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Hello, and welcome to Noon Conference hosted by Modality.

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Noon Conference connects the global radiology community through free live

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educational webinars that are accessible for all and is an opportunity

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to learn alongside top radiologists from around the world.

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Today, we are honored to welcome Dr.

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Brian Midkiff for a lecture entitled Renal Transplants and

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Complications.

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Dr. Midkiff completed his radiology residency at Brown University,

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Rhode Island Hospital, followed by a fellowship in abdominal imaging

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and intervention at Beth Israel

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Deaconess Medical Center.

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He is on the abdominal imaging and oncologic imaging staff at

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UMass Memorial Medical Center.

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At the end of the lecture, please join Dr.

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Midkiff at a Q&A session where he will address questions you may have on today's

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topic. Please remember to use the Q&A feature to submit your questions so we

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can get to as many as we can before our time's up.

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With that, we're ready to begin today's lecture. Dr.

1:00

Midkiff, please take it from here.

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All right. Hopefully, you can see my screen okay. Hi, I'm Dr. Brian Midkiff.

1:06

Nice to meet you. I'll be talking today about the imaging of renal transplants

1:10

and complications.

1:14

Our objectives for today are going to include gaining familiarity

1:18

with basic transplant anatomy and imaging modalities,

1:23

to gain experience with common transplant complications

1:27

and their associated imaging appearances,

1:30

and also to gain knowledge and take a little bit of a deeper dive

1:35

into some of the different subtypes of complications, including parenchymal,

1:38

vascular, and urologic.

1:43

Our outline for today, we'll start by taking a look at a couple of unknown

1:47

cases,

1:48

talk a little bit about the background of renal transplants and our imaging

1:52

modalities, but then really hoping to spend the majority of

1:56

the time talking about common complications that we see with transplants.

2:02

In the big picture,

2:03

transplant imaging is interesting, and it's meaningful patient

2:07

care, and so I'm hoping to share some of the ways that these cases are

2:11

really so engaging and unique.

2:15

So I'll start with this unknown case first, and I'll let you take a look at this

2:19

for a moment while I describe it. So this is a

2:22

grayscale ultrasound image, longitudinal image of a right

2:26

lower quadrant renal transplant.

2:29

And as you take a look here, I'll sort of draw your eyes

2:32

anteriorly to the cystic-appearing area.

2:35

You can see that this area looks pretty anechoic.

2:38

It looks pretty circumscribed and thin-walled and so really

2:42

looking mostly like a simple cystic area.

2:45

The only thing that might give you slight pause is that there's not a significant

2:49

amount of increased posterior through transmission. There's a little bit.

2:53

You can see a little bit of increased through transmission behind it, but not a

2:56

lot.

2:57

And so for evaluating renal transplants, it's always important to do a

3:01

good Doppler evaluation.

3:04

And as you can see here on color Doppler,

3:07

really prominent vascularity in this area, this prominent

3:10

swirling yin-yang appearance, and this was a case of a pseudoaneurysm.

3:16

Let's do another case.

3:18

This is another longitudinal image of a right lower quadrant

3:22

renal transplant. And as you take a look at this, you can

3:26

recognize that it's a power Doppler image, and you may

3:30

be kind of struck by how diffusely

3:33

decreased the vascularity of this transplant is.

3:37

Even on power Doppler imaging, seeing essentially no significant

3:41

flow or perfusion throughout the renal parenchyma.

3:44

So considerations could be something like an arterial thrombosis

3:48

where the entire graft is diffusely devascularized and has no flow

3:52

at all. But when we put the spectral gate out in the parenchyma, we get

3:56

these waveforms, and you can see that there's actually a sharp systolic

4:00

upstroke, but the diastole is very abnormal.

4:03

The flow rapidly drops, the flow reverses,

4:07

as you can see here.

4:09

And these findings are consistent with renal vein thrombosis.

4:15

So let's do one more case before we start.

4:17

This is an axial contrast-enhanced CT image through the pelvis

4:21

at the level of the bladder.

4:23

And as you can see, there's numerous small foci of gas kind

4:27

of tracking and dissecting along the urinary bladder wall.

4:31

There's a little bit of urinary bladder wall thickening.

4:33

There's some adjacent inflammatory stranding on both sides.

4:36

And so this would be consistent with emphysematous cystitis.

4:40

This patient also had a left lower quadrant renal

4:43

transplant.

4:45

And as you take a look at these images, you can see that the gas and the

4:49

infection has ascended into the transplant kidney with this really

4:53

diffusely gas-filled appearance of the collecting system consistent with

4:56

emphysematous pyelitis. And you can also see some urothelial thickening

5:00

and enhancement, and this turned out to be pyonephrosis.

5:05

So that's a couple of unknown cases to kind of introduce the topic

5:09

of some of the variety of things we can see with renal transplant imaging.

5:13

For an introduction to renal transplants, renal transplants are the

5:17

treatment of choice for end-stage renal disease.

5:21

They offer a longer life than dialysis.

5:25

They offer a higher quality of life than dialysis.

5:29

Kidneys are the most commonly transplanted organ worldwide, as

5:33

you can see here,

5:34

accounting for around sixty-five percent of global

5:38

transplant surgeries each year.

5:41

There's around twenty-eight thousand new cases each year in the US,

5:46

and also in the US, kidneys make up around eighty-six percent of the

5:50

national organ waiting list. So a lot of patients involved and

5:54

a lot of cases.

5:58

For a review of basic anatomy, we could talk a little bit about the donor

6:02

and the recipient.For the donor, the left kidney is generally

6:06

favored.

6:07

Surgeons prefer the left kidney because the left renal vein is longer, which helps

6:11

to facilitate surgical anastomosis.

6:14

But in some cases, they may end up choosing the right due to other

6:17

factors. For example, the left kidney may have multiple

6:21

accessory renal arteries, which can make preserving the vascular

6:25

supply more difficult and tenuous, and so in some cases, they may choose the right.

6:31

For the recipient, the kidney is typically placed in the extraperitoneal pelvis

6:35

on the right side, if the right side is available.

6:38

So you can see that in the diagram over here,

6:41

that the kidney is placed on the right with the associated anastomosis.

6:45

You can see the iliac artery, iliac vein, and I'll also draw your

6:49

attention to the ureteral bladder anastomosis

6:53

here. You can kind of see that the native ureters are tucking behind, but that the

6:56

implanted ureter is placed much more anteriorly.

7:01

So that's an overview of anatomy.

7:03

In terms of our imaging modalities, ultrasound is really going to be

7:07

the primary imaging modality of choice.

7:10

Ultrasound has a ton of benefits. Doppler

7:14

imaging offers really excellent vascular evaluation.

7:18

And by vascular, I sort of mean in a

7:22

multifactorial way. You can really assess parenchymal perfusion.

7:26

You can do detailed assessment of arterial flow, a detailed assessment

7:30

of venous flow. So it's a really nice comprehensive evaluation of the transplant

7:34

vasculature. And there's other advantages as well.

7:38

You get a really thorough evaluation of the collecting system.

7:41

Is there hydronephrosis? Is there debris, like infection or blood products

7:45

in the collecting system?

7:47

And then also it's useful for fluid collections.

7:50

Transplant patients often have multiple different fluid collections.

7:54

There may be post-op hematomas, seromas.

7:57

Later on, you can develop abscess.

7:59

So hopefully you can kind of sense here, ultrasound really covers a wide range, has

8:03

a lot of advantages.

8:05

As we're moving into talking about imaging, I do want to mention one important

8:08

consideration, which is to always read the operative

8:12

note. Always. Always read the operative note.

8:16

You'll find that there were complications during the surgery you don't know about,

8:19

vascular anastomosis that were atypical, possible

8:23

complications they may be worried about, and that kind of knowledge is

8:27

going to make your imaging and your reporting much more accurate.

8:30

So definitely recommend reading the operative note in every case.

8:34

So I have an example of that on the image on the right side of the screen

8:38

here. If you were already looking over here, you may have noticed one or

8:42

two slightly atypical things about this image.

8:45

For example, it's labeled MRAs instead of MRA, meaning that

8:49

there's multiple main renal arteries, and so you can see a couple different areas

8:53

of inflow into the right kidney, in this case with two

8:58

main renal arteries.

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This is the kind of detail that you get from reading the operative report.

9:04

So really helpful to be aware of the vascular supply, any

9:07

alterations, and make sure you're not missing something important when you're doing

9:11

your thorough assessment with ultrasound.

9:15

A great second-line modality in multiple different

9:19

ways is CT. And I've got a couple of different kinds of CT

9:23

examinations listed here. For example, CT has really high

9:27

sensitivity for infection, and you can just think about how

9:30

clearly contrast CT shows pyelonephritis, for example, or foci

9:35

of gas or abscess. So CT has a lot of added value.

9:39

But sub-specialized exams can add extra value.

9:42

For example, CT urogram can be

9:45

highly diagnostic and accurate for assessing ureteral leak.

9:49

Is there a leak? Where is it located?

9:51

And doing the delayed phase urogram really shows that accurately.

9:54

Or is there an obstruction or a stricture?

9:57

Where is the ureteral stricture? How long is the stricture?

10:00

CT can really define all that.

10:03

And then there's also CT angiogram, which once you've done your Doppler

10:06

evaluation and you may be worried about an arterial stenosis or thrombosis,

10:11

CTA will give you really gold standard evaluation of where it's located,

10:15

how long that narrowing or occlusion is for interventional radiology

10:19

planning or for surgical planning.

10:21

I've got a couple positive cases on the right here.

10:24

This is a renal transplant artery stenosis.

10:28

Hopefully, you can see right here, this kind of high-grade focal narrowing right at

10:31

the anastomosis of the renal artery with the iliac artery.

10:35

And on the other side here is a venous stenosis.

10:37

This is the renal vein with significant focal narrowing as it

10:41

approaches the iliac vein. So a couple of values of CTA and CT venogram

10:44

here. I'll briefly mention other modalities can be helpful

10:48

as well. For example, a nuclear renogram is sort of

10:52

uniquely able to assess function and excretion if you do a

10:56

30-minute renogram with excretory curves.

10:59

Other modalities can help as well, but with ultrasound as

11:03

first-line and CT as second-line, you have a lot of useful tools at your

11:06

disposal.

11:09

All right. So we've made it through the first couple parts of our outline, saw a

11:12

couple of cases, did some of the background anatomy, and talked about imaging

11:16

modalities.

11:18

And I'd really like to move into sort of the main part, talking about some of these

11:22

complications.

11:24

It can be a complex topic, and I'd like to try to

11:28

organize it in kind of a systematic way that makes it a little bit more

11:31

straightforward. So I'm going to start with a chart first, kind of laying

11:35

everything out.

11:37

So this is sort of an overview chart of a lot of the major

11:41

renal transplant complications.

11:43

These are a lot of the common ones and things that I want to talk about today.

11:47

So if you look across the top, you can see these different columns here.

11:51

These are immediate complications.

11:53

These may be things occurring within one to two days,

11:57

during the first week for sure. Early complications that may occur a few days

12:01

later or one to two weeks, and then later complications.

12:05

So the columns are organized by timeframe.And the rows are

12:09

organized by type. So some of the main categories include

12:13

parenchymal complications of the transplant, vascular

12:16

complications, or urologic complications.

12:20

And so what you can do is you can follow these across, where early

12:24

parenchymal complications might include ATN or acute rejection, later

12:28

one might be chronic rejection or urologic.

12:31

You can see a leak early on, or you can see a stricture later.

12:35

So what I want to do today is go through some of these cases and some of these

12:37

categories, and then I'm going to bring this chart around and show it

12:41

again at the end and really hopefully bring it to life a little bit.

12:45

Now, after we get to see some cases and put it in some context and have

12:49

some mental images to go with it, hopefully, this will kind of bring it to life a

12:52

bit. So this is how we're going to go through it.

12:55

These are the categories we're going to do.

12:56

We'll talk about parenchymal and vascular first,

12:59

and then talk about urologic, which is a little bit more straightforward with

13:03

things like leak or hydronephrosis, and finish up with these last couple of

13:07

categories after that. So let's talk about parenchymal complications

13:11

first.

13:12

ATN is pretty fast. ATN

13:16

is a pretty rapid complication. This is something that's most often going to

13:20

occur two days postoperative, sort of in the two- to three-day range.

13:24

The primary cause is going to be any kind of ischemic insult

13:28

to the transplant.

13:30

It doesn't really matter what the cause is.

13:32

I've got a couple of causes listed here.

13:35

For example, there could be prolonged ischemic time of the kidney before

13:39

it's implanted. That would be one example of an ischemic risk.

13:42

Another one would be increased blood loss.

13:45

You can see here hypotension or blood loss during surgery, which

13:49

could cause decreased perfusion of the kidney, and that could risk an ischemic

13:52

insult. But the common thread is some kind of ischemic insult to the

13:56

kidney that then manifests as ATN after it's implanted

14:00

and after it revascularizes.

14:02

This is a case up here on the right showing some of the findings,

14:05

including decreased diastolic flow.

14:08

You've got this really nice initial systolic upstroke, but then look

14:12

how low the flow is during diastole.

14:14

I've got a couple of slides from this case on the next image as well, and you're

14:18

going to have elevated resistive indices as well.

14:21

Decreased diastolic flow and elevated resistive indices can be seen in

14:25

other entities as well, which we're going to talk about.

14:28

So these findings are most useful, and you can be most accurate

14:33

when you combine these findings with other factors, including the

14:37

patient's risk factors. For example, let's say you read the operative note,

14:41

there was prolonged ischemic time. You know the patient's at risk.

14:45

And then the timeframe, you're seeing this maybe thirty-six or forty-eight hours

14:48

post-op. If the imaging fits the history and the timeframe, you're going to be

14:52

more accurately able to identify ATN.

14:55

So these are the images from that case.

14:57

This patient presented two days postoperatively.

15:00

They had decreased output and elevated creatinine.

15:04

And I'll just let you think about that as a clinical scenario.

15:07

What if I told you decreased output, elevated creatinine?

15:12

And multiple things come to mind. There could be graft dysfunction or

15:15

rejection, but for example, you could get this with obstruction.

15:19

If there was hydronephrosis, it could present the same way.

15:22

So ultrasound's going to be indicated to help sort out some of the differential

15:25

clinical concerns. This patient's ultrasound showed decreased

15:29

diastolic flow, as you can see on the image I already showed you.

15:32

And this is an image out in the parenchyma also showing decreased

15:35

diastolic flow

15:37

and with elevated resistive indices between zero point nine and one point

15:41

zero, which is pretty elevated.

15:44

However, clinically, the main concern was ATN.

15:48

This was two days postoperative. There was concern for ischemia before it was

15:52

implanted, and this was the imaging appearance.

15:55

So the patient was managed conservatively. They waited.

15:59

They did routine follow-up imaging.

16:01

And if you take a look at this follow-up ultrasound three weeks later,

16:04

look at the difference in the diastolic flow.

16:07

It was basically almost like a flat line here, hardly any velocity.

16:11

And now you see this much more robust diastolic flow.

16:14

So the resistive index dropped to a normal level of zero point seven one, and this

16:18

was consistent with ATN.

16:21

So at this point, I'm going to kind of pause for a second.

16:25

I've been throwing around this term RIs, resistive indices,

16:29

and just want to make sure that everyone's kind of on board and comfortable with

16:32

the terms that we're using. So we'll do a brief aside about the

16:36

resistive index. It's a calculable flow parameter derived from the

16:40

shifts during one cardiac cycle. And you're going to be interested in the

16:44

difference between the peak systolic velocity and the end

16:47

diastolic velocity.

16:49

It's pretty simple to calculate.

16:52

You can see the equation is here, and I promise this

16:56

is the only equation in my lecture today, just this one.

16:59

But you can see it's pretty simple.

17:01

Peak systolic velocity minus end diastolic over peak

17:05

systolic.

17:06

It's useful to help assess the resistance in a system, and as

17:10

resistance to flow increases, the resistive index will increase.

17:15

It doesn't identify any one specific pathology, but if you

17:19

have a high resistance system, which could be ATN

17:23

or rejection, or like we saw, it could be renal vein

17:26

thrombosis. If you have a high resistance system, then there's

17:30

need to look further to identify what the cause is.

17:32

So this is a very helpful landmark of possible pathology that's going on.

17:36

So that's resistive index, and there's a normal example here just to help highlight

17:40

that. This was a kidney perfusing very well.

17:43

Peak systolic is fifty-two, end diastolic is twenty, and that

17:47

leads to an RI of point six two. You can plug it into your equation here.

17:51

Peak over end-- Systolic over end diastolic works out to zero point

17:55

six two.

17:57

I thought one or two of you may double-check this, so I actually double-checked

18:01

it myself before I showed it, and it really does work out to zero point six two.

18:05

And the number that you see should match what you're seeing on the imaging.

18:09

This looks like a low resistance system, and when you look at the waveforms,

18:13

sure enough, there's a really robust ample diastolic flow.So those two

18:17

should match.

18:19

All right, so let's move on to the other two parenchymal complications.

18:23

A little bit about acute rejection and a little bit about chronic rejection.

18:27

So acute rejection can also have elevated resistive indices,

18:31

which again, can overlap with ATN, but ATN is a little bit earlier.

18:35

This is going to start occurring a few days later.

18:38

Also, another useful difference is you'll start to see morphologic

18:42

changes in the kidney itself. It can start to look enlarged,

18:46

more swollen, more edematous.

18:49

You can start to get loss of the corticomedullary junction,

18:52

and also kind of a unique appearance where the medullary pyramids start to

18:56

look more hypoechoic or darker. So I'll kind of

19:00

direct your attention to the top image on the right here.

19:02

This is a grayscale image of acute rejection, and you can see the

19:05

corticomedullary differentiation looks kind of unusual.

19:09

The medullary pyramids look kind of unusual, and there's this more hypoechoic

19:12

appearance.

19:14

And then down here is Doppler imaging,

19:16

and you're going to see really decreased diastolic flow and an

19:20

elevated resistive index of around 1.0.

19:23

Really high RI, and this was a case of acute rejection.

19:28

You might be looking at this and thinking, "Hang on.

19:31

Doesn't this really overlap with what I just said about ATN?"

19:35

The decreased diastolic flow, the elevated resistive indices, and yes,

19:39

there's definitely some similarity there.

19:41

So again, it's useful to correlate with other factors. ATN occurs earlier.

19:45

This occurs a little bit later, and typically, as acute

19:49

rejection starts to begin and progress, you'll start to see more of these

19:52

parenchymal changes, and that can help you tell it apart from maybe an initial

19:56

concern for ATN.

19:58

All right, let's move on to chronic rejection.

20:01

And unfortunately, chronic rejection is the most

20:05

common cause of chronic kidney transplant failure.

20:09

The imaging is pretty striking. The kidney will start to look much

20:13

more echogenic. You'll see decreased blood flow.

20:18

This is a nice example up here on the top right, where there's a

20:21

normally functioning and perfusing allograft, lots of color Doppler

20:25

vascularity, next to a chronically rejected one.

20:28

You can see this is more echogenic and sort of what a striking

20:32

difference of the Doppler vascularity.

20:34

Really poor flow and perfusion in this chronically rejected kidney.

20:38

On CT, you may see calcifications, as well as the

20:42

smaller size of the allograft. This is a CT image of chronic

20:45

rejection. You can see it's small, sort of barely bigger than the

20:49

adjacent psoas, and that there's multiple calcifications as well.

20:54

So those are the findings of chronic rejection.

20:57

So let's move into vascular cases next, and I'm

21:01

gonna start by showing an unknown case, let you take a look for a

21:04

second.

21:06

This is a color Doppler image,

21:10

longitudinal color Doppler image of a right lower quadrant renal transplant.

21:14

And whereas you can see really robust color flow at the upper

21:17

polar and inter polar areas,

21:20

you're probably struck by how decreased and essentially totally

21:24

absent flow is here to the lower pole.

21:28

And so this appearance is consistent with a segmental infarct in a

21:32

transplant kidney.

21:35

So for vascular complications, there's a couple of different arterial ones that are

21:39

gonna be important for us to cover, thrombosis and stenosis,

21:43

as well as things like pseudoaneurysm, like that case we saw earlier,

21:48

and a couple of venous complications as well, including thrombosis.

21:51

So let's talk about arterial thrombosis first.

21:55

Renal artery thrombosis is an early

21:58

complication, with the majority occurring during the first week, even as early as

22:02

24 to 48 hours.

22:06

When I first learned this, I found this really counterintuitive,

22:10

I don't know if anybody else might be feeling that way, where

22:14

we're talking about thrombosis occurring before stenosis.

22:18

And one would think you would start with stenosis first.

22:20

The stenosis would narrow, it would progress, and it would basically progress

22:24

to thrombosis.

22:26

With transplant imaging, it's totally backwards.

22:30

Thrombosis occurs first, often due to injury to the

22:34

artery during surgery. For example, there was a small surgical

22:37

injury. There was an intimal flap that ultimately led to a thrombosis.

22:41

There's focal kinking. But thrombosis is an earlier

22:45

complication, and stenosis comes later.

22:49

Patients will have a sudden onset of anuria,

22:52

as basically the whole kidney no longer has blood supply.

22:55

You'll have acute renal failure, pain.

22:59

Arterial thrombosis is overall the most common vascular

23:03

cause of loss of the transplant,

23:06

and it can be segmental, as we saw in this case over here, or it can

23:10

be complete.

23:13

So these are two positive cases, and these are both on power Doppler imaging.

23:17

And really, you're gonna notice a total absence of flow

23:21

within the graft. You can see on power Doppler imaging, both of these kidneys

23:25

show essentially no flow throughout whatsoever.

23:28

Total absence of any arterial venous flow and no detectable

23:32

waveforms.

23:34

Now, it's possible you might be looking at these images and thinking about the case

23:38

I showed earlier of the renal vein thrombosis, which also

23:42

had really no significant flow in the kidney.

23:45

And the difference there is when we did waveforms in the parenchyma, we did get a

23:49

systolic upstroke, and then we got that reversal of flow in diastole.

23:52

So there were findings on spectral Doppler.

23:55

That's not really gonna be the case with arterial thrombosis.

23:58

With no arterial inflow, there will be no systolic upstroke and

24:02

no flow, and kind of as it says here, typically, really no detectable

24:06

waveforms in the transplant itself.

24:09

So that's renal artery thrombosis.

24:12

Stenosis, as I mentioned, occurs a bit later.

24:14

It's usually more delayed than thrombosis,

24:17

most frequently occurring around three to six months

24:20

postoperative.It's not rare. It can occur in more than

24:24

10% of patients, and the most often site is at the

24:28

anastomosis, which is around 50% of cases.

24:31

This is an example case here on the right.

24:34

And as you take a look at this,

24:36

couple of things might catch your eye.

24:39

First of all, there's really markedly elevated velocities.

24:42

Check out the velocity here of over 600 centimeters per

24:45

second. You can also see an artifact here called aliasing,

24:49

and that's when really high velocity flow can be incorrectly displayed

24:53

as reversed, this little sort of blue area in the middle of the orange.

24:58

High velocity flow aliasing, and this is going to be concerning for renal

25:01

artery stenosis.

25:04

So talking about stenosis,

25:08

there's an important consideration I kind of want to highlight, which is that

25:12

stenosis can look a couple of different ways depending on

25:15

where you image. If you image at the area of the stenosis

25:20

or if you image more distally, you can see different imaging appearances.

25:24

At the stenosis, you're going to see really elevated velocities

25:28

like we just saw,

25:29

200 to 250 centimeters per second or higher, and you may see

25:33

aliasing or other things like spectral broadening.

25:37

Spectral broadening is when the area under the curve gets filled in due to really

25:40

turbulent flow.

25:43

A helpful way to help increase the accuracy is also to compare to the

25:47

flow in the adjacent iliac artery.

25:49

So if your main renal artery is more than double the velocity, a

25:53

ratio of more than two compared to the iliac artery,

25:57

that's going to increase your sensitivity and accuracy for stenosis.

26:01

So if you take a look at the images on the right here, I've got a couple different

26:04

labels on these.

26:06

You can see the top image is the main renal artery, and the lower image is the

26:09

iliac artery. And you can kind of compare the velocities for

26:13

yourself and take a look at the difference.

26:16

In the renal artery, we're seeing over 400 centimeters per second,

26:20

whereas in the iliac it's under 100.

26:23

So over 400

26:25

over a number of less than 100, your ratio is going to be higher than four,

26:29

really, really elevated in this case of renal artery stenosis.

26:34

So these are the findings if you're looking at the area of narrowing,

26:38

but it can look completely different if you image distally, and

26:42

this can kind of help increase your accuracy because you might identify these

26:45

findings at different points. What if we look distally?

26:48

If we look distally to the stenosis, you're going to have really diminished flow,

26:52

and that's because there's this upstream bottleneck where the blood flow is really

26:56

narrowed at the stenosis with decreased blood flow getting through.

27:00

So you're going to see lower velocities and dampened waveforms if you look more

27:04

distally. And so this is what's called Tardus Parvus

27:08

waveforms, and you can see the definition here.

27:11

Tardus refers to the prolonged slow systolic upstroke,

27:15

and Parvus is this diminished or rounded peak.

27:18

So here's a couple cases here, and I'll draw your attention to this case first.

27:22

Think about what a systolic upstroke should look like.

27:26

You should have a spike. You should have, like, a really towering high

27:30

vertical spike during peak cardiac contractility as

27:33

systole gets underway. Instead, you see this kind of gradual incline,

27:37

almost like at a 45-degree angle. That's too slow.

27:41

That's delayed. And then additionally, these peaks are kind of like dampened

27:45

and sort of rounded and blunt in these lower peaks, and it's reflected in the

27:48

measurements here. You're seeing lower velocities around 20,

27:51

and so this is a Parvus-Tardus waveform.

27:55

Let me show you another one over here as well.

27:57

This is quite a similar example. Where is the high

28:01

systolic peak? You don't see it at all.

28:04

You get these kind of sort of undulating, rounded appearances as you

28:08

go. So when I was first learning the appearance of Tardus

28:12

Parvus and I looked at this, I thought it looked kind of like, almost like

28:16

rolling hills.

28:18

And I don't know if anyone may be a fan of the "Lord of the

28:22

Rings" movies or books, but when I see what looks like

28:26

rolling hills, it kind of reminded me of the Shire.

28:29

That was actually how I learned this.

28:31

And hobbits, they sort of live in these dwellings that are carved into these

28:33

rounded hillsides.

28:35

If you're not familiar with the Shire,

28:38

this is the Shire. And if you take a look here, you can see these sort of rounded

28:41

houses they live in that are buried under the ground.

28:44

If they're kind of hard to see here, you can see these little chimneys coming out

28:47

the top. Here's a couple of sort of close-up views.

28:50

But look at this sort of rounded dome shape with, like, a gradual

28:54

slope and no peak. So you can take a look at this shape and kind of compare

28:58

it to here. I don't know if that may help anyone remember Tardus Parvus, but it

29:02

helped me when I was first learning.

29:05

All right. So let's move on to a couple of other vascular cal-- complications.

29:09

First thing to talk about is pseudoaneurysm.

29:13

So these are most often discovered around one to three months

29:16

post-transplant. But technically, they can really occur

29:20

at any later time as well. One of the main risks is the number

29:24

of biopsies that these patients get.

29:26

If they're worried about acute rejection, if they're worried about chronic

29:28

rejection, these patients actually often undergo frequent biopsies of the

29:32

transplant, and that's going to increase the risk of pseudoaneurysm.

29:35

So they can also occur,

29:37

as you see here, months or even years later,

29:41

and they can be related to inflammation at the suture line or secondary to prior

29:45

biopsy.

29:46

The risks of pseudoaneurysm are really

29:50

significant. They can dilate, they can enlarge, and they can

29:54

rupture, really resulting in catastrophic hemorrhage.

29:58

And there's a sample case here. You can see this really swirling,

30:02

really prominent vascularity with that yin-yang appearance consistent with

30:05

pseudoaneurysm. And I want to actually show you a little bit more about this case

30:09

on the next slide.

30:11

So this was a case that was discovered on an

30:14

incidental three-month follow-up ultrasound.

30:18

The patient came in for routine three-month imaging, and this is what we saw

30:22

first on the gray scale. We saw this rounded area.

30:25

And kind of like the earlier case, it's pretty

30:28

anechoicIt's pretty circumscribed and thin-walled, and

30:32

I actually think this shows even better posterior increase through

30:36

transmission. Look how bright the ultrasound signal is back here.

30:40

But we put color Doppler on, and look at the amount of vascularity.

30:44

Patient went to CT angiogram. You can see here on the axial contrast

30:48

enhanced CT, this is the pseudoaneurysm,

30:51

and this is a coronal MIP image. And these images show

30:55

that it was arising at the vascular anastomosis just

30:59

outside of the kidney. This was extrarenal.

31:03

Talking a little bit more about pseudoaneurysm, this is the case I had shown

31:07

earlier. So these can be intrarenal, like this case,

31:11

or extrarenal, like the last one I just showed.

31:14

They can appear as a simple cyst or a little bit of a complex

31:17

cyst. And if I could make

31:20

one teaching point, if I could say one key thing, it would be that

31:24

evaluating any cystic area within or around the

31:27

transplant with color Doppler is the key.

31:30

You see a rounded thing, you see an anechoic thing, you see an area of

31:34

fluid, Doppler, Doppler, Doppler.

31:36

Make sure it's not a pseudoaneurysm in the kidney or next to the kidney, just like

31:40

these cases.

31:41

And then when you do, we kind of talked about the classic appearance already

31:45

with this really prominent swirling yin-yang vascularity internally.

31:49

This case ended up going to IR for treatment,

31:52

and here's images from that. You can see where the pseudoaneurysm was.

31:57

The coil occluded the neck, and you're kind of left with a small

32:01

segmental infarct, but the rest of the graft was otherwise preserved.

32:07

So let's do another unknown case as we go forward

32:11

here. So top image is a grayscale image, and the

32:14

bottom image is color Doppler.

32:18

And probably the first thing you're noticing is on the color Doppler image,

32:22

these really prominent tubular structures with a really

32:26

significant amount of color Doppler flow and vascularity,

32:30

almost like a tangle of vessels. And if you're looking at this and thinking

32:34

about arteriovenous fistula or AVF, you are

32:37

exactly correct. These are surprising in terms

32:41

of how often they can be occult on grayscale imaging.

32:45

If you're looking up at this image, which is the same interpolar area, it doesn't

32:49

really look that bad.

32:51

These can be much more apparent on color, and they can be kind of occult on

32:54

grayscale, especially if they're small.

32:56

So once again, there's the point of doing a really good color Doppler

33:00

evaluation of the kidney.

33:03

So the most common cause of AVF is going to be iatrogenic, which is

33:06

biopsy. These are relatively common, occurring in around 10% to

33:10

20% of patients.

33:13

The good news about AVF is that the

33:16

majority will close spontaneously.

33:19

Actually, around 70% heal spontaneously,

33:23

and only around 30% will persist. The ones that persist

33:27

can manifest a few of the different symptoms that I've listed here.

33:31

You can see some of the ways that they can present.

33:34

Really large ones, for example, could potentially increase the risk of high output

33:37

heart failure from a really large AVF.

33:40

But if I could just pick one symptom, it's the hematuria.

33:44

Gross hematuria

33:47

is the most commonly associated and what you'll most often see with these

33:50

cases.

33:53

This is a couple of other cases. I mentioned earlier, these can potentially be

33:57

pretty occult on grayscale, and this one down here is a good example of that.

34:02

You can see, for example, that on the grayscale, there's really no discernible

34:06

abnormality toward the lower pole.

34:09

But if you take a look over at color Doppler images, this is a longitudinal

34:13

image and a transverse image, you can see really, really prominent

34:17

marked vascularity at the lower pole in this case of AVF, but

34:21

hard to see on grayscale. So a good Doppler interrogation to

34:25

identify these is really going to be key.

34:27

You'll see high velocity flow. If you're able to actually identify the

34:31

draining vein, you can see arterialized flow in the draining

34:34

vein. So the case up here on the right

34:39

is kind of a smaller central AVF, but I wanted to show it

34:43

just to sort of highlight the flow dynamics.

34:46

First of all, look at the systolic velocity.

34:49

You're pushing around 300 centimeters per second.

34:52

Really, really high velocity flow.

34:55

But what's maybe just as interesting is what happens during diastole.

34:59

The velocity hardly goes down at all.

35:01

And if you can sort of see where this peak of systole is hitting around 300,

35:05

it goes down just a little into diastole, and diastolic flow is coming in at

35:09

around 200 centimeters per second, even through

35:13

diastole. So this is really, really, really

35:17

robust, hypervascular, prominent flow, in this case of

35:21

AVF.

35:23

So as we wrap up talking about vascular complications, I

35:27

did want to touch on venous also. This was the case I showed

35:30

earlier of renal vein thrombosis.

35:33

In these cases, you'll also see significantly elevated

35:37

resistive indices. There is going to be high vascular resistance,

35:42

and maybe if you think about it, this isn't really much of a surprise.

35:45

You've got a total outflow obstruction.

35:48

No blood can leave the kidney. It's swollen, it's backed up,

35:52

it can't empty, and you're trying to force more blood into a system that's

35:56

already swollen and can't drain. So that's going to be a really high resistance

36:01

system, and you're going to see these kind of waveforms here.

36:04

Low diastole, reversal during diastole.

36:07

If you can get good images of the main renal vein, you'll also see

36:12

the thrombosis. You'll see loss of flow in the main renal vein, and the kidney

36:16

can also start to sort of swell and become enlarged

36:19

just due to the increased blood volume that it can't empty.

36:23

So I want to show you another case here about the renal vein for a moment.

36:28

This was a patient where concern about the renal vein was first

36:31

identified on the Doppler imaging.

36:33

So I'll draw your attention to the Doppler images firstAnd taking a look,

36:37

you can see the arterial flow during systole

36:42

looks pretty good. This is a sharp upstroke.

36:45

Your velocities are pretty good. You're hitting up around 60 centimeters per

36:48

second, so the initial systolic arterial inflow looks pretty

36:52

good. But diastole is a different story.

36:55

It drops very rapidly, diastolic flow is low, and then

36:59

look at the second half of diastole.

37:01

There's essentially no flow during the second half of diastole, and you're seeing

37:05

that on cardiac cycle after cardiac cycle.

37:08

So this was interpreted as concerning for possible renal vein pathology,

37:12

concerning for maybe a really high-grade stenosis,

37:16

or a developing occlusion based on these findings.

37:19

And look at the resistive index of 0.97. Really, really elevated.

37:24

So the patient went to CT venogram,

37:27

and I want to show you a couple of coronal images from the CT venogram.

37:31

And you can see a really large amount of thrombus throughout the renal

37:34

vein. And unfortunately, this was actually quite extensive.

37:38

It went from the renal vein through the external iliac vein.

37:42

It went all the way up the common iliac vein, all the way to the

37:46

insertion with the IVC. So really, really prominent case of venous

37:50

thrombus that was first questioned based on the Doppler

37:53

findings.

37:57

All right, so

37:59

I want to tell everybody great job.

38:01

We've made it through a lot of complications so far.

38:03

We covered these different parenchymal complications, different vascular

38:06

complications,

38:08

and so we'll move into some of the later ones here.

38:10

These are a little shorter and a little bit more straightforward, talking about

38:14

urologic and a couple of other complications.

38:17

The goal is really to give an overview of all the things that can be commonly seen,

38:21

so we'll touch on urologic and these other ones as well.

38:25

So ureteral leak is an early phase complication,

38:29

typically going to be most common during the first one to two

38:33

weeks. The most common site where you're going to see it is

38:37

right at the anastomosis, right where the ureter is implanted on the

38:41

bladder. This is typically due to distal ureteral

38:45

ischemia.

38:47

That's the most common cause, but there's other causes as well.

38:50

For example, there could be technical error at the site of the

38:54

anastomosis, an incomplete seal or suture

38:58

failure. So there's different causes, but a common thread here

39:02

is they all occur at the anastomosis.

39:04

Whether it's ischemia, whether it's suture failure, you're going to want to look

39:07

closely. I had mentioned earlier how the ureteral

39:10

implant is more anterior toward the front of the bladder, and so these cases

39:14

I'm going to show you are going to show leaks in those locations.

39:17

This was a patient that had a kidney transplant on the left, and you can see

39:20

extravasation just anteriorly, right from that anastomotic

39:24

site.

39:26

So this was a positive leak on the left side.

39:29

This other case is a positive leak on the right side, but you can sort of

39:33

see how it's that same characteristic location. It's anterior.

39:37

It's at the ureteral anastomosis.

39:39

You can see extravasation here on the axial image.

39:42

This is a sagittal MIP image. They were trying to treat the patient

39:45

conservatively with a stent, hoping this would heal and close, but you can see the

39:49

extravasation on that sagittal image as well.

39:53

Other ways to diagnose

39:56

this can be clinical.

39:58

For example,

39:59

you can aspirate fluid and send it for creatinine.

40:02

That's going to be accurate as well.

40:04

But doing a good CT urogram protocol, you really need

40:08

nice delayed phase imaging, giving time for it to go through the ureters, fill

40:12

the bladder, and leak. A good delayed phase CT urogram is going to be

40:16

highly sensitive and also really show you anatomically the

40:20

exact site of concern.

40:22

So that's ureteral leak. Let's talk a little bit about hydronephrosis.

40:27

What are some of the causes, and how much should you worry when

40:31

you see that a transplant has dilation?

40:34

So there can be a couple of initial early causes and then other

40:38

causes that can develop over time.

40:41

So the early causes include ureteral edema.

40:44

This can occur really in the immediate postoperative period.

40:47

If there's focal swelling at the anastomosis where they attached it, focal

40:51

edema can narrow the lumen, and it can cause upstream

40:54

dilation. You can get blood clots or debris in the collecting system,

40:59

chemonephrosis, kind of clogging it up, and those can be some early causes

41:03

as well.

41:04

Other causes can develop more over time.

41:06

For example, fluid collections can really compress the ureter,

41:10

and fluid collections are a cause of ureteral obstruction and

41:14

hydronephrosis. These can be early or late.

41:17

For example, a postoperative hematoma or seroma,

41:21

or after that, a collection like an abscess.

41:24

Other late complications, late causes of

41:28

hydronephrosis include developing a ureteral stricture.

41:32

That's not going to be an early one. Those take time to develop.

41:35

So talking about hydronephrosis, let's look at one or two

41:39

cases. This is an axial CT image on the right.

41:42

This was a non-contrast CT, and you can see a large

41:46

loculated fluid collection, which turned out to be a urinoma.

41:49

But this is really the fossa where the transplant should be

41:53

sitting. Because this is loculated, you can see the mass effect.

41:56

Look how the kidney is sort of pushed far posterior.

41:59

It's pushed against the psoas, it's pushed against the sacrum, and

42:03

there's hydronephrosis because this collection compressed the ureter.

42:07

So fluid collections can cause hydronephrosis as well, and this was

42:10

caused by a urinoma.

42:13

Moving into other late phase causes.

42:17

I mentioned other collections. For example, lymphocele can develop later.

42:21

And so if we take a look at this longitudinal grayscale image,

42:25

you can see hydronephrosis in the transplant kidney, and then there's this

42:29

collection, which is a sort of a circular collection.

42:32

If you could imagine kind of a donut shape, it's wrapped around the

42:36

ureter, and you can see the ureter just going into here and then disappearing,

42:39

getting compressed, causing hydronephrosis secondary to a

42:43

lymphocele.As transplant kidneys

42:47

survive longer and last longer, they can also potentially develop

42:51

routine complications. So the image on the right is hydronephrosis

42:55

in a kidney that was obstructed by a calculus, so of a more standard

42:59

cause. And you can see here this calculus starting to migrate towards the

43:02

proximal ureter, causing upstream hydronephrosis.

43:06

You can also see the really nice sort of dark shadowing here behind this calculus,

43:10

confirming that it's a stone.

43:13

And then there's one more late-phase cause of hydronephrosis that I want to

43:16

touch on, which is stricture. Let's talk about that for

43:19

a minute. So this is a case of ureteral stricture,

43:24

and this is kind of a coronal oblique MIP

43:28

image, kind of meant to show the stricture in plane.

43:31

So you can see the stricture here, this sort of area of long segment

43:34

narrowing,

43:36

causing upstream dilation, upstream hydronephrosis.

43:39

This is a later complication. Patients can have pain or decreased

43:43

function due to the kidney being unable to empty properly.

43:47

This is also most often due to ischemia or due to

43:50

suturing as well. This is an example of what a ureteral stricture can look

43:54

like.

43:57

All right. Let's start to move towards our final section of complications here.

44:01

Last couple things we want to talk about.

44:03

And so I'm going to talk about fluid collections, and I left this slide

44:08

blank at first as kind of a self-test.

44:11

So I'll ask you, as we've been going through these slides, we've

44:15

talked about a few different kinds of fluid collections.

44:18

We've mentioned a couple different kinds.

44:20

So can you name two or three of the collections that we've looked

44:24

at?

44:25

Can you name maybe four different collections?

44:27

What's some of the usual suspects we're going to be worried about around the

44:32

kidney in a post-transplant patient?

44:35

And so I'll pull up a representative list for you here.

44:38

These are some of the main ones that we're worried about.

44:41

These are attempted to be organized by timeframe.

44:45

So things like hematoma and seroma

44:48

might strike you as really early postoperative complications.

44:51

Those are going to be very early. As you start to move a few days

44:54

postoperative, things like a urinoma can develop or abscess can

44:58

develop, and then longer-term things like lymphocele, which can take

45:02

weeks to months.

45:04

So I mentioned these are the usual suspects.

45:07

If you can take a look at the first letters of these words,

45:12

it spells out HUSUAL, and HUSUAL

45:16

is not a word. I know it's not a word, but this was as close as I could get it to

45:19

the usual suspect, and this was kind of the way that helped me learn and remember

45:23

these. If you can remember the HUSUAL suspects, this helps you

45:27

organize possible collections for your differential diagnosis,

45:31

kind of sorted by time, what's earlier and what's later.

45:36

So let's talk about a couple of these collections in a little bit more detail.

45:40

First, we could talk about hematoma.

45:42

These are classically going to be hyperdense on non-contrast CT.

45:46

You can see the image on the right,

45:48

really prominent case of hematoma.

45:51

There is a lot of blood products in front of the kidney, under the kidney,

45:55

and there's this really, really large hematoma wrapping around the back of the

45:58

kidney, sort of extending well up the retroperitoneum, large volume of blood,

46:02

in this case, a retroperitoneal hematoma.

46:06

On CT, hematomas classically look more echogenic

46:10

internally.

46:11

That can evolve with time. Older hematomas can start to look more hypoechoic,

46:16

but they're going to pretty consistently have no internal Doppler flow.

46:20

So I want to talk a little bit more about hematoma with a couple of sample cases

46:24

on the bottom here. Hematomas can sometimes occur in

46:28

certain locations that are more concerning, and a great example of that is

46:32

a subcapsular hematoma. So if you take a look at this first case here,

46:37

you can see this sort of echogenic, complex-appearing collection.

46:40

The hematoma is sort of really following the posterior

46:44

outline and contours of the kidney.

46:45

It tapers at the upper pole, tapers at the lower pole, and has this really

46:49

thickened appearance. But if you take a look at the underlying allograft, take a

46:53

look at the transplant, it's getting compressed.

46:57

The back of it, you can actually see here, is indented.

47:00

So this kidney is starting to get compressed, starting to get squished,

47:04

and when you look at the same case with Doppler imaging,

47:07

we can see, once again, decreased diastolic flow

47:12

and elevated resistive indices. So not surprisingly, you're

47:15

looking at a high-resistance system.

47:18

You're crushing and compressing your kidney.

47:20

It's going to make it harder to force blood flow into a kidney that's being

47:24

squeezed like that. And so these are examples of subcapsular hematoma.

47:27

There's another one here on the right.

47:29

This is another subcapsular hematoma, once again, kind of like deforming

47:33

and indenting the posterior aspect of the kidney there.

47:36

So that's hematoma.

47:39

Let's touch on urinoma briefly. This case on the right is the CT that I

47:42

showed you earlier. Patients with urinoma often have

47:46

decreased urine output and swelling as the urinoma starts to enlarge or

47:50

expand, and they'll also have a rapid rise in

47:54

creatinine as well.

47:56

I did want to show one nuclear medicine image.

47:58

So that's the bottom left image here. This was a nuclear renogram.

48:01

You can see there's a right lateral projection and an anterior projection,

48:05

and this is extravasation of tracer sort of near the upper pole,

48:09

coming out superiorly and then tracking laterally around the kidney as well.

48:13

And this was a urine leak that formed a urinoma.

48:17

And one more fluid collection to touch on

48:20

is lymphocele. I mentioned this can occur a bit later.

48:24

If you sort of take all fluid collections over time,

48:28

lymphocele is overall the most common.

48:31

It typically occurs four to eight weeks postoperatively, but they can

48:35

occur much later, even months or years later as well.

48:40

Not surprisingly for lymphocele, it's going to be caused by damage

48:44

to lymphatics, transection, inadequate ligation

48:49

of the iliac lymphatics during surgery.Unfortunately,

48:53

these tend to recur after aspiration.

48:56

You can see these really large fluid collections on this coronal CT here.

48:59

This was a lymphocele. And you might hope that aspiration would be curative.

49:02

You could take the fluid out, reduce the mass effect.

49:05

But unfortunately, they do tend to recur.

49:07

Patients often need sclerotherapy, or surgery for

49:11

definitive treatment.

49:14

All right. So let's move toward our final unknown case.

49:20

This is a grayscale image, and I'll let you take a look for

49:24

a second.

49:25

And as you start to look at the image, you notice that the anterior part

49:29

looks pretty normal. There's good cortical fitness, good cortical

49:33

echogenicity, but it's a different story posteriorly.

49:36

You have these ill-defined echogenic areas, and maybe more

49:40

ominously, you have this appearance, which is called dirty shadowing.

49:44

Unlike the clean or dark shadowing behind a stone, this is sort of

49:48

dirty, almost partially echogenic shadowing, and you can see it emanating from

49:52

these areas here. And this is going to be consistent with gas.

49:56

And so this was a case of emphysematous pyelonephritis.

50:01

So the etiologies for abscess and infection can change a little bit over

50:05

time in post-transplant patients.

50:08

In the post-surgical period, it's often due to things like surgical contamination,

50:12

catheter infections, hospital-acquired, but sort of the

50:16

group here is post-operative in the hospital, post-surgical

50:20

complications.

50:22

Later months are a different story.

50:24

The patients go on chronic immunosuppression, and that can lead to

50:28

infections that are more opportunistic.

50:30

Things like CMV, PCP, fungal infections, more

50:34

opportunistic risk in these immunosuppressed patients, or severe

50:37

infections, like this case of gas-forming infection that ascended to the

50:41

transplant kidney. So these patients are at higher risk as well going

50:45

forward from their immunosuppression.

50:49

This was the case that I showed you earlier.

50:51

And this is a CT showing emphysematous pyelonephritis.

50:56

So, let's do a couple of wrap-up slides to finish up.

51:00

These are the objectives that we talked about earlier, gaining familiarity with

51:03

basic transplant anatomy and modalities.

51:07

Gaining some experience with common transplant

51:10

complications and the different imaging appearances.

51:14

And then getting to do, hopefully, a little bit of a deeper dive

51:18

into some of the different subtypes, talking about parenchymal complications,

51:22

vascular and urologic.

51:25

I mentioned we would come around to this

51:28

table again, and hopefully, this now comes a

51:32

little bit more alive, having seen these cases and being able to put them in

51:36

a bit of context. So let me run through

51:40

this for a second. We talked about parenchymal complications, things

51:44

like ATN or acute rejection.

51:47

This was acute rejection with these sort of morphologic changes,

51:50

irregular corticomedullary junction, hypoechoic pyramids, et cetera.

51:54

And then we talked about chronic rejection, which was a bit more straightforward.

51:58

We talked about vascular complications.

52:01

This was a case of renal artery thrombosis, talking about how

52:05

thrombosis occurs earlier, but stenosis occurs

52:09

later, as do these sort of post-biopsy complications.

52:12

We talked about urologic complications, things like leaks that occur

52:16

during the early phase, whereas other entities like strictures occur

52:20

later.

52:22

We talked about fluid collections, and if you kind of run across the row

52:26

here, early things were seroma and hematoma, and later ones were things

52:30

like lymphocele. This was that subcapsular hematoma compressing the

52:33

kidney. And then lastly, we talked about infection in that early

52:37

period versus later period, and this was a more severe case of that

52:41

emphysematous pyelonephritis. So hopefully, this table comes a little bit

52:45

more alive and kind of gives you a framework.

52:47

It can be a little bit of a complicated topic, but approaching it in a

52:51

systematic way can be really helpful.

52:54

So I'll wrap up on the next couple slides.

52:56

I wanted to introduce myself for 10 seconds, just to say that I'm a real

53:00

guy. I'm not AI. I'm a person.

53:04

My wife and I are lucky to have five kids. This is us zip-lining.

53:08

I thought I'd have to read their X-rays, but fortunately, everybody did great.

53:12

But this is what I wish you, is the joy of radiology and all the amazing

53:16

things we can do at work and the joy of family at home.

53:19

And I do have a quick thank you slide.

53:21

Ashley Whitehurst was super supportive and helpful.

53:24

Modality is wonderful to give us this forum to share topics that mean a lot to

53:27

us. I've got the best colleague in the world, Lacey McIntosh, and I

53:31

do want to thank the audience for a minute.

53:34

Whether you're watching this now or whether you're watching it later,

53:38

thank you for letting me share a topic that I enjoy.

53:42

You came to enhance your knowledge.

53:44

You came to learn and grow, and that's an admirable thing.

53:48

Thank you for contributing to our field and all the things that we can do, and I

53:52

appreciate you.

53:54

And so here's a reference slide, some of the great resources.

53:58

And

53:59

that's all I have for now, and we'll look towards taking some questions. Thank you.

54:05

Fantastic. And thank you, Dr. McGiff, for sharing

54:09

that lecture and

54:11

those little bits about yourself at the end too.

54:16

At this time, we will be opening the floor for any questions from our audience.

54:20

You may submit your questions through the Q&A feature.

54:24

All right. So, opening up a couple of questions here, and I'll see if I can

54:28

give good answers to a couple of these.

54:31

One of the questions was, can we differentiate ATN

54:35

versus acute rejection?

54:37

And so definitely ATN versus acute rejection

54:42

is a little tricky. They both occur early phase,

54:45

and there can be some overlap with those elevated resistive indices

54:49

and low diastolic flow. The main differences is ATN's a little

54:53

bit earlierTypically around 24 to 48 hours,

54:57

maybe 72 hours, and that's a little bit of an earlier timeframe than

55:01

acute rejection. And then also you can start to see more

55:05

parenchymal changes in acute rejection, that corticomedullary change,

55:09

darker pyramids. So it can be a little bit difficult, but the timeframe

55:13

helps, and if you see grayscale changes, that can help, too.

55:18

All right, let's see what else.

55:22

There's a question about telling a seroma, urinoma,

55:26

and lymphocele.

55:28

That's probably the toughest question because you picked all the ones that are

55:31

anechoic. A hematoma is going to be echogenic, but a seroma can be

55:35

anechoic,

55:37

and lymphocele can be anechoic, and so can a urinoma.

55:40

So one thing that helps is the timeframe.

55:42

If it's a couple of days postoperative, two days postoperative,

55:46

it's likely a seroma. If you're five, six, seven days

55:50

and you still see a bunch of simple fluid and you see a clinical change,

55:54

there's decreased urine output,

55:56

the creatinine is starting to rise, then you can worry more about

56:00

urinoma.

56:01

And then lymphocele occurs later, so the timeframe helps.

56:04

So the two things that help me is the timeframe and then the clinical

56:08

scenario, because urinoma usually has clinical manifestations as well.

56:11

That's a great question.

56:15

Let's see. Moving forward, looking for other stuff.

56:18

Is hydronephrosis ever a normal finding after

56:22

transplant? Yes. I would say yes. If you're in the

56:26

first couple of days postoperative, it's very common to

56:30

have focal edema at the anastomotic site.

56:33

That's just from surgical manipulation.

56:36

The surgeon is handling the distal ureter, handling the bladder, anastomosing it,

56:40

and during the early phases, you can get a little bit of healing and swelling

56:43

there, and the swelling narrows the ureter.

56:45

So in the first few days postoperative, you can see transient hydronephrosis.

56:50

The best thing to do is closely follow it clinically and with imaging.

56:54

Is the creatinine starting to go down?

56:57

You might check it 24 hours later. Is the hydronephrosis starting to go

57:01

down? So it can be normal and transient, but it deserves close

57:04

follow-up clinically with labs and with imaging.

57:09

All right, let's see what else.

57:15

All right. That looks to be most of the questions for now.

57:19

So I appreciate it, and those are great questions, by the

57:23

way. And thank you very much for the input. I appreciate it.

57:28

Dr. Midkiff, thank you for your lecture today,

57:32

and thanks to everyone here who participated in this noon conference and

57:35

asked such great questions.

57:38

You can access the recording of today's conference and all our previous noon

57:42

conferences by creating a free account.

57:44

We'll also email out a link to the replay later today.

57:48

Be sure to join us next week on Thursday, June 11th at 12:00 PM

57:52

Eastern, where Dr. Mohit Aggarwal

57:56

will deliver a lecture entitled Salivary Gland Masses.

58:00

You can register for it at medelity.com and follow us on social media

58:04

for updates on future noon conferences.

58:07

Thanks again, and have a great day.