Interactive Transcript
0:50
Good afternoon, everybody, and, um,
0:52
uh, welcome to the case-based review.
0:54
So we'll get started right away.
0:57
Uh, the goal is to try and show case examples
0:59
of clinical scenarios, you know, that we need
1:02
to be aware of as majors, especially those
1:05
where we can make an impact and difference.
1:07
And I'm also going to provide some take-home points so that
1:10
you can take those and use them in your clinical practice.
1:16
So the first case is, um, it's actually a two-part case.
1:21
I'm going to show you two patients, uh, two different
1:24
patients who, uh, have a very similar clinical presentation.
1:28
And they both have the same primary disease entity.
1:32
So the first one is a 52-year-old female
1:35
patient who is known to be hypertensive,
1:38
has diabetes, longstanding diabetes,
1:41
and has been experiencing right upper
1:42
quadrant pain for the past three weeks.
1:45
The pain is not related to eating, and she doesn't
1:48
have any blood per rectum, diarrhea, or constipation.
1:52
So let's dwell into the images.
1:54
So looking at the axial contrast-enhanced images,
1:58
and you can see oral and IV contrast has been given.
2:01
So as I'm going to scroll through these, um,
2:04
you can see there's a little bit of ascites,
2:05
in the liver, maybe some fatty infiltration,
2:08
uh, in the liver parenchyma itself,
2:11
a little bit of peritoneal stranding.
2:14
And you can see right here, the small bowel
2:16
mesentery showing a little bit of stranding as well.
2:19
As we march our way down, contrast-filled
2:22
uh, small bowel loops, and we start getting
2:26
into the area of the bowel that is abnormal.
2:29
So what you're seeing here is
2:31
basically the bowel is not distended.
2:34
Um, there is no, uh, mucosal thickening, uh, because if
2:41
you have linear or nodular mucosal thickening, then that
2:44
has a certain differential, or if you have, um, dilatation
2:49
that goes along with it, that has a certain differential.
2:51
So again, ascites.
2:53
What you're seeing is thickening of, um, uh, you're
2:57
seeing basically, uh, low-density thickening of
3:02
the submucosal layer of the bowel wall, which is
3:04
referred to as the "water halo sign," if you will.
3:08
So these are the axial images.
3:09
Now let me show you the coronal, and again,
3:13
scrolling through this, you are seeing the
3:15
distal jejunum, essentially the area of bowel
3:18
that is affected, a fairly long segment of bowel.
3:22
Again, no nodular or linear mucosal thickening.
3:25
There is no distension, but there is,
3:28
uh, the so-called water halo sign, or
3:30
low-density thickening of the bowel wall.
3:34
And again, has, uh, ascites to go along with that.
3:37
And there is a little bit of mesenteric, uh, stranding
3:40
with prominence of the, of the Vasa Recta.
3:45
So that's sort of the first patient.
3:47
You're seeing the axial and coronal images.
3:50
Again, these are just the summary images showing
3:52
the finding on the axial and the coronal, uh, plane.
3:56
The second patient is a 46-year-old woman who has
4:01
a longstanding history of recurrent abdominal
4:03
discomfort that has led to multiple hospitalizations.
4:08
And now she comes back with the same
4:10
complaint and gets admitted this time over.
4:13
So she has severe abdominal pain.
4:15
Again, there is no history of, uh, any, uh, passing any
4:19
blood or any vomiting or nausea, just severe abdominal pain.
4:23
So let's look at the axial image of this
4:26
particular patient as we march our way down.
4:28
Again, oral
4:29
and IV contrast has been administered.
4:33
So compared to the prior patient, this patient has,
4:37
um, a thickening of the stomach wall, which again is
4:40
low density or sort of fluid in density, if you will.
4:44
There is ascites in this patient as well.
4:47
And again, compared to the prior case where the
4:49
predominant finding was in the distal small or in the
4:52
distal jejunum, in this case, it is the duodenum, the,
4:56
the, the, uh, the second, third, and fourth part of the
4:58
duodenum leading into the jejunum, where you see the
5:01
abnormal finding. And this is the classic water halo
5:04
sign where there is thickening of the submucosa with
5:07
low density seen in the, um, in the wall of the bowel.
5:11
Again, there is some ascites to go along with it.
5:13
So that's on the axial.
5:15
Let's see on the coronal images.
5:18
The same finding you can see here is the duodenum, the
5:21
duodenal C-loop as it makes its way to the duodenal or
5:23
jejunal junction, and the classic low-density within the
5:28
bowel wall, which is thickened, but there is no dilatation
5:31
and no linear or nodular thickening of the mucosal folds. So
5:36
and again, there is some ascites in this patient as well.
5:40
Here's just a 3D image showing the,
5:43
um, the same again, the summary.
5:45
So these two patients, we have the first patient
5:47
where the predominant finding is in the distal
5:50
jejunum, the second patient where it is the duodenum
5:53
and the proximal jejunum, which are affected.
5:56
Now, as I mentioned to you, when you have
5:58
water halo, or you see low-density bowel wall,
6:03
um, it's important when you look at a bowel
6:05
and approach a patient with a bowel, as I said,
6:07
you want to make sure there is no dilatation or
6:10
distention, which these two patients don't have.
6:13
Then do you have linear or nodular thickening?
6:15
Because that leads to a certain differential,
6:17
which these patients don't have.
6:19
And then comes the question of having, um, thickening
6:22
of the submucosal or the bowel wall and, and
6:26
depending on the, um, on the density we see on CT.
6:30
So low, low density, as you see here, which is
6:33
called the water halo sign typically has the
6:37
two I's as the, um, differential, which is
6:40
inflammatory, uh, etiologies or ischemic etiologies.
6:45
Uh, then it can be pus in which case it's infection, or it
6:50
can be blood in which case there is bowel wall hemorrhage.
6:53
which is slightly more higher in density
6:56
than what you're seeing in these cases.
6:58
And then finally, it can be cells, and
7:00
which is typically seen in lymphoma.
7:03
Now, you know, of those entities, as I said,
7:05
this is low density, so it's water halo, which
7:08
means it's either ischemic or inflammatory.
7:11
It's too long a segment typically, and proximal
7:14
small bowel ischemia is not as common as it
7:16
is in the distal bowel or in the large bowel.
7:20
So, you know, that makes ischemia lower on the differential
7:23
and neither of these two patients has had any intervention.
7:27
And so that leaves, leaves, leaves us with inflammation.
7:30
So the question is can we resolve the etiology of the water
7:36
halo sign in these two patients in terms of inflammation?
7:41
Uh, can it be Crohn's or inflammatory bowel disease?
7:43
Again, the distribution is a little atypical.
7:46
That typically happens distally in the
7:48
small bowel as opposed to proximally
7:50
in the, uh, in the small bowel.
7:53
So let's look at the history a little bit.
7:55
Case A, this patient was, I told
7:57
you, was a diabetic and hypertensive.
7:59
So she has been taking an ACE inhibitor for hypertension.
8:04
And case B, which is the second case who
8:06
has been getting recurrent episodes, has
8:08
a brother who has a similar condition.
8:11
He gets a rash and abdominal symptoms.
8:14
And then in addition to the abdominal pain, she
8:17
also gets swelling in the tongue on separate occasions
8:20
and also gets a rash that, that accompanies it.
8:24
So given the history in these two different
8:27
patients, the question is in terms of differential
8:30
diagnosis, which do you think is the most common,
8:34
um, or most likely diagnosis in these two patients?
8:38
So you have these five options: Crohn's enteritis,
8:42
infectious enteritis, angioedema of the bowel
8:45
wall, bowel wall metastasis, or lymphoma.
8:48
All right.
8:50
So a hundred percent got it right.
8:51
It is angioedema of the bowel wall.
8:53
And, um, again, the water halo sign, typically with
8:57
the history in these two different, uh, different
8:00
patients, uh, the same etiology, which is angioedema.
9:03
And if you look at the classification of angioedema,
9:07
you can see that it can be, uh, acquired in
9:10
which case medications are the commonest one we
9:13
see in our emergency setting and ACE inhibitors.
9:16
are the most common, although NSAIDs
9:18
are, NSAIDs can also lead to it.
9:21
If it is hereditary, it's because of C1, um,
9:24
uh, you know, enzyme, um, uh, C1 esterase,
9:30
inhibitory enzyme deficiency, which leads
9:32
to, um, uh, the, the symptoms that we see.
9:35
And typically they have skin rash as well as,
9:38
um, you know, recurrent bouts that happen, which
9:41
was seen in the, in the, in the second patient.
9:44
Irrespective of what is the etiology in terms of,
9:47
you know, whether it's idiopathic, it's secondary
9:49
to medications, or is it a, a hereditary angioedema,
9:53
the underlying mechanism is increased capillary
9:56
permeability, which leads to, um, edema of the bowel wall.
10:00
And ultimately that is what is
10:02
seen as the, uh, water halo sign.
10:04
The important point to remember is, uh, that although
10:08
the diagnosis is clinical awareness of this entity.
10:11
is, and its characteristic imaging appearance can lead or
10:15
sway the, uh, uh, the, uh, clinicians to this particular
10:19
diagnosis when the radiologist raises the concern.
10:22
And although imaging follow-up may not usually be
10:25
indicated, um, complete remission of the abnormal findings
10:28
may support the clinical diagnosis of, uh, angioedema.
10:32
So that's sort of in a nutshell.
10:33
So the take-home message here is if you
10:35
get proximal small bowel water halo sign,
10:38
correlate with the history and think of.
10:41
angioedema, whether secondary or
10:43
hereditary in the differential diagnosis.
10:45
So that was the first case.
10:46
Excellent.
10:47
We move on to the second case.
10:49
Second case is a 57-year-old male patient who
10:53
comes with abdominal pain and microhematuria.
10:56
And as is the case in a lot of instances, you
10:59
know, an ultrasound is asked and I'm going
11:01
to show you the ultrasound static images.
11:04
So we are looking at the right. There's no hydronephrosis,
11:07
looks like the right kidney is fairly unremarkable.
11:10
There are no stones we see, no masses, no cysts.
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And then we come to the left side.
11:15
Compared to the right side, you can see, if you
11:18
see the outline of the left side, there appears
11:19
to be dilatation of the collecting system.
11:22
And there appears to be a hypoechoic
11:24
lesion centered in the renal sinus.
11:27
And if you put the Doppler flow on,
11:28
it's not a very vascular lesion.
11:31
You can see vessels around it, but not typically within it.
11:35
You know, a little bit of flow at the periphery,
11:37
but really not a very hypervascular lesion.
11:40
But clearly there is hydronephrosis and dilatation of
11:42
the collecting system, as you're seeing in these images.
11:47
And so, you know, he has microhematuria, has abdominal
11:51
pain, and the question is what is causing, uh, the
11:54
dilatation of the collecting system on the left?
11:56
And what is the reason that you're seeing
11:59
that hypoechoic area in the left renal sinus?
12:02
Okay.
12:02
And so because of those reasons, the
12:04
patient gets a hematuric protocol CT.
12:07
And so what I'm showing you on the, on the left
12:09
is the, um, uh, is the contrast-enhanced images.
12:13
The image on your right are the delayed,
12:15
delayed, uh, nephrographic, um, uh, phase images.
12:19
So a little bit of blunting of the, um, of
12:22
the window level so that you can appreciate
12:23
the filling of the collecting system.
12:25
So as we march our way down, you can see that there is
12:29
clearly an infiltrative mass, uh, that is present, centered
12:34
in the renal sinus, and you can see the parenchyma,
12:39
a normal parenchyma on the periphery, is enhancing.
12:43
You can see the right kidney is
12:45
showing excretion of contrast.
12:46
There is paucity of excretion of contrast on
12:49
the left, and you can see that the mass extends
12:53
beyond the renal sinus into the proximal ureter.
12:56
You can still see there is enlargement of the, uh, the
12:59
ureteric lumen there with filling defects seen within it.
13:03
And as we come down, you can see that there
13:06
is now the ureter becomes normal in caliber.
13:09
So I'm going to show you the coronal
13:11
images where it's a little bit better seen.
13:12
In addition, if you look on the axial images,
13:15
there also is an enlarged lymph node in the left
13:19
common iliac location and also a few scattered
13:22
small nodes higher up, which are not enlarged, but
13:24
the largest is seen in the common iliac location.
13:27
Immediately distal to the point where the ureter is
13:30
transitioning to, uh, from the enlarged to normal caliber.
13:33
And these are the coronal images showing the
13:35
same, the portal venous and sort of the, um,
13:38
the delayed excretory phase, if you will.
13:41
And again, you can see that the infiltrative mass
13:44
originating in the renal sinus, uh, extends to the, uh,
13:47
parenchyma, uh, and also extends into the proximal urethra.
13:52
Here is the enlarged node that we saw on the axial image.
13:55
And here it is on delayed.
13:56
You can see that there is contrast excretion on the
13:58
right, but there is no perceptible contrast seen in
14:02
the collecting system on the left, indicating that
14:05
clearly this mass is compromising the renal function.
14:08
The renal vein appears to be normal in caliber.
14:10
There is no extension into the renal vein.
14:13
So all we see in summary is an infiltrative mass.
14:17
Which is, um, sort of, uh, centered in the renal sinus,
14:21
is encroaching on the renal sinus, obliterating the renal
14:25
sinus, is causing obstruction to the renal collecting
14:28
system on the left, compromising the renal function.
14:32
There is a small little stone here, which is, you know, just
14:34
probably an incidental thing seen in the left upper dilated
14:36
upper polar calyx, and there is accompanying adenopathy.
14:40
There is no extension into the renal vein.
14:41
So those are some of the summary of the findings.
14:44
And given that this patient has not frank,
14:47
but microhematuria and abdominal pain, the
14:49
question is what is your most likely diagnosis?
14:52
So these are the options,
14:57
renal cell carcinoma, transitional cell carcinoma,
15:00
some kind of chronic renal infection or lymphoma.
15:07
So the majority of you, um, thought about transitional
15:10
cell carcinoma and about 15 percent thought about lymphoma.
15:15
Now, it's interesting, um, you know, if you look
15:17
at the size of the lesion that is infiltrating the
15:20
renal sinus, um, one would expect, uh, typically
15:25
with transitional cell carcinomas to have frank
15:27
hematuria, which this patient didn't have.
15:28
Now, that's not a, you know, it's not a distinguishing
15:32
feature, but that should lead you to the, to the
15:34
fact that something else perhaps is going on here.
15:37
And the correct answer is lymphoma.
15:40
Although, you have to give a differential and this
15:42
patient ideally needs to have tissue sampled to make
15:45
the answer or to, to arrive at the correct answer.
15:48
This patient did have a nephroureterectomy and I, I'm
15:50
going to tell you a little bit about why that was done.
15:53
Uh, and, and this turned out to be follicular lymphoma.
15:56
Clearly, you can see that the mass is sort of
15:58
arising in the renal pelvis and ex, was extending
16:01
fairly low down into the, um, uh, into the ureter.
16:05
So when you look at the differentials of infiltrative
16:07
renal masses, uh, you know, this was, somebody
16:10
has actually looked at that and what they found
16:12
was the overwhelming majority was between renal
16:15
cell carcinoma and transitional cell carcinoma.
16:17
Those two would be the commonest
16:19
infiltrative renal masses that you would see.
16:22
But the, but lymphoma is a distinct third and you know,
16:25
it's important to keep that in mind and, and sort of,
16:28
uh, mentioned that in the differential, if, if somehow
16:33
the clinical symptoms or the clinical features don't fit
16:36
or something else is going on, which doesn't make sense.
16:39
And then metastasis is being the least common.
16:41
So, you know, keep in mind about lymphoma.
16:44
And so in terms of taking home point is
16:46
don't forget lymphoma in the differential
16:48
diagnosis of infiltrative renal masses.
16:50
Now, biopsy may help.
16:52
Now, this patient interestingly presented in the last
16:55
week of March. And, you know, there was a time when
16:58
COVID things were sort of evolving and, uh, the, the
17:02
surgeons were apprehensive that if they waited for a
17:04
biopsy and if the patient didn't get a biopsy and, and
17:07
this was indeed a transitional cell carcinoma, then
17:10
he would have probably, um, the lesions would have,
17:13
the lesion would have spread and perhaps become, uh,
17:17
inoperable at that point and therefore a biopsy was not
17:21
done and they went straight to a nephroureterectomy.
17:23
One could make the argument if they had biopsied and
17:26
found it to be a lymphoma, the, you know, they could
17:28
have spared the surgery, but in this case, um, I, what,
17:32
which I didn't show you was a split renal function.
17:34
Um, nuclear medicine study was performed on, there was
17:37
barely any renal function on the kidney on that side.
17:40
And so it wouldn't have helped much, even if
17:42
they had found a diagnosis of lymphoma, they
17:44
probably would have taken the kidney out.
17:46
But under normal circumstances, you know, that is one
17:49
indication for doing a renal biopsy is if you see, if you're
17:52
suspecting lymphoma because clearly that can be managed non
17:55
surgically, uh, rather than doing an aggressive surgery.
18:00
But the bottom line is, you know, if
18:01
you have an infiltrative lesion, keep
18:03
in mind RCC, TCC are the commonest.
18:06
Don't, uh, don't forget lymphoma in the differential.
18:11
Alright, moving on to the next case.
18:13
This is a 58-year-old, uh, uh, female patient who comes to
18:17
the emergency room with persistent lower abdominal pain.
18:20
It's dull, aching, uh, is not related to
18:24
eating, is not related to, um, any kind of
18:26
exercises, just there throughout the day.
18:29
And she was worried what was going on.
18:31
So let's look at the CT images.
18:33
So let's start with the axial first.
18:36
So, um, and you can see this is, you know, sort
18:39
of a, um, uh, hematuria, uh, dual, uh, split
18:43
bolus, uh, study where, um, part of the contrast
18:47
has been given earlier to pacify the collecting
18:49
system because we were not sure what to expect.
18:52
And so there's contrast excretion here and
18:54
also enhancement of the parenchymal organs.
18:56
And so as we march our way down.
19:00
You can see that there is a large low-density lesion.
19:03
You can perhaps appreciate some septation if
19:06
you window it within this lesion and they,
19:10
they likely are showing some enhancement.
19:14
Here's the uterus.
19:16
You can see the sigmoid right here.
19:18
And, um, These are the round ligaments on either side.
19:21
So the question is, and you can see the ureters are coming
19:24
all the way, um, to the bladder and they seem to be, uh,
19:28
And so it is, you know, a, a mass that is arising from
19:33
the renal pelvis, uh, extending up into the lower abdomen.
19:37
Uh, we couldn't identify the, the, uh, ovaries.
19:40
So the assumption is being a, uh, you know, middle-aged
19:44
woman, this likely is a, um, adnexal or primary ovarian.
19:48
pathology.
19:48
Here is the coronal showing the same thing.
19:52
A large low-density mass which is arising
19:56
from the right sort of right adnexal region.
19:59
It's causing some extrinsic compression of the bladder.
20:03
Again, you can appreciate the subtle
20:05
septations which are likely enhancing.
20:09
And there's no obstruction to bowel.
20:12
We don't see any changes of bowel wall thickening
20:15
or anything within large bowel and a good amount
20:17
of contrast has been administered as you can
20:19
see there's adequate opacification of both
20:22
the small and large bowel in this instance.
20:24
And here is a sagittal image again showing its
20:27
relationship to the uterus, um, causing
20:30
an extrinsic, uh, compression. You can see it's
20:33
causing extrinsic compression on the bladder.
20:35
And again, the septations are seen nicely.
20:37
So that's sort of in a nutshell
20:39
what was seen on the, in the CT.
20:42
So the question is, um, what is the
20:44
site of origin of the lesion seen on CT?
20:47
And that should be a fairly straightforward and easy answer.
20:50
Let's see what
20:54
in a low-density lesion arising from the pelvis with
20:57
septations that seem to be enhancing we don't see any
21:00
neural nodularity or any kind of neural enhancing nodule,
21:11
okay, so 100 percent got it right it's the it is an
21:13
ovarian mass. And, you know, that was a fairly easy ask.
21:18
Um, so, uh, subsequently, we performed an MR
21:22
just to get a better, um, you know, better
21:26
assessment of the morphology of the lesion.
21:28
And as opposed to CT, you can see on MR, this is a CT scan.
21:31
fat-saturated T2-weighted image.
21:33
You can nicely appreciate the septation within the mass.
21:36
There are some areas that are a little bit less
21:38
brighter than the other areas, although predominantly
21:41
the mass is showing homogeneous, uh, signal intensity.
21:44
And here's the normal appearing,
21:47
uh, uterus reading into the cervix.
21:48
Here is the SAG fat-saturated T2-weighted image
21:51
again, showing nicely the outline of the uterus.
21:54
There is some free fluid, but here is the primary
21:57
lesion, multiloculated, um, So again, as you all
22:01
know from a differential perspective, um, when you're
22:03
looking at pelvic masses, ovarian masses, the, it's
22:08
the, the four sort of buckets we try and put them for
22:11
assessment in terms of differential is, is it unilocular?
22:14
Is it multilocular?
22:16
Is it a mixed solid and cystic lesion, or is it a predominantly solid lesion?
22:23
And so, this would fall into the multilocular category.
22:25
And, you know, just statistically, the commonest lesions
22:28
typically in a female pelvis are epithelial lesions.
22:31
So, epithelial neoplasms arising from the ovary.
22:35
So, again, here's a coronal fat-saturated T2, nicely showing
22:38
the multiloculated nature of the lesion. We don't
22:42
see a discrete solid nodular component on the T2.
22:46
This is a post-gadolinium enhanced fat-saturated image.
22:49
Again, the septae are enhancing, but we don't
22:53
see any distinct nodule within the lesion or in the wall of the lesion.
22:59
Here is the coronal again showing the same
23:07
finding, where you can see the septations are
23:10
predominantly peripheral and enhancing.
23:13
And here is a sagittal delayed image.
23:23
I'm not sure what this probably was, like a proton density
23:26
type of image, but... So here's, in summary, the appearance of the lesion,
23:31
which, so far, we have ascribed her pain to a pelvic lesion
23:36
that is likely arising from the ovary.
23:41
And in terms of differential, we have put this lesion
23:44
from a morphologic perspective into a multilocular
23:48
cystic lesion, likely arising from the right ovary.
23:52
And so, you know, the common etiology in that
23:55
instance is, as I said, you have to think about
23:59
epithelial lesions, typically a borderline or a
24:02
benign epithelial lesion arising from the right ovary.
24:08
If it was malignant, you would expect to see
24:10
more nodularity with early enhancement, um,
24:13
which is not seen in this case.
24:16
Now, it's interesting, if you look at the coronal,
24:18
CT images of the same patient, I just want to show you
24:22
these images one more time because that gives you a
24:25
clue as to the etiology of this specific entity.
24:30
So take a couple of seconds
24:32
to look at these coronal images.
24:36
And having seen that, what is the most
24:39
likely diagnosis in this particular case?
24:42
Is it a primary ovarian epithelial neoplasm?
24:45
Is it a large pelvic nerve sheath
24:47
tumor arising very close to the ovary?
24:50
Is it an ovarian metastasis with a GI
24:52
primary, or is it an ovarian germ cell neoplasm?
24:58
So it looks like, um, you know, there is a sort
25:02
of an equal distribution, um, uh, of the bulk, the
25:05
majority answered A, which is a primary ovarian
25:08
epithelial neoplasm, or D, ovarian germ cell neoplasm.
25:12
And then a few of you selected one each.
25:16
It's a pelvic nerve sheath tumor and ovarian metastasis.
25:19
Now, it's not an ovarian germ cell
25:21
because we don't see any fat, neither.
25:24
I showed you only the fat-saturated images on the
25:26
MR, but on the CT, there clearly is no fat density
25:30
seen, so that's going to be extremely unlikely.
25:32
So that can be excluded very safely.
25:35
The primary ovarian epithelial neoplasm still remains high
25:37
on the cards, but the reason I'm showing you this
25:40
case is, uh, you know, you have to be very careful.
25:43
You pay attention to the GI tract when you're
25:46
looking at ovarian lesions.
25:50
This was an ovarian metastasis of the GI primary.
25:53
So, where is the primary?
25:54
So, if you look at the coronal images again, uh, again, there
25:58
is oral contrast here, and you can see right here, there is
26:01
a fluid-filled distended appendix with some calcification.
26:05
And this was a, um, a mucinous adenocarcinoma
26:09
arising in the appendix with ovarian metastases.
26:12
So, you know, keep in mind, uh, this is
26:15
one, um, very important take-home point I
26:18
would like you to, uh, uh, to keep in mind.
26:20
So, uh, this was the finding on the scan and
26:24
here is a PATH report, uh, when they went in.
26:27
Uh, she had a right, uh, salpingo-oophorectomy,
26:30
which showed secondary involvement.
26:31
by a low-grade appendiceal neoplasm, and the
26:34
appendix did have a mucinous adenocarcinoma
26:38
with perforation and mucin extravasation.
26:40
The left ovary was fine, only had surface deposits.
26:43
So why am I showing you this case?
26:45
I'm showing you this case because this is a paper
26:47
from the PATH literature written by one of our
26:49
pathologists, and the important point here to take
26:52
home is that the appendiceal mucinous neoplasms have
26:56
a propensity to spread to the peritoneum and ovaries.
27:00
And, and the, the reason you need to understand
27:03
that is because it doesn't, um, there can be a
27:07
disconnect between the size of the appendiceal
27:09
lesion and the size of the ovarian metastasis.
27:12
And so you can have a relatively, you know, benign
27:15
fluid-filled distended appendix as was seen in this
27:18
case, but have a large metastatic deposit in the ovary.
27:22
And why is it important to make that distinction?
27:26
When they go in and do cytoreduction, there is a slight
27:29
varying point of view in terms of surgical approach and
27:33
post-surgical or neoadjuvant therapy if
27:36
a GYN oncologist is dealing with it or a
27:38
GI oncologist is dealing with the patient.
27:42
So let me show you two other
27:43
examples, a couple of other examples.
27:45
Here is a patient who has a fluid-filled distended appendix.
27:48
Do not ever discount that.
27:50
This patient also has a little bit of
27:51
peripheral calcification, and this also was
27:53
a mucinous adenocarcinoma of the appendix.
27:56
Here is a different patient which
27:58
this patient was called appendicitis.
28:00
In the emergency room.
28:02
And again, if you look closely, there is a, um,
28:05
fluid-filled distended appendix, and this was
28:07
actually perforated, uh, uh, uh, tumor with, with
28:11
mucin surrounding the cancer mimicking appendicitis.
28:15
They went in assuming it was appendicitis and found
28:18
cancer and then had to do a staged, uh, a staged
28:22
right colectomy at a later time point with, uh, you
28:26
know, with debulking, uh, of the mucinous deposits.
28:30
And here is another example.
28:31
This patient was thought to have a right ovarian lesion.
28:34
So here is an ovary on the ultrasound.
28:37
You can see there is a lesion in
28:38
very close proximity to the ovary.
28:40
And this is what was measured as a complex ovarian lesion,
28:44
or right adnexal mass arising from the ovary.
28:46
On CT, you can see it's a fluid-filled distended lumen
28:50
of the appendix with calcifications at the periphery.
28:52
So it can dip down fairly low on the
28:55
right side and mimic an ovarian neoplasm.
28:59
So the take-home points are: remember
29:00
ovarian metastases can and do occur.
29:04
They can be predominantly cystic.
29:05
They can be multiloculated cystic.
29:08
Or they can be solid and cystic masses.
29:11
The low-grade appendiceal mucinous neoplasms can spread
29:14
to the peritoneum and the peritonea, even though the
29:18
primary tumor does not look sinister or obviously invasive.
29:22
So this is very important to keep in
29:23
mind is there can be a disconnect.
29:25
So don't ever, ever discount the fluid-filled appendix.
29:28
In fact, you know, nowadays, whenever we see an
29:31
ovarian lesion, the first thing we do is look
29:33
at the appendix and make sure there is nothing
29:35
going on there or look at the rest of the bowel
29:37
and make sure there's nothing going on there.
29:39
So, so that's sort of the take-home message here.
29:43
All right, moving on to the next case, we have a 19
29:46
year-old, um, uh, young male patient from Chile who
29:51
was referred for abdominal pain and microhematuria.
29:55
The patient doesn't have any history of any surgery
29:57
in the past or any other medical condition.
30:00
You know, the mother says that he goes to school and then
30:03
comes back in pain and, you know, she took him to the
30:08
emergency room in Chile and they found microhematuria and
30:11
he has been worked up, and no one knew what was going on.
30:16
And so the patient had a CT,
30:17
which was a hematuria protocol CT.
30:19
So let me show you the non-contrast run first.
30:22
Obviously, in this case,
30:25
but this is sort of the early phase of enhancement.
30:28
And as we go down, you can see the kidneys
30:31
bilaterally show symmetric enhancement.
30:33
And, you know, if there were any obvious
30:36
stones, we would have seen it by now.
30:37
And we clearly don't see any hydro.
30:39
We don't see any renal masses.
30:41
We don't see any stones as we go down into the pelvis.
30:45
Here is the enhanced aorta.
30:52
So here is the right psoas muscle.
30:53
Here is the left psoas muscle.
30:55
I'm not going to have you, you know, spot the abnormality,
30:58
but it's right here in front of the right common iliac.
31:02
So keep an eye on that particular,
31:04
focal lesion, if you will.
31:08
And coming down into the pelvis, again, nothing obvious
31:11
to explain the patient's hematuria.
31:16
So let's look at the bone windows
31:19
sort of opacifying the collecting system
31:21
to see if there's any filling defects.
31:23
And again, we haven't seen any hydronephrosis.
31:25
I'm marching my way down.
31:26
You can see the ureters are bilaterally opacified, really.
31:30
And this was the lesion I was pointing out earlier,
31:34
not in any proximity to the ureter, not causing
31:39
any obstruction to the right, and there is a nice,
31:41
entry into the bladder.
31:46
Now, moving on to, this is slightly, the
31:50
soft tissue of the delayed scan, and again,
31:53
the same thing here, you can see the ureters
31:58
are nicely opacified, haven't seen any mass lesion,
32:00
but this is the area that we are looking for.
32:02
You know, talking about.
32:06
And so, between the I-minus and the enhanced images,
32:11
this particular lesion showed 35 Hounsfield unit change.
32:14
So it was an enhancing lesion.
32:17
So I pointed out the area of abnormality
32:19
as was seen on the axial scan.
32:21
And let's look on the coronal.
32:24
So again, we're looking at the early arterial and
32:26
sort of the, uh, you know, slightly delayed,
32:29
uh, if you will, the nephrographic phase images.
32:33
And so as we stroll our way, you can
32:35
see the vessels are nicely enhanced.
32:37
And this is the area of concern
32:39
you can see between here and.
32:41
Moving on.
32:41
It's just showing sort of brisk enhancement
32:46
and nothing else.
32:48
So, you know, young patient with, this
32:51
is not really retroperitoneal, a little
32:52
bit lower than what you would expect.
32:54
But one thing you always think about is, you know, am
32:56
I missing something in terms of looking at the testis?
33:01
So an ultrasound was performed and this is the
33:04
ultrasound image of that particular lesion itself.
33:07
So you can see it's hypoechoic, well-demarcated.
33:10
Um, it measures about six centimeters in long axis.
33:14
And on the Doppler, it does show some flow,
33:16
although it's not markedly hypervascular.
33:19
So it's not a vascular, um, vascular structure.
33:22
Again, here you can see there is some
33:25
increased flow seen in parts of the
33:27
lesion, but not really a vascular structure.
33:32
And then I'm going to show you a clip of the
33:37
testes bilaterally, you're looking at the right
33:39
and the left testes, and as we scroll through
33:44
this, you can see that the testes are normal.
33:47
We don't see any local masses within the testes
33:51
because, you know, one in especially in the second
33:54
and third decades, you think about intra-testicular
33:57
lesions with retroperitoneal, um, masses.
33:59
But in this case, the testes are absolutely normal.
34:04
And so subsequently, a PET CT was
34:06
also done just to kind of assess.
34:08
And, uh, you can see that there is some moderate activity,
34:11
but really it doesn't show a lot of, uh, uptake as you
34:15
would expect in something that was floridly FDG avid.
34:20
So again, a 19-year-old patient complaining
34:22
of microhematuria and abdominal pain.
34:25
All you see is a solitary lesion, which is well demarcated,
34:29
uh, in the low retroperitoneum or in the common iliac
34:31
region on the right side, appears to show brisk enhancement,
34:35
change about 35 units in terms of Hounsfield units.
34:38
Uh, the testes bilaterally are unremarkable.
34:42
And so that's, this is sort of in a nutshell, what
34:44
the lesion appears like in terms of enhancement.
34:47
And this is what it looks like on the, and
34:50
this finding, as we already discussed, there is
34:52
no splenomegaly or any other adenopathy seen.
34:55
And so the question is, what is your most likely diagnosis?
34:59
Are we dealing with an extra adrenal pheochromocytoma, a
35:02
benign neurogenic tumor, metastatic adenopathy, infectious
35:07
or inflammatory adenopathy, or neurogenic lesion?
35:12
Again, the patient is 19 years of age.
35:15
Uh, as I said, the testes were negative
35:18
bilaterally, doesn't have any other symptoms
35:24
except abdominal pain.
35:29
Okay.
35:29
So, um, uh, there is sort of a tie between
35:32
a pheochromocytoma and a neurogenic tumor.
35:35
A few have called it a neurogenic lesion and
35:37
the, uh, the three and four were not selected.
35:39
And clearly it's not metastatic because
35:41
we don't see anything in the testes now.
35:43
Could it be some other primary?
35:44
It's possible, but we don't see any other.
35:47
Extradrenal pheo, which typically happens in
35:50
the organ of Zuckerkandl in close proximity
35:52
to the inferior mesenteric artery and vessels.
35:55
The patient is not symptomatic.
35:57
Now that doesn't guarantee that it's not a.
36:00
It cannot be an extra adrenal pheo if the patient has
36:02
any kind of congenital predisposition, which again,
36:05
there is no syndromic possibility it could be a benign
36:09
neurogenic tumor. That seems like the most likely
36:13
possibility and they can briskly enhance and you
36:16
know, they can be benign. But this was an inflammatory
36:19
adenopathy and this patient had Castleman's disease.
36:22
So this is the other sort of entity
36:24
I want to make you aware of.
36:26
It's not as uncommon, you know,
36:27
we have seen a fair number of cases.
36:30
And so the classic path feature is hypervascular
36:32
lymph nodes with hyalinization of vessels,
36:34
which leads to the brisk enhancement we see.
36:37
And the reason why it's, um, you know,
36:40
it's a little bit near and dear because Dr.
36:42
Kesselman was at MGH, um, I was a
36:46
pathologist here in our hospital.
36:49
And so, you know, it can be uni or multicentric, but
36:52
the key features on, on imaging are you see nodal
36:57
lesions that show homogeneous brisk or intense enhancement.
37:01
There are three distinct patterns.
37:02
The most common is you see a solitary non-invasive well
37:05
circumscribed mass, as was seen in this particular patient.
37:09
The second is a dominant infiltrative mass.
37:12
So it kind of looks like an ill-defined well
37:14
lesion, but does show brisk enhancement.
37:16
And the last type is the matted multiple lymph nodes,
37:19
which is the least common of the three features.
37:22
So just to show you some additional
37:23
examples, this is another patient here.
37:26
You can see there is a large, uh, nodal
37:28
mass in the left side, fairly bright on
37:31
T2, uh, showing, um, a brisk enhancement.
37:34
And this was biopsied to be Castleman's.
37:37
And here is an example of the multicentric nodal
37:40
lesions, where in this particular patient, you're
37:42
seeing multiple nodal lesions in the right inguinal and
37:45
right pelvic region that are showing brisk enhancement.
37:48
So when you have hypervascular nodes, especially
37:51
if they are solid, I mean, solid and, and, um, and
37:55
single, consider Castleman's in the differential.
37:58
It's not that rare an entity.
38:00
And, you know, again, from an imaging
38:02
perspective, you can guide, uh, the, um, uh,
38:06
the, uh, the diagnosis towards that direction.
38:09
Of course, you need a biopsy to, to, you know, make the,
38:13
uh, to make the correct diagnosis, but at least you can
38:16
suggest it, especially if there is lack of any primary
38:19
and there is no evidence of metastatic adenopathy.
38:22
So hypervascular nodes, especially if it is
38:24
solitary, think about Castleman's disease.
38:29
Moving on to the next case, this
38:30
is a 59-year-old male patient.
38:33
who went to get his annual physical
38:35
exam done by the primary care physician.
38:39
The PCP, as part of the exam, does, you know,
38:43
a digital rectal exam and feels increased
38:45
firmness on the right side of the prostate.
38:49
The patient did have a recent PSA drawn, and
38:51
it was 2, so it wasn't really, you know,
38:53
increased, and the PSA density was fine as well.
38:58
So, has a prostate MRI done at an outside
39:02
institution where they comment on a 3.
39:04
2-centimeter pyrexial lesion, and he's referred to us
39:08
for a fusion-guided biopsy because the institution
39:11
where the MRI was done didn't have a fusion
39:13
apparatus, so they wanted us to do a fusion biopsy.
39:16
So I'm going to show you images from the MRI.
39:19
So let's start with the axial T2-weighted images first.
39:22
So as we scroll through, you can see the normal seminal
39:24
vesicles, a little bit of bladder outlet changes,
39:28
it's some thickening and increased trabeculation.
39:30
And as we come to the mid prostate, you can
39:33
see on the left side, there is the normal
39:35
peripheral zone and the transitional zone.
39:37
But on the right side, what you see is there is a lack
39:40
of the zonal differentiation that appears to be a
39:43
well-circumscribed lesion that is encompassing or
39:47
involving the transitional and the peripheral zones.
39:49
Okay.
39:51
And it extends right from the base
39:53
and goes all the way to the apex.
39:55
So that's what it looks like, just a magnified
39:58
view, and let's look at the coronal now.
40:00
So again, looking at the levator muscles as we come
40:03
down, you have the seminal vesicles coming down.
40:07
Here's the ejaculatory ducts coming in.
40:10
So again, the same thing here.
40:11
Look at the left side.
40:13
This is the normal central zone.
40:15
This is the bright signal from the, um,
40:18
uh, from the normal peripheral zone.
40:20
This likely is related to prostatitis on the left
40:22
side, but on the right side, you can see that there
40:24
is, you know, you're losing out on that, on that zonal
40:28
differentiation, and there is this area that goes all the
40:31
way from the base to the apex, like you saw on the axial.
40:35
And here is a magnified view of the, uh,
40:38
the coronal image as, as you can see it.
40:41
So clearly, there is an abnormal,
40:43
um, abnormality seen on the T2.
40:46
Now let's see the diffusion and the enhanced images.
40:48
So the top, you're looking at the high B value.
40:51
This is a B value of 2000, and this is an ADC image.
40:53
So as we scroll, you can see that the entire right
40:56
side is showing very bright signal on the high B value.
41:00
Marked signal loss on the ADC images.
41:04
Anteriorly, there is an area which shows much more
41:07
darker signal on the ADC and also brighter signal
41:10
on the B value of 2000 than the rest of the region.
41:14
So that's sort of what you see on
41:16
the diffusion again here.
41:18
And then as we look on the gadolinium-enhanced
41:20
images, this is the early phase of enhancement.
41:24
You can see that that whole area is enhancing early.
41:27
But this area that shows, um, heightened or
41:31
darkened ADC or more restricted
41:34
diffusion clearly shows a lack of enhancement
41:38
or there is rim enhancement in that location.
41:40
So the whole area is abnormal, but this area, which
41:43
is, uh, showing more restricted diffusion, and the rest
41:47
clearly shows, um, lack of enhancement or there is
41:50
peripheral sort of rim-like enhancement in that location.
41:53
So that is sort of the, uh, in a
41:55
nutshell, the, uh, the finding.
41:57
So the question is, what is your most likely diagnosis?
42:00
And here, these are your four options.
42:03
Uh, diffuse high-grade Gleason grade cancer, as was
42:05
called on the outside; they call it a Pyrex 5 lesion.
42:09
Is it BPH with normal asymmetric
42:11
peripheral zone due to prostatitis?
42:13
Is this a patient with granulomatous prostatitis
42:16
or are these post-biopsy changes on the right?
42:23
So remember, the PSA was 2.1,
42:25
the PSA density was not abnormal, but the PCP
42:32
clearly felt something rock-hard on the right side
42:36
on the digital rectal exam.
42:41
So yes, I think 100 percent, you got it correct.
42:44
The patient does have granulomatous prostatitis.
42:46
The patient had a history of high-grade, um, uh, superficial
42:50
bladder cancer for which he was treated with BCG.
42:54
I didn't give you this history, but
42:55
you know, you guys didn't need it.
42:57
And this patient has a case of granulomatous prostatitis.
43:01
And on the biopsy, they found dense granulomatous
43:04
inflammation with scattered microabscesses, which was
43:07
consistent with the diagnosis of granulomatous prostatitis.
43:10
So it can mimic cancer.
43:12
That's why we have to be aware of this entity.
43:14
And, you know, it's, it's a prior BCG therapy that is typically
43:19
the clinical scenario in which we
43:21
see this particular, uh, finding.
43:23
It's not very common in those patients,
43:26
but the point is, we don't scan everybody
43:29
that gets BCG therapy with a prostate MR.
43:31
Perhaps if we do, we will see more
43:33
cases of, uh, granulomatous prostatitis.
43:37
Um, so the debate is, is it an ongoing active
43:39
infection or is it hypersensitivity, and the presence
43:42
of granulomas and, and lack of organisms that can
43:46
be cultured from these biopsies, um,
43:50
suggest that it's likely a hypersensitivity reaction.
43:53
Um, slightly higher percentage in those patients where you
43:58
see the findings on those coming for prostate
43:01
MR for prostate cancer and they have the relevant history.
44:05
Um, and, you know, the, the, um, recommendation
44:10
is, uh, if the patient does get, um, obstructive
44:14
symptoms after this therapy, is, you
44:16
know, think about gynecomastia, uh, prostatitis,
44:18
and you can do an MR and, and, and prove it.
44:22
So the take-home message here, it can mimic
44:23
clinically significant cancer, can, it
44:25
can sometimes cause elevation of the PSA.
44:28
In about half the cases, it can; in
44:30
this patient, there was no elevation.
44:32
The clue is, you know, unlike prostate cancer,
44:34
which enhances homogeneously, uh, typically these
44:38
patients show peripheral rim-like enhancement.
44:40
Now this particular sign is not very
44:42
sensitive, but it is very specific.
44:43
So when you see this, it's very likely that this is,
44:46
that it is granulomatous inflammation and not cancer.
44:50
So this is typically what cancer enhances like.
44:52
This is a Gleason 8 tumor in the left peripheral zone.
44:54
You can see it's homogeneously enhancing.
44:57
And in this particular case where
44:59
this patient had BCG therapy,
45:01
you can see there is an area on the right side on
45:04
the T2 showing marked restricted diffusion, and on
45:07
the DCE showing peripheral rim-like enhancement.
45:10
There's also a smaller area on the left, same
45:12
thing showing peripheral rim-like enhancement.
45:14
So if you see that, think about granulomatous prostatitis.
45:18
And suggest that, uh, instead of a, you know, regular,
45:21
um, run-of-the-mill, uh, high-grade prostate cancer.
45:26
Moving on to the next case, uh, this probably will be the
45:28
last case, um, uh, it's a 50-year-old male patient being
45:32
treated for presumed renal infection with antibiotics.
45:36
Uh, and shows very little improvement of symptoms,
45:39
uh, continues to have vague abdominal pain,
45:42
weight loss, and occasional low-grade fever.
45:45
So remember, he, he is on antibiotics and,
45:48
you know, has been, uh, written off as
45:51
somebody having recurrent bouts of UTI.
45:54
And what he says is despite taking the antibiotics,
45:57
I'm not seeing any improvement in my condition.
45:59
And so a contrast in studies performed, so you can
46:02
see this is the axial CT images as we scroll through.
46:05
You can see on the axial images that there are
46:07
these peripheral low-density areas bilaterally,
46:11
cortical-based extending into the renal site,
46:13
into the medullary portion, not into the sinus.
46:17
It doesn't look like there is a lot of perinephric
46:19
There's some perinephric stranding, but not a lot
46:21
of perinephric stranding. But they are multiple bilateral
46:26
and not causing any hydronephrosis and not leading to
46:30
any, um, you know, any mass-like features, if you will.
46:35
So, and let's, let's look on the coronal again, better
46:38
appreciated on the coronal low-density areas, bilaterally,
46:42
uh, cortically-based extending into the med lab, but not
46:45
really into the renal sinus, no obstructive symptoms, uh,
46:48
no other adenopathy in the retroperitoneum as we saw, and
46:51
none of the other organs show any kind of visceral changes.
46:54
So, the question is, what is your diagnosis?
46:57
Is it multiple renal abscesses, IgG4 disease, is
47:01
it renal tuberculosis or is this renal lymphoma?
47:06
Again, none of the other organ systems
47:08
are involved in this particular patient,
47:12
you know, his chest x-ray was normal,
47:15
didn't show any changes in the chest x-ray.
47:18
Um, all he has is these symptoms and has been taking
47:21
antibiotics for quite some time with no improvement.
47:27
Perfect.
47:28
100 percent of you got it right.
47:29
This is IgG4 disease.
47:31
Um, so again, it's, you know, it is sort of a, not
47:36
a new, but it's a multi-system, uh, inflammatory
47:40
disorder that can lead to mass-forming lesions.
47:43
Thank you for joining us.
47:43
It's marked by IgG4-positive plasma cells in the affected
47:47
organs, typically seen in the lacrimal glands, but
47:51
you can see it in the abdomen and pelvis, the pancreas,
47:54
kidneys, and the retroperitoneum that can be affected.
47:57
The kidneys, uh, in terms of a GU infection, are a
48:00
representative organ and collectively, when you see
48:04
the lesions referred to as IgG4-related kidney disease.
48:08
And so they can present with unexplained renal
48:10
dysfunction and imaging abnormalities as we saw here.
48:13
These patients typically have elevated serum
48:16
IgG4 levels, although about, you know, one
48:20
fourth can have normal serum IgG4 levels.
48:22
So that's something important to keep in mind.
48:25
And the, the real, uh, sort of, um, therapeutic, uh,
48:29
intervention in terms of giving corticosteroids and
48:32
there is a dramatic response that these patients show.
48:36
It's important to remember that the IgG4 spectrum
48:38
in the kidneys can have varying patterns.
48:41
So what we saw was bilateral, round, or wedge
48:44
shaped areas, predominantly cortical-based.
48:47
Now remember, lymphoma can do the same thing.
48:49
So that's one common differential
48:50
that you have to keep in mind.
48:51
But that's the most common presenting feature for IgG4.
48:55
You can have diffuse patchy involvement.
48:58
You can have a rim of soft tissue surrounding
49:00
the kidney as you see in the pancreas.
49:02
And just to show an example quickly,
49:04
this is a non-contrast study.
49:06
You see that there is a lot of soft tissue or low
49:08
density that surrounds the retroperitoneum, as
49:11
well as the kidneys, um, mainly on the right side.
49:13
And this was biopsy-proven IgG4.
49:16
Again, better seen on the coronal where you
49:18
can see the soft tissue line that surrounds.
49:21
The kidney.
49:22
There is also low-density areas within the
49:23
kidney itself, but there is a lot of soft
49:26
tissue surrounding the aorta.
49:29
There is a different patient where
49:32
there is perinephric soft tissue.
49:33
In this case, there is calcification.
49:36
So that can also be seen with IgG4.
49:38
The differential here would be amyloid.
49:40
That can sometimes mimic, you know, this particular
49:44
finding, but this was biopsy-proven IgG4. You can
49:47
have bilateral nodules in the renal sinus. You can
49:50
have diffuse thickening of the renal pelvis and
49:52
I can just show you a 3D MIP of a case here. The
49:56
patient has diffuse circumferential thickening of
49:00
the renal pelvis that was proven to be IgG4 again.
50:03
It's very difficult to preemptively make the diagnosis,
50:07
you need to get a biopsy, but suffice it to say that
50:09
it can mimic an invasive renal sinus tumor.
50:15
And then finally, you can get a solitary mass-like lesion.
50:18
And that's what is seen in this case where it
50:21
looks like there is a lesion, non-contrast and
50:23
contrast-enhanced, which is infiltrating into
50:25
the adjacent liver parenchyma.
50:29
And this turned out to be IgG4.
50:33
And so that's, that's sort of the coronal image
50:36
showing, coronal and sagittal images showing depiction
50:38
of the involvement of the liver.
50:42
So the takeaway here is that IgG4 can
50:44
mimic both neoplasms and infection.
50:47
You know, if the patient is not responding to
50:49
therapy, if the symptoms persist, especially if
50:51
the lesions are multifocal and affect the kidneys
50:55
bilaterally, you know, then think about IgG4.
51:00
So I think in the interest of time, I'm going to stop here.
51:02
If there are any questions about the cases that
51:04
we have seen thus far, I'll be happy to answer.
51:09
I am not seeing any questions pop up so far, Dr.
51:11
Harrison Ghani.
51:16
So I guess everything was very clear and you
51:18
know, you guys got most of the cases right?
51:20
So it sounds like you're a great teacher
51:23
and we—Oh, here's one that just popped up.
51:26
For IgG4, is there always antibiotic administration?
51:30
And the answer is no.
51:31
But remember, these patients don't, uh, typically
51:34
present with classical findings.
51:37
So they are assumed to have either a tumor or infection.
51:41
And so not infrequently, they will be put
51:44
on, you know, antibiotic therapy, thinking
51:46
that these are abscesses.
51:48
And when they don't respond to therapy, that's
51:50
when you need to start thinking of IgG4.
51:52
So it's not always, but frequently, I would say.
51:57
Thank you.
51:57
Thanks again.
51:57
Thank you.