revascularization are observed on the duplex ultrasound or on the next day, we routinely perform the angiography. Then we could cessate the thrombolytic therapy, and if necessary, acute or elective additional intervention to correct underlying lesions,

or to establish patencies. We check the wound and then we follow-up these patients every six weeks, three months, 6 months, and one year after thrombolytic therapy. So these are the patient characteristics, mostly of these were male, 70 years,

and five of them were native bypass, and five were a bypass occlusion, venous or prosthetic. And two of them had multiple occlusions, whether Rutherford class 1 or 2A. And these were the first 10 patients that were treated with Urokinase and I will present here

the results of these 10 patients first. So, very important, there were no deaths, no severe adverse events, and it was technical feasible. The flow at the duplex examination was there after 24 hours, but most of our patients actually had it already after 6 hours.

The amputation rate, right now, is zero. And also no bypasses were now needed. So we will continue this MUST trial right now and January we probably will have the inclusion of the group with the Alteplase, which I'll present next year.

And we think that microbubbles with Urokinase is a safe combination right now. We will further include the groups of adults placed and further optimalisation of the microbubbles technique with nanobubbles. Had a talk about that yesterday, so you can look it up.

And nanobubbles are nanoparticles of 5 to 500 nanometers, which are very small, they do not penetrate the endothelial barrier of the doubt and it damage. And it can carry the thrombolytics actually to the side the aorta catheter need it. You can also make the magnetic paste,

which means you can paste these patients on the MRI. Then you can have local treatment of thrombolytic therapy. So thank you for your attention.

right now here's a different case is a 49 year old male who presented to the emergency department after vomiting a lot of blood vomiting was the key word there it's going the other direction so that's an upper GI bleed all right and

when we talk about upper GI bleeds there's a lot of different causes for upper GI bleeds the most common are ulcers but there's mallory-weiss tears of the esophagus there's just esophagitis or gastritis

there's different cancer vascular malformations fistula is varices which I'm not going to talk about but varices on the venous side in a patient with portal hypertension these are all causes of upper GI bleeding now

once again we might treat them medically we might look at them with endoscopy and potentially cauterize something embolization usually is used when and when endoscopy is not successful all right or certainly surgery but an upper

GI bleeds embolization is a lot more attractive of an option all right so here's another picture what do you think you up for it nope you turned me down all right who wants to who wants to tell me what they see how about you how about

you guys you can team up together what do you think so what do you seeing so let's look at that together so this is a seal EF is an anagram of the celiac axis you want to think it through you want to volunteer you see a filter we don't care

about that yeah all right that's fair so you see the catheter going up right in the middle and it's going right into the celiac axis all right what I want to draw your attention to is right in the middle of the screen a little bit over

to the left is again a blobby thing all right that's extravagant of contrast and the vessel that that's coming off of is the gastroduodenal artery so I want you to see that if you look at the catheter you

can see the shadow of the catheter right up going up from the bottom that's going into the celiac axis and the big vessel going over to the left side of the screen is the proper hepatic artery that the common hepatic artery excuse me and

the first vessel heading south from there is the gastroduodenal artery that blood vessel is supplying the end of the stomach and the beginning of the small intestine and what you see is the extravagant coming off now what it's

very important if you're dealing with bleeding patients whether it's in dusky whether it's hemoptysis or GI bleeding anything like that we're looking for that type of blob appearance which just mean the contrast is no longer

constrained by the artery it's free into space okay usually the way we were built is that the blood vessels the biggest they ever are near the heart as they leave the heart they get progressively smaller until they reach

the tips of your fingers and the tips of your toes if there's any place that you see where it gets big small then big again that's not normal okay that's not normal and now we just got to figure out what's

the abnormal part is it the small part or the big part all right in this particular case it's that big blob that's big it doesn't belong there all right but in the upper GI system there's lots of collateral vessels so we can

just go in and we can put coils right in the gastroduodenal artery and we can embolize that and we can do it safely because we know that there is alternative routes for blood to flow now the one thing we have to do here and

this is an important concept for any abnormal bleeding whether it's trauma or other causes is we always look for the backdoor so in this particular patient we did an angiogram of the superior mesenteric artery there's another vessel

going to the intestines and it's nice cuz we have the coils there you can get a sense that it's possible for blood to flow from a branch of the superior mesenteric artery backwards into the GDA and so we just want to make sure that

that's not happening because we can do the best job ever with an embolization procedure but if we don't get the front door and the back door we're gonna fail patients will come back with recurrent bleeding and at least in my experience

that's a big reason why people do come back so we think we do a great job in two or three days later people come back with abnormal bleeding it's weak because we didn't address both sides of the pathology all right so here's another

year old patient diagnosed with

glioblastoma lesion is located on the left frontal lobe this is done after radiation and surgery the image to your left is just a regular MRI with contrast gadolinium is the one used this time we always be the drum in the context of

choice is gadolinium in our institution you could notice the big size of the glioblastoma lesion onto the left frontal lobe of the patient as indicated in the round ring patient went for treat radiation and surgery look at the two

images to your right the one in the middle is done Pet MRI without the contrast take a note on the area where the lesion was before there is normal uptake but you don't notice any abnormal uptake and on to your right is post

treatment MRI is that those two are done the same day and with gadolinium the deletion the area where the the ring it is enhanced by the contrast but look at it there is no hypermetabolic uptake that means that the lesion is not viable

so the malignancy is not viable this time this scan is done to evaluate the effectiveness of the treatment it's a good sign before I go to the third case

okay stent graft deployments once you've ballooned you basically pass the sheath over the balloon all the way down to the portal circulation the reason for that

is the Viator stance has a bare portion that's captured by the sheath so your sheath has to be deep into the portal circulation so when you unsheath it it opens up and then you pull back so it snags on your portal venous entry so

it's a feel thing and a visual at the same time for the operator okay so your sheath has to be deep in the portal circulation so that dilates put your sheath all the way down this is a run just to make it look pretty for you guys

and then you basically deploy the Viator stent via tourists and like I said has a bear portion that's captured by the plastic here and that plastic sheath basically transfers the capture of the bare

portion from plastic to your entry or access sheath okay as a ring to it and put it in has a feel to it that ring has to be right there it's very common for people starting off to deploy it inside the sheath up so it's a kind of a feel

thing to actually make sure that it's actually in there snug with it with the sheath okay then you push the stents all the way into the sheath now the bare portion is captured by the sheath you remove the plastic it's over over and

done with and then you pass pass your your stent all the way down to the portal vein and then unsheath it like a wall stents let it open pull everything back till it snags on the portal venous entry sites and then unsheathed the rest

of it which is the covered portion and that stays constrained by the cord and then you pull then you pull the cord keep key portion here is this is the ideal tips and ideal ace tips is a tips from the portal vein bifurcation to the

a patek vein IVC junction okay that's an ace tips it's usually a straight tips it's the straightest tips you'll see it runs parallel to the caiva okay rookies will be doing tips down out in the

periphery and Deliver okay they'll be fishing for small portal veins out of his small hepatic veins and at the end their tips is gonna be like a big seat like a big C loop okay it'll be a longer tips with more stance and it won't be an

aggressive decompressive tips okay but an ace tips is a more aggressive central tips straights it comes from the portal vein bifurcation to the paddock vein IVC Junction that's kind of like an ace tips

okay unsheath it and then and you and then you pull the cord to basically deploy it and this is kind of a reenactments the Styrofoam cup is the portal vein the sheath is in there now over the wire there's no wire in the in

the reenactments and then you unsheath the bear portion so it opens up okay and then you pull everything back till it catches on the portal vein okay you move the sheath all the way back and

then you pull the cord you see the cord right there you pull the cord and it basically opens up the covered portion okay and it opens up from the portal venous end so it actually capped catches it right away catches that portal venous

entry sites there's no slippage and so basically rips open tip to hub okay and that's kind of your final product and then you go in and and then you go in and balloon okay so here it is ballooning put the sheath

over the balloon sheath is deep into the portal circulation you put the tips in your unsheath to cut the the the bare portion let it flower open you pull everything back to like snags you unsheath the rest of the stunt and then

you pull the cord okay and then you dilate with 8 or 10 or whatever so this is visit with the debilitation and that's kind of your final product ideal

- Frank, thank you very much for your invitation. This is my disclosure. I think that all vascular surgeons are asking ourself following question. Is diameter of triple A the sole indicator for surgery? To ask for this question since about 20 years, we are interesting with function in aging with a PET CT

using 18F-FDG which allows the evaluation of the regional glucose metabolisms. And shows the presence of an inflammatory reaction at the level of atherosclerotic tissue infiltrated by the inflammatory cells. During our pilot study, we observed that

the uptake of the FDG was also stated with the unstable triple A. And during several studies, we were observed that FDG uptake not only show of predicted rupture but it predict also the site of the rupture

in triple A patients in Thoracic Aortic Aneurysms as well as Aortic Arch Aneurysm as you can see. Here is very easily we are find, you can observe FDG uptake and this patient we performed MRI and you can see here, free iron particles, it's same area of every velope. Starting increase FDG uptake

and this patient refused operation and come back three months later to rupture. Of course FDG is not specific for aneurysm or disease. We can found FDG uptake in cancer disease, infection or arthritis or arthritis and reason why several authors interested with different kind of biomarkers

and sodium fluoride F 18 each one of those one. And it's injections indicated for diagnostic PET imaging of bone to define areas of altered osteogenic activity. The primary clinical use of sodium fluoride PET is in detection of osseous prostate cancer metastasis. But some authors, all of them start to use it for

evaluation of the plaque metabolism in high cardiovascular risk subjects. One group from United Kingdom and leaded by a Dr. Newby from Cambridge, they performed several very nice studies using this marker in coronary artery disease for plaque rupture

and for evaluate aortic stenosis to accumulation of the calcification in the aortic leaflets. And also for carotid stenosis and they, during this several studies, they demonstrated that 18F sodium fluoride, selectively binds to microcalcification coronary

and carotid atherosclerotic plaques and that are associated with plaque vulnerability and rupture. More essentially he interested, they interest also the triple A and they called this study the SoFIA study and it concern about 72 cohort patients

and 20 study population. And it is very nice picture of the patients with positive 18F sodium fluoride uptake. It is specific for one and reason why it is left right in red color here, but anyways, very easy to show the infusion images uptake

at the symptomatic aneurysms. And they divided their cohort study in three levels of Tertile 1, Tertile 2, Tertile 3 according to sodium fluoride uptake from low uptake to increase uptake and they observed that the growth rate,

increased growth rate, aneurysm repair and rupture and aneurysm repair alone, it was significantly higher in the patients in Tertile 3 group. And they concluded that Fluorine-18 sodium PET-CT

is a novel and promising approach to the identification of disease activity in patients with triple A and is an additive predictor of aneurysm growth and future clinical events. My conclusion is 18F-FDG and 18F Sodium Fluoride however,

not specific for inflammation. Therefore, new imaging tracer for a more accurate inflammation detection and therapy evaluation are needed. We need specific markers of angiogenesis and inflammation to predict the triple A evolution and potential rupture.

Thank you very much for your attention.

let me show you a case of massive PE

this launched our pert pert PE response team 30 year-old man transcranial resection of a pituitary tumor post-op seizures intracranial frontal lobe hemorrhage okay so after his brain surgery developed a frontal lobe

hemorrhage and of course few days after that developed hypotension and hypoxia and was found to have a PE and this is what the PE look like so I'll go back to this one that's clot in the IVC right there and

that's clot in the right main pulmonary artery on this side clot in the IVC clot in the right main pulmonary artery systolic blood pressure was around 90 millimeters of mercury for about an hour he was getting more altered tachycardic

he was in the 120s at this point we realized he was not going the right direction for some reason the surgeon didn't want to touch him still to this day not sure why but that was the case he was brought to the ir suite and I had

a great Mickey attending who came with him and decided to start him on pressors and basically treat him like an ICU patient while I was trying to get rid of his thrombus so it came from the neck because I was conscious of this clot in

the IVC and I didn't want to dislodge it as I took my catheters past it and you see the Selective pulmonary and on selective pulmonary angiogram here and there's some profusion to the left lung and basically none to the right lung

take a sheath out to the right side and do an injection that you see all this cast of thrombus you really see no pulmonary perfusion here you can understand why at this point this man is not doing well what I did at this point

was give a little bit of TPA took a pigtail started trying to spin it through aspirated a little bit wasn't getting anywhere he was actually getting worse I was starting to feel very very nervous I had remembered for my AV

fistula work that there was this thing called the cleaner I don't have any stake in the company but I said you know I don't have a lot to lose here and I thought maybe this would be better than me trying to spin a pigtail through

the clock so the important thing about the cleaners it does not go over a wire so you have to take the sheet out then take out the wire then put the cleaner through that sheath and withdraw the sheath

you can't bareback it especially in the pulmonary circulation the case reports are poking through the pulmonary artery and causing massive hemorrhage and the pulmonary artery does not have an adventitia which is the outer layer just

a little bit thinner than your average artery okay so activated it deployed it and you started to get better and this is what it looked like at the end now this bonus question does somebody see anything on this this picture here that

made me very happy on this side this picture here that made me feel like hey we're getting somewhere I'm sorry the aorta the aorta you start to see the aorta exactly and that that was something I was not seen before the

point being that even though this doesn't look that good in terms of your final image the fact that you see filling in the aorta and mine it might have been some of the stuff I had done earlier I can't I can't pinpoint which

of the interventions actually worked but that's what I'm looking for I'm looking for aortic blood flow because now I've got a hole in that in that clot that's getting blood flow to the left ventricle which starts to reverse that RV

dysfunction that we were concerned about make sure I'm okay with time so we'll

- Lymphatic, so it's fun, actually, not to talk on venous interventions for once. And, naturally, the two systems are very different. But, on the other hand, they're also related in several ways and I will come back to that later. I have no disclosures, maybe only my gratitude to this man, Dr. Maxim Itkin,

who actually got me started in the field, and was gracious enough to supply me some of his material. And who is also responsible for making our lives way easier over the last years. Because in former times, we needed to do, to visualize the lymphatic system,

we needed to do pedal lymphangiography and that was very, very cumbersome. It took a long time and was very painful for the patient. And he introduced the ultrasound guided intranodal lymphangiography,

and that's fairly easy for most of us. With ultrasound you find a lymph node in the groin, you puncture that and you can control the needle position with contrast enhanced ultrasound and once you establish that position, you might do a MR lymphangiography.

Thereby showing, in this case, a beautiful, normal anatomy of the thoracic duct. I need to say, the variations in lymphatics are extreme. So, you can also visualize, naturally, the pathology, like for example, pulmonary lymphatic perfusion syndrome.

What's going on there. Normally, lymph courses up through thoracic duct, but in this case, you kind of have a reflux in the bronchial tree and lymph leakage. And you can image that again, beautifully with MR, which you can show extensive leakage

of lymph in the lung parenchyma. So you can treat that. How can you treat that? By embolization of the thoracic duct. But first we need to get into there, and that's not a very easy thing to do.

But now, again, with access to a lymph node in the groin, you can push lipiodol, and then visualize the cisterna chyli and access that transcutaneously with a 21/22 gauge needle and then push up a O-18 wire high up in the thoracic duct.

First you deploy some coils to prevent any leakage of glue inside the venous system, and then by microcatheter, you infuse glue all the way down, embolizing the thoracic duct. So, complete different group of lymphatic disorders is oriented in the liver and hepatic lymphatic disorders.

And maybe not everybody knows that, but 80% of the flow in the thoracic duct is caused by the liver and by the intestine. And many times in lymphatic disorders, there needs to be a combination of two factors. One factor is a venous variation of a,

sorry, an anatomical variation in lymph vessels and the other one is that we have an increase in lymph flow. And in the liver, that can be caused by a congestion of the liver, for example, cirrhosis, or a right side, that's congested heart failure.

What happens then is you increase the flow, the lymph flow, tremendously and if you also have a variation like in this case, when the vessels do not directly course towards the cisterna chyli, but in very close contact to the abdomen,

then you can have leakage of the lymph and leakage of proteins, which is a serious problem. So, what is then, to do next? You can access the lymph vessels in the liver by percutaneous access in the periportal space,

and induce some contrast and then later, visualize that one back, visualize that with dye that you can see with an endoscopy, thereby proving your diagnosis, and then, in a similar way,

you can induce lipiodol again with glue, embolizing the lymph vessels in the liver, treating the problem. In summary, popularity of lymphatic interventions really increased over the last years mainly because novel imaging,

novel interventional techniques, new approaches, and we all gained more experience. If you would like, I would guess that, we are at a phase where we were at venous, like 10, 15 years ago. If we are a little bit positive,

then the future is very bright. And within 10, 15 years, we find new indications and probably have much more to tell you. Thank you for your attention.

people were thinking about the covered

portion actually actually would be occlusive in that paddock veins a lot of people are concerned about that this could be kind of like a but carry you're gonna actually occlude flow in the paddy vein caused thromboses that didn't pan

out at least clinically okay it didn't pan out and that's another advantage of actually accessing very close to the paddock vein IVC junction that's where the biggest vein is so you don't get a lot of occlusive problems okay but

usually clinically it does not pan out so the bigger the hepatic vein the more likely you have a lot of room around your your graft you won't be occlusive to the paddock vein that's more important for for transplants than other

than others I told you it's rare this is actually a very rare case of such that where you actually have a segmental segmental kind of but carry after a tips okay and you know this is actually from a form of venous outflow from the ematic

vein this is a perfusion defect typical it's a wedge right typical perfusion defect in the liver that's how you death so you know this is vascular this is a perfusion problem but you've got hepatic artery readout artery the red arrows

running into the segments and you have portal vein running into the segments so what's the problem it's actually a paddock vein occlusion okay by the stents subclinical no no clinical complaints you let it be

in the patients usually recover okay treat the patients and not the images okay on the other side if you put their tips too deep sometimes you actually get thromboses of the portal vein branch

again you get a call from hepatology you've got portal vein thrombosis is the patient doing okay yes treat the patient and not the images they usually resolve this it's not not a big problem another technical problem

I'm gonna focus mostly on technical for you guys this is a but key area okay and the but carry especially in the acute stage the liver is not like a cirrhotic liver is big liver is actually engorged okay so it's very large usually

your needle is too short to even reach the portal vein okay that's a big problem okay because your access needle is too short for a very large engorged the portal vein so this is as deep as it

goes do I have a see that that do you see that needle tip that's as deep as the needle tip goes okay the portal vein is a good distance away okay luckily this is a co2 porta gram luckily I'm actually in a small branch right

there I just hit it on you know and on this is not the there's not a needle tract this is just luckily hitting it a little branch and on so I'm actually accessing the portal vein and I can do a co2 porta gram here okay

typical inexperienced person would say you know this looks good I'm lucky I'm in a branch but it's a nice smooth curve I'll just pass a wire down and I'll balloon it and I'll put a stent in it's a nice curve and you know so it's my

lucky day I don't need to extend my needle or get a bigger longer needle to reach the portal vein here's the problem with this and this is exactly what this is exactly what this is they pass a wire and it looks beautiful just put a stent

and go home okay here's the problem this is actually the small branch access sites this is actually where you really need to access world vane but your needle is not long enough okay

what we found out is that if you are in a small in a small portal vein no matter how much you balloon it it will come down again and it will be narrow so believe it or not if you go sideways in a portal vein and rip it open with a

balloon it will stay open but if you go down of small portal vein and balloon it open it will always contract down okay so you cannot do a tips simply by ballooning and putting a stent in in this case okay what we do is we actually

denude the vein itself we actually rip it off okay and make it a raw parenchyma and we do that with a Tortola device we literally rip off the paddock the paddock portal sorry the portal vein endothelium and media and adventitia rip

it off make it completely raw as if it's an access as if it's a liver brain coma which is which it is now and then we then we balloon dilates okay rip it off denude it angioplasty it's okay and then put the stent and see that aggression

despite all that aggression of ripping it off it still has an hour kind of an hourglass shape to the to the tips okay that little constraint there that's the hepatic venous access sites this is the parenchymal tract to see nice and open

with a balloon but the but the actual vein that we've been through despite our aggression in actually ripping it off it's still narrowed down but this is as good as it gets okay

- The title is Why Open Surgery is Still the Best Treatment for Juxta- and Pararenal AAAs in Good Risk Patients: Technical Tips. This slide demonstrates the trends of AAA repair in our university, my institution. After the introduction of EVAR in 2007 in Japan, more than half of AAA was treated with endovascular repair.

However, open repair also remains the mainstay. After the introduction of EVAR, comparing the percentage of open repair with renal artery clamping between pre and post EVAR, there was a significant increase. Recently EVAR with fenestrated graft and snorkel technique

has been performed for the treatment of JAAA in high risk patients with favorable outcome. However, open surgery is typically used as first-time treatment in low-risk patients. We demonstrated the outcome with results in Journal of Vascular Surgery in 2018.

Among 451 open surgery, 111 underwent repair of JRAA aortic aneurysms. In hospital death was less than 1%. This study suggests that open repair of juxtrarenal and pararenal aortic aneurysms can be done safely. We will show the technical tips for juxta-

and pararenal AAAs. Operative approach, manipulation of the left renal vein, method of anastomosis and method of reconstruction of the renal artery. The position of proximal clamps were decided based on the anatomy of the aneurysmal neck,

which was two approach. One was transperitoneal approach. Proximal clamp site, it's placed in inter-renal was suprarenal, which is proximal upwards. Like this 3DCT, if the orifice of the renal artery and the SMA are at the same level,

we choose supra-celiac clamping. In those cases, we user a transabdominal approach with left-sided medial visceral rotation. As you can see the descending colon and pancreas, spleen and stomach are rotated anteriorly and medially, leaving the left kidney, adrenal gland, ureter

and gonadal vein in situ. Using this approach, we can control the orifice of the celiac artery and the SMA and both renal arteries and therefore we can directly clamp all of these arteries. After exposure, the proximal anastomosis was made without PCPS.

After finishing the proximal anastomosis, the clamp was then moved down to the graft to perfuse the renal arteries. The next, manipulation of left renal vein. This is a dissection of renal vein and dissection of the branches

such as the adrenal vein or gonadal vein frees the left renal vein and makes it easier to expose the proximal aorta and to perform proximal anastomosis. The next is on the left side with the division and stump closure.

Divide the renal vein proximally to the adrenal vein and gonadal vein and they close the stump by 4-0 prolene running sutures. On the left side it's a very rare case, but sometimes re-anastomosis in the vein. We demonstrated renal artery clamping and left renal vein

division during abdominal aortic aneurysm repair. That's not in itself compromised for long time renal function. In reaction to that, we demonstrate that in publication in Journal of Vascular Surgery, the division had no significant impact

on CRD for up to two years during follow-up. Then this is initially pressed on posterior and ends on anastomosis was performed by placing a 3-0 Prolene suture in the posterior wall and continued anteriorly in a running fashion. Regarding the renal artery perfusion,

perfusion it with cold ringer solution undertaken. The bypass graft for the renal artery was anastomosed to the main body or limb of the main graft in advance, then the main body was anastomosed to the aorta. During the aorta clamping, the renal artery was perfused with chilled solution.

Finally we demonstrated the technical tips for juxta- and pararenal AAAs. Thank you for your attention.

- Few aspects of vascular surgery are more controversial than the management of neurogenic TOS as you heard earlier from Dr. Illig. I will propose that recurrent neurogenic TOS and persistent neurogenic TOS are even more of a challenge to deal with. Persistent neurogenic TOS

occurs in 10 to 15% of patients, and it's really the individual who fails to show any improvement following decompression. Recurrent, 15 to 30% of individuals who have some degree of partial or complete relief after the initial decompression.

This may be insidious or acute, and most often occurs somewhere within a two-year time frame. It could be a missed original diagnosis. Or it may be a secondary insult, a new stretch injury to the plexus,

incomplete rib resection, ectopic bands, scar tissue formation around the plexus, or pec minor syndrome. Pec minor syndrome is a frequent cause of recurrent and/or persistent neurogenic symptoms.

Its co-existence is over 50% of patients with neurogenic TOS. Sanders recognized in 2003 that pec minor causes the majority of recurrent neurogenic TOS symptoms. What is it?

Well the pec minor originates in the second, third, fourth, and fifth ribs, inserting on the coracoid process, which is part of the scapula. Muscle hypertrophy, spasm, and fibrosis will constrict those structures underneath,

which would be the axial artery vein and posterior to that will be your plexus. This was first described in '45 by Wright. Lord and Stone did five decompressions for what they defined as "hyperabduction syndrome." It was lost at some point,

rediscovered by Thomas then Doctor Sanders in 2004, who studied it prolifically, defined it as a sub-set of neurogenic TOS. There's a plethora of literature in this present day and age supporting pec minor syndrome.

Etiology: majority of people have trauma, most often in motor vehicle accident with a whiplash type of injury. Repetitive shoulder strain and spontaneous events can occur, inducing hyper-induction of the shoulder. Clinical symptoms are similar

between neurogenic and pec minor: weakness, pain in the neck, clavicular, anterior chest wall, trapezius region and then paresthesias, most often in the ulnar distribution. Isolated pec minor does happen. Typically these individuals

have fewer head and neck symptoms. And you'll notice the intensity of symptoms are significantly less. On your examination it's your standard TOS examination. Unfortunately provocative maneuvers are not as rewarding. You'll find that with isolated pec minor,

these individuals have fewer head and neck symptoms, typically with rotation, tilt, scalene compression. There's nothing really to see. But they do have point tenderness over the infraclavicular region, directly on top of the pec minor.

And you'll notice that with contraction of the pec major, the symptoms will be minimized. Sanders noted the three most common findings with pec minor syndrome are: tenderness to palpation in the subcoracoid space, ULTT and EAST.

You'll notice that in some of these patients who do have persistent or recurrent symptoms, quite likely, pec minor tenderness was missed in the original diagnosis. A thorough history and physical certainly is beneficial. Unfortunately there's no test or exam

that is pathognomonic for this. Appropriate imaging should be completed to rule out other pathology. And then a selective pec minor muscle block not a plexus block, but a minor block, a muscle minor block,

should be considered. EMG testing has mixed results. When you look at your muscle block, typically done with a baseline examination, you'll then inject lidocaine 4 cc with ultrasound guidance 45 degree angle to avoid dropping in the lung.

Inject in a two to three centimeter area. And what you're looking for is resolution of your tenderness, improvement of your symptoms, at rest and with provocative maneuvers. For those ones who have an unsuccessful block

you may want to consider repeating it, or consider performing a scalene block. For those individuals that do have pec minor syndrome, conservative therapy, which is range-of-motion and stretching, tends to work well, 50% resolution in eight-week window.

For those individuals who fail pec minor tenotomy, low-risk out-patient procedure, relatively quick recovery time. A variety of approaches have been defined in the literature. Here's one approach with a patient

previously undergoing neurogenic decompression with a superclavicular approach, this is the anterior axillary approach, with a two to three centimeter vertical incision in the anterior axillary line. The subcutaneous divide at the pec fascia

is open and the muscle is elevated with a Deaver retractor. You'll trace this up to the coracoid process, and with that being the case, you'll transect two to three centimeters of the pectoralis minor muscle,

and then release any fascial bands or accessory muscle around the neurovascular bundle. These patients have done well. With isolated tenotomy you'll see that there's an improvement anywhere from 90 to 100%. However, you need to take into consideration

a good number of these people have combined neurogenic TOS and pec minor syndrome. And with that being the case, the success may be a little bit less. So in summary, pec minor syndrome is a frequent cause

of recurrent or persistent neurogenic TOS. Isolated pec minor tends to have fewer head and neck symptoms. Diagnosis is aided with a block. And tenotomy appears to be safe and effective. Thank you.

so we're just gonna like hop over to the clinic side and kind of discuss how we work up or what are the things we look for when we see the patients in clinic

so a lot of patients are referred to us by urologist so we have to have a urology on board to to better take care of this patient we can't treat this patient you know by ourselves so a lot of patients are referred to us by our

neurology team if they don't have a urologist we have to refer to them to erosions first before we can even work them up or PAE so we won't make sure that patient you know doesn't have any underlying cancer that we know of so we

want to make sure that we check their PSA levels because this high high patient can ask actually I predict a decent progression and actually our risk for acute urinary retention you want to make sure that you get

urinalysis a lot of patience wet with lots is not only due to pph you could also be secondary to UTI or if patient has some type of bladder tumor or bladder disorder so it's kind of good to know to understand some of the lingo

that urology uses so once they see the urologist they do some your dynamic studies and one of the popular ones are these non-invasive studies called euro flama tree and the post-void residual do you offer the Euro excuse me you heard

from a tree usually we will measure the flow rate and the volume of the patients so what they do is they they would pee in this special funnel and the final obviously they go in private but this final is connected to some machine that

can actually measures how fast and how much their voiding and so normally it's about 25 miles per second but if it's anywhere less than 13 to 15 it can suggest obstruction and use the obstructions usually due to BPH some of

us a very low flow rate such as like say less than ten or six you have you want to be a suspicious of some type of you to neutral structure after they do that usually what they'll do is they take a post void residual is basically scan so

they'll put that little probe above the bladder and they'll see how much is left in a bladder if it's 150 that she usually indicates in complete emptying someone who has greater than 200 that may suggest patients having some type of

bladder dysfunction so a lot of its patients to us at least woke up with some type of imaging and the ones that at least our physician selects is the MRI patient do get a CT angiogram which can also evaluate the pelvic Anatomy and

arteries however the process the mr process actually gives a better illustration of the prostate a tissue to see if there's any suspicious for cancer for example you can also display the president atomy and characteristic up

the gland so most patients do get MRI or at least we get them to get MRI to measure the actual volume in literature they will tell you that a patient can get a trance rectal ultrasound but I'm not sure how many

guys in here would like a probe stuck up their butt to get to get their prostate measured so unless you wanted to get pissed at you just supporter I am right so when we see the patient you obviously want to review their HMP more

importantly you'll want to check their comorbidities there's social history whether it is smoke or not because they're gonna that's gonna have an impact on how we stay patients and how you can predict their anatomies

obviously someone's died who is diabetic or who has a history of smoking you could expect for them to have a greater degree of atherosclerosis and again the first thing that we would get the patient why we walked in is we go in

that scoresheet the IPSS score and so that's gonna give us an idea of how bad this symptoms are so if they come in to us with a score of say you know they're mildly symptomatic I'm not sure how much to pee a procedure with would help them

because how much more lower can we get their scores down so a lot of patients we would treat are in the moderate to severe category and their quality of life score should be for the most part will be about three or higher you also

want to make sure the trusted results since this is Andrew Graham procedures you will make sure that they have a pretty decent renal function patients with lots a lot of them may have some degree of renal insufficiency so we have

to be careful make sure we watch that lab value so this is some of the screening criteria that a lot of us may use so patients who I have refractory to medications for the six months someone has a high IPSS core grain 13 or

qualifies score greater than three process volumes gotta be at least 40 grams we sometimes get patients with a high score but they're positive volumes around 30 we usually usually wouldn't treat those

patient because we can't basically treat or shrink the prostate any any lower than that you someone who has an abnormal urine Flo and someone who maybe refractor to medical therapy these are just a list of

exclusion criteria the ones that should my party set out someone who has prostatitis or current approximate infection you definitely want don't want to treat those patients chronic renal failure and relatively maybe coagulation

factors that could be patient dependent sometime sometimes we could optimize them to get this arteriogram procedure and prostate and bladder malignancy also this somewhat also relative we do treat patients with prostate cancer it just

depends on what course of treatment they're on currently so once we had screen the patients and and deemed them to be a candidate we reviewed the patient we review in detail the procedure with the patient so you want

to let them know that it's a our angiogram procedure that will go through the either the growing or sometimes the radio and the procedure itself you can take anywhere from one for one to four hours and sometimes longer depending on

how complicated their arteries feeding the prosthetist more importantly we want to educate them about the side effects okay we have to let them know that a lot of their symptoms might actually worsen during the first few days after the

procedure so if they have the Syria now urinary continence they actually may get really worse especially for the first few days okay we have to go over the complication with the patients that can include a public infection ischemia or

any vessel related complications that pseudoaneurysm or bleeding so we have to basically have a basic knowledge of how do we combat this side effects and these are just some of the list of side effects that

are mentioning or at least we also used a PI radium it helps I guess to numb up the prostate urethra we have to educate the patient that this can change the color of the urine so we always make a note to our patients that if you are

going to take this medication please call us that way we don't kind of shock you and we also know that the change of color is from the pair radium and not from anything else the tripping or oxybutynin

it helps reduce bladder spasm we would normally use it for a patient who go somewhere to Foley our patients would go some Foley tends to have a great degree of bladder spasm Coley's a lot of spatially get constipated for multiple

reasons being better that or they and she is soft and there's also the over-the-counter azem so this is just a sum of the standard medications that we would give all our patients all of them will get about cipro for seven days

we'll give them some type of anti-inflammatory Asia usually is ibuprofen were prescribed 800 a tid if needed anti-acids since it's just to protect your belly or their stomach from the ibuprofen minimum we'll get a stool

softener at least for the first three days or if they got developed loose toast and we would ask them to stop it and the medications for pain that we would get them as Norco just in case and I would say like more than half these

patients don't even need Norco at best they'll probably use ibuprofen you know just to minimize the inflammatory side effects that I get it also helps out with post embolization that sometimes we'll get and I believe so I don't I'm

not sure if I'm messing about post embolization syndrome patient do can get these symptoms and a lot of symptoms can vary they can get some body slug or fever malaise and the degree the symptoms were may bear from patient to

patient and a lot of symptoms are described kind of like a flu-like symptoms and we also want to reiterate a patient that the symptoms are temporary and it should get better over to at least at first week or so so patients on

warfarin we have a lot of patients on warfarin for whatever reason whether they had a recent cardiac intervention we want to assure that we stop those medications at least before the edge ground procedure so it's very important

that you have a good rapport or whoever and have prescribed him the coumadin whether it's a cardiologist or the surgical team and a lot of dissipation may need to be crossover outside like a short-acting

anticoagulation such as Lobo Knox at least in our practice we ask the patient to this condition discontinue your aspirin unless they're you know they have a recent cardiac intervention we may leave it leave them

on aspirin metformin as very important since we did it is a natural procedure we want to at least hold have the patient hold the metformin the morning of the procedure and maybe a couple of days after and someone who are

allergic to contrasts we will make sure that we're prepared to premedicate a patient and also be prepared in case there's a severe reaction and the pre medication as we know will give them some type of a standard metal prednisone

will they'll take it like twelve seven or one hour before and they also gets unbearable and preoperatively or one hour before the procedure and during the clinic we also determine the level of anesthesia so since this procedure

usually takes a long time we always get it with our anesthesia team is just more for patient comfort it's not really for pain okay I couldn't imagine laying a table for several hours at the time so we all shop anesthesia on board just

really for patient comfort so we're just

this is just happens to be a biliary

other classification system with bismuth how where the injury occurs and this is really germane after surgery so you'll see most of these actually after misadventure with bluish surgery and and like I said the most common ones

actually after laparoscopic surgery but we have barrier so we have oncological have two extremely complex three sections of the liver now and and we the advent and certainly rise are more balloon complications this is an example

of what we might do in the complex setting this patient had explorers in cholangitis primary cylinder current charges received a transplant and the transplant liver had a recurrence and with recurrent explorers and cholangitis

there was just no way we could cross it but even with a long-standing billy we drain frequently if you drain most obstructed systems a day or two passage across an inflamed structure it makes it much more easy and you will see their

people get brought back for their secondary tube with laryngitis sometimes this is not possible so we actually have made attempts to cross this there's no other way so we happen to use a sharp organization so we happen to use a

transept own needle and use a sharp needle go breakthrough sometimes analysis of the CT scan is a very important you really want to know what's between your one side and what's on the other side and the more even more fun

thing to do now is using our rfy off-label and we'll burn our way through and create the track that actually has a much better patency rates and even sharp organization your allow essentially coring of sort of in chronically

inflamed fibrotic tissue and allows you a chance of keeping this open it's just example of how you benchley burrow through with a shop another case with a sharp needle creating a track really that's not

natural because this is obviously a transplant patient and it's the only way through even done what we've done is stick the intestine first and then put us in a punch our way through polio stay out and

then thereby restoring the the track and they are sort of you have to be just really created with biliary disease when it comes to chronic obstructions or high-grade obstructions so like I said with benign the disease frequently it's

post-operative and so they will present in multiple different ways and most of the times they're just leaking in the intraperitoneal ich you you're you essentially peritoneal cavity will reabsorb it so patients get jaundice is

essentially it hi arrays but Rubens and you'd really can diagnose in many ways and really just dealing with this can be problematic and then so we've been dealing with bluish structures and and oh sorry benign Ballou strictures

post-operative benign Ballou strictures in a more labor-intensive way we actually leave tubes in for six months which is probably a little more than most people must be not a benign the Lewis structures are managed with three

months of stinting with a minimum of twelve French tube so that's a reason why some of these patients will get kalanchoe pasties multiple bluie a drained Rhys tenting it and tube exchanges and changed up this way and

then this is just happens to be the British is worth a typical we will get access cross the stricture kalanchoe plastic stretch out this benign structure and then place a tube in for as long as you can to keep it open and

fro asses of between three and six months there's a classic example someone who obstructed that they said this looks very smooth it doesn't look ugly and looks okay doesn't look like a cancer we sometimes what I so biopsy if it has any

suspicious appearance and then get across you can see even with a balloon how tight the structure can be with a high pressure balloon and there after placing achievement for again three to six months we actually err on the side

of caution almost our patients have six months of intubation which is quite long difficult and this is our experience what we do then is when do you remove it to actually have a sort of a step-by-step process we have a it's not

really medical clinical trials actually just if a flow clinical trial what we'll do is get the tubing bring a patient back and we actually cut the tube so there's only the access through the parenchyma of the liver is preserved but

nothing through the structure we will cap the tube is since you can maintaining access and see if the patient doesn't make sure that doesn't get fever the stricture is maintained and then we'll bring the patient back

after a week to do a balloon whiticus test that's really just a modification of a urinary radhika test we're going to take pressure measurements after slow contrast injections to make sure it remains the

patency and for us the data suggests we can essentially and predict over 90% who will be staying free if they pass the Whittaker test in keeping the monetary reading less than 20 centimeters of

water and really it allows us to manage these because of how many patients have what procedures at our institution we have a large volume of patients that we actually follow and it's a you know our fellows think it's the most common

procedure Billu intervention had this is actually not that coming everywhere else and this is what I believe tests we have a pro forma that we fill in and the contrast has been ejected in

certain rates per minute and so this test takes about 30 minutes we make sure that there's the predictive value of in less than less pressure building up over higher high contrast injection rates will give us a great prediction of no

longer needing the tube and then stone

so these are a lot of slides most limited you know I'm talking I'm talking to you guys I'm talking showing you a lot of technical stuff you know and a lot of slides and I'm gonna talk mostly technical of you know how tips and dips are done kind of a step by step so even

the title it's kind of a workshop step by step of how basically you do you do tips and dips and what and and what are they so in general when you have when you have this is basically kind of out flow spleen spleen dumps blood into the

portal vein the mesentery dumps blood into the portal vein portal vein goes into liver liver does its thing and then dumps the blood into the eppadi veins to the right atrium okay for that because the liver is connected with the spleen

and the guts in series unlike any other organ basically the liver has to be a low-resistance organ because the portal circulation is low-pressure look the liver has to be a low-resistance organ with liver disease especially liver

cirrhosis you actually get increased resistance and in the liver with that disease and you get basically a backup of the blood flow in the portal circulation and increases the pressure in the portal circulation that's kind of

the genesis of or the pathogenesis of portal hypertension backing up circulation the spleen and in the guts then you get ascites and hydra thorax that's kind of think of it as weeping of fluid into the pleural space and into

the and into the perineum part of it is oncotic part of is osmotic basically think of it nutritional and pressure driven causes at the same time we all have potential portosystemic connections in other words they're there but they're

not connected or they're not opened up in plumbing they hold them bleed valves or pressure valves when the pressure is high and you know they start weeping or leaking you know in your in your basements we have the same thing

we have so many portosystemic connections there are about 55 named ones there are innumerable ones that are actually that are actually not named the common ones that we know are because of because of bleeding is esophageal

varices that's the connection usually between the left gastric vein and the azekah can be hazardous system you can also get gastric varices and that's usually connecting between a spleen and the left renal vein through a gas renal

shunts you can get also all sorts of connections even down in the internal hemorrhoids we get actually portal hypertension hemorrhoids and bleeding and so many numerous other shunts that we just don't have time to cut to cover

it to cover all these so the general to the general thought of treating all these complications of portal hypertension is to decompress the system to reduce the pressure and that's along the lines of years and decades of

surgery shunts that were placed and now tips ism largely replaced all these surgical shunts with the exception of Vancouver and Tampa okay that they still do some surgical actually a lot of surgical shunts most most other places

in North America converge to a tip to a tip shunt the the advantage of the tips of over surgical shunts is the usual what we hear is minimally invasive it you know it's a quick recovery less morbidity and mortality areason for

white tips has beaten the surgical shunts is the transplant era all these surgical shunts are actually extrahepatic so when you go for a transplants and liver hits the buckets they actually have to go and shut down

these shunts wherever they created them steena renal portal cable in the tips it goes out with a liver in the bucket so there's no complication of transplantation that's the real advantage of tips over surgical shunts

and that's why it's become very very prevalent in in in North America with a transplant error when approaching gastric varices just briefly another way is a BRT Oh which is to go basically into the left renal vein go up the shunt

and specifically screw rows the stomach and that's not the that's not this kind of subject of our of our discussion here I'm gonna talk to you

thank you so much for inviting me and to speak at this session so I'm gonna share with you a save a disaster and a save hopefully my disclosures which aren't related so this is a 59 year old female she's lovely with a history of locally advanced pancreatic cancer back in 2016

and and she presented with biliary and gastric outlet obstructions so she underwent scenting so there was a free communication of the biliary system with the GI system she underwent chemo and radiation and actually did really well

and she presents to her local doctor in 2018 with ascites they tap the ascites that's benign and they'll do a workup and she just also happens to have n stage liver disease and cirrhosis due to alcohol abuse in her life so just very

unlucky very unfortunate and the request comes and it's for a paracentesis which you know pretty you know standard she has refractory ascites and because she has refractory ascites tips and this is a problem because the pointer doesn't

work because a her biliary system is in communication with the GI system right so there's lots of bugs sitting in the bile ducts because of all these stents that have opened up the bile duct to list to the duodenum and so you know

like any good individual I usually ask my colleagues you know there's way more smart people in the world than me and and and so I say well what should I do and and you know there was a very loud voice that said do not do a tips you

know there there's no way you should do a tips in this person maybe just put in a tunnel at drainage catheter and then there was well maybe you should do a tips but if you do a tips don't use a Viator don't use a covered stand use a

wall stunt a non-covered stunt because you could have the bacteria that live in the GI tract get on the the PTFE and and you get tip situs which is a disaster and then there was someone who said well you should do a bowel prep you

like make her life miserable and you know give her lots of antibiotics and then you should do a tips and then it's like well what kind of tips and they're like I don't know maybe you should do a covered said no not a covered tonight

and then they're you know and then there was there was a other voice that said just do a tips you know just do the damn tips and go for it so I did it would you know very nice anatomy tips was placed she did well

the next day she has fevers and and her blood cultures come back positive right and you can see in the circle that there's a little bit of low density around the tips in the liver and so they put her on IV antibiotics and then they

got an ultrasound a week later and the tips that occluded and then they got a CT just to prove that the ultrasound actually worked so this really hurt my gosh to rub it in just to rub it in just just to confirm that your tips occlude

it and so you know I feel not so great about myself and particularly because I work in an institution that defined tip seclusion was one of the first people so gene Laberge is one of my colleagues back in the day demonstrated Y tips

occludes and one of the reasons is because it's in communication with the biliary system so bile is very toxic actually and when it gets into the the lining of the tips it causes a thrombosis and when they would go and

open these up they would see green mile or biome components in the in the thrombus so I felt particularly bad and so and then I went back and I looked and I was like you know what the tips is short but it's not short in the way that

it usually is usually it's short at the top and they people don't extend it to the to the outflow of the hepatic vein here I hadn't extended it fully in and it was probably in communication with a bile duct which was also you know living

with lots of bacteria which is why she got you know bacteremia so just because we want to do more imaging cuz you know god forbid you know you got the ultrasound of her they because she was back to remake and

you know that and potentially subject they got an echo just to make sure that she doesn't have endocarditis and they find out that she has a small p fo so what happens when you have a thrombosed tips you go back in there and you do a

tips or vision you line it with a beautiful new stent that you put in appropriately but would you do that when the patient has a shunt going from one side of the heart to the other so going from the right to the left so sort of

similar to that case right and so what do we do so I you know certainly not the smartest person in the room we've demonstrated that so I go and I asked my colleagues and so the loud voice of saying you know I told you this is why

we don't practice this kind of medicine and then there was someone who said why don't we anticoagulate her and I was like are you kidding me like you know do you think a little lovenox is gonna cure this and then the same person who said

we should do a tunnel dialysis tile the tunnel drainage catheter or like a polar X was like how about a poor X in here like thanks man we're kind of late for that what about thrombolysis and then you

know the most important WWJ be deed you guys are you familiar with that no what would Jim Benenati do that's that's that's the most important thing right so so of course you know I called Miami he's you know in a but in a big case you

know comes and helps me out and and I'm like what do I do and you know he's like just just go for it you know I mean there are thirty percent of the people that we see in the world have a efo it's very small and it probably doesn't do

anything but you know I got to tell you I was really nervous I went and I talked to miner our colleagues I made sure that the best guy who was you know available for stroke would be around in case I were to shower emboli I don't even know

what he would do I mean maybe take her and you know thrombolysis you know her like MCA or something I don't know I just wanted him to be around it just made me feel good and then I talked to another one of my favorite advisors

buland Arslan who who also was at UVA and he said why don't you instead of just going in there and mucking around with this clot especially because you have this shunt why don't you just thrown belay sit and then you

know and then see what happens and so here I brought her down EKOS catheter and I dripped a TPA for 24 hours and you know I made her do this with local I didn't give her any sedation because I wanted and it's not so painful and I

just wanted her to be awake so I could make sure that she isn't you took an intervention location you turned it into internal medicine I I did work you know that's that's you know I care right you know we're clinicians and so she was

fine she was very appreciative I had a penumbra the the the Indigo system around the next day in case I needed to go and do some aspiration thrombectomy and what do you know you know the next day it all opened up and you can still

see that the tips is short the uncovered portion which is which is you know past the ring I'm sorry that which is below the ring into the portal vein is not seated well so that was my error and and there was a little bit of clot there so

what I ended up doing is I ended up balloon dilating it placing another Viator and extending it into the portal vein so it's covered so she did very

- [Sergio] Good morning everybody. I really do thank you for the opportunity to reason with you about the lower limbs venous kinetics and the consequent impact on drainage direction. I have no conflicts of interest to declare, particularly because this talk is all about physics and about those laws of physics

that rule the venous drainage. We could say that the drainage occurs along our Italian leg, along a deep venous highway, a saphenous freeway and along several tributary and perforated roads.

But we could also say that we could divide the anatomy of our lower limb into three different compartments. So the tributary one's above the fascia, the saphenous one in between the fascia layers, and the deep venous one below the fascia. In this kind of network, talking about physics,

we could apply the Bernoulli's principle which, to make it simple, states that whenever there is an acceleration, a lateral pressure drop occurs. Which introduces the Venturi's effect as a potential aspiration of blood

from a slowest toward a fastest vessel. But actually, up to now, we couldn't say this for sure and say that venous network because we have really few data on the literature about the velocity values that we have in the different segments of the different compartments.

So the aim of this investigation, in the first physiological part, was to evaluate the different velocity values of different segments, understanding if the Venturi's effect could be applied inside this network, and then looking at the pathological cases.

So we have 36 lower limbs of healthy controls, and we assess all the velocity segments in the different segments of the three different compartments, evoking the flow both by active dorsal flection maneuvers of the foot, and by compression/relaxation

of the calf of course. So we compared all the different values of all the different velocities with the two different maneuvers, and we created several tables and we performed several statistical tests to see

how these velocities were behaving in the different compartments. So it's pretty interesting to notice that there are segments of our venous networks in which if we are performing the vocation of the flow with two different maneuvers, we are going to have

significantly different values of velocity. So for example, this happened in the external iliac vein, in the femoral vein, in the posterior tibial vein, and the tributary veins. If you look at the graph, we realize that there is a gradient of velocities

that is decreasing in physiology. While we are moving from the deepest, toward the most superficial compartment. And if we take all these velocities we assess together, we see that there are three different groups of velocities basically, statistically speaking,

that almost totally overlap the anatomical compartments, with some exception. So if you look over here for example, you have the posterior tibial vein that belongs to the deep venous system of course, in terms of anatomy, but not in terms of velocities.

Which means that the velocity we reported were significantly different from the ones belonging to the deep venous compartment. The same thing for the short saphenous vein, which demonstrated to of course belong to the saphenous compartment in terms of anatomy

but not in terms of velocities. If we move toward the pathological part of this, and we look at the 40 chronic venous disease patients we assessed in a model in which we considered incompetent tributary as the segment you see over there, depicted as C.

Compared to the adjacent GSV trunk, A and B. It's interesting to notice how the peak diastolic velocity and the diastolic time average velocity are actually significantly higher in the tributary compared to the GSV in pathological cases.

And if we look at the resistance index, it's interesting to notice how the segment in B, so the GSV trunk below the confluence, is actually higher. Like indicating a sort of preferential road of drainage toward the incompetent tributary.

This introduced the Venturi's effect, so now we can see the Venturi's effect could play a role inside the venous network. In physiology with a gradient that is increasing in terms of velocity, so potential aspiration while we are going toward the deepest compartment.

And the gradient that is subverted in pathology, where we have tributaries that are going faster when they are incompetent, compared to the GSV trunk, so leading to potential aspiration. But our blood is not a newtonian fluid, our vessels are not ideal conduits,

so we have to admit some things we know that we know, and that's of course the newtonian physics. Kn we know that we don't know,

and that's the application of the newtonian physics inside the human body. And then unkn things we don't even know that we don't know. That's the in-vivo validation

of these physical models. Independently by what we know and by what we don't know, I totally agree with profe tters and starting from today we know that Venturi's effect could play a role inside the venous network. Thank you.

other things that we look at tools that we use include the ankle and toe brachial indices those are these at blood pressure comparisons between the

arm and the foot or the toe the great first toe we use segmental pressures your blood pressures and multiple levels down the leg pulse volume recordings which look very similar with cuffs down the leg but they're looking at the size

of the leg per heartbeat PPG's which is basically pulse ox for the four individual toes TCP o2 which is very important and not used enough which is looking at the oxygen tension within the tissue itself and skin perfusion

pressure so ABI as I mentioned as a comparison the arm and the leg pressures and people with CLI often have an ABI less than point for the pressures gonna be less than 50 millimeters in mercury so the ABI may be falsely elevated

people who have chronic kidney disease because the vessels get calcified and they don't compress very well when you blow up the cuff increasing it above 0.45 after if it's been below that is somewhat predictive of wound healing but

not that helpful at the time of an angiogram so as the higher the two pressures is often used to calculate this because you have two pressures and each leg right you have it dorsalis pedis pressure that

you can get and you have posterior tibial so the way that you do in ABI is you look at the higher of the two and compare that to your arm pressure so just remember if your ulcer is being supplied by the vessel that's got the

lower pressure than your ABI is could be normal you could still have CLI so again not always that helpful the toe brachial indices is a it is a little bit more helpful people with diabetes only because the toe arteries tend not to

calcify as quickly in these patients less than 0.75 is considered abnormal and increasing it up into the normal range of course is predictive of fluid wound healing so limitations these only really look at

the macro vascular so that you know the named ves blood vessel patency they don't really tell you what's going on at the level of the capillaries and a recent meta-analysis suggests that neither of them can be consistently

relied upon as okay it came to a normal range we're definitely not gonna get an amputation now so I think I really do have to press both buttons each time so the systolic pressure measurements for segmental pressures you basically look

at the pressures on multiple levels of down the leg a drop of greater than 20 is considered significant and then severity of a number of lesions can't be totally determined from that again this only really tells you what's going on in

the named vessels pulse volume recordings these are cuffs that are looking at the volume of the limb with each pulse it's helpful and patients would they have non compressible vessels because the leg actually has a it's a

microscopic but detectable increase in size with each pulse and so this is better in people who have non compressible vessels and changes in PVR's often will actually precede angiographic findings CTA findings and

recent publication from the s from the society vascular surgery however calls into question their usefulness compared to a bi alone the good pictures are coming soon so this is an example what you may see in

the chart for some of your patients with critical limb ischemia so this is actually segmental pressure and pulse while recording from where I trained in Miami and basically what we're looking at is a combination of things on one of

these sheets so the pressures are listed in the middle but each sheet is going to be different depending on your institution so you're looking for a big drop and pressure from one level to the next so if you look for example in the

middle at the right leg you know there's a 176 in the arm and then there's a 126 in the high thigh normally because of gravity you should have an increase in flow at that level so that's already I have normal on the right side and then

progressing down any grade any drop greater than 20 suggested that something may be abnormal at that level PPG's these are really good for detecting what may be going on at the foot or lower levels so you transmit an infrared

signal through the toe and then try to see how much of that light comes out the other side essentially and so the amount of it it's depending on how much bloods in the digit and the flow the flow of the blood vessels so if you had a

previously flatlined signal then restoring a pulsatile signal is considered a and it you know an approved marker of tissue perfusion so this is essential in patients who have distal ulcers particularly in the level of the

toe because restoring you see you've probably all seen those of you that work in labs that do a lot of peripheral disease seen an angio graphic result where you get flow down to like the mid foot but you see no perfusion down to

the digits and unfortunately that's often not going to be enough to heal a wound so the PPG's are something I try to get in all patients who have tote tote ones so there's an example of a patient who

has flatline and all five digits on the right foot and we recant alized their anterior tibial artery and had flow all the way down there and there was a wound blush in the toe and this is the restore pulsatilla T in all five digits the next

day so at our institution now and also I've modeled after what it was with my training which is the day after the procedure we keep all these patients overnight we get an ABI i segmental pressures and pulsefire

recordings and PPG's and anyone who has flat waveforms in them in their foot level or anybody with a toll sir and if possible we try to get a duplex which you get which I'll go over next it's not always reimbursable at all institutions

if you do them in the same day though so TCP o2 as I mentioned is something that's a little underutilized I think the the task two recommendations that we actually use to stratify the different types of disease and perf arterial

disease suggest that all patients with CLI should have this testing done but it's hard because patients have to not smoke and not drink coffee or tea the morning of the exam and that's hard to get patients to do you have to keep the

room temperature controlled and so it's office availability is limited so an improvement values greater than forty millimeters of mercury in the area surrounding an ulcer suggests that it's going to have successful healing so we

often will do this before we take the patient for an angiogram as a baseline and then bring them back afterwards and if we're if we have a very large increase that you know that's a good sign but of course we're our goal is

usually to be greater than forty and it's one of the few of these tests that's actually useful in patients who don't have Doppler signals so this is a totally not fake wound on this right foot this is example of what it looks

like you basically put multiple probes around the area of the foot and you're testing for the different oxygen tensions skin perfusion pressures is analogous but slightly different basically you're inflating a cop over

different areas of tissue and until the blood flow stops and then slowly deflating it until you can detect light being transmitted through that area again greater than thirty values or predictive of wound healing a lot of

numbers and there will be a test at the end of this so this is a chart kind of showing the ischemic wounds healing likelihood is correlated with an increase in the skin perfusion pressure so if you're less than 30 you're

unlikely to heal if you're greater than 40 it's most likely not an excuse mcquown and you should start looking at other ideologies like venous disease or neuropath neuropathic disease or infection duplex ultrasound is extremely

- Thank you. These are my disclosures. So, iliac artery can be your friend or your worst enemy, with cases of significant iliac artery occlusive disease. This doesn't mean you can't do it, but I always teach my fellows to give it the full meal deal.

I don't hesitate to dilate with the seven or eight millimeter angioplasty balloon, and then I'll follow that up with the dilators, and that gives me a good idea, if the dilator doesn't go up, it's time to consider some other route.

Rarely, I will do a conduit, and I usually will do this either with a purse-string in the distal common iliac artery, or a proper conduit with a synthetic graft, especially if I'm going to combine that with an ileofemoral bypass.

The thing to remember is you not only have to get the device up, you have to be able to turn it, and that's why I use those tips or tricks. Endovascular gear, we've already seen today a few speakers talk about some of the catheters and sheaths they like to have on the shelf.

I'll just take you through these. These are the specific ones I like to make sure I have. A stiff glide, and a Amplatz Super Stiff with a once centimeter tip, can again be your friend but also your enemy, so you have to treat those wires with respect.

And some people forget about that old trick of being able to put three 018 wires through a five French catheter, and that can sometimes get you deep into a superior mesenteric artery or a renal artery. Sheaths, I personally don't like

the angled sheaths from Cook. I find the Ansel One and Ansel Two sometimes work against you. I prefer to use the Raabe sheath, which is a straight sheath. The disadvantage of the Raabe sheath

is it comes with a very stiff dilator. So the tip here is just open the Ansel One, take out the High-Flex dilator from the Ansel One and put it up your Raabe sheath and that'll get you to where you want to be. The steerable sheath, Josh Adams did a great presentation.

It's an outstanding sheath. The only thing I would worn you is if you ride a tricycle through your whole life you won't be very good on a bicycle. So don't get too used to using a steerable sheath. Every once in awhile, just use it with the

old-fashioned catheters and wires before you, and open up the steerable sheath if you really need it. Beware short and downgoing renals. This is a trick sometimes you can use. Stephan Haulon showed this. You can drop, if you can't get any catheter

or sheath to follow, just drop a reverse catheter in, do the rest of the fenestrations, open up the top cap, and then put up a Coda balloon with your ipsilateral access, and you can use that Coda balloon to form a roof, and you can get any catheter or wire

to get into that tough renal artery. Beware of tortuosity, this really is your enemy. This, I have a low threshold just to go to a retroperitoneal exposure for either a direct puncture or conduit. There's nothing more demoralizing than deploying

a fenestrated graft, and if a lot of torque is built up into that because of those tortuous iliacs, you will see those fenestrations start to move as you deploy each stent, and that's sometimes an irretrievable situation. Renal artery occlusive disease used to be

a contraindication for fenestrated graft. It is no longer. Although, renal artery calcified and downgoing renals can really be a big problem, and always believe the CT, don't believe the angio. This is an angiogram of the same patient.

This does not depict what the real true story is. And with these particular cases, you know, most people in the room do not have access to customized fenestrated grafts, which sometimes you can use to help you with these cases. So this is a case that's interesting,

and what we did here is we basically came from above, pre-stented these with covered stents, and then that made the fenestrated graft on a second stage procedure, much easier. I didn't have to use any contrast. I could use these as my markers for the renals,

and in this particular case, I was able to use a steerable sheath for that short renal, and you can see how much that trajectory of that renal changed with that covered stent as well. Finally, this is a case that kind of highlights a lot of different tips and tricks.

This is a large aneurysm, juxtarenal with common iliac aneurysms, significant iliac and femoral artery disease. And so again, we kind of customized this. I'm not a big fan of snorkel and parallel grafts, but in this particular case I saw its use.

So I made a fenestration for the left renal and I planned to use a snorkel for the right because I couldn't get any kind of configuration to fit with the renal artery and SMA being on the same plane. So here I used that same balloon

for the iliac occlusive disease, to get the device up. You can see the issues here. There's the left renal coming off. I decided to fenestrate that and put a snorkel in the right renal, and this is what I did.

I was afraid that that fenestrated graft was going to cover the renal, so I came down from above just to mark the left renal. As I deployed the graft, I got out of the scallop, snared from the top, and then I brought a sheath down through the scallop, and I actually catheterized

the left renal from a downgoing perspective, and this worked quite well. I was able to snorkel right and then fenestrate the left, and we had an excellent result. And my final tip for you is don't go chasing endoleaks

with these long fenestrated procedures. If you have done the right procedure, all those endoleaks will seal. Thank you.

stamp placement we talked a little bit about it I'm gonna talk to you a little

bit more about it and ideal stance is a straight stance that has a nice smooth curve with a portal vein and a nice smooth curve with a bad igneous end well you don't want is it is a tips that T's the sealing of the hepatic vein okay

that closes it okay and if there's a problem in the future it's very difficult to select okay or impossible to select okay you want it nice and smooth with a patek vein and IVC so you can actually get into it and it actually

has a nice hemodynamic outflow the same thing with the portal thing what you don't want is slamming at the floor of the portal vein and teeing that that floor where where it actually portly occludes your shunts okay or gives you a

hard time selecting the portal vein once you're in the tips in any future tips revisions okay other things you need it nice and straight so you do not want long curves new or torqued or kinks in your tips you

a nice aggressive decompressive tips that is nice and straight and opens up the tips shunt okay we talked a little bit you don't want it you don't want to tee the kind of the ceiling of the of the hepatic vein another problem that we

found out you want that tips stance to extend to the hepatic vein IVC Junction you do not want it to fall short of the paddock vein IVC Junction much okay much is usually a centimeter or centimeter and a half is it is acceptable

the problem with hepatic veins and this is the same pathology as the good old graft dialysis grafts what is the common sites of dialysis graft narrowing at the venous anastomosis why for this reason it's the same pathogenesis veins whether

it's in your arm for analysis whether it's in your liver or anywhere are designed for low flow low turbidity flow of the blood okay if you subject a vein of any type to high turbot high velocity flow it reacts by thickening its walls

it reacts by new intimal hyperplasia so if you put a big shunt which increases volume and increased flow turbidity in that area in that appear again the hepatic vein reacts by causing new into our plays you actually get a narrowing

of the Phatak vein right distal to the to the to the Patek venous end of the shunt so you need to take it all the way to the Big C to the IVC okay how much time do I have half an hour huh 17 minutes okay

Viator stents is one way let's say you don't have a variety or stent many countries you don't have a virus then what's an alternative do a barre covered stem combination you put a wall stent and then put a covered stance on the

inside okay so put a wall stent a good old-fashioned you know oldie but a goodie is is a 1094 okay you just put a ten nine four Wahl cent which is the go to walls down so I go to stand for tips before Viator

and then put a cover sentence inside whatever it is it's a could be a fluency it could be a could be a vibe on and and do that so that's another alternative for tips we talked about an ace tips as a central straight tips and it's not out

and fishing out in the periphery okay this is an occlusion with a wall stance this is why we use think this is why now we use stent grafts this is complete occlusion of the tips we're injecting contrast this is not the coral vein this

is actually the Billy retreat visit ptc okay that's a big Billy leaked into the into the tips okay and that's why we use covered stance I'm gonna move forward on this in early and early and experienced

- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro

or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire

because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,

or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,

very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D

in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--

radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about

to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.

So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where

the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist

to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here

to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric

reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I

mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic

close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to

understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.

Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use

Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.

We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.

You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.

Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial

phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,

the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,

very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone

and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.

In other words can offer higher value in patient care. Thank you.

I'm the FDG is have a radio pharmacy located on the second floor no New York State does allow nuclear medicine

technologist and nurses to inject the con the FDG isotope I know in other states one in particular is is New Jersey the the nurses are not allowed to inject isotope and the technologist has to do it also in addition certain

isotopes and certain scans the ducts have to inject the contrast like the the cervical Lin scintigraphy and some so my question has to do with discharge instructions so just like you give them that little card that they keep with

them so they trigger some radiation alarm and a bridge or on a highway do you give them discharge instructions about if there's small children at home that they're not sitting in their lap for extended period what kind of

instructions do you give on discharge after these patients so we when they come in coupled with the screening forms that they fill out we have some instructions attached to it and does that does have

the discharge instructions but we reiterate to them you know if they have small children or babies and pregnant women and just try to keep their distance for the next 12 to 24 hours just to until the really activity has

wear off so the FDG is like two hours almost for the half life FDA FDA has 60 minutes 116 minutes half life and usually by 12 hour by the 12 hour period they're mostly background radiation okay thank you

we had they have a written instruction like it's like a packet that we give into the market that we do to the patient and the patient have accessed to the web portal that they have and they can be the instructions from there

this is correct so betta bar is still investigational for the most part the only way you can build for it is two different scans you build for a pet and you build for our mr so you've got to get approval for both what you are not

going to get reimbursed for is the registration and that's where it gets a little bit challenging because then you need a radiologist who is both certified uncredentialed to read a pet and an mr so right now most institution bill it as

two different procedures so that's why you that's how we get the approvals just a little information on the side I went back to this case study because I forgot to tell you that in order for the PET CT to have as clear image as the pet MRI

the pet portion I mean the city portion and the pet city would have to be done diagnostically and that this would expose the patient to radiation three times that's why they prefer the pet MRI because yeah the reason why we do it if

we do it mostly for for for pediatrics and it's it and it's because of radiation because you know like our my team is saying you you are going to have this patient have constant follow-up so if you can reduce the amount of

radiation they have from a younger age as we all know it work in radiology DNA injuries occur when you're younger then more is more severe than than later our MRI the pet MRI injection they're all lined with lead and our MRI the pet

MRI room is actually lined with lead so we don't really have Needham let aprons we don't know we don't have wear aprons they are allowed to go to other appointments after they are pet MRI usually with the FDG most of the

radiation after the Tessa's finish is gone they're not more than what not more than radioactive than background radiation so they are are safe to be around people yes that's more for precautionary

measures yes no they go straight to the PACU so we our MRI table is detachable we have an area for where we keep our inpatient bay area we have a structured ready for them to go into right after the test and the

anesthesiologist and if they are Pediatrics the pediatric nurse is with them and they go straight to pack you do like probably like probably less than ten a week right now some weeks we are busy we do for how we do that much some

it varies like we'll do three or four but we are trying because the reimbursement that's one of the big issue our institution is actually eaten eating the cost for some of these to provide a patient with less radiation

especially or pediatric population we have one pet MRI machine for the whole institution three at the main campus we have two we have multiple and other regional sites so the yes

no less than 15 GFR except for the EU vist less than 30 then we notified the radiologists eeeh this is harder to so you this is the it's a linear contrast as opposed to the Catalan bettervest which is

macrocyclic so it's easier for the body to get rid of well there yes well they're only they're already getting dialysis so it's really not much of a harm yes we do patients on dialysis but we make sure the dialysis is done within

24 hours after receiving the contrast yes um sometimes you know you just have it to have it we don't require it for all the tests if you have it we have it we check if it's already in the chart we

acknowledge it you know we don't require for outpatient we don't require but in patients we do all right anything okay so Bernie pet/ct the scanning time for pet/ct is about 30 minutes to 45 minutes Patsy pet/ct is about 30 to 45 minutes

with the pet MRI sometimes they they order dedicated pet MRIs so that is a little longer you have to take note that we do a whole body scan whole body scans for even just for a regular MRI is at least an hour so we try to eliminate

just you know having them have to have to or point to different appointments and just one waiting room one waiting time so that cuts down the response for the patient themselves yes we do for adults it's 12 for the

whole body and then for the pet brain it's about 10 if I'm not mistaken and then plus or minus 10% and then the pediatric doses are cultured calculated base of their height and their weight and there are all protocol by a

radiologist because we have a lot of whole-body protocols we have the bone survey actually that's about 30 or 40 minutes and yes that's an hour and then we have longer whole body protocols diseases

specific and sometimes they try to depends on what the patient's diagnosis is we have whole body scans where they have to check the bone marrow and that needs to be from tips of the toes and tips of the fingers and that can be a

challenge especially if the patient is tall because that has to be in sequest sequestered and sequential patient and positioning is also a challenge alright thank you so much thank you thank you so much

[Applause]

my talk is titled extremely obvious IR and I think as we move through these slides you guys are going to be able to pick up really quickly on why I elected for that title so this is a patient this is a 67 year old male he had an Evo repair in 2014 in 2015 he

underwent two repairs for persistent type 2 endo leak and this was done via transsexual approach in 2018 we got a CTA that demonstrated an enlarging aneurysm sac so here's just some key critical images from the CT I had the CT

and its entirety today but I had to like panic dump a lot of slides off of my powerpoint I'm always the girl at the airport that you see transferring things from one suitcase to the other like right when it's about to get onto the

airplane so what do we notice about where we see the contrast in these in these images so is it anterior is it posterior anyone its anterior so what if I told you that we see contrast in the anterior sac but this patient has an

included ima where is it coming from so we get the CTA we see any large aneurysm sac we see it an endo leak we bring them into clinic we go through the routine things the patient denies abdominal pain they deny back pain and so we go ahead

and all of our infinite wisdom and we schedule them for a trans cable approach to repair what we call a type 2 and delete now one of the most the most important key sentences from the workup is we say this is likely a type 2 in the

leak but a feeding vessel is not identified okay so our usual algorithm at UVA if we get a patient we do a CTA we bring we see any sort of endo leak if we cannot identify a feeding vessel usually what we do and you can let me

know if this is the same at your practice or if it's different we'll bring them in and we'll do some dynamic imaging from an arterial approach and we'll try to see you know is it really type 2 can we identify a feeding vessel

and oftentimes what happens in those situations is you you identify oh it is a type 2 we just see where it was from and we're gonna have to bring them back and we're gonna have to put them prone and we're gonna

have to stick the stack directly so we thought we were gonna outsmart it this time like we we were gonna just identify that it was typed to you right from the get-go do I have the play button or do you have the play button awesome all

right so this is our trans cable access so what we're doing these days to do our trans cable access and our fenestrations is we're actually using a t lab kit so we're using the transjugular liver biopsy sheath and we're putting our

65-centimetre cheap a needle through that so everything's going great so far we see our sheath in access goes smoothly I might have gone for two slides can you hit the I'm not sure yeah go ahead and hit that nope go ahead and

go one for slide and then just play that video for me yes please awesome so this happens pretty quickly can you play that video again and just keep playing it through on a loop and so we do an injection from our microcatheter from

our trans cable approach and what do you guys noticing where are you noticing the contrast tracking yeah in the red circle [Music] it is now right so everybody at UVA is is a proficient Monday Morning

Quarterback let me tell you so we see the contrast tracking down outside of the iliac limb so now we're all going okay can you go ahead all right go ahead and play this video all right so we get access into the femoral artery

just to make sure because at this point we're hoping against hope we haven't put this on the patient we haven't put this patient on the table MANET made a trans cable puncture only to identify that this patient does in fact have a type 1

B in delete but our arterial access proved that is exactly what we did the junction of the yes we did we did a trans cable puncture to identify that it was a junction leak so that's a problem right because we have

this action going on right so we have a trans cable puncture as dr. Haskell just adapt ly summarized we have a trans cable puncture we've done nothing so far but identify that this patient has the type 2 in a week so it is a micro

catheter right it's just it's just a party foul and then it was the fellow's dream because you pull out and there's nothing to hold pressure on there's nobody's dream at that point so I want to stop here and I want to just take a

moment you guys can live my psych at night so do you ever your so my normal algorithm for my patient since I come in in the morning I look at the patient's chart I review their prior imaging and I try to

do all of these things before looking at my attendings plan because one of the things that I realized is that challenges me to try to figure out what's my plan for the patient what do I think the most appropriate inventory

would be and every once in a while you see something in the plan that doesn't quite jive and you're like there's this is likely a type 2 in the league although a feeding vessel is not identified so I have two options at this

point I either walk down to the reading room and I say hey someone tell me what's going on we don't identify that type - is it worth doing a diagnostic imaging or anyway I just roll with it and this

was a day where I elected to roll with it and so I just want to take a moment and reiterate it's always important for all of us to you know you have a voice and use it and you want to bring up these

things that's sometimes we all start going through the motions where you work with someone that you trust a lot it's really easy to say like Oh someone's smarter than me caught that right so going back it's like it's like that

terrible joke what is the radiologists favorite plant the hedge mmm that's what that is it's like well it could be but it might be and ray'll right you go ahead and play this so this is just our walk of shame as

we're casually embolizing our track out of our trans cable approach and here we are back in clinic so again this is a 67 year old manual with recent angiogram that demonstrates significant type 1b endo leak and we plan for an extension

of the left aortic lab so we bring the patient back we do a standard comment from our artery approach we get into the internal iliac we identify the iliolumbar all kit all standard things we drop an amp at Sur plug to prevent

any sort of further type to end a leak into the limb that we go ahead and extend we put in the iliac limb we balloon it open we'll go ahead and play this video and our follow-up angiogram reveals a resolved type to end a week so

ultimately we did it so what are

and what makes things complex is when the Louie system is inhospitable to the easy procedures when the ducts are dilated I think most operators find this

really relatively easy to get a tube in but once it's under lay that it really makes it tricky you either have a disease of the Blooey systems such as sclerosing cholangitis in flammond ich ins of the power duct architecture and

the wall itself all surgeons have gone in in misadventure transected cut the wrong duct and so cholecystectomy is are frequently the most common ones we misidentified and right posterior duct inserting below

and they cut that or even cancers is there not sometimes Calandra carcinomas such as cat skins - matrix of the ones right at the middle of the tree those ones make it challenging to sometimes get through sometimes they're so severe

in the severity of a structuring that it's it's very difficult to get through and sometimes we have to use sharp organizations and then like I said post surgery and with the advent of your gastric sleeves and gastric bypass

surgery this has become a much more common place and so frequently I think bluie interventions are on the rise again whereas I think they went out of favor for a few years in the 2000 mainly the GI became so aggressive with a

slanting Denova stenting and middle stenting then and bluie disease came down somewhat in high AR but this is all on the upswing again now with much more patients with with a bariatric surgery so in terms of intervention and your

your procedures in the room for difficult access and again a unviolated Ballou systems is actually not that insignificant even very experienced operators is going to be the most challenging procedure of the day and

it's vital to actually know your options and for we will actually a pacify the blue system with anything that has yellow stuff so frequently surgical drains that are adjacent to the leaking site sometimes we will check them and

sometimes you just got to be careful not inject too much sometimes their pacifiers and obliterates a field so much so you can't see anything your procedures pretty much done I also use known in distance gee I frequently would

be the first group to go in and try address below a leaking and they'll plate in the stands even though it doesn't cross the leaking site or it's inadequate for a decompression so we frequently would just stick the

indistinct directly and start our procedure that way so we know we're going through deliver through some bad structures but you we use a very very small caliber needle and stick the in distinctly and then once we use that

sometimes we'll place a wire knowing the fact that this is not our final track to a destination we'll put a wire in and then put that into any peripheral duct and then stick our skinny wire and so that's another way another way is

actually once you original PTC's been obtained with its optimal not will use mix lidocaine jelly with contrast media and mix it and make it a real thick slurry and that sometimes is a really good way to keep

the contrast from making out really really quickly he sounds quite logical but it's actually a very cute trick so that's another thing to consider every now and then you can actually use gas because it doesn't dissipate so if you

take co2 and there's at large dilated ducts you can actually put co2 and visualize that very nicely particularly specifically in the left lobe of the liver tends to dive into Phi the ventral left duct very nicely with gas but

sometimes it's not always easy if it is gas filled intestinal tract and then use control actress and I'll show you what that looks like on a picture and then high-grade lesions every now and then we have to use sharp aura colonization and

really the packing of the wire and your who should be your Russia sheet a needle from a tip set every now and then we will use a cardiology transept or needle the skinny a needle and really that sometimes with a high-grade multi

sclerosing agent of sclerosing cholangitis sometimes that is the only way through and sometimes we will use even rfy and drove our way through with high-power so this is a little bit what what it would look like if you had a

lack called a transaction we couldn't specify the billary system from about 30 passes of a routine and ptc axis that we should be stuck a central duct we pointed the wrong way contrast we float much faster than we could to get a

second axis so we just put a wire and it immediately then we actually stuck our wire and used our wire to get down and this is a cute way of getting using just a structural element even though you don't actually managed to keep contrast

in there to allow you to identify here's an example of a patient who had a Whipple procedure and a surgical master moses leak and it was under laid it difficult to pacify patient also has rapid respiration so some of these

patients are from the ICU they breathe very very high frequency and it's actually very difficult unless you get general anesthesia sometimes the risk outweighs the benefits of putting people under

for some of these that we will just as soon as if get pacified the blue system put a wire and again another example where we stuck a wire then we actually use that to gain a second axis and pacify the other system left atrophy

this is a patient with a very very small left lobe and we use the right axis it's a very acute angle from the left hand side we actually spin just stuck put in a snare and we stuck a snare we pull the wire out from the left through the white

and out the skin and then pushed it down using a stuff and that's why I'm taking your snare from Lord lift out the let right and then put in from the right hand side up the skin then you push that all the way through into the right hand

side and how you have power lateral axis so just there are some cute tricks that you can do to and make your procedures more successful and this is the other way you may do it sometimes you can only get to the lift system from the right

the hilar cholangiocarcinoma here high central high low lesion we could get our CAFTA from the right to the left that there's no way we could get from left to right so all we did was stay our Y from right to left and it comes out the skin

and then using a peel away she you put the wire down from the right hand side then you said she go from left access all the way up the skin on the right you exchange being glide wire put it in the pillow sheath and the right stolle

feeder that aren't all the way and you pull your pillow as sheath and now you have left access and right axis and sometimes it's the only way to get our lateral axis this is commonly found when surgeons require bilateral tube for a

cholangiocarcinoma classic in Palmyra section where they use the Blooey tube to feel their way up and look at the end of the tumor and so sometimes we do

- The Chairmans, Doctor Reed, thank you very much to accept our data or hypothesis. This is a little bit different of the other subject. I have no disclosure. So, very sure that the type A and B dissections are potentially lethal diseases.

Typically silent with progression. But we know variation point, or the focus, we know now in the last 20 years that 29 genes, when they are not the codes but they are weakening factors after our, therein, and we want to demonstrate here,

that in description or hypothesis is that the intimal and the medial injuries of the aortic wall, in the thoracic aortic anarithmias and dissections are caused primarily only from one type of kinetic forces which appears on the aortic wall in three different forms: That is the pouc

e-entry, the cl entry that is wall haematom. This is the same aortic dissections in three forms. We don't think that the wall stress and the wall force are significant factors.

Seeing that factors come from the vorticis, Leonardo already described. Even different levels, and most typical is the sinus of valsalva, main flow way is not contact with the sinus vawe turbulence. There is the main flow, actually the laminal flow

is not real, it is a parabolic, rotating pressure and the blood mass vawe sliding on the endothelium. Endothelium, that is the multilayer, non-thrombotic, in the sagital view, in a vawe form surface, and on the vawe form surface, induced low scale vorticis, and the main flow is sliding on theses vorticis.

This is a very difficult kinetic situation. Any geometrical changes makes significant side-vortex development, and kinetic and turbulence differences. Here you can see the rotating parabolic mass vawe, sliding on the endothelial.

And when this vorticis, the main vorticis effect on the wall are the same place as the most frequent entry line of the Type A dissection. In this case, and other uncular and right sinus. Here we are, actually the human aortic dissections and the aneurysms are developing mainly

behind the side-branches and valves-behind turbulences and vorticis. Here gene factors are stored not really on the 29, mostly in the TGF-B pathways, and the smooth muscles and cells. And genes, after all, this is not relevant,

although there is two theories: The genetic theory and the hemodynamic theory. You can see on the right side that it's two different bicuspid valve, causes different turbulences and different velocity and different forces of the aortic wall.

Any forms of the form changes of the vessels cause turbulences and also different poststenotic vorticis. Here and then, had a print, imprint of the endothelial structure changes, endothelial surface changes,

and endothelial migration in the middle column, as you see and on the graphic. Here you can see the different velocity turning point of the dilated aorta and the replace aorta. Even in the bisupidal and the tricuspidal, you can see the diameter and their form

are the length and the heights are different of the turbulences and the turbulence formed here. You can see, we can close out the sheer stress, because that you can see, in the stress points they are the small curvature in the bicuspidal and the tricuspidal aortic wall.

Although, the typical point of entry on the main curvature. But a very important difference, is the left ventricul ascension and angulation. Different flow and velocity forces. And also,

pressure point with the typical Type A/Type B dissections. The main pressure is in the ascendance, although the typical ended underneath are near the left subclavian artery, but the flow is, we can see the right side are the speed, are the largest displaced.

Numbers of possible re-entries are dependent from the size and the location of the main entries and re-entries. That is, different type of type arch, form, flow, and a means different re-entry size and location as you can see.

In this case, also, bare stent vibration by turbulence can cause different turbulences and side-vortex formation, as you can see on the right side. And back to the vorticis. The vorticis this kinetic force that would be a hypothetic,

hypothesis, our hypothesis, it comes from the vortex merge, ita-filaments and double vortex, double the phalanx form. And by to reach that, they give up light, heat,

velocity changes, and kinetic force. Here that is the double-helix form and also when at the collision of this that I'm speaking about, these are the forces, and they are very high scale forces. Not the same scale as the sheer wall, and the wall forces.

So, the conclusion and then, the take home message, is we conclude that the gradient between significant turbulence-vortex merge or collision generated kinetic force divided by the wall resistance is the deciding factor about endothelial injury and the real potentially fatal aortic vawe dissection.

It gives us a realistic prognosis and can determine the seriosity of the aortic wall injury, we can differentiate a simple endothelium injury to the life threatening type A or type B dissection. We need in the future develop a new imaging programs form NMR or CONTRAST TEE transform this visualization,

this image into kinetic vectors. We need a prognostic calendar for time related aortic wall changes based on genetics and patients symptomatic. And need a device to measure in vivo online aortic vessel wall resistance.

And at the end a cartoon. Actually, black holes are also, you can see, as vorticis. And this force cannot be only positive, it can be only negative, a vacuum, as in the tornadoes. But can rise in the aortic wall.

That is positive or negative force can be. Thank you very much for your attention.

so just a compliment what we everybody's talked about I think a great introduction for diagnosing PID the imaging techniques to evaluate it some of the Loney I want to talk about some of the above knee interventions no disclosures when it sort of jumped into

a little bit there's a 58 year old male who has a focal non-healing where the right heel now interestingly we when he was referred to me he was referred to for me for a woman that they kept emphasizing at the anterior end going

down the medial aspect of the heel so when I literally looked at that that was really a venous stasis wound so he has a mixed wound and everybody was jumping on that wound but his hour till wound was this this right heel rudra category-five

his risk factors again we talked about diabetes being a large one that in tandem with smoking I think are the biggest risk factors that I see most patient patients with wounds having just as we talked about earlier we I started

with a non-invasive you can see on the left side this is the abnormal side the I'm sorry the right leg is the abnormal the left leg is the normal side so you can see the triphasic waveforms the multiphasic waveforms on the left the

monophasic waveforms immediately at the right I don't typically do a lot of cross-sectional imaging I think a lot of information can be obtained just from the non-invasive just from this the first thing going through my head is he

has some sort of inflow disease with it that's iliac or common I'll typically follow within our child duplex to really localize the disease and carry out my treatment I think a quick comment on a little bit of clinicals so these

waveforms will correlate with your your Honourable pencil Doppler so one thing I always emphasize with our staff is when they do do those audible physical exams don't tell me whether there's simply a Doppler waveform or a Doppler pulse I

don't really care if there's not that means their leg would fall off what I care about is if monophasic was at least multiphasic that actually tells me a lot it tells me a lot afterwards if we gain back that multiphase the city but again

looking at this a couple of things I can tell he has disease high on the right says points we can either go PITA we can go antegrade with no contralateral in this case I'll be since he has hide he's used to the right go contralateral to

the left comment come on over so here's the angio I know NGOs are difficult Aaron when there's no background so just for reference I provided some of the anatomy so this is the right you know groin area

right femur so the right common from artery and SFA you have a downward down to the knee so here's the pop so if we look at this he has Multi multi multiple areas of disease I would say that patients that have above knee disease

that have wounds either have to level disease meaning you have iliac and fem-pop or they at least have to have to heal disease typically one level disease will really be clot against again another emphasis a lot of these patients

since they're not very mobile they're not very ambulatory this these patients often come with first a wound or rest pain so is this is a patient was that example anyway so what we see again is the multifocal occlusions asta knows

he's common femoral origin a common femoral artery sfa origin proximal segment we have a occlusion at the distal sfa so about right here past the air-duct iratus plus another occlusion at the mid pop to talk about just again

the tandem disease baloney he also has a posterior tibial occlusion we talked about the fact that angio some concept so even if I treat all of this above I have to go after that posterior tibial to get to that heel wound and complement

the perineal so ways to reach analyze you know the the biggest obstacle here is on to the the occlusions i want to mention some of the devices out there I'm not trying to get in detail but just to make it reader where you know there's

the baiance catheter from atronics essentially like a little metal drill it wobbles and tries to find the path of least resistance to get through the occlusion the cross or device from bard is a device that is essentially or what

I call is a frakking device they're examples they'll take a little peppermint they'll sort of tap away don't roll the hole peppermint so it's like a fracking device essentially it's a water jet

that's pulse hammering and then but but to be honest I think the most effective method is traditional wire work sorry about that there are multiple you know you're probably aware of just CTO wires multi weighted different gramm wires 12

gram 20 gram 30 gram wires I tend to start low and go high so I'll start with the 12 gram uses supporting micro catheter like a cxi micro catheter a trailblazer and a B cross so to look at here the sheath I've placed a sheet that

goes into the SFA I'm attacking the two occlusions first the what I used is the micro catheter about an 1/8 micro catheter when the supporting my catheters started with a trailblazer down into the crossing the first

occlusion here the first NGO just shows up confirmed that I'm still luminal right I want to state luminal once I've crossed that first I've now gone and attacked the second occlusion across that occlusion so once I've cross that

up confirm that I'm luminal and then the second question is what do you want to do with that there's gonna be a lot of discussions on whether you want Stan's direct me that can be hold hold on debate but I think a couple of things we

can agree we're crossing their courageous we're at the pop if we can minimize standing that region that be beneficial so for after ectomy couple of flavors there's the hawk device which

essentially has a little cutter asymmetrical cutter that allows you to actually shave that plaque and collect that plaque out there's also a horrible out there device that from CSI the dime back it's used to sort of really sort of

like a plaque modifier and softened down that plaque art so in this case I've used this the hawk device the hawk has a little bit of a of a bend in the proximal aspect of the catheter that lets you bias the the device to shape

the plaque so here what I've done you there you can see the the the the the teeth itself so you can tell we're lateral muta Liz or right or left is but it's very hard to see did some what's AP and posterior so usually

what I do is I hop left and right I turned the I about 45 degrees and now to hawk AP posterior I'm again just talking left to right so I can always see where the the the the AP ended so I can always tell without the the teeth

are angioplasty and then here once I'm done Joan nice caliber restored flow restored then we attacked the the common for most enosis and sfa stenosis again having that device be able to to an to direct

that device allows me to avoid sensing at the common femoral the the plaque is resolved from the common femoral I then turn it and then attack the the plaque on the lateral aspect again angioplasty restore flow into the common firm on the

proximal SFA so that was the there's the plaque that you can actually obtain from that Hawk so you're physically removing that that plaque so so that's you know that's the the restoration that flow just just you know I did attack the

posterior tibial I can cross that area I use the diamond back for that balloon did open it up second case is a woman

- Thanks again, and thanks to Dr. Vieth for the kind invitation again this year. I am on the scientific advisory board for the device. So remotely monitoring flow in vascular structures is not a new concept, Dr. Vieth and colleagues actually reported this several years ago. But the technology has finally caught up with that concept.

So this device involves a microsensor which is a piezoelectric polymer, bluetooth technology to then wirelessly transmit this data for external processing. At this meeting in the past we've reported our initial in vitro results with the bench top model

showing the concept is possible on the bench top, both to determine degree of stenosis, and actually location of the stenosis, distal or proximal to the sensor. There's also in-vivo data in an animal model, an ovine carotid bypass model,

which shows the ability of the sensor to transmit through the tissue under physiologic conditions. We then use this to also show the ability of the sensor to detect stenosis and occlusion in an in-vivo ovine carotid model. Most recently, we've actually done a human

proof of concept trial in AV fistula patients, using an external patch containing the sensor and the transmitting equipment. Seventy six patients were studied, that were coming in to and angio suite for fistulograms and or angioplasty

for their fistula and their access, and measurements were taken at that time, both pre and post evaluation. We found 100% success, both in acquiring data and in storing this data remotely.

And the findings were actually corroborated by the fistulogram that was then performed. Eleven patients actually didn't have significant stenosis, and 65 had stenosis or occlusion, and you can see the data, which is generated by the device,

in the lower bars, showing both stenosis, on the left, and occlusion on the right, and juxtaAnastomotic stenosis of 75% in the lower blue bars. Additional sensors can be placed on the device. This can be done with new microsensors, which can be placed right next to the original sensor.

Phonoangiography can give volumetric flow rates, accelerometers can be placed, which can actually show thrills and pulse and generate acoustic data. Photplethysmography sensors can be placed, and thermal sensors can be placed

to generate such data as hematocrit, degree of stenosis, heart rate, possibly even blood pressure in the future. Some of these sensors have been placed, and there's a high correlation when they're used to Transsonic flow probes under pulsatile flow conditions

to show that we can actually generate information on flow, both peak and lack of peak, and it's very accurate in terms of its comparison to these Transonic flow probes. You can also detect hematocrit. So the sensor can actually be utilized to show

hematocrit in human blood samples with a strong correlation to standard measures of hematocrit and hemoglobin using the device. Detection of blood volume is also possible with these new added microsensors. There's peak detection of the photoacoustic spectrum,

which can allow a determination of total blood volume. So the concept is to acquire the raw data through whatever array of sensors are desired. Initially, right now, we're still using the piezoelectric sensor to really just monitor flow and stenosis.

Signal processing can then be performed using machine learning. This has actually being placed into the algorithm, so that machine learning can accumulate and analyze the data. For clinical metrics which can then be

acted upon by the clinician. There will be a trial beginning in 2019 in Europe, again utilizing an external patch sensor, and dialysis access patients to see if we can acquire real time, remotely monitored information, and then alert the clinicians appropriately to

predetermined clinical criteria. This is the current variation of the patch. It is worn for 7 days, is sweat and waterproof. It could actually be worn longer than that, but we're going to have the patients change the device after 7 days.

It's easy to apply, comfortable to wear, it does have this multi-modal sensor capacity. It can add up to ten sensors on the device to generate both optical, acoustic, thermal, and mechanical information, and it will automatically monitor the patient's dialysis

access over which it's placed. The battery life is 2-3 months, but we're going to change the patch, each one, after only seven days, so that won't be an issue. And you can automatically measure, you can actually generate as much data as you'd like,

but we're going to generate at least eight pings, or eight data acquisitions per day. So the real time fluid management is also possible with this device. You can actually utilize this to generate, hopefully, both flow information and

information on fluid volumes. So this is our timeline. We'll start the trial in 2019. We hope to have FDA approval for hematocrit, flow, stenosis, and cardiac output in Q1, Q1 and Q4 of 2020, and we look forward to

presenting the data at further meetings here in the future. Thank you very much.

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