Interactive Transcript
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Hello and welcome to Case Crunch, rapid case
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review for the core exam hosted by Medality.
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In this rapid-fire format, faculty will show key images
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along with a multiple-choice question, and you'll respond
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with your best answer via the live polling feature.
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After a quick answer explanation,
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it's on to the next case.
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Today, we're honored to welcome
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Dr. Claire for the GI board prep case review.
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Dr. Brookmeyer completed her radiology residency,
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chief year, and body MR fellowship at Johns Hopkins.
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She's on the faculty in the Body Division at
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Johns Hopkins Department of Radiology
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and also serves as the course director for the
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medical student clinical electives in radiology.
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Questions will be covered at the end if time allows.
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So please remember to use the Q&A
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feature to submit your questions.
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With that, we are ready to begin today's board review.
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Dr. Brookmeyer, please take it from here.
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Hello, everyone.
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My name is Claire Brookmeyer.
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I am on the faculty at the Johns Hopkins
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School of Medicine, and I am very excited
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to present to you my GI board review.
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So, our plan for the day
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is to do a rapid-fire case review.
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I want us to get through as many questions
1:10
as possible because more is more.
1:13
So, I'm going to give you a strategy
1:14
for getting through these questions.
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I will present to you the question stem,
1:18
including the images, and I want you to try and
1:20
answer before looking at the answer choices.
1:23
This is a way to help you avoid getting distracted
1:26
by the distractors. Use everything on the images.
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And then, please hold your questions to
1:31
the end, and I will stick around to answer
1:32
any questions regarding all the cases.
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So, one question to get us warmed up—
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are you a resident, an attending physician,
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just here for the cases, or other?
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All right, and I see most of us are here cramming
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for the course, so this is the right time to do it.
1:58
All right, let's go ahead and
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get started with our first case.
2:03
So, best diagnosis—so I'd like you to take a look
2:07
at the images, formulate what you think is going on,
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and here are your answer choices.
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All right, it looks like we have an even split
2:29
here between internal hernia and a volvulus.
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So here, the best answer choice is a volvulus.
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And really, the key here is identifying
2:37
that there is this mesenteric whorl.
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So here, we have an acute closed
2:41
loop small bowel obstruction.
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There is lack of enhancement of the involved bowel loop,
2:46
uh, of the walls of the involved bowel loop, indicating
2:49
that there is some degree of bowel ischemia.
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And if this is acute, if this is acute,
2:54
this is truly a surgical emergency.
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So, why are the other answers incorrect?
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Well, partial small bowel obstruction
3:00
is an incomplete answer, and it really
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doesn't account for the mesenteric whorl.
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Same thing with the internal hernia.
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While you can have a, um, a closed-loop small bowel
3:08
obstruction that results from an internal hernia,
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those are typically much more sac-like,
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with sort of a mushroom appearance, and really aren't
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characterized so much by this mesenteric whorl here
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that I've identified by this orange arrow.
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Um, acute embolic mesenteric ischemia, while it
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would account for the ischemic bowel, would not
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account for this mesenteric whorl here in the middle.
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Next question.
3:35
All right.
3:36
19-year-old male, previously healthy,
3:38
presenting with abdominal pain.
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What is your best diagnosis?
3:44
I'm going to let this image stack scroll.
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For a while, and then I'm also
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going to give you sequential images.
3:54
Here are three sequential images
3:55
from that scrollable stack.
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And here are your answer choices.
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All right, looks like the majority of us did choose
4:14
the correct answer, which is a left peritoneal hernia.
4:17
So, really identified by this left upper quadrant, um,
4:20
sac of bowel, um, originating near the DJ junction.
4:26
So, why are the other answers incorrect?
4:28
Well, a right-sided peritoneal hernia would
4:30
really have the sac of bowel on the right side.
4:33
Peterson's space hernia is an acquired hernia after
4:36
a Roux-en-Y surgery, and I haven't shown you any
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uh, post-surgical changes here in the abdomen.
4:40
And then the foramen of Winslow
4:43
hernia.
4:43
While it can also cause a loop or a sac
4:46
of small bowel on the left side of the
4:48
abdomen, you would expect to see bowel and
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mesentery between the portal vein and the IVC.
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That's the point of showing you this axial image here.
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You can see that there's no mesentery or bowel
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here between the portal vein and the IVC.
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So that excludes a foramen of Winslow hernia.
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So, you should really be able to
5:08
differentiate between these hernias.
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The left periduodenal is much more
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common and occurs at the DJ junction.
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The right periduodenal is less common and is
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typically associated with non-rotated bowel.
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And then the foramen of Winslow hernia, which is
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in fact a distractor for the left periduodenal,
5:24
really should be identified with mesentery
5:26
or bowel between the IVC and the portal vein.
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All right, next case. Best diagnosis?
5:36
Look at everything on the images, formulate your plan.
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And here are your answer choices.
5:53
All right, looks like we have a pretty even spread.
5:55
Uh, the correct answer here is a femoral hernia.
5:59
So, the key to distinguishing between, uh,
6:01
the femoral hernia and the inguinal hernia
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is really where the inguinal ligament is.
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So, femoral hernias occur, uh, medial to
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the femoral vessels, which this one is.
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So, here are the femoral vessels,
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and then here's the neck of the hernia.
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Importantly, it is inferior and
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posterior to the inguinal ligament.
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So, the inguinal ligament,
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I've identified here by these yellow arrows.
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And you can see that as we move from anterior
6:24
to posterior through these sequential
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slices, the hernia neck is posterior to the inguinal ligament.
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These are much more likely to incarcerate
6:33
because they have a narrow neck.
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So, why are the other answers incorrect?
6:37
Well, the obturator hernia originates
6:39
between the pectineus and obturator, and it's
6:41
usually associated with pelvic floor laxity.
6:43
These are a lot easier to see on axial images.
6:46
And then the inguinal hernias—the neck of the
6:48
hernia is superior to the inguinal ligament.
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So, because this is such an important distinguish,
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an important thing to distinguish, I've brought
6:57
up a companion case of an inguinal hernia.
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Here, you can see that the neck of the hernia
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originates superior to the inguinal ligament,
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which I've identified here by the yellow arrows.
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In contrast to the case that we had,
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where the neck of the hernia is posterior.
7:12
Okay. It's an important distinction here.
7:17
Alright, next case. Best diagnosis?
7:20
Take a look at all of the images.
7:23
Formulate your thoughts.
7:29
And here are your answer choices.
7:40
Alright, perfect.
7:40
Everyone here got scleroderma?
7:42
Scleroderma is, in fact, the correct answer.
7:45
So, scleroderma in the gut is really identified by
7:48
impaired gut motility, so you can have a patulous,
7:51
fluid-filled esophagus, and then things that look like
7:53
obstructions because of the impaired gut motility.
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So, a pseudo-SMA syndrome, where the proximal
7:58
duodenum is dilated, and then a pseudo-obstruction,
8:01
where there's diffuse dilation of the bowel.
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If you see interstitial lung disease at
8:06
the lung bases, that's a nice tip-off that
8:08
you're probably dealing with scleroderma.
8:09
So...
8:12
So, why are the other answers incorrect?
8:13
Well, celiac disease on CT is really identified
8:16
by dilated bowel and, on fluoroscopy,
8:19
byt the jejunal and ileal fold reversal.
8:20
Eosinophilic enteritis really, um, identified by
8:24
diffuse bowel wall thickening, and it's quite rare.
8:27
And then adhesive small bowel obstruction
8:28
really wouldn't explain the esophageal
8:30
and lung findings that I gave to you.
9:55
Next case.
9:59
Take a look at the images.
10:08
And here are your answer choices.
10:18
This was part one of the question.
10:19
We're going to move on to part
10:20
two before we go over the answers.
10:26
All right.
10:27
Here's the follow-up question.
10:37
Good.
10:38
All right.
10:39
So we will go over the answer choices.
10:41
So the best diagnosis here was toxic
10:43
megacolon, and the majority of you chose that.
10:45
So, toxic megacolon, really identified by this complete
10:48
loss of haustra, and the mucosal irregularity here.
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And so, these tiny little pseudopolyps—
10:53
that’s from the mucosa, that’s ischemic, and it's dying,
10:56
and it's starting to slough off into the lumen.
10:59
And it’s part of this pattern
11:00
of this marked colonic dilation.
11:03
So, why are the other answer
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choices here incorrect?
11:06
Well, large bowel obstruction and Ogilvie's
11:08
syndrome, while they can cause dilated
11:09
colon, really wouldn’t explain the loss
11:11
of haustra and the mucosal changes.
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Ulcerative colitis, when it's uncomplicated,
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really shouldn’t have this much colonic dilation
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and also would not have these mucosal changes.
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And then for the follow-up question, the correct answer here
11:26
was to discuss with the team that it is contraindicated.
11:29
That is the correct answer,
11:29
and that's what the majority of you chose.
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Remember that in toxic megacolon, enema is
11:33
contraindicated because there's a risk of perforation.
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That colon is, uh, that colonic wall is dead,
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and ischemic, and, um, can risk perforating.
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And in fact, if you look closely at this
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image, at the yellow arrows here, you can see
11:46
that this patient had actually already perforated,
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and there's a little bit of pneumoperitoneum.
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Next case. This is a scrollable stack of images,
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so I'm going to let it play for a while, and then
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I'm going to give you sequential images as well.
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So I'll let this play.
12:13
And here are your sequential images if you
12:15
were to be able to scroll through them.
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You will be able to manipulate how fast you
12:20
scroll if you're given a stack on the exam.
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And here are your answer choices.
12:44
All right, looks like the majority of
12:45
you chose the correct answer,
12:46
which is, in fact, Meckel's diverticulitis.
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Remember, this is a omphalomesenteric duct remnant.
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Complications in adults—think much
12:53
more about small bowel obstruction and
12:55
diverticulitis, less likely bleeding.
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And then, of course, the rule of twos
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that is always harped on—2 percent of the
13:00
population, 2 feet from the ileocecal valve,
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and it's usually symptomatic before age 2.
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So, follow-up question to this.
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What is the next best step?
13:21
All right, looks like the correct answer eked out.
13:25
The next best step here is a surgical consult.
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Well, I think some of us gut-react,
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and we go to the free pertechnetate scan.
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Remember that this free pertechnetate scan
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is a distractor, and it's really to evaluate
13:35
for a gastrointestinal bleeding source.
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It's only going to be 60%
13:39
positive predictive value in adults.
13:41
This patient's problem is
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predominantly the diverticulitis.
13:45
And so, just like appendicitis,
13:47
it needs a surgical consult.
13:49
We haven't said anything about this patient bleeding.
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We just know that this diverticulum is inflamed.
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All right, next case.
13:58
Best diagnosis?
14:02
Formulate your thoughts.
14:09
Here are your answer choices.
14:19
All right, 100% correct.
14:21
I love it.
14:22
Uh, so the correct answer here is,
14:24
in fact, epiploic appendagitis.
14:26
And you can see that there is this small, ovoid fat
14:29
density here arising from the descending colon.
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Um, and you have a central dot sign, um,
14:35
which corresponds to this thrombosed vascular pedicle.
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When you see this central dot sign, it is
14:40
really pathognomonic for epiploic appendagitis.
14:43
So, the real infarct.
14:45
And so, you should be able to tell
14:46
the difference between these two.
14:47
Epiploic appendagitis happens in the
14:49
descending colon, the rectosigmoid.
14:51
The fat density is smaller.
14:52
It's in the one to three-centimeter range.
14:55
Ovoid, and again, when you see that central dot sign,
14:57
you know right away it's epiploic appendagitis.
14:59
In contrast, an omental infarct is
15:01
much more likely to be right-sided.
15:02
They are much larger.
15:04
They are typically less well-defined.
15:05
And depending on the size and how much necrosis
15:07
is going on, you can get central liquefaction,
15:10
like I've shown you in this example here.
15:14
All right, next case.
15:20
I'm going to let this CineStack scroll for a
15:22
minute, and then I will also give you still images.
15:33
Here are your still images.
15:43
And here are your answer choices.
15:54
All right, we're going to move on
15:56
to Part 2 of this question.
16:01
What is this patient at increased risk of?
16:04
And here are your answer choices.
16:05
Read all of the answer choices.
16:16
All right.
16:17
So, answer— the correct answer to
16:19
Part 1 of this question is ulcerative
16:20
colitis, which the majority of people got.
16:23
This is a really nice example of that lead
16:26
pipe colon that we are often taught about.
16:28
So, chronic repeated inflammation of the colon leads to
16:32
this featureless pattern with complete loss of haustra.
16:35
You can also see neural fat deposition in some cases.
16:39
It tends to involve the entire
16:40
colon, and especially the rectum.
16:42
And so, here I've given you arrows pointing out
16:44
this lead pipe appearance of the colon.
16:49
So, what is this patient at increased risk of?
16:51
They're at increased risk for both
16:52
toxic megacolon and colorectal cancer.
16:55
This is a friendly reminder to
16:56
read all of your answer choices.
16:59
So, why is perianal fistula incorrect?
17:01
That is a much more typical finding in
17:02
Crohn's disease, and that's because Crohn's is
17:05
transmural, and so it has more fistulization.
17:09
And also, ulcerative colitis, while it tends to involve
17:12
the entire colon, typically spares the anal canal.
17:18
Moving on to our next case. Best diagnosis—take a
17:23
look at the images, including this scrolling image.
17:30
I'm going to let it play for a while
17:31
before I give you your answer choices.
17:45
All right, and here are your answer choices.
17:56
Perfect.
17:56
It looks like the majority of people got the
17:58
answer correct, which is, in fact, a marginal ulcer.
18:01
So, the key here is identifying that there's lots of
18:04
inflammation in this patient who is post-gastric bypass,
18:07
and the inflammation is all at the gastrojejunostomy.
18:10
So, this happens when gastric acid crosses the
18:13
GJ and enters the jejunum, and it makes the
18:15
jejunum really angry and inflamed because it's
18:17
not used to receiving all of that acidic fluid.
18:20
And so, here you can see that there is wall
18:22
thickening, and surrounding fat stranding, and
18:25
outpouching here at the gastrojejunostomy.
18:28
So, why are the other cases incorrect?
18:30
Well, while these are all other
18:31
complications of a gastric bypass, they don't
18:35
apply—they don't fit these imaging patterns.
18:37
So, afferent loop syndrome is a type of
18:38
small bowel obstruction in the right upper
18:40
quadrant involving the afferent loop.
18:42
Gastro-gastric fistula is really identified
18:44
by fluid, or if you're lucky enough to have
18:46
given oral contrast in the excluded stomach.
18:48
These patients typically have weight gain.
18:51
And then, a GJ stomal stenosis—you might think of that
18:53
as a bowel obstruction involving the gastric remnant.
18:57
So, you'd expect to see a dilated
18:58
gastric remnant and a dilated esophagus.
19:04
All right.
19:05
This is the same patient as the last case,
19:08
but two weeks later. What is your best diagnosis?
19:13
Take a look at the images. Form your thoughts.
19:22
And here are your answer choices.
19:32
Perfect.
19:33
And the majority chose the correct
19:34
answer, which is a pyogenic abscess.
19:37
So, here we can see that there's this, um,
19:40
coalescing intrahepatic collection, and if you're
19:43
lucky, you can see a double target sign, either
19:45
involving the entire rim of the collection or,
19:47
in this case, just the posterior margin,
19:49
and that's really indicative of a pyogenic abscess.
19:52
So, what is the double target?
19:53
Well, I zoomed in here, and I'm really showing the
19:56
double target here, just along the posterior margin.
19:59
That's when there's central necrosis,
20:00
this enhancing rim of granulation tissue,
20:04
and then perilesional inflammatory edema.
20:06
So, that makes up your double target.
20:09
Okay.
20:11
Next case.
20:14
Take a look at the images and formulate your thoughts.
20:23
And here are your answer choices.
20:33
Use everything on the images.
20:38
All right.
20:39
All right.
20:39
Looks like we were a little more
20:40
evenly split here between sclerosing peritonitis
20:43
and pseudomyxoma peritonei.
20:45
The correct answer here is sclerosing peritonitis.
20:49
So, the key here is identifying
20:51
these sheet-like peritoneal calcifications.
20:55
What this is really getting at is what's the
20:56
differential for sheet-like peritoneal calcifications.
20:59
You could think about prior bacterial peritonitis,
21:02
chronic peritoneal dialysis, and sort of what goes
21:05
along with that is secondary hyperparathyroidism.
21:07
So, the key here is really to use
21:09
everything that's on the images.
21:10
So, this patient's native kidneys are really atrophic.
21:13
You can infer that they are on dialysis.
21:17
So, sheet-like peritoneal calcs, very
21:18
characteristic of sclerosing peritonitis.
21:23
So, the other answer choices—why are they incorrect?
21:25
Well, let's talk about pseudomyxoma
21:26
peritonei since that was the distractor here.
21:28
You really want to think much
21:29
more about scalloped margins.
21:31
You typically don't see this degree of sheet-like
21:34
peritoneal calcs, especially if it's prior to treatment.
21:37
So, that would be highly unusual.
21:39
The other answer choices—peritoneal mesothelioma,
21:42
you'd be much more likely to see masses or cysts,
21:45
not so much the peritoneal calcifications,
21:48
and the diffuse ascites, and then peritoneal
21:50
carcinomatosis, you'd be much more likely
21:52
to see omental caking or nodules.
21:54
Um, really the identifying feature
21:56
here is these sheet-like peritoneal calcs.
22:03
Alright, next case.
22:05
Formulate your thoughts.
22:14
And here are your answer choices.
22:23
Alright, looks like we, uh,
22:26
were also not quite sure here.
22:27
Um, so the correct answer here is littoral cell angiomas.
22:30
These were half proven.
22:32
So, what this is really getting at
22:34
is, um, what's your differential for
22:36
multiple hypoenhancing splenic lesions?
22:38
Well, you think about things like METS, sarcoid,
22:41
um, and then you get down to these, um, other benign
22:43
things like littoral cell angiomas, um, and peliosis.
22:47
So, why are the other answers incorrect?
22:50
Well, splenic infarcts—the morphology here is wrong.
22:52
Those tend to be more wedge-shaped and subcapsular.
22:55
These are much more intraparenchymal.
22:56
Echinococcal cysts.
22:58
The APR would really need to show you these,
23:01
like, clearly defined daughter cysts in order
23:03
for you to confidently make that diagnosis,
23:05
and I have not pictured them here for you.
23:07
And then post-traumatic pseudocysts—these are true
23:09
cysts, they don't have any intralesional enhancement.
23:12
On these images, you can clearly see that,
23:14
um, this lesion is taking up contrast between
23:16
the arterial and the venous phase, and so this
23:19
definitely has some, um, internal vascularity to it.
23:25
Alright.
23:26
Best diagnosis.
23:29
Take a look at these images.
23:36
And here are your answer choices.
23:46
So, it looks like we also had an even split here.
23:49
So, um, when I'm dealing with an MR case that has
23:54
multiple images, I start by identifying each sequence.
23:59
So here we have a T2 coronal, a T1 fat-sat
24:03
pre-contrast, and then a T1 post-contrast subtraction image.
24:08
So we can see that we've got some T2 shading and
24:11
some intrinsic T1 hyperintensity within this lesion.
24:14
This combination of signal between T1 and T2
24:18
is very characteristic for blood products.
24:20
You could think of that just like
24:21
you would for an endometrioma.
24:23
You can see that there's no intralesional enhancement.
24:26
You also notice that the stomach and
24:28
the proximal duodenum are quite dilated.
24:30
So, the correct answer here is a duodenal hematoma.
24:33
So, causes of duodenal hematoma—blunt abdominal
24:36
injuries is by far the most common, although it can
24:38
also be caused by an underlying coagulopathy.
24:40
Nearly a third of these cases present with proximal
24:43
small bowel obstruction, like this case did.
24:46
It's typically associated with
24:47
other solid organ injuries.
24:49
Um, this particular, uh, patient, um,
24:52
had dropped a barbell on his stomach.
24:55
So, um...
24:58
The ABR can show you common things like duodenal hematomas
25:02
in uncommon ways, for example, on an MRI.
25:05
Um, but just remember to break it down by, um,
25:09
each sequence and then really, um, think about,
25:12
you know, what blood looks like on, um, on an MRI.
25:19
All right.
25:20
Next case—best diagnosis.
25:22
Use all of the images. Formulate your thoughts.
25:31
And here are your answer choices.
25:41
Alright, and the majority chose the correct
25:43
answer here, which is, in fact, pseudocirrhosis.
25:46
So, this happens after treatment of diffuse
25:48
liver metastases, typically with breast cancer.
25:51
Um, and you get hepatic capsular
25:53
retraction and fibrosis.
25:54
Um, and these patients may or may not have,
25:56
uh, clinical evidence of liver failure.
25:59
So, why not the other answer choices?
26:01
Well, really, the only distractor here is cirrhosis,
26:04
and it might have a very similar appearance to this
26:07
post-treatment scan, but it wouldn't fit with the
26:09
history, and I've given you the pre-treatment imaging.
26:11
It really wouldn't, um, explain the
26:12
diffuse, um, FDG-avid hepatic uptake.
26:17
All right, next case.
26:21
You can just go ahead with the answer choices.
26:32
All right, it looks like the majority of you
26:33
did, in fact, choose the correct answer choice,
26:36
which is primary sclerosing cholangitis.
26:39
You can see that there is both
26:40
intrahepatic and extrahepatic biliary ductal dilation, and stricturing,
26:45
very characteristic of PSC.
26:48
That's why the other answer choice is incorrect,
26:50
while primary biliary cirrhosis really only affects
26:53
the intrahepatic ducts. AIDS cholangiopathy,
26:56
while it can involve both the intra-
26:58
and extrahepatic ducts, really occurs in very sick individuals,
27:01
people who have a CD4 count less than 100.
27:03
It does not fit the history I've given you.
27:06
And also, um, tends to have
27:08
papillary stenosis, which I have not pictured here.
27:11
Recurrent pyogenic cholangitis, really
27:14
identified by really dilated intrahepatic
27:16
ducts with filling defects from stones,
27:18
again, which I have not pictured here.
27:22
So, pertaining to this patient,
27:23
here's a follow-up question.
27:26
What are they at increased risk for?
27:29
Read all of your answer choices.
27:39
All right, looks like the majority chose the right
27:41
answer here, which is A, B, and C, meaning cirrhosis,
27:44
cholangiocarcinoma, and gallbladder carcinoma.
27:47
So, I think we are all very much aware of the
27:50
increased risk of cirrhosis and cholangiocarcinoma.
27:52
We see that on a day-to-day basis.
27:55
These patients have a 400 times increased risk
27:57
of cholangiocarcinoma compared to the general population.
28:00
Sometimes, we forget about their
28:01
increased risk of gallbladder cancer.
28:03
They have a lifetime risk of about 3% to 14%,
28:06
which is about 10 times that of the general population.
28:08
So, this patient is at risk for all of these things.
28:16
All right, next case. I'm going
28:18
to give you sequential images.
28:23
What is your best diagnosis here?
28:34
All right, 100% got the right
28:36
answer here, which is, in fact, aspiration.
28:38
What I have given you is basically a
28:40
bronchogram—just massive aspiration.
28:43
You can see that, um, the airways here at the
28:46
lung bases are actually really dilated and
28:47
bronchiectatic, and so this patient's probably
28:49
been chronically aspirating for a while.
28:56
All right, best diagnosis.
29:10
All right.
29:10
The majority here got the correct
29:11
answer, which is, in fact, lymphoma.
29:14
So, when in the mesentery, you're going
29:15
to look for it to encase the vessel.
29:17
So, you can see here that there's
29:18
all this lymphadenopathy that's
29:20
working its way around the vessels.
29:22
That's the sandwich sign.
29:24
And then, also in the retroperitoneum, it will encase
29:27
the aorta and IVC and lift it off of the spine.
29:30
So, very characteristic appearance for lymphoma.
29:39
Next case.
29:41
Look at all of your images.
29:52
It looks like the majority here did get the correct
29:54
answer, which is a lymphangioma, identified by this
29:59
low-density fluid signal mass that is
30:03
conforming and insinuating around the
30:05
existing structures. On ultrasound,
30:08
it has this really characteristic honeycomb appearance,
30:10
and they can be both intraperitoneal or extraperitoneal.
30:13
Lymphoma, mesothelioma, and nodal mets are
30:16
incorrect because those would be much more likely
30:18
to be solid in appearance and have much more
30:21
enhancement on post-contrast CT.
30:30
All right, next case.
30:41
So, we have an even split, but the
30:42
majority did eke out the correct answer
30:44
here, which is a serous cystadenoma.
30:48
So, these are typically honeycomb
30:50
or microcystic in appearance.
30:52
On a contrast-enhanced CT, those really
30:54
tiny honeycombs or microcysts, they can
30:57
look kind of solid around the periphery.
31:00
But on a T2 sequence, you can clearly see
31:04
that these are, in fact, just tiny little cysts with
31:07
these very thin, fine septations throughout it.
31:10
Very occasionally, they can
31:11
be oligocystic or polycystic.
31:13
What I've given here is the much
31:14
more classic microcystic.
31:17
The tip-off here that this is a serous cystadenoma,
31:20
is this central stellate calcification. Ansd so, you can
31:23
see even on the T2 that there's this architecture
31:27
forming here towards this central stellate process.
31:30
And on the CT, you can see that it's all calcification.
31:33
So, when you see this morphology and
31:36
this architecture, it's a very characteristic
31:38
appearance for a serous cystadenoma.
31:41
Mucinous cystic neoplasm is much more likely to
31:43
be unilocular or just a few large cysts.
31:48
A pancreatic neuroendocrine tumor, you'd really
31:50
need to show some sort of hypervascularity
31:51
to confidently make this diagnosis.
31:54
And a SPEN, while they can have calcifications,
31:57
really, this architecture with a central stellate
32:01
calcifications is much more characteristic of a serous cystadenoma.
32:08
Next case.
32:12
Use all of the images.
32:23
All right, looks like the majority did get to the
32:25
correct answer, which is a focal nodular hyperplasia.
32:29
So, as I mentioned earlier, when I'm dealing with these
32:32
questions that have multiple sequences or images,
32:35
I start by identifying each one that I'm looking at.
32:38
So, here we've got a T2.
32:39
We can see that there's a central
32:42
T2-hyperintense scar in the middle, but the,
32:44
the parenchyma of this
32:46
lesion is actually, like, very subtly T2 bright.
32:49
Barely above background liver.
32:52
On this out-of-phase image, which we identify by this
32:55
India ink artifact, there's no intralesional fat in it.
32:59
Here, we have an arterial phase image where
33:00
we see that the majority of it is really
33:02
hypervascular, except for this central scar.
33:05
And then, this is an EOVIST scan, so this is
33:07
a hepatobiliary phase. You can tell because
33:09
there is some retained
33:11
contrast here in the intrahepatic bile ducts.
33:13
You can see that there is uptake
33:15
slightly above that of background liver.
33:18
So, FNH lesions, you can think of them as
33:20
stealth lesions because they're almost
33:22
isointense on T1, T2, and venous phase imaging.
33:26
What tips them off is if you're lucky enough to
33:28
get this central scar, which is T2 bright and has
33:30
very delayed enhancement. And then, the majority of
33:32
the lesion is arterial enhancing, and then there's
33:34
persistent uptake similar to or above that of
33:37
background liver on the delayed hepatobiliary phase.
33:43
Hemangiomas are characterized by peripheral
33:46
discontinuous nodular enhancement,
33:49
and poorly differentiated HCCs and
33:50
metastases really shouldn't have this
33:53
persistent uptake on the hepatobiliary phase.
34:00
All right, next case.
34:02
Best finding, best diagnosis for
34:05
the finding at the yellow arrow.
34:07
Use all of your images.
34:18
All right, looks like the majority of
34:19
you got to the correct answer.
34:21
So, this is in fact a dropped gallstone.
34:26
All right, this is in fact a dropped gallstone.
34:29
So we can see that there is this punctate
34:31
hyperdensity here along the hepatic capsule in
34:33
this patient who has, in fact, had a cholecystectomy.
34:37
This punctate hyperdensity is intrinsically
34:40
T1 bright, so this is a T1 FAT SAT sequence.
34:44
And then, this is a subtraction image.
34:47
You can tell because the fat is almost all the way dark,
34:49
but there is still contrast in the vessels, and you can
34:52
see that there is no enhancement within this lesion.
34:55
So, this is consistent with a dropped gallstone.
34:57
So, when you see this intrinsic T1 hyperintensity,
35:01
that really helps you narrow your differential.
35:03
So you want to think about
35:04
intrinsically T1 bright stuff.
35:05
So, things like subacute blood, cholesterol—like
35:09
cholesterol gallstones, melanin, and proteinaceous debris.
35:14
So dropped gallstones, they tend to
35:15
occur along the hepatic capsule, as well
35:17
as dependent areas in the abdomen.
35:18
So, along the hepatorenal
35:19
recess or the pericolic gutters.
35:22
This is a case of an uncomplicated gallstone, but
35:25
they can develop some pretty significant complications,
35:27
including inflammation, abscess, and fistula.
35:32
Good job on this case, guys.
35:34
Let's do the next one.
35:39
Read all of your answer choices.
35:50
All right.
35:51
And it looks like the majority of patients did,
35:53
or the majority of students did, in fact, get to
35:56
the correct answer, which is "any of the above."
35:58
So, what this question is getting at is,
36:00
what is your differential for linitis plastica?
36:03
So, here we can see that the stomach wall is
36:06
diffusely thickened, and we've got complete
36:08
loss of the normal gastric fold pattern.
36:10
So, this is very characteristic of linitis plastica.
36:14
So, what can cause linitis plastica?
36:17
Well, you can have a primary adenocarcinoma, like a
36:19
signet ring cell carcinoma, lymphoma, or metastases,
36:24
especially from breast, can cause this appearance.
36:27
So, any of these things can cause a linitis
36:30
plastica appearance, and you just needed
36:31
to recognize this, this, um, appearance.
36:40
All right, next case.
36:41
This is part one.
36:44
There will be two parts.
36:56
It looks like we have an even split.
36:59
Let's do the second part.
37:01
And then we will come back and
37:02
talk about the correct answer.
37:15
Good.
37:15
Okay.
37:17
So, let's talk about the correct answer to the first one.
37:19
So, this post-liver transplant ultrasound.
37:22
So, let's look at what we are actually presented with.
37:27
So, we are given the prior exam,
37:29
which was four days post-transplant.
37:31
You can see on this exam, we did have a normal or a
37:36
nearly normal arterial waveform where we have a clear
37:38
systolic peak tapering off towards end-diastole.
37:43
On the current exam, which is two days later,
37:45
or six days post-transplant, you can see that
37:48
we've lost that normal arterial waveform.
37:51
That is a very concerning finding in the early post-
37:53
operative period, and you must interrogate that quickly.
37:58
So, really what you're left with is, um,
38:00
a CT angiography or an MR angiography.
38:03
And between those two options, a CT angiography
38:05
is much faster, um, and is, um, much more
38:08
practical for a very sick post-transplant patient.
38:11
It is inappropriate to wait 24 hours on this exam.
38:15
Um, this is clearly a change and a
38:17
loss of a normal arterial waveform.
38:18
And that is very concerning, um,
38:20
for acute arterial pathology.
38:22
Do not leave this alone.
38:24
Um, if you do no further follow-up,
38:27
um, you really haven't interrogated
38:29
what's going on with the artery.
38:33
So, here I've given you the CT angiography.
38:37
And this shows that there is, um,
38:39
an early hepatic artery thrombosis.
38:40
So, you can see that there is a
38:41
cutoff of the celiac artery here.
38:45
And then you can even see that there's
38:47
really no, um, contrast-enhanced vasculature,
38:51
no contrast-enhanced artery, um, anywhere
38:53
along the length of the porta hepatis here.
38:56
Early hepatic artery thrombosis is really the most
38:58
feared complication because it has a very high
39:00
morbidity and mortality in the early postoperative
39:02
appearance— in the early postoperative period.
39:05
So, in ultrasound, you're really looking
39:07
for this loss of waveform, like I showed
39:09
you in the first part of this case.
39:12
So, typically, it starts out with a high resistive
39:13
index, which can be really hard to differentiate
39:16
from just, like, early postoperative edema,
39:18
but then it progresses to slow flow and parvus tardus,
39:21
and eventually loss of flow, which is what we
39:23
were seeing on that six-day post-op ultrasound.
39:28
So the next steps, depending on your
39:30
institution, will either be CT angio,
39:34
catheter angio, or straight to surgery.
39:36
That depends on the clinical picture
39:38
and your institutional practice.
39:44
All right, next case.
39:47
Oh, I wanted to show you one quick thing.
39:48
So one of the distractors here is a late
39:50
hepatic artery thrombosis. Um, it doesn't fit the
39:52
early post-op time period that I've given you.
39:54
And also, um, this often develops,
39:56
um, slowly and over time.
39:58
And so you'd be much more likely to see
39:59
collateral vessels, which we don't see here.
40:05
All right.
40:08
Next case.
40:10
Take a close look at the image.
40:21
All right.
40:21
Looks like the majority of
40:22
people got this answer correct.
40:24
Um, so the correct answer here
40:26
is gastroesophageal reflux.
40:27
This is a case of feline esophagus, and that's really
40:31
where you get this very striped appearance with these
40:33
very thin, one- to two-millimeter circumferential folds
40:36
that involve the lower, um, two-thirds of the esophagus.
40:39
And they're very transient when you
40:41
are, um, doing fluoroscopy in real time.
40:45
Uh, these are associated with gastroesophageal reflux.
40:49
So are the other answers incorrect?
40:50
Well, CMV is really identified by large, flat ulcers.
40:54
Candida has these discrete, small, shaggy plaques.
40:57
And then scleroderma has this, um, distal dilation
41:00
and poor emptying of the lower esophagus.
41:06
All right.
41:06
Next case.
41:09
Best diagnosis for the CT finding at the arrow.
41:20
All right.
41:21
It looks like we had sort of an— we weren't sure here.
41:24
Um, so, uh, the correct answer
41:26
here is actually focal fat, and so,
41:31
um, I've given you an in-phase and out-of-phase
41:33
sequence, and you can see that there's, um,
41:34
loss of the signal here between the in-phase
41:37
and the out-of-phase, and that accounts for
41:39
the hypodensity that's in the pancreatic head.
41:43
And we go back and we look at this T2
41:45
sequence and really see there's not really any
41:47
pancreatic parenchymal or peripancreatic edema here.
41:51
Um, and there is preserved, um, normal
41:53
intrinsic T1 signal hyperintensity
41:56
in this part of the pancreatic head.
41:57
So groove pancreatitis, autoimmune pancreatitis, and
42:01
pancreatic adenocarcinoma would not fit that appearance.
42:04
For autoimmune pancreatitis, groove
42:06
pancreatitis, you really expect to see some
42:08
T2 signal, and pancreatic adenocarcinoma,
42:11
you'd expect to see loss of
42:12
the normal T1 hyperintensity.
42:15
But the in-phase and out-of-phase images here really
42:17
seal the deal, particularly this area here
42:19
where you can see that there's loss of signal.
42:29
All right, next case.
42:31
Best diagnosis.
42:41
All right, looks like the majority
42:42
here did get the correct answer.
42:44
And so that is von Hippel-Lindau, um,
42:50
uh, von Hippel-Lindau.
42:51
So VHL in the abdomen.
42:52
Think about pancreatic and hepatic cysts.
42:55
In particular, this nearly complete cystic replacement
42:58
of the pancreas is very characteristic of VHL.
43:01
You can also get pancreatic serous cystadenomas,
43:03
pancreatic neuroendocrine tumors, and renal cell
43:06
carcinomas, which I've shown you here. I've given you
43:08
a picture of a mixed cystic and solid enhancing, uh,
43:11
renal mass, um, to help sort of tip us off that
43:14
we are dealing with a syndrome here of VHL rather than
43:17
other, uh, other types of isolated pancreatic cysts.
43:28
All right.
43:29
Best diagnosis in this patient with
43:32
a remote history of gastric sleeve.
43:44
All right.
43:44
Looks like the majority did get this correct.
43:46
So this is a case of atrophic gastritis.
43:49
You can see that there is complete
43:50
loss of the normal gastric folds.
43:53
When you see this complete loss of normal gastric folds,
43:55
there's really two things you want to think about.
43:57
A late-stage atrophic gastritis,
44:00
as well as linitis plastica.
44:02
So why are the other answers incorrect?
44:04
Well, while this tubular configuration is, um, is
44:09
characteristic of a post-gastric sleeve patient,
44:12
you should have normal gastric
44:14
folds, even after a gastric sleeve.
44:16
This patient does not have normal gastric folds.
44:19
Zollinger-Ellison syndrome
44:21
should have hyperplastic folds.
44:24
This patient's folds are completely gone.
44:26
And then a gastric stricture, while a known
44:27
complication of a gastric sleeve, is not pictured
44:30
here. Usually, that's, um, a short segment
44:32
involving the mid or distal pouch.
44:37
So this brings us to the end.
44:38
Here's a quick summary of all the diagnoses
44:40
that we have seen, um, and I've given you a
44:43
pretty, uh, wide-ranging distribution across
44:46
the gastrointestinal imaging, um, mimicking the
44:50
distribution that the ABR has for their blueprints.
44:53
I'm going to stick around to go over any questions
44:55
that you have about any of the cases that we've seen.
44:57
I hope that this was useful and that you got
44:59
to see a lot of different types of cases.
45:03
Thank you very much for joining.
45:05
And please give feedback on this session.
45:07
Thank you.
45:09
Thank you so much, Dr. Brickmeyer.
45:10
901 00:45:10,480 --> 00:45:11,550 That was great.
45:11
You got through so many cases.
45:14
Um, if people have questions, please go
45:15
ahead and put those into the Q& A box.
45:18
And I think there's one in there already.
45:20
Could you please repeat the MR pattern for blood?
45:23
Sure.
45:25
So, um, so think about an endometrioma, right?
45:28
Subacute blood, you're going to see intrinsic
45:30
T1 hyperintensity and, like this, T2 shading.
45:33
So that's exactly what's going on here.
45:35
T1 bright, mild T2 shading.
45:40
It's like an endometrioma, but
45:41
it's, it's in the duodenum.
45:43
And it's just because it's a hematoma.
45:45
And so this is a process that happens
45:46
as the blood starts to break down.
45:48
And so it's part of a sort of subacute process.
45:53
So, T1 hyperintensity—please have a differential
45:55
ready to go for intrinsically T1 bright stuff.
45:58
Subacute blood, cholesterol,
46:01
melanin, proteinaceous debris.
46:06
You covered everything then.
46:07
No questions.
46:09
Sounds good.
46:09
All right.
46:10
Well, please fill out feedback on this session.
46:12
Um, and thank you very much for attending.
46:14
Thank you so much, Dr. Brookmeyer, and for everyone
46:17
else for participating and attending, of course.
46:19
Um, you can access the recording of today's case review.
46:23
We will be sending that via email in a couple of days,
46:25
so be on the lookout for that.
46:27
Be sure to join us Wednesday,
46:28
May 8th, with Dr. Judy Squires.
46:30
She'll lead us in a rapid review
46:31
of pediatric imaging cases.
46:33
You can register for that on our website,
46:36
or in that email we'll send, or follow social
46:39
media for updates on future case reviews.
46:42
Thanks again for learning with us,
46:43
and we will see you soon.
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