- [Alicia] The AVIR is pleased to announce the recipient
of this year's prestigious Shari Ullman Gold Medal Lecture award as Dr. Wael Saad. Dr. Saad completed his medical education at AnChans University in Cairo, Egypt. He then completed a vascular surgery internship at Johns Hopkins University.
His radiology residency at the University of Rochester, and his interventional fellowship at the Institute of Radiology in Washington University. Dr. Saad has been internationally recognized for his expertise in liver disease, including transplantation, hepatobiliary disease,
and portal hypertension. He has over 240 publications, as well as over 70 book chapters. He's a manuscript reviewer for numerous journals, including the Journal of Vascular and Interventional Radiology, the Journal of Clinical Imaging,
The American Journal of Roentgenology, Cardiovascular and Interventional Radiology, and Radiology. He serves on the editorial board for the American Journal of Roentgenology, and the Journal of Clinical Imaging Services.
He serves on several committees with the Society of Interventional Radiology, and the Radiologic Society of North America. One of the most obvious testaments to his passion for education has been demonstrated by his role in founding the Middle Eastern Endovascular Therapy Symposium.
It was founded in 2017, and it's hosted in Cairo, Egypt. It is the first, true regional IR and endovascular conference. MEET provides a comprehensive IR experience for its attendees through MEET IO, MEET aorta, and MEET stroke.
Subsequently, MEET has funded the Egyptian Board of IR, a two year IR fellowship, with an SIR United States IR curriculum, and SIR AVR board examiners. Dr. Saad is an avid supporter of both the AVIR and ARIN. Not only has he graciously been willing to present for the
organization on many occasions, he was an integral component of the Regional Michigan Chapter success. Those who know him can attest without hesitation that he is a natural educator, and makes tremendous effort to teach his
physician, nurse and technologist colleagues alike. For those reasons and so many more, the AVIR is humbled to have the privilege of honoring Dr. Saad as this year's Gold Medal lecturer. (audience applause) - [Dr. Saad] Well, it's truly a great honor to be here
in front of you, and receive this award, and I really appreciate that from AVIR and special thanks also to Siemens for the support for this organization. Without their support and sponsorship, this actually cannot actually happen.
I learned that by doing the conference in the Middle East that it takes a lot of work and a lot of passion and support from industry to actually support our functions. So I'm truly grateful and truly appreciative. The award is from AVIR. There are ARIN members here as well, so I did not know
that there are nurses here as well. My talk is focused primarily on AVIR but definitely we'll talk about the important role that nurses play. Another thanks that I have to give is to the University of Virginia.
I spent five of my best years at the University of Virginia as a faculty. That is a very special place with very special people that work there. And when I think of special people, I actually think of the techs, the nurses, and the physicians,
in that order, that actually work as a team, and actually help one another, and actually stick it out with one another. And as far as faculty, as far as teaching, it's a very, very special place in my heart. I'm gonna say things about IR techs,
and this is kind of my take on things.
I've been practicing IR, including training, for about over 20 years now. And I've worked in four universities in the United States, one in the United Kingdom, and three in the Middle East.
Over these 20 years, I have seen techs and nurses being treated in different ways. So let's just focus on the United States. Over these years, the techs and nurses were treated in different ways, depending on different schools and different thought processes
by the physicians. I have been to institutions where techs-- and the Michigan techs that are sitting here today have heard this talk before. This is the golden retriever talk. That's what they call it.
I've been to institutions where techs are no more than fetchers. And when I was at Virginia talking to tech students I always told them, when you're looking for jobs, beware of the hook. They told us, "What's the hook?"
and I told them the hook on the wall. That hook on the wall go inside their rooms and look if there's a hook on the wall where they go, where the tech kind of guesses, and in a better communication environment is told what they're planning to do,
and goes and starts putting what she or he predicts what the catheters and gadgets are gonna be for the procedure. Because their role, usually, in that setting is to go fetch. Go get me a cobra.
They run off, go get a cobra and come back. That's the golden retriever kind of treatment. I think, in my personal opinion, that is very old school. It is still carried today, in places that are still hanging onto the old days.
I've been in institutions where techs are, actually on the other extreme, an integral role in the procedure itself. The anatomy, what needs to be done, actually giving suggestions and actually educating physicians as well.
Off the record. They do a lot of education for physicians. I believe the new school, the latter, is actually where you need to be as techs. You have evolved to be an integral profession, involved in procedures, expecting what is next,
understanding the disease process, understanding the anatomical difficulties, and the technical difficulties and the platforms needed. Anticipating what might be next, suggesting what might be next. And I think you have evolved into this very important
and integral profession. As medicine in the United States and around the world gets stressed economically, I think this is actually in nurses' and techs' favor to step up, to be the professionals that they are, to blossom as far as the potential that you are.
Actually getting more involved with physician decisions, and with procedural decisions as well. You are no longer working with the control freak IR that you're not allowed to touch the table, you're not allowed to move the table, you're not allowed to touch anything.
All your job is to go fetch. I don't believe in that and I don't condone that. And I hope this eventually fades out throughout all our institutions. Thank you.
I can't stress, also, the importance of the nurses.
I again, like I told you, I've been in four to five universities in the United States. Uniformly, invariably, the nurses always feel that they're left out. They feel that they're a little bit on the side,
and they're not in the focus of the procedure. And unfortunately that's inevitable because you've got the physicians and the techs focusing on their monitors, while you're focusing on your monitors. They're talking technical plumbing stuff,
you're dealing with medicine. You are the people that are actually taking care and actually doing the medicine in this procedure, okay? You will highlight if there's a problem to the physician but primarily, you are actually taking off of this plane and landing this plane safely.
Taking care of these patients. You are actually the medical core of this procedure. The other guys are just doing the plumbings, okay? So that is very important as well. We need to always stress that. That you are an integral part.
You do feel left out, it's inevitable, because everybody's focusing on something that you're not focused on. If you're focusing on what they're focusing, that's not a good thing, okay? And so it is very, very important that we have
strong nurses, good nurses. Strong personality nurses that actually can step up and speak up when something's going wrong. And we do really appreciate that, especially as physicians as we mature and we actually see the input from all the members of the team.
Thank you very much.
Okay. So I'm gonna talk about splenic artery embolization. And this is a subject, even on the physician side,
on the program side, SIR guests, SIRCE, Middle East, they're giving this talk to talk about, for 15 minutes, splenic artery embolization. And I don't think even the people that are putting the program actually understand as physicians, that this is a really big subject.
This is a diverse, diverse kind of group of procedures, it's not even a diverse procedure. And it all depends on actually... It's not working. Okay. It all depends on what you're treating,
and how you're treating it. This is actually the most important slide of the whole talk. If you want to focus on something, just focus and remember this slide. This is a group of indications for ...
Sorry guys. For splenic artery embolization. It's trauma, splenic artery aneurysm exclusion, NOHAH syndrome, which is splenic steal and liver transplant, HyperSplenism and portal hypertension. HyperSplenism and portal hypertension actually
overlap a lot. They're not synonymous, but they overlap a lot. Commonly, very commonly, when you find portal hypertension there's HyperSplenism, and if there's HyperSplenism sometimes there's portal hypertension, extrahepatic portal hypertension.
And the approach, technically, towards these disease processes, are different. With trauma, which I'm not gonna talk about today, because I don't have enough time for it. Trauma, you are actually going focused on a target area that's bleeding and either embolizing that
specific bleed, or embolizing the vicinity if you can't get to that specific bleed.
Splenic artery aneurysms, you're basically trying to exclude the aneurysm while maintaining as much flow to the spleen as possible. Transplant, liver transplant with splenic steal,
what you're really trying to do is not necessarily block the splenic artery, but just impede the flow in the splenic artery. I'll explain all of these in following slides. HyperSplenism and portal hypertension is actually you're trying to kill parenchyma.
You're trying to reduce the actual splenic bed. You're actually, this is a distal artery, or end artery particle embolization. So this is a whole group of procedures, a whole group of technical strategies of actually treating and so you have to know exactly what you're doing
and why you're doing it. And these kind of-- I'm gonna follow with some technical things of how we proceed with this. So starting off with splenic artery aneurysms. And with splenic artery aneurysms, you'll get a lot of debates on you do a proximal embolization,
you do distal embolization, proximal's better than distal. It really depends. That's a very superficial approach to things. It depends on what the disease process is. So in general, with splenic artery aneurysms,
you try to be as proximal as possible, just proximal to the aneurysm, keeping as much collateral to the actual spleen itself. Okay? It is not a splenic reduction, it is not an end artery embolization.
This you can actually apply these principles you can actually apply to all visceral aneurysms, especially all branches coming out of the celiac axis.
You can do that with the spleen, you can do that with the hepatic artery, for example. So here you've got a splenic artery aneurysm. Yeah. So ideally, what you wanna do with a splenic artery aneurysm is to actually exclude the aneurysm itself while
maintaining maximum flow to the spleen so you don't kill the spleen, okay? The best approach to that, if you can do that, which is not common, actually quite rare, is to actually put a stint graft across the splenic artery, excluding the aneurysm itself,
and letting it thrombose. That's the ideal situation, which is the rare situation. Rarely you can actually do that. This is more common with older people, middle-age to older people. It is also more common with women,
in childbearing or later stages in life age. With age, our splenic artery actually toils and turns more and more, it actually becomes more and more redundant and ectatic, and becomes more coiled. And it's more common to find coiling and difficult anatomy with women as well.
Theories behind that is pregnancies, estrogen, being kind of a relaxant to muscles, and actually causes more ectasia to the splenic artery. So the older you are, the more likely-- the patient is a woman, the more likely there would be actually tortuosities and this makes it very difficult to
put a stiff platform up there for a stint graft to actually cross over and actually purely exclude the aneurysm and maintaining full flow to the spleen
Next approach, which is the most common approach and the most technically feasible approach usually is to actually cross the splenic artery,
go distal, coil embolize the spleen, splenic artery distal to the aneurysm and then pull back and coil embolize proximal to the aneurysm itself and that's the most common one and that's the most technically feasible because you can do that with more flexible, lower platforms with microcatheters and catheters.
With younger physicians, I'm gonna show you a procedure. You will find that they're actually coiling in the aneurysm itself and putting a lot more coils in the aneurysm itself, which there's nothing wrong with that, you're just putting a lot-- too much coils in procedure. But ideally, this is what you need to do.
And the reason for that is you need to go as distal as possible in the splenic artery, but just proximal to the aneurysm to provide collateral flow to actually circumvent or bypass the aneurysm and actually continue to revive and keep the spleen alive.
That's basically the whole idea of doing this. The distal embolization is for prevention of back bleeding from these collaterals. So whenever you're embolizing in any celiac axis branch, it's not only the splenic, it's the splenic, the hepatic, the GDA, pancreatic audidenal,
you always have to embolize, whether it's a bleed or an aneurysm, distal and proximal because of all those collaterals and that back bleeding that you actually will pre-fill or re-bleed from the bleed, so this is a typical example where you don't have to go distal to prevent that back bleeding from
filling up that aneurysm. This is an example of a very tortuous splenic artery, with a large splenic artery aneurysm, with an eggshell calcification. So this is the aneurysm here, and what they did was embolize right across the splenic aneurysm from distal
in the aneurysm as well as proximal. And that's the aneurysm kind of excluded.
Sometimes it is so tortuous that we can't even get a microcatheter across, and that's a problem. So what do we do there? In the old days, if you can't do that,
and you can't cross the aneurysm then the best way is to actually puncture the aneurysm self-percutaneously and put coils and thromen through the needle as well. We've been able to reduce the incidence of that by doing the Fong procedure, which is not, it's kind of like a cowboy way of doing it,
but it actually reduces the amount of times that we actually have actually gone to actually percutaneously puncture the aneurysm. What we do is we actually use glue. We actually use a very thick glue. And what we hope for is that we deploy this thick
glue plug and let it run in the aneurysm, go to the distal end and actually plug the distal splenic aneurysm-- splenic artery. And that is basically your distal coil equivalent. And then you put coils or glue to finish it off. And most of the time it works, sometimes it doesn't.
And when it doesn't, sometimes you kill the spleen. They key thing is to make thick, thick glue, okay? I know it's kind of like, 60% of the time, 100% of the time it works, or something like that. But it's pretty hairy, but we've been able to do that with minimal complications.
A thick glue, 1:1, fire it as a plug, it rotates through the aneurysm, goes distally, and then you actually coil it or glue proximally. This is an example of that. Large aneurysm. This is actually the inflow artery in the red arrow,
the outflow artery out of the aneurysm is the other red arrow, the smaller arrow at the top. And then there's another branch sneaking proximally around the aneurysm, not involving the aneurysm going to the spleen. That's good.
That's a good sign. There's a nice collateral that can grow, that actually can revive the spleen if you take out most of the spleen. That's the distal pancreatic tail. We were unable to cross this aneurysm. In fact we were barely into that aneurysm.
What we did was just deploy that thick glue. Sorry guys, it's not working for me here. This is what we have. This is actually that little piece of glue is actually in the distal outflow artery, okay? And the rest of it, this is actually in the inflow artery,
and we basically excluded this with just purely glue, without any coils. This is the kind of follow up imaging of the patient with an excluded aneurysm and a largely live spleen by actually excluding it this way.
This is another example. This is a complex aneurysm. This is an aneurysm that's actually involved the common trunk of the SMA and the splenic artery. So we can't embolize the splenic artery. That's not a good thing.
This shows you a lot of teaching points, a lot of technical teaching points about the management of these complex aneurysms. So this is a complicated... This is a complicated aneurysm. It involves the common trunk of the SMA and the celiac axis.
So the plan is, we need, going down low, is actually the SMA, so what we need to do is to embolize the splenic artery, proximal as possible, okay, to allow as much collateral as possible to go to the spleen. Do a stint graft from the aorta into the SMA to exclude the aneurysm and then thrombose it.
The embolizing material in this case, plugs, it could be coils as well, would do the same principle of preventing back bleeding into the aneurysm. So you're kinda seeing all these principles being put together in this complex procedure.
So the first thing, we went up to the splenic artery and we embolized it with plugs, okay and that's kind of embolized, and then we went into the SMA and put balloon expandable stints and excluded the aneurysm. Here you see the aneurysm with the eggshell calcification,
see this anatomy perfectly, almost on the dead lateral. We put the stint grafts. On our follow up CT, the aneurysm had shrunk partially thrombosed, but still there is still more flow in the aneurysm. So this most likely kind of like a type 1 endo leak
into the aneurysm. The patient was on Plavix and on Aspirin. So technically, what you can do is to put another stint proximally and close that kind of type 1 endo leak. What we chose to do is actually stop the Plavix and stop the Aspirin, just stop it,
'cause they're anticoagulants, stop it for a month and follow up CT. That helps actually thrombose it. Okay so instead of subjecting a patient to another procedure, you just stop the Aspirin and Plavix for a month. Maybe that's enough to help it thrombose.
Then resume the Aspirin and Plavix, and that's all we needed to do is just stop the Aspirin and Plavix. Kind of several technical and medical teaching points
in that case. The next subject, which is splenic steal syndrome, which is a very complex subject.
Splenic steal syndrome, or NOHAH, that's non-exclusive hepatic artery hyperprofusion basically means that the hepatic artery's open, but there's slow flow in it, so it's not anatomical. This is a hemodynamic problem. It is not an anatomical defect.
It's not a thrombosis, it's not an aneurysm, it is not a stricture, it is not a kink. The artery is a wide open pump, but flow is going through it very slowly. The idea on this is to go as proximal as possible and is to impede flow, slow down the flow,
not necessarily shut it off, but slow down the flow significantly. Go proximal as possible to allow collaterals to keep the spleen alive. It is not a splenic artery embolization where you use particles.
And the etiology of this is numerous, it's diagnosis of exclusion, it's diagnosed in less than 1.5% of liver transplants in the United States and Japan. For some reason it is diagnosed at 25% in Germany, so somebody's overcalling it and somebody's undercalling it.
Over the years, I can tell you, 10 years ago, most transplant surgeons in the United States did not believe in it. Now they're believing it more and more, they're calling it more and more. It probably is happening in 1-2% of transplants
in the United States, not 25%. This is a perfect example where the hepatic artery is open, the hepatic artery is so slow that the actual splenic vein catches up with it. The splenic vein actually catches up with the flow in the hepatic artery.
That's how slow and stagnant that hepatic arterial flow is. Your differential diagnosis is a fistula. It's that there's a fistula between the hepatic artery, that's kind of differential diagnosis. However, this is truly a splenic phase. You see the spleen.
Contrast has gone right through the spleen up, down the splenic vein and caught up with the hepatic artery, so this is a true, slow flow in the hepatic artery in a transplant. Initially, we thought that the best way to deal with this is to actually embolize the spleen and there are two types.
There's a GDA spleen, and a splenic artery steal. So there's a GDA steal, which is even rarer, and a splenic artery steal. So initially we thought that the best way to deal with this is just to embolize the spleen, because this is splenic steal.
The spleen is stealing flow from the hepatic bed. Simple, simple thought process. Embolize the spleen, or embolize the GDA in case if it's a GDA. But it's actually a lot more complicated than that.
This is basically kind of your anatomy in hemodynamics.
Celiac axis gives supply to the spleen, gives supply to the hepatic artery, and there's increased flow to the spleen for some reason. Then flow goes back from the gut and spleen back to the hepatic graft by the portal vein. This is kind of your general circulatory
kind of hemodynamics. What the Japanese for years have been talking about was a small for size graft, a completely different syndrome, called small for size graft. In other words the liver is actually too small
for the amount of portal flow that's coming to it. It's an undersized graft. So for example, a transplant in a kid put in an adult. The liver is too small for the amount of portal flow that's actually coming at it.
And what they found out was that there was slow flow in the hepatic artery as well, and they didn't know how that went about. So for years, the Germans were talking about splenic steal, and the spleen is stealing blood flow, the Japanese were talking about
there's a small size graft and there's increased portal flow, but as a coincidence we're looking at hepatic or slow arterial flow. Then, kind of the Americans came along and actually put it all together for them. This is probably a constellation of syndromes and problems
that are occurring at the same time. One can predominate, one can be the only sole problem, or it could be a group of problems. What happens when you increase flow to the liver by the portal vein, there is actually something
called the HABR, the hepatic artery buffer response. This is a partly-reciprocal, poorly understood relationship between the portal vein and the hepatic artery. If you increase portal flow to your liver right now when you eat, if you take a big meal,
portal flow will increase to your liver and your hepatic artery's gonna slow down, because 20% of flow to the liver is from the artery, and 80% goes from the portal vein. If you eat a lot, your portal vein flow increases, your hepatic artery compensates by dropping down to
maintain that flow to the liver. That's kind of a partly-reciprocal relationship. So when you put a small graft in a patient, with relatively high flow, too much flow for the portal vein, the hepatic artery slows down. Okay?
So this is not just a steal phenomenon, this may also be a response or a reflex response to a high flow situation. The graft- and just to add a little bit more detail to this- the graft could be small, or the graft could be non-compliant and poor.
A poor graft, as well, can do the same thing. So it could be a big graft that's not functioning that well, and/or stiff, that would do the same thing as well. Okay? So increased portal flow, decreased hepatic arterial flow.
Let me give you another layer of complexity to what's going on with the hemodynamics of this. This is actually a balance of two things: think of it as a pivot or a balance on two aspects. One pivot is on the arterial side of the house. This is actually a balance between the hepatic arterial
resistance and the splenic arterial resistance. Things that would increase the hepatic artery resistance will give preferential flow to the spleen. So it may not be a splenic problem, it could be actually a liver problem. A stiff graft is a problem.
A poor graft is a problem. A huge subcapcillar hematoma in the liver that's compressing the liver, increasing the resistance of the spleen, of the liver, would cause hepatic arterial flow to go towards, preferentially, towards the spleen. So it's a balance between hepatic and splenic arterial beds.
The other side of the house is the veinous side, which is what we talked about a little bit before. It's either the quality or size of the graft versus the amount of portal flow there is. If the portal flow is increased, with a good graft, or is it a poor graft with normal portal flow?
So this is a balance between two things. This is quite a complex procedure. Quite a complex hemodynamics and causes. Be as it may, that's all academic.
The treatment of this is the same. It's to break the cycle.
And the best way to break the cycle is a splenic artery embolization. You embolize the spleen, whether it's gonna be steal, you're emnbolizing the splenic artery. Whether it's portal flow, increased flow, or a liver that can't handle portal flow,
you still embolize the spleen to actually close the circuit and reduce that portal flow coming back to the liver, and both work. So all what I told you as far as the complexity and the reasons is actually academic. The treatment is the same.
It's splenic artery embolization. As proximal as possible, to allow as much collateral. This is what we've done here, where we've embolized the spleen proximally. I'll show you this. This is just after an embolization.
You see numerous collateral left gastric hiploic arcade reviving the spleen. The spleen is alive and well. We've embolized it. This is before and after. This is a true splenic steal procedure,
before and after embolization, frame for frame. Same injection rates, same catheter, same catheter position, same frame rates, no cheating, okay? Frame for frame. You inject, and you actually see initially there's
absolutely no flow in the hepatic artery, now you've got more flow in the hepatic artery, running almost parallel with the splenic bed. You've basically tilted that back towards flow in the hepatic artery, regardless of what the cause is.
Is it a big spleen that's stealing blood? Or is it a graft portal, you know, scale problem? These are just some pretty kind of hemodynamics analysis of what gestalt I just showed you on different slides of increased flow to the liver and decreased flow to the spleen.
Hypersplenism and portal hypertension, which is basically parenchymal reduction. I'm gonna-- how many minutes do I have? 10 minutes? 10 minutes, okay. So this is the other one, which is,
you're not trying to exclude aneurysms, you're not trying to impede flow, you're actually trying to kill spleen. You're trying to reduce splenic volume. This is an end artery splenic artery embolization. Completely different technique.
Completely different inventory except the microcath. HyperSplenism is basically splenomegally with reduction of blood cells. We usually do it for thrombocytopenia but it also could be neutropenia, okay? Neutropenia is actually a double-edged sword.
Sometimes we can't embolize because the white blood cell is so low that it's a high infection rate, so they actually have to boost up the white blood cells for us before we actually do the embolization to try to reduce the risk of infection.
Okay, so even in really bad thrombocytopenia, and there's actually neutropenia, we would actually have to wait. The hemooncologist would actually give drugs to increase and boost immunity, increase the white counts, so we can actually embolize the spleen.
Ideally, old school, you have to embolize at least 60-75% of the spleen. So, old school IRs would actually go in and whack the spleen 70-80%, once and for all. So usually, there are two ways to do this. One way is to actually just go to the splenic artery
and spray the spleen with particles, whether it's gel foam, any form of particles, PVA, embospheres, whatever. Bland particles. And actually just spray the spleen and hope for the best, that 25% of it's still alive.
Okay and you do it, you know, you play it by ear. Embolize a little bit, watch, repeat it and such. That's kind of one way of doing it. And that's also the way that you would actually have to be forced to have to do it if you can't reach the splenic branches.
Another way is to actually take out the lower 70-80% of the spleen, sparing the upper pole, and you usually try to spare the upper pole, because that's the closest to the lung. If there's a lot of pain involved, and there is a lot of pain involved with a spleen,
if the pain is higher up in the upper pole, you get a lot of splinting, they don't take a deep breath in you get atelectasis, you get fever, you get fever along with post-embolization syndrome, which also gives you fever, and now you're kind of in the fog of fevers and is this post-embolization?
Is this atelectasis? Is this splinting, or is it the worst of your fears, which is the spleen is dead and it's liquefied and you're getting infection and an abcess. So what we try to do is minimize the pain with the splinting and the atelectasis by sparing the upper pole.
At least in theory. An interesting paper came out and they actually showed how much of the spleen they took out, and what the results were. So when you take out more than 70%, which is by the book, old school way of doing it,
which is the majority of the IRs that you work with are gonna be doing this. They're gonna be taking a whack of the spleen 70-80%, biting the bullet, and then seeing what happens. You get a 50% complication rate.
Complications could be pain, it could be fever, it could be liquefaction. But you get very good results with neutropenia. Okay? If you do 50-70% you still get pretty good results with lower complications.
If you embolize less than 50%, you get okay response but it's not durable. It's only for six months and you get no complications. So here's my school. Here's the new school. What we do is we actually reach that 75%
but we reach it through two to three sessions. We take it bit by bit. What we do is we do a first session, 25-30%, where we take a whack of the lower pole, not the upper pole, so we can bring them back again. Because if you give it to them at the top,
and they really hurt, they'll never come back. (laughs) So you make sure they come back, at least for another session. Okay, so you take the lower pole out first. Some people, and I'll show you an example,
they'll take the middle portion out first, and then they'll take the lower pole and the last top pole at the very end. But another way is take the lower pole, then you take the upper pole. And then if you need to do some more,
you take a part of the middle portion. Okay, and this is an example of a very large spleen. I'm just running it through for ya. Going for the lower branches, lower pole, to-- actually, sorry, we went for the middle portion first,
this is the example of the middle portion. Took that out. And this is kind of your post. After the first session. Second session we took out more. Which is the lower pole.
Third session, we went for the upper pole and we took out the upper pole. Then we did-- and I'll show you the results, and this is what you see. So first time, it's 100% baseline of the parenchyma, we took it down to 62% residual, 46% residual,
and after the third time we actually brought it down to 25%, no complications, no pain, they keep coming back after a month and a half, and they were very well stabilized. And this is actually the same patients with the results. Platelet counts go up as the splenic volume goes down.
We're taking it gradually, piecemeal, instead of taking just one bite at it originally. The same thing with portal hypertension. I don't have time to talk about portal hypertension, but it's the same kind of technique, the same kind of approach.
It is phased or staged and it's basically going after the parenchyma. Thank you very much. (audience applause)
Any questions? Yes go ahead.
- [Woman] What was the timeframe between each session? - [Dr. Saad] We play it by ear. So it's a minimum of four to six weeks. We do a CT before clinic visits CT make a decision on whether we need to proceed see the patient see how they're doing
how they-- if you take the wind out of 'em then we're gonna give it more time. If we see liquefaction, we'll give it a little bit more time without infection. With kids a lot of them are kids as well we actually work around the school schedule.
So we can actually do it in the summer when they're free spring break so there's a lot of other things that we kind of play along with. But at least four to six weeks. Okay very good. Any more questions?
Any more questions? Okay thank you very much. Thanks. (audience applause)
Disclaimer: Content and materials on Medlantis are provided for educational purposes only, and are intended for use by medical professionals, not to be used self-diagnosis or self-treatment. It is not intended as, nor should it be, a substitute for independent professional medical care. Medical practitioners must make their own independent assessment before suggesting a diagnosis or recommending or instituting a course of treatment. The content and materials on Medlantis should not in any way be seen as a replacement for consultation with colleagues or other sources, or as a substitute for conventional training and study.