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and previous noon conferences by creating a free account.

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Today we're honored to welcome Dr. Kevin Chang

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for a lecture entitled MRI

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of the Pancreas Basic Anatomy and Pancreatitis.

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Dr. Chang currently serves as the section chief

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of abdominal imaging

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and director of MRI at Boston Medical Center

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and Associate Professor

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of Radiology at Boston University Banian

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and at School of Medicine, as well as adjunct professor

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of diagnostic imaging at Brown University

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Albert Medical School.

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He's worked across multiple practices, health systems,

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and hospitals over the past 20 years in a wide variety

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of academic, private practice

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and hybrid clinical settings, caring for a wide variety

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of patient populations

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before dedicating his current practice

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to the care of the underserved.

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At the end of the lecture, please join him in a q

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and a session where he will address questions you

1:07

may have on today's topic.

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Please remember to use that q

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and a feature to submit your questions so we can get to

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as many as we can before our time is up.

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With that, we're ready

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to begin today's lecture to entertain.

1:17

Please take it from here.

1:19

Thank you very much for the, uh, the kind invitation

1:22

that give you guys a talk about, uh, MRI of the pancreas.

1:25

Usually the stop takes, uh, uh, a couple hours.

1:28

I've decided to, to divide it up in the first half

1:31

of the lecture that I usually give is, uh,

1:33

regarding basic anatomy as well as pancreatitis.

1:36

So basically non, uh, lesions

1:39

and, uh, non-malignant findings in the pancreas.

1:43

These are my disclosures.

1:46

MRCP was first introduced in 1991, so it's been

1:49

around for many decades.

1:50

Prior to MRCP, um, uh, ERCP was the way to,

1:53

to visualize the pancreas and the pancreatic duct,

1:56

and 40 to 70% of, of diagnostic ERCPs were negative.

2:00

So, Mr. MRI and Mr.

2:02

RP has largely supplanted ERCPs as well

2:05

as percutaneous transa cho angiograms

2:07

and the imaging of the pancreatic and the biliary treat.

2:10

And the advantages are that it's non-invasive.

2:12

It avoids, um, complications related to pancreatitis due,

2:16

you know, perforation, hemorrhage, sepsis,

2:19

and, uh, risks of sedation.

2:20

It's definitely a, also a cheaper exam than any RCP, uh,

2:23

does not involve ionizing radiation

2:26

and involves less operator skill and patient preparation.

2:29

It also allows for more accurate depiction

2:31

of the ductal diameter of both the biliary

2:34

and the pancreatic duct without the distension

2:36

using, um, contrast.

2:38

And there's a lower failure rate for, uh, MRPs, um,

2:42

but it does depend on patient cooperativity

2:45

and, um, in some sequences depend on

2:47

breath holding capabilities.

2:49

So, um, indications, clear indications for MRCP include, um,

2:54

obstructions in the GI tract, esophageal gastric

2:56

or duodenal obstructions, um, structuring

2:59

or edema at the Ular Vader, uh, presence of peram due

3:03

with needle diverticula can sometimes also make

3:05

ERCPs more complicated.

3:07

Uh, in terms of trying to cannulate the ula.

3:10

Also, per surgical, post-surgical anatomy can also

3:13

complicate, uh,

3:14

or make some ERCPs more difficult, uh,

3:16

specifically bowel reconstruction, including cholo,

3:19

doco enteric or pancreatic enteric anastomosis, as well

3:22

as gastro ostomies.

3:24

And then, um, depicting the, the ductal anatomy beyond

3:28

or upstream from an obstructing lesion is also a, a,

3:30

a great indication for MRCP

3:33

and clearly, uh, it's a, it's a great test in patients

3:36

that have had an incomplete or a failed ERCP.

3:38

There are some disadvantages to MRCP,

3:40

however, the, the spatial resolution of, uh,

3:44

MRI is less than that of, uh, the fluoroscopic images

3:48

of pain during an ERCP.

3:50

So this can limit the visualization

3:52

of small peripheral ducts.

3:53

It also clearly lacks the therapeutic

3:55

or, uh, pathologic diagnostic capabilities of more invasive,

3:59

um, uh, modalities,

4:00

but it can be helpful for the guidance

4:02

of those kind of procedures.

4:04

And it's not, oftentimes, it's not

4:06

as specific in differentiating malignant from benign causes

4:09

as obstruction,

4:11

although, uh, the use of, um, IV contrast can help look

4:14

for an obstructing mass.

4:16

Um, there are also other, other limitations that can, uh,

4:20

reduce your image quality, especially in patients

4:22

with large volumes of, um, fluid in the abdomen,

4:24

like in ascites

4:25

or in patients that have difficulty

4:27

with cooperation and breath holding.

4:29

And then there are a variety of susceptibility artifacts

4:31

as well that can limit visualization of the ducts.

4:34

So, basic principles behind Mr.

4:36

RCP, basically the images,

4:39

the imaging is based on the inherent T two weighted contrast

4:42

between slow flow fluid containing structures, uh,

4:44

versus the background organs and soft tissues.

4:47

Fluids have much longer T two relaxation times than

4:51

the adjacent soft tissues.

4:52

And the, and very heavily weighted T two weighted sequences

4:55

can depict these structures

4:57

with a higher relative signal intensity than the adjacent,

4:59

uh, fat and organs, which have a,

5:02

a shorter T two relaxation time.

5:04

When you image with a long, uh, echo time,

5:06

it helps the suppressive background signal

5:08

and improves, increases the contrast

5:10

and noise ratio of these structures.

5:13

For, uh, the technique for MRI, basically,

5:16

there isn't usually much patient preparation necessary,

5:20

but in the elective situation, um,

5:24

be having a patient be MPO for two to four hours prior

5:27

to the exam can certainly help

5:29

by reducing any residual fluid in the stomach

5:31

and the duodenum, uh, allowing you

5:33

to better see the adjacent ducts.

5:35

Um, an alternative can be giving some kind

5:39

of a negative oral contrast agent, uh,

5:41

I think gastro mark was taken off the market,

5:43

but anything else that can reduce your, um,

5:46

T two relaxation time for fluids such as, uh,

5:48

certain fruit juices

5:50

or even um, gadolinium, um, diluted, uh,

5:53

fluid can also help, uh, reduce, um, the,

5:56

the T two signal intensity of, uh, GI tract fluid.

6:01

Um, you can also give oxygen by nasal cannula

6:04

to help patients with breath holds.

6:06

And then the planes of imaging,

6:07

we will usually acquire them in the axi

6:10

and the coronal planes,

6:11

although some of the coronal fixed side images can also,

6:14

um, be acquired.

6:16

We're using various o liquidities

6:17

to better demonstrate the entire, um, length

6:21

of the pancreatic duct.

6:22

And we use both multis slice, uh, thin cuts, as well

6:25

as thicker slab images.

6:28

And then some supplementary, um, sequences

6:31

that we can use include, uh, 3D uh, pulse sequences

6:35

that acquire a volumetric, uh, volume

6:38

to better depict the anatomy, um, using thinner cuts.

6:42

And there's a bunch of different techniques for the 3D.

6:45

Um, uh, volumetrically acquired pulse sequences as well,

6:48

including, uh, multis slice 3D single shots, as well as, um,

6:53

uh, 3D grace

6:54

or gradient echo spin echo, um, hybrid type of images.

6:58

Some of them are, uh, fast enough now

7:00

that you can actually acquire the volumetric data

7:02

set in a single breath hold.

7:03

So this can certainly help in some patients

7:05

that have difficulty with, um, with, uh, longer breath holds

7:09

or inconsistent respiration that, uh, limit the utility

7:13

of some of the respiratory triggered free breathing pulse

7:16

sequences that can take a couple minutes to acquire basic

7:21

protocols include, um, axial single shots, uh, with

7:24

and without fat saturation, um, coronal, uh, images, uh,

7:29

thin cuts or,

7:30

or thick s labs, as well

7:32

as we usually will acquire T one weighted, uh, in

7:35

and out of phase images just to cover the pancreas, to look

7:37

for, um, the presence of, uh, fatty structures.

7:40

We use diffusion weighted images as well.

7:42

And then, uh, we will do an axial T one fats at pre

7:46

contrast, uh, even without, uh,

7:48

even when you're not giving IV contrast

7:50

to cover the pancreas because the intrinsic T one

7:53

hyperintensity of the, um,

7:54

pancreatic parenchyma is important to see.

7:57

Uh, and then obviously we will repeat

7:59

that pulse sequence in multi phases following the

8:01

administration of IV contrast when you're looking for,

8:04

um, abnormal enhancement been.

8:08

So in terms of planning for the, uh, the images, uh,

8:11

alpha axial plane, basically, uh,

8:13

we acquire thick slab images.

8:15

They can be a variable slice thicknesses to,

8:18

to depict the biliary, um,

8:19

or to, to depict the pancreatic ductal tree, as well

8:22

as the biliary ductal tree.

8:24

Um, the thinner their slabs are the less, um,

8:27

contamination there may be from adjacent fluid containing

8:30

structures, but the less

8:31

of the anatomy you're gonna be able to see.

8:33

There are also other techniques such as, um,

8:36

radial slab techniques

8:37

where you do these multiple coronal oblique, um, sequences

8:39

to cover the entire pancreatic

8:41

and biliary tree in, in different projections.

8:44

And then for 3D, um, 3D volumetric, uh, acquisitions, um,

8:50

you can do respiratory triggered, um, pulse sequences

8:54

where the, uh, slices are acquired at end at, uh,

8:57

end expiration for each, um, breath, um, cycle.

9:01

Or, uh, you can, uh, use some of these accelerated, um,

9:04

3D sequences

9:05

to acquire the whole volume in a single breath hold.

9:08

There are various pitfalls as well to be aware of.

9:11

Susceptibility artifacts will lead to, uh, loss of, um,

9:15

signal in fluid containing structures.

9:17

These could be related to surgical clips, metallic stents,

9:20

presence of gas, either in the adjacent bowel

9:23

or within the biliary or at the pancreatic tree.

9:26

Uh, it's, uh, helpful to correlate the, these appearances

9:30

with the gradient echo in

9:31

and outta face sequences to look for evidence

9:33

of susceptibility, which would, uh, manifest as,

9:36

as blooming on the endphase images compared

9:38

to the out phase images, as well as correlating

9:40

to any prior studies like, uh, x-ray or, or CT exams.

9:44

Uh, motion artifacts can also, um, uh, show up in, in some

9:48

of our images, uh, includes vascular pulsation artifacts

9:51

and, uh, biliary flow artifacts,

9:52

which can decrease your T two signal within, um,

9:56

flowing structures, uh, containing fluid.

9:59

And then you can get, uh, very pseudo filling defects like,

10:01

um, adjacent extrinsic structures like,

10:03

uh, crossing hepatic artery.

10:05

When you're looking at the bile ducts, um, the presence

10:07

of intraductal debris

10:09

or blood can look like, uh, filling defects in the,

10:12

in the ducks as well as, uh, gas in the ducks.

10:15

New mobilia or even gas in the pancreatic tree,

10:18

stringer oti contraction can also, um,

10:20

look like a stricture.

10:21

So it's important that some of those, uh,

10:23

fixed slab images get repeated multiple times, uh, over time

10:26

to try to, um,

10:28

visualize the entire tree at multiple time points to, to try

10:32

to image between a peristalsis

10:35

and then overlapping fluid containing structures in the

10:38

stomach or the duodenum or even the spinal canal

10:40

or, uh, ascites can also, uh, obscure visualization of the,

10:44

of the ducts.

10:46

Here's an example of, uh, an artifact, uh, in this case, uh,

10:50

on, uh, in visualizing the biliary tree,

10:53

there's this big signal void here in the, in the right, um,

10:56

hepatic tree.

10:58

And on a, uh, on a gradient echo sequence,

11:00

you can see this huge signal void, uh, in affecting the,

11:04

the right lobe of the liver.

11:05

And on a CT scan, you can see that that's related

11:08

to a metallic clip, uh, in the Porto Hepititis region.

11:12

So there's, uh, an example of susceptibility artifacts,

11:14

which can, uh, limit your visual visualization

11:18

of the biliary pancreatic tree.

11:19

On MRI. These are some maxalt weighted, um,

11:23

pulse sequences without fat saturation.

11:26

And, uh, in this case,

11:27

you can see there's a filling defect within the, uh, the,

11:31

the, the bile duct here within the duct.

11:33

But the important finding is

11:35

that it's on the anti dependent side of the lumen.

11:37

So that tells you that you're looking at, uh,

11:39

gas rather than a stone,

11:41

which would dependently layer along the dependent side

11:43

of the, of the, um, of the bile duct.

11:47

And then in this patient with, uh, findings

11:49

of chronic pancreatitis with this beaded look

11:51

to the pancreatic duct, you can see there's a, a loss

11:56

of signal in the, the common hepatic duct here,

11:59

which looks like it's transverse to the direction

12:02

of the biliary tree here on a,

12:04

on a thinner cut, a thinner slice.

12:06

Here, you can better see that, uh, that, uh, filling defect

12:09

that's, uh, a funny shape for,

12:12

for something like a, a stone.

12:14

And the reason for this appearance,

12:15

which you can also see here on this ERCP faintly, is

12:18

that there's a crossing vessel on this angiogram.

12:21

So this is the, uh, the extrinsic impression from a crossing

12:24

white hepatic artery simulating a, uh, narrowing

12:27

or a stenosis stenosis in the bi biliary tree.

12:31

This is an example of sphincter of ODI contraction.

12:33

You can see there's a focal narrowing here in the distal CBD

12:36

and an otherwise normal, uh, caliber pancreatic duct.

12:39

And, um, and that's just from, uh, intermittent, uh,

12:43

contraction of the sphincter of odi.

12:47

Here's another artifact here

12:48

where you can see there's a dilated pancreatic duct

12:51

with some side branch radicals

12:52

that are visualized here as well.

12:53

And, um, this structure over here looks like a stomach.

12:56

So this is a fluid filled stomach,

12:58

which when the fixed slab includes the, uh,

13:00

gastric g lumen can make it difficult to visualize the, uh,

13:03

pancreatic duct in that location.

13:06

And the solution to

13:07

that is just basically making the slab thinner

13:10

or just looking at your other sequences, um, to look around

13:14

behind or in front of the, um, these, these, uh,

13:16

fluid containing structures.

13:21

Next topic is gonna be embryology.

13:23

So, um, it's important to realize how the pancreas develops

13:28

as an embryo and a fetus, uh, to better understand some

13:31

of the anatomic variations that I'm gonna show

13:34

to you in a little bit.

13:35

So, basically, your, your, your, um, embryologic, um, origin

13:40

of the GI tract and the and and GI structures.

13:43

There's a kind of a gi tract here with little buds

13:47

that start to form that will eventually become the liver

13:50

and the, the gallbladder

13:52

and bile ducts, as well as, uh, the pancreas.

13:54

And the pancreas actually forms from two different buds.

13:57

Um, there's the, what's called the dorsal on log

14:00

and the ventral onlo, and these two little buds here.

14:03

And over the course of development, they, uh,

14:06

start to branch off.

14:08

And the ventral onlo, this tiny little, um, accessory part

14:11

of the pancreas swings around the right side

14:13

and the posterior side, dorsal side of the GI tract

14:17

swings over to the posterior margin of the, uh, the, the,

14:22

the dorsal on login

14:24

and eventually fuses the form, uh, the posterior half

14:27

of the pancreatic head.

14:31

And then the pancreatic duct forms,

14:33

there's the main pancreatic duct in the body

14:35

and the tail of the pancreas.

14:36

And then, um, the, the duct usually will, the majority

14:39

of the duct will drain as a duct

14:40

of rear song here towards the, the sphincter of OTI

14:44

and the amva.

14:45

And then there's variable appearance of the accessory, um,

14:48

pancreatic duct, also known as abductive Santorini.

14:52

This is a Grey's Anatomy photo of the, uh, of the pancreas.

14:56

And you can see here the pancreas is, um, basically, uh,

15:00

enveloped by the c sweep of the duodenum.

15:03

And, uh, you can see where the

15:06

ular forms along the medial portion of the second portion

15:08

of the duodenum.

15:10

And, um, and then in, in addition, the pancreas also, um,

15:14

uh, envelopes itself

15:16

around the superior mesenteric artery in vein.

15:19

And the, the mesenteric, uh, artery in vein help

15:22

to define the anatomy of the pancreas here.

15:24

So in relation to the pancreas, these are the anatomic terms

15:28

that we use to describe the different, uh,

15:30

locations in the pancreas.

15:31

You've got the pancreatic head, which is everything

15:33

to the right patient's, right of the mesenteric vein.

15:37

You've got the, um, pancreatic neck, which is just in front

15:40

of the, the mesenteric vein, the superior mesenteric vein.

15:43

And then the rest of the pancreas is divided in half by body

15:46

and tail portions.

15:47

And then there's an ate process, which is, um,

15:50

which is posterior to the mesenteric vein as well,

15:53

that tiny little, um, uh,

15:56

ventral the pancreatic ventral part that the, the, the pars

15:59

that the portion that used to be the ventral on

16:01

log of the pancreas.

16:04

There's also, um,

16:05

multiple ductal confluence variants that can occur.

16:08

Uh, you see the smooth muscles wrapping the, uh,

16:10

the confluence between the common bowel duct

16:13

and the pancreatic duct at the, uh, ula of Vader.

16:17

They, this common channel can be a varying lengths.

16:20

You can have a short common channel,

16:21

or no common channel at all,

16:23

where the ducts drain separately at the Ula.

16:26

Or you can have a long common channel

16:27

where sometimes the sphincter doesn't quite

16:30

envelop the entire confluence.

16:32

And this can result in reflux of pancreatic fluid, at least.

16:36

The theory is that there may be reflux of pancreatic fluid,

16:38

which can theoretically increase your risk

16:40

for choli doco seals.

16:42

And, uh, cholangiocarcinomas perhaps from chronic irritation

16:46

of the biliary re tree from pancreatic enzymes.

16:51

So the major ductal variants, uh, are, are here basically,

16:55

you, I showed you the, the typical

16:57

or the conventional ductal anatomy where you have most

17:00

of the drainage via the, the, um, the duct of ung

17:03

or the, um, the, the, the main pancreatic duct

17:06

and the duct of ung with, uh, variable, uh, appearances

17:10

or, uh, obliterated appearances of the accessory duct

17:13

or the duct of santorini.

17:14

Sometimes when the fusion of the ventral and the dorsal

17:18

and loin is incomplete, uh, drainage can, there,

17:22

there may be incomplete, um, convergence of the duct of ong

17:27

and the main pancreatic duct.

17:29

And the, in this case, the, the main pancreatic duct may,

17:32

um, drain completely by the duct of Santorini

17:35

or the accessory duct in what's called a

17:37

bank, a pancreas disease.

17:39

Vum. This is a abnormal, anatomic variant seen in about 10%

17:42

of all patients.

17:44

Uh, not all, uh, pancreas di vum.

17:47

In fact, most pancreas deum cases are not associated

17:50

with recurrent pancreatitis,

17:52

but a minority are, um, literature says 20 to 45%.

17:57

I see. I think that's, that may be on the higher side

17:59

as we increasingly recognize the, uh, the, the how common,

18:03

uh, pancreas deum is.

18:05

But, um, this is a, a variant

18:07

that you can see in 10% of individuals.

18:09

And then when the accessory duct is tortuous, um,

18:12

some people call this anep pancreatic.

18:14

I'm not sure if it's that much of a clinical relevance,

18:18

but it's just an interesting finding to, to see with a name.

18:22

This is a case of pancreas DI disease.

18:25

You can see the, the main pancreatic duct drains via the

18:28

duct of Santorini, and the duct of zone is separate,

18:30

basically, um, just draining the sennet process on

18:34

as a separate onset duct.

18:36

And the typical appearance is

18:37

that the common bowel duct in the pancreatic duct kind

18:39

of cross over each other, um,

18:41

and don't converge, uh, at the level of the pancreatic head.

18:44

And this is a 3D image showing you how, uh,

18:47

they are separate on ct.

18:49

Also, you'll see that the pancreatic duct will cross

18:52

anterior to the common bile duct

18:53

and drain separately from the CBD.

18:58

There is a variant of, uh,

19:00

of the visum called the dominant dorsal ducts.

19:03

So you may have, uh, what looks like conventional anatomy,

19:05

but if the majority of the drainage ends up happening via

19:09

the duct of santorini rather than the duct of then

19:12

functionally, they may, uh, function more like a duct, uh,

19:17

more like a pancreas di vum rather than a, um, uh,

19:20

rather than just conventional ductal anatomy.

19:23

Rarely, I guess, some of these patients can be, uh,

19:26

can have a, a, a recurrent pancreatitis, in which case, um,

19:30

a dominant dorsal duct syndrome may be present.

19:35

And then this, and they call this when the,

19:38

the ductal sanin is a little bit more dilated than the, uh,

19:42

the duct of, uh, this can be called a Santorini seal.

19:45

And then this is a little tortuous, um, duct of Santorini,

19:50

um, the so-called anep pancreatic.

19:55

Alright, another congenital variant

19:58

that's worth describing is, is the anular pancreas.

20:01

So if that ventral on login, that ventral bud

20:03

of the pancreas, um, doesn't completely migrate

20:07

around the dorsal half of the, the GI tract to, um,

20:12

converge on the pancreas if it, if it does that,

20:14

but it drags some of the ventral on login around,

20:18

and there's incomplete migration,

20:21

the pancreas may form a ring around

20:24

that second portion of the duodenum.

20:26

And this is called an annular pancreas.

20:28

And this, um, 3D image here, you can see

20:30

that there's narrowing of the lumen of the duodenum,

20:33

and sometimes you'll see a duct also, um, associated with

20:37

that anular, uh, parenchymal, uh, remnant of the pancreas.

20:43

And sometimes you'll see that pancreatic duct, uh, portion

20:46

of the pancreatic duct encasing the duodenum as well.

20:50

Um, this is seen in one in 2000 individuals,

20:52

and, uh, 10% of these cases may, may obstruct the duodenum.

20:56

They don't, most of them do not, uh,

20:58

but when they do, they often, uh, will present

21:00

as a pediatric patient this finding,

21:02

or as a neonate with this finding.

21:04

And it can be a cause in these cases

21:06

of gastric outlet obstruction

21:08

or biliary obstruction or pancreatitis.

21:13

Here are, um, multiple cases of, uh, an anular pancreas.

21:16

I'm showing it to you both in CT here

21:19

where you can see in this minimal intensity projection.

21:21

You can see there's a duct around the lumen

21:23

of the second portion of the duodenum here, as well

21:26

as excess pancreatic tissue around that second portion

21:29

of the duodenum on the this,

21:31

on these two coronal images here.

21:34

And you can see this very well on, on MRI as well.

21:37

So this is a, a great use of that.

21:39

Um, non-contrast T one fat saturated image

21:42

where the intrinsic T one hyperintense pancreatic tissue is

21:46

seen here to encase the, the second portion of the duodenum.

21:52

Next topic is ductal stones.

21:54

So, um, the CBD is identified in, in the, uh,

21:57

almost every MRCP and the sensitivities

22:00

and specificities in the, uh, the accuracies

22:03

for depicting ductile stones, whether it's, uh,

22:05

biliary ductal stones, which we more commonly look for,

22:08

or even pancreatic ductal stones is, uh,

22:10

certainly much better than that of ultrasound or ct.

22:13

It's now basically the test of the initial test of choice

22:16

for evaluating for ductal stones.

22:18

And there's an example of a stone in the common bile duct,

22:22

which looks like a filling defect distally plus minus, uh,

22:25

upstream, um, ductal dilatation on a thin cut,

22:29

you can better see that little meniscus sign

22:32

of a filling defect around filling defect within the lumen

22:35

of the distal duct here.

22:38

And when you're looking at, um, the coronal images,

22:41

whether it's a fixed slab

22:42

or a maximum intensity projection from a 3D, uh,

22:46

single shot, um, it's important to realize

22:49

that the maximum intensity projection images, uh, the,

22:53

the only, the maximum intensity pixels being projected

22:55

forward for you to look at,

22:57

and that may obscure visualization of smaller stones

23:00

that are, that are in completely obstructing the duct.

23:04

So it's, it's still important

23:05

to look at the source images in these 3D um, pulse sequences

23:09

to, to identify the individual stones

23:12

that may be obscured on the maximum intensity projections.

23:17

Here's an example of a stone within the pancreatic duct.

23:20

Um, I, I suppose some of these could form, uh,

23:23

theoretically from reflux in the CBD,

23:25

but more commonly they're identified in the setting

23:28

of chronic pancreatitis, uh, possibly from erosion of some

23:31

of the parenchymal calcifications into the duct, the,

23:34

the calcifications that you often see in the, in the, in,

23:37

in the setting of chronic chronic pancreatitis.

23:40

But they look just like a biliary stone.

23:42

Uh, here's a dilated pancreatic duct here at,

23:45

at the pancreatic neck and head,

23:46

and you can see there's a round filling

23:47

defect here distally.

23:49

And it'll look just like, um, like any other kind

23:51

of ductal calculus.

23:56

And when you're differentiating stones from strictures,

23:58

basically there are some features that help you, um,

24:01

make this differentiation, whether it's in the biliary tree

24:04

or in the, or in the pancreatic duct.

24:07

Um, malignant strictures tend to look more focal

24:11

with long segments of involvement and irregular margins

24:14

and maybe some asymmetric shouldering.

24:16

So these are examples of, uh, some, some, uh, long axis

24:19

and short axis views of the duct and,

24:21

and how they might appear, uh, in both views.

24:24

Whereas a, uh, benign stricture tends

24:27

to be a shorter segment.

24:29

It looks more, um, symmetric and smooth

24:32

and regular, uh, versus a stone, which will look like a, um,

24:36

a rounded filling defect with, uh, with a,

24:39

a meniscus sign here.

24:40

And it'll look more like a, uh,

24:42

circumscribed filling di defect within the dilated duct on

24:46

the transverse fuse.

24:49

And, uh, this is an example of, uh, the difference

24:52

between a stricture here

24:53

where you see the asymmetric shouldering

24:55

and long involvement of the, um,

24:56

of the distal CBD versus a filling defect in the distal CBD.

25:02

So, the next topic, you know, one

25:04

of the reasons why I discuss stones here is

25:06

'cause, um, one of the main reasons why we do MRI, uh,

25:09

in the setting of pancreatitis is to look for an etiology.

25:13

You know, they don't need us

25:14

to make the diagnosis of pancreatitis.

25:16

We don't always see the findings of pancreatitis on MRI.

25:20

Um, uh, they, the clinically, they'll, they'll know

25:24

that the patient has pancreatitis based off, uh,

25:27

elevated serum lipase and, and clinical presentation.

25:30

Um, but the, one of the main causes for pancreatitis is, uh,

25:33

gallstone cause gallstone pancreatitis.

25:35

So we're looking for the presence of gallstones, whether

25:38

or not they actually see them obstructing the duct or not.

25:41

But it's important to recognize the imaging features

25:43

of acute pancreatitis.

25:45

Typically, the, um,

25:46

the hallmark is gonna be per pancreatic edematous changes

25:49

the T two hyperintense signal, uh, either within the,

25:53

the pancreatic parenchyma

25:54

or the adjacent tissues, plus minus adjacent fluid, uh,

25:58

or fluid collections.

26:00

The pancreatic parenchyma itself may also appear

26:02

swollen and a deus.

26:03

And you may see not just per pancreatic fluid collections,

26:07

but, uh, the presence of pseudocysts, um,

26:10

or other complications depending on how long standing the,

26:13

um, the B of pancreatitis is.

26:15

Um, you can also look for evidence of necrosis, um,

26:19

in the form of either inhomogeneous enhancement

26:22

or areas of, uh, non enhancement.

26:25

And then what MR is particularly good at detecting is

26:29

the presence of hemorrhage.

26:30

So hemorrhage is going to look T one hyperintense even prior

26:34

to contrast administration.

26:36

And, uh, and MRI is also going to be a, a good way to look

26:40

for other alternative, um, causes other than gallstones, um,

26:44

for a pancreatitis, whether that's an anatomic

26:47

or an obstructive cause.

26:49

Here's a typical case of acute

26:52

and interstitial pancreatitis on, uh, MRI.

26:55

These two images are T two weighted fat saturated images in

26:59

the axial and the coronal plane here.

27:01

And you can see, um, a lot of T two hyperintense, uh,

27:04

edema within the interstices of the pancreas, as well as,

27:08

uh, uh, in the per pancreatic soft tissues

27:11

throughout the retroperitoneum.

27:12

It looks like it's extending into the,

27:14

the perineal space on the left side as well.

27:17

And then there's also some ascites in a peri splenic

27:20

and upper abdominal distribution.

27:22

And in the coronal images here, you can see a lot

27:25

of per pancreatic, um,

27:27

T two hyperintensity edema surround the pancreatic head.

27:30

And the third and the,

27:31

and the, um, the all around the duodenal sweep on, uh, pre

27:35

and post contrast, uh, T one fat saturated images.

27:38

You can see the preserved intrinsic T one hyperintensity

27:41

of the pancreas here, which does look a little swollen.

27:45

Uh, and then following contrast administration, you,

27:49

you will, you'll, you'll be looking

27:51

for homogeneous enhancement, uh,

27:53

to exclude necrotizing pancreatitis.

27:57

You're also gonna be looking

27:59

for other complications following, uh,

28:01

contrast administrations parti play particular attention

28:04

to the vessels, looking for any erosion

28:07

of arterial structures causing a pseudo aneurysm

28:10

or the thrombosis of the struc, other structures,

28:12

especially the spinal vein and, uh,

28:14

and superior mesenteric vein and portal vein.

28:18

Here is another typical appearance for acute pancreatitis.

28:21

Here you're seeing, uh, peripancreatic fluid collections on

28:24

the T two non-fat saturated image on,

28:27

uh, T one weighted images.

28:28

You're looking in particular at the intrinsic T one, uh,

28:32

signal for the pancreas.

28:34

In this case, you're seeing that there's a relative, um,

28:37

decrease in signal intensity in the pancreatic tail.

28:40

And, uh, with fat saturation,

28:42

you can also see hemorrhage extending, uh, anterior

28:45

to the pancreatic head.

28:46

In this particular case of a patient with, uh,

28:49

hemorrhagic pancreatitis

28:50

and following contrast administration, the lack

28:52

of enhancement in that pancreatic body tail here, uh,

28:55

which show you that there's also, um, the presence of, uh,

28:58

a necrotizing pancreatitis in the body tail as well.

29:04

And yet another case here, axial T two weight image.

29:07

Without fast saturation, it can be a little more difficult

29:09

to pick up the, um, the edema that you see better when you,

29:13

uh, look at a T two weighted pulse sequence

29:15

with fast saturation present.

29:17

So here you, again, you see the, um, the edema

29:19

and the pancreatic parenchyma here,

29:21

peri pancreatic T two hyperintensities consistent with, uh,

29:24

peri pancreatic edema.

29:26

And then looking at that, um,

29:27

pre contrast two unweighted image, um,

29:30

you can see there's a little bit

29:31

of in homogeneity in the pancreatic neck here, better

29:35

to evaluate that following contrast administration here,

29:39

where it's more obvious that in that pancreatic neck area,

29:42

there is an area of non enhancement, uh, which, um,

29:46

you can use the subtraction images

29:48

to make it even more apparent, uh, where there's a lack of,

29:52

of, uh, enhancement, especially if there's any in any, um,

29:56

heterogeneity on the pre contrast two weighted images

30:00

or if there's, um, presence of hemorrhage on that, uh,

30:03

pre contrast image, it may be easier to see that, uh,

30:07

on a subtraction image

30:08

where you subtract the pre contrast image

30:09

from the post contrast image.

30:11

And then in that same area of non enhancement,

30:13

you're seeing some very subtle mild CT hypo bone intensity,

30:17

which, uh, is another feature that you can see in, uh,

30:21

necrotizing pancreatitis.

30:23

So here looking for non enhancement T two hypo intensity,

30:26

as well as, um, uh, the other features that we,

30:29

we've discussed, um, in the setting

30:31

of interstitial embolous pancreatitis.

30:34

And yet another case here of, uh, necrotizing pancreatitis.

30:38

I'm showing you a CT here showing you the para pancreatic

30:41

fluid in addition to steatosis on the MRI, you can see

30:45

that edema to even better effect.

30:48

And then on the pre contrast T one weighted images,

30:52

you can see there's intrinsic TT one hyperintense signal

30:55

with a little bit of heterogeneity in the tail, kind

30:58

of subtle, but much more obvious following contrast

31:01

administration, where in the pancreatic body,

31:04

you're seeing this area of non enhancement, which in

31:07

retrospect, looking at that T two added image, again,

31:09

correlates to an area of subtle T two hypo intensity.

31:14

And the time interval between these two images

31:17

is about two days.

31:19

So that might be one explanation

31:21

for why you see the necrosis better on the MRI than than you

31:25

did on the, on the CT scan.

31:27

But, um, I think because ga gadolinium enhancement is

31:31

so much more apparent on an MRI, oftentimes the diagnosis

31:35

of necrotizing pancreatitis can be easier

31:37

to make on the MRI than on the initial ct.

31:43

Alright, another case in this case here,

31:46

I'm showing you a CT where there's relative hypo bone

31:48

enhancement in the, uh, ONT process of the pancreas here,

31:53

as well as, uh, presence of stats on the MRI on, uh,

31:58

T two weighted images with and without fat saturations.

32:01

You can see there's a little bit of focal, um,

32:04

uh, edema in that area.

32:06

But, um, on the T one pre contrast image,

32:10

you can see there's T one hyperintensity in

32:12

that uncinate process suggesting that, uh,

32:15

if it's more intense than the regular, um,

32:18

paren pancreatic parenchyma that may be suggestive

32:21

of hemorrhage in that location.

32:24

And then following contrast administration

32:27

and subtraction, you can see that area

32:29

that's hypertense on the pre contrast images subtracts out

32:33

from post contrast images, suggesting

32:35

that there's an a small area

32:36

of focal hemorrhagic necrotizing pancreatitis.

32:40

Uh, definitely, uh, something that would be easier

32:42

to pick up by MRI than on the initial ct.

32:47

And keep in mind that hemorrhagic pancreatitis is a,

32:52

um, a more urgent finding than other cases of pancreatitis

32:56

because of the, the theory behind the, um, the,

33:00

the hemorrhage is that it's thought

33:01

to be related to vessel erosion.

33:03

So, um, the finding

33:05

of hemorrhagic necrotizing pancreatitis should prompt, uh,

33:08

surgical consultation and possible intervention.

33:12

So that brings us to the, uh, Atlanta classification system,

33:17

uh, the revised Atlanta classification for pancreatitis.

33:19

So, acute pancreatitis is divided up into

33:23

two broad categories.

33:24

There's the interstitial emus, uncomplicated pancreatitis,

33:27

you know, uh, or non necrotizing pancreatitis versus

33:30

necrotizing pancreatitis.

33:32

So that's the first distinction you make based off, uh,

33:35

areas of non enhancement.

33:37

And then when you have fluid collections, uh, associated

33:40

with the pancreas, um, there, there's further branching

33:44

of these collections, depending on the time course,

33:46

whether it's, um, roughly within, uh, four weeks

33:49

of disease onset or longer than four weeks of disease onset,

33:52

basically trying to differentiate just per pancreatic fluid

33:55

collections from, uh, more organized collections,

33:59

which could represent either pseudocysts

34:01

or areas of Waldorf necrosis,

34:03

depending on whether you're talking about interstitial ems,

34:06

pancreatitis, or necrotizing pancreatitis, um,

34:10

less than four weeks after disease onset.

34:11

These pancreatic fluid collections are just, uh,

34:14

called acute per pancreatic fluid collections.

34:15

Whereas when you start to see a wall forming around them

34:19

and they start looking like they're more organized

34:22

and potentially drainable if infected, um,

34:25

we would call those pseudocysts.

34:26

And these tend to look more T two hyperintense

34:28

and, uh, simple in appearance on, uh, on mr if they're, um,

34:33

uncomplicated without infection or, or, um,

34:37

or, or other debris.

34:39

Whereas in the presence of necrotizing pancreatitis,

34:41

these fluid collections are called either acute necrotic

34:44

collections, if it's within, um, uh, their earlier onset,

34:47

uh, after disease onset, or if they are more organized

34:51

and walled off, that's when we call them

34:53

walled off necrosis.

34:55

And, um, walled off necrosis doesn't necessarily mean, uh,

34:59

they're sterile or infected.

35:01

That, that the distinction between, uh,

35:04

sterile collection versus an infected collection is largely

35:06

a clinical, um, differentiation.

35:09

Um, however, sometimes we can imply that, uh,

35:12

there's a higher likelihood

35:13

that a collection might be infected if we see gas

35:15

collections within it, and

35:16

that might be better seen on CT than mr,

35:20

and both these collections can be either intraparenchymal,

35:23

peripancreatic, or combined.

35:25

So this is the, uh, the revised

35:27

Atlanta classification system.

35:30

I'm gonna show you an example of a pseudocyst here.

35:33

Um, when you see a fluid collection next

35:35

to the pancreas in the setting of pancreatitis, uh,

35:37

if it communicates with the, the pancreatic duct,

35:41

that's even more, um, consistent with, uh, pseudo syst,

35:45

although you don't necessarily have to see that,

35:46

um, that appearance.

35:48

60% of pseudocyst will resolve spontaneously over time,

35:52

although, um, more complex pseudocyst,

35:55

either if they're enlarging, if they're hemorrhagic,

35:57

or if they're infected, some of these may require, um,

36:00

drainage, whether it's surgical,

36:03

endoscopic, or percutaneous.

36:05

And, uh, aspiration

36:06

of these collections usually yields aase.

36:09

There's another view of, uh,

36:11

of a slightly more complex sum case of, uh,

36:14

pancreatic pseudocyst,

36:16

where you have a per pancreatic fluid collection here

36:18

with a T two dark wall and, uh,

36:20

and lack of internal enhancement.

36:25

So next we're gonna go into some of the complications of,

36:28

um, of pancreatitis.

36:30

This is an ultrasound in somebody with a, uh,

36:32

pancreatitis presenting with abdominal pain,

36:35

elevated serum lipase.

36:37

Um, and, uh, on ultrasound, they saw

36:40

what they call the mass in the pancreatic head.

36:42

So this prompted further evaluation by ct.

36:46

And on the CT scan, you can see there is something

36:49

that looks mass like in the pancreatic head region, uh,

36:53

with some vessels displaced

36:55

or a faced, uh, along the medial margin here.

36:59

And then this was further evaluated by MRI

37:02

for a suspected pancreatic mass on, I'm, I'm,

37:06

I'll show you the, um, uh, I think for one reason

37:09

or other patient could not get, uh,

37:12

IV contrast, unfortunately.

37:13

But on the in and out of phase T one weighted images here,

37:15

you can see that, um, there are some areas

37:19

of intrinsically T one hyperintense signal,

37:21

which look different

37:22

with India ink artifact compared to the adjacent fat.

37:25

And on the TT weighted image,

37:27

there's some T two signal heterogeneity.

37:29

But because of this appearance with the, um, kind

37:32

of a T two signal heterogeneity in the center,

37:35

the peripheral margin of T one hyperintensity,

37:37

which looks different from the adjacent fat on the outer

37:40

phase images, the possibility

37:42

of a pseudo aneurysm was raised.

37:45

And, uh, whether you do it by CTA or MRA,

37:47

or if you just look at your arterial phase post contrast,

37:50

uh, MRI images, you're looking for, um, uh,

37:56

you know, a, uh, collection

37:58

or a structure attached to vessels, um, that's, uh,

38:01

consistent with a, uh, communication of the arterial tree.

38:05

So in this case, this was a pseudo aneurysm of the, um, of,

38:09

uh, the region of the, either the pancreatic duty or,

38:12

or GDA portion of the pancreas.

38:14

And any, uh, arterial structure around the pancreas can,

38:17

can, um, present with a pseudo aneurysm, uh, in somebody

38:20

with, uh, acute pancreatitis.

38:23

Other things you'd be looking for on those Mr.

38:25

A and MRV images

38:27

or the venous phase images would be, um, presence

38:29

of thrombosis as well as in in, in adjacent structures.

38:34

And then, um, here's another case of, uh,

38:37

a patient presenting with, uh, abdominal pain on CT and Mr.

38:42

TT weighted pulse sequences without fast saturation.

38:44

Here on the ct, you can see that there's, uh,

38:48

some wispy per pancreatic fatty stranding,

38:53

as well as a swollen appearance of the pancreatic, um,

38:56

parenchyma here, especially in the body

38:58

and tail, you can see there's also a kind of a, uh, uh,

39:04

a, um, margin.

39:05

There's a sharp, uh, encasement

39:07

of the pancreatic body on the CT images

39:10

and on the MR images, you can see that the, the, um,

39:14

pancreatic parenchyma look appears swollen.

39:17

There's, there's less of the feathery appearance

39:19

that you typically see, uh, on the, on MRI.

39:23

Um, and here, there, there also happened

39:25

to be some tiny little, uh,

39:27

cystic foci, which we will ignore.

39:29

But on the post contrast, MT one weighted images here,

39:32

you can see again that same appearance of, um,

39:35

perp pancreatic fatty stranding,

39:36

but also this sausage case appearance of, uh, of this kind

39:41

of, uh, enhancing capsule around the pancreatic body.

39:47

And in that case, this is a pa, a patient

39:49

with autoimmune pancreatitis.

39:51

This is that, that soft education, uh, appearance

39:54

of the pancreas is typical for autoimmune pancreatitis.

39:56

I'm showing another example here, multi-phase CT pre

40:00

and post conscious CT here, showing you

40:02

that diffuse swollen appearance of the pancreas, loss of

40:04

that, um, feathery soft tissue

40:07

and fat, uh, appearance of the pancreatic parenchyma

40:10

with a relative smooth margin, which shows, uh,

40:13

what looks like, uh, an area

40:15

of differential enhancement encasing the pancreatic body

40:18

entail here, also shown to good effect on the MR images

40:22

for the same patient T two fat saturated image.

40:24

Here, you could see that, um, sausage casing appearance, uh,

40:28

on the TT weighted images

40:30

and on the post contrast images as well.

40:33

So you can see the pancreatic parenchyma here with that, uh,

40:36

rind of tissue around the body and tail.

40:41

So, autoimmune pancreatitis, um,

40:42

type one autoimmune pancreatitis is associated with, um,

40:46

elevated serum IgG four.

40:48

So it is a common finding, uh,

40:51

and can be the presenting finding in patients with

40:53

IgG four related disease.

40:56

Keep in mind if, um, in these cases, if you're,

40:59

if you're proposing the, the possibility

41:01

of an IgG four related disease,

41:03

there are all their extra pancreatic findings

41:06

that you can look for to help, um, uh, increase your,

41:10

your confidence in making that diagnosis.

41:12

Many of these patients can present with, uh,

41:14

sclerosis and cholangitis.

41:16

They can also show renal pseudo masses or,

41:19

or, uh, areas of, uh, uh, uh,

41:22

interstitial nephritis in the kidneys.

41:24

They can present with retroperitoneal fibrosis.

41:27

You can see lung nodules

41:28

and ground glass opacities in the lungs as well.

41:31

Um, it is basically an immune mediated

41:33

fibroin inflammatory disease.

41:35

The typical imaging appearance in the pancreas,

41:38

which I showed you before, was this sausage pancreas with a,

41:42

a smooth, uh, appearance of the parenchyma with loss

41:46

of the loation and the variable appearance of this halo

41:49

or capsule of tissue around the pancreas.

41:52

Um, there may be a delayed enhancement relative

41:55

to a normal pan, to a normal pancreas.

41:58

And, um, there can be ductal narrowing

42:01

of the pancreatic duct in these areas without

42:04

upstream dilatation usually.

42:06

And typically, they don't show as many pseudocysts

42:11

as other cases of, uh, interstitial emus pancreatitis,

42:14

and can show less relative retroperitoneal fluid

42:18

and inflammation compared to other cases of pancreatitis.

42:21

And if the, if this diagnosis is being entertained, uh,

42:25

usually the next step is a trial of steroids,

42:28

and then you can follow up the images to see if it improves.

42:33

Here's, uh, an example of, uh,

42:35

extra pancreatic manifestations

42:37

of an IgG four related autoimmune pancreatitis.

42:40

In this case, this patient had renal lesions here,

42:43

which can look like renal masses.

42:45

Uh, um, it's difficult to differentiate from immuno masses.

42:49

Uh, they will look hypo.

42:52

The, the ones I've seen can look hypo enhancing

42:54

and diffusion restriction.

42:55

Sometimes they don't look very mass, like, uh,

42:58

it could look like a, an a bilateral lon nephritis, um,

43:02

without the clinical features, uh,

43:04

or, um, typical symptoms of pyelonephritis.

43:08

In this case. This patient also had a, a rind of soft tissue

43:11

around the aorta in a patient with, uh, an aortitis related

43:15

to IgG four related disease.

43:17

And here again, you can see T two hypo intensity,

43:19

renal masses, uh,

43:21

and, uh, uh, soft tissue around the aorta, as well

43:24

as an enlarged prostate, which is another finding

43:27

that you may see in some of these cases.

43:29

Uh, uh, prostatitis.

43:31

Other areas that can be, uh, affected by, um,

43:35

this autoimmune inflammatory response include the salivary

43:39

and the lacrimal glands.

43:40

So you can present with a, a sal Adenitis, um,

43:44

periorbital tissues, uh, lymph nodes, the thyroid gland.

43:48

You can present with a thyroiditis, uh, as well

43:50

as a prostatitis.

43:52

There are also findings

43:53

that have been described in the testes and the breasts

43:55

and in the pituitary gland.

43:58

So if you can make that diagnosis based off,

44:00

based off the spectrum of findings, oftentimes you'll,

44:03

you'll look like a, a hero,

44:04

because oftentimes, uh, the radiologist is the first one

44:08

to propose this diagnosis.

44:10

Um, the next topic is going to be, uh,

44:15

chronic pancreatitis.

44:16

So repeated bouts

44:17

of pancreatitis can result in atrophy and fibrosis.

44:20

Um, the, an imaging characteristic for this is not just, um,

44:24

dilatation and bead

44:26

and stricturing of the, the main pancreatic duct,

44:28

but you also see more side branch ectasia.

44:32

And the, uh, the biliary tree may also be dilated due

44:36

to fibrosis in the pancreatic head.

44:38

And, uh, now, RCP is, um, better than, uh,

44:42

better at characterizing moderate and advanced diseases, uh,

44:44

and not as good at being able to see earlier, uh, disease

44:49

as the side branch ectasia may be below the resolution

44:52

of MRI is a typical example of, uh,

44:56

chronic pancreatitis on a coronal thick lab image.

44:59

You can see, um, uh, dilated duct here

45:02

and side branch radicals, again here, dilated, uh,

45:05

pancreatic duct and, uh, biliary tree, um, with

45:10

that typical beaded appearance that's characteristic

45:13

for chronic pancreatitis.

45:15

And then the, um, last, um,

45:19

pancreatic functional related, um, topic I wanted

45:22

to address was, uh, secret

45:24

and enhanced, um, functional MRC ps.

45:27

Uh, we don't do a lot of these, but, um, but,

45:30

but some, you know, rarely we will get this, um, request

45:34

to evaluate pancreatic ductal function

45:36

or to better visualize the pancreatic tree by stimulating it

45:40

with, uh, with, uh, intravenous secretine.

45:43

So it's usually given

45:44

as 0.2 milligrams per kilogram dose by weight.

45:48

Uh, and you inject it very slowly over one minute.

45:51

And then you, uh, you obtain, um, fixed lab, um,

45:56

MRCP images, uh, at various time points over, um,

46:00

the, the course of the next couple minutes.

46:02

And then you get, uh, kind of a time course exam here, uh,

46:06

where the pancreatic duct should dilate in a

46:09

normal pancreas.

46:11

And then you can also try to quantify the amount of juices

46:14

that get end, that end up being excreted into the, uh,

46:17

duodenal lumen to try to, um, get a sense of, uh,

46:21

pancreatic exocrine function.

46:23

And then it also allows you

46:24

to get a better look at the sphincter of OD to assess

46:27

for any sphincter of OD dysfunction, as well as to, uh,

46:31

better evaluate the rest of the pancreatic ductal tree,

46:34

especially if it's a non dilated pancreatic, uh,

46:37

ductal, uh, duct.

46:40

And then I think the last topic I'm going

46:42

to talk about today is, uh, evidenced by this case here.

46:47

So I'm showing you a CT here, very similar to some

46:51

of the other cases I've shown you already

46:53

before, where you've got a CT image showing, uh,

46:57

peripancreatic fluid fatty stranding, a relative area

47:01

of non enhancement in the pancreatic neck.

47:03

But I'm gonna tell you, the presentation here is,

47:06

is not the same as the previous cases.

47:09

This patient didn't present with, uh, with, um, you know,

47:13

indolent abdominal pain.

47:15

This was a, a trauma patient who, uh,

47:18

suffered blunt abdominal trauma.

47:20

So, um, when you see non enhancement

47:23

or hypo enhancement in the pancreatic neck,

47:25

especially when it's right in front of the, um,

47:28

midline structures like the vertebral body, um,

47:33

you want to entertain the possibility

47:36

of pancreatic ductal transection for which MRCP is a, uh,

47:41

an excellent, uh, modality

47:42

to better evaluate the pancreatic, uh, the presence

47:46

of pancreatic, um, injury, as well as the status

47:49

of the pancreatic duct.

47:51

So here's a T one weighted outer phase image showing you

47:54

relative hypo intensity, uh, compared

47:57

to the intrinsically T one hyperintense pancreatic body.

48:01

And on the T two weight fa fast saturated image, here,

48:04

you can see a normal pancreatic duct caliber in the

48:07

pancreatic body with this area

48:09

of transection T two hyperintense laceration through the,

48:13

um, the pancreatic parenchyma.

48:16

And when they, when that laceration that you see on, on MRI

48:20

extends to involve at least 50% of the, um, thickness

48:25

of the pancreatic parenchyma,

48:27

there's a very high association with, um, uh,

48:30

a duct laceration.

48:33

So, um, so the main finding is a, a laceration

48:37

that's deeper than 50% of the thickness,

48:40

and then you'll oftentimes see the peripancreatic fluid

48:44

as well, which may be related to, to pancreatic, um, leaks.

48:49

This is what it looks like following contrast administration

48:52

during arterial and the venous phase.

48:53

Here you can see that lack of enhancement, again, not

48:56

to be confused in this case with necrotizing pancreatitis,

48:58

but, um, uh, pancreatic laceration involving, in this case,

49:02

more than 50% of that pancreatic, uh, thickness extending

49:05

to, to beyond the, um, the course

49:09

of the expected pancreatic duct.

49:12

And then on the fixed side images, again,

49:14

you can see the pancreatic duct of normal caliber

49:16

and then narrowing and non

49:18

visualized in the region of injury.

49:22

And, uh, this is a diagnosis it's

49:24

otherwise very difficult to make clinically

49:27

or on, uh, even on on ct,

49:30

but it's an important diagnosis to make

49:32

because, uh, it's, um, associated with very high

49:37

morbidity and mortality.

49:38

Mortality can be up to 20 to 50%, uh,

49:41

when the duct is disrupted.

49:42

And oftentimes the diagnosis is delayed, um,

49:46

because of, um, there's usually

49:49

multiple other associated injuries, uh,

49:51

when you do see a pancreatic duct, um,

49:53

or a pancreatic, um, laceration, uh,

49:56

hemorrhage in other organs, fistulas abscesses, sepsis.

50:00

There's a, there's a bunch of other, uh, complications

50:02

that are generally seen in these kind of patients with a,

50:06

with a very variable

50:07

and non-specific pre clinical presentation.

50:11

And then that might prompt, uh, any RCP to

50:14

actually demonstrate the ductal leak, uh, directly

50:17

with a contrast injection.

50:20

Alright, so that's a summary of, uh, my part one talk

50:24

for MRI of the pancreas.

50:25

We went over MRI principles and techniques,

50:28

and we went over a whole bunch of imaging pitfalls, uh,

50:31

particularly to MRI.

50:33

We went over the anatomy,

50:35

not just the embryologic development of the pancreas,

50:37

but, uh, ductal development

50:39

and the resulting ductal variants

50:40

that you can oftentimes see.

50:42

We went over stones and strictures, uh,

50:44

and the differentiation of those two

50:46

str, uh, findings on Mr.

50:48

Mrm RCP, as well as the, uh, findings of pancreatic

50:52

or, uh, findings of pancreatitis, both acute

50:54

and chronic, as well as various complications of, uh, of,

50:57

um, pancreatitis, including,

50:59

including necrotizing pancreatitis.

51:02

Um, we touched upon some

51:04

of the para pancreatic food collections as well as, um,

51:07

pseudo aneurysms.

51:09

And then last but not least, I wanted to touch on the topic

51:11

of, uh, pancreatic duct transections.

51:14

And, uh, with that, thank you very much.

51:17

I'm open to questions.

51:21

Thank you so much for sharing your lecture, Dr. Chang.

51:23

Yes. We will open the floor now for any questions.

51:27

If you've got a question, please pop that into the q

51:29

and a feature of Zoom, so we can work through as many

51:33

as we can before we need to close.

51:35

Okay, it looks like I have to stop sharing

51:37

to be able to see the, um,

51:39

Yeah, you might have to. No,

51:41

I found it. Awesome.

51:42

Mailbox box.

51:43

Okay, so let's see, multiple questions here.

51:55

Uh, so someone's asking about the sensitivity

51:57

of imaging findings of acute pancreatitis CT versus MRI.

52:01

I think they're both great for it.

52:03

I mean, keep in mind that, um, the, the goal

52:07

of imaging is not to make the diagnosis

52:09

of acute pancreatitis,

52:10

but to, uh, to evaluate for complications of pancreatitis

52:14

and causes of pancreatitis, whether that's gallstones,

52:18

whether there's biliary obstruction,

52:20

pancreatic ductal obstruction,

52:22

and obstructing mass in the pancreas,

52:24

or any of the other etiologies that I showed you.

52:27

I think MRIs better than CT in terms of the sensitivity

52:31

for finding the, uh,

52:32

the inflammatory changes in pancreatitis,

52:34

but I'm not sure exactly what the, the, the,

52:36

the actual numbers are behind that.

52:39

Um, uh, the other, the next question would be, uh,

52:43

how would you distinguish between focal necrotizing

52:45

pancreatitis and, uh,

52:46

hypo enhancing pancreatic adenocarcinoma?

52:48

That's an excellent question. There can be overlap.

52:51

We can't always differentiate focal pancreatitis

52:54

from a pancreatic mass.

52:56

Um, uh, that is definitely a, a known pitfall for

53:01

imaging of the pancreas.

53:02

Um, but, um, features would be, um, uh,

53:07

when I see a focal finding in the pancreas associated

53:11

with upstream ductal dilatation, uh, especially if there's,

53:13

uh, the lack of clinical findings that you'd typically see

53:16

with, uh, focal pancreatitis be more suspicious for, uh,

53:21

pancreatic adenocarcinoma.

53:22

In those cases, certainly follow-up imaging could also help,

53:25

um, resolution of findings.

53:27

You know, basically pancreatitis tends to be a waxing

53:30

and waning phenomenon, so

53:31

it should change an appearance over time.

53:33

But if, uh, if you have a persistent finding,

53:36

especially in the absence of, uh, pain

53:38

or elevated serum lipase

53:39

or other, uh, features that you typically associate

53:42

with pancreatitis, uh, that would certainly raise the, uh,

53:45

suspicion for, uh, pancreatic adenocarcinoma in, in,

53:49

in addition to the, the usual serum markers that you can,

53:51

um, run to, to elevate your, your suspicion for an a,

53:56

an focal adenocarcinoma.

53:59

And then there's certainly features

54:00

of pancreatic adenocarcinoma,

54:02

which I can get into in a part two of this lecture where,

54:05

um, you'd be, uh, more suspicious of an adenocarcinoma like,

54:08

um, um, vascular involvement, vascular encasement, um,

54:13

and, uh, obviously the presence of metastases.

54:19

All right.

54:24

So next question is, what do you do when you

54:28

find pancreatic calculi in the pancreatic head

54:32

and a dilated pancreatic duct, but you don't see a tumor

54:37

or in a pat or a mass in a patient

54:39

who never had pancreatitis?

54:42

Um, if I'm reading that correctly,

54:49

um, pancreatic calculus is not a typical feature

54:54

for a pancreatic mass.

54:56

So if I see a pancreatic ductal calculus, I,

54:58

I'll definitely mention it, especially if there's a,

55:00

an upstream d dilated duct.

55:03

Uh, it's a feature that we can see in the setting

55:05

of chronic pancreatitis.

55:07

Um, I think it's up to the gastroenterologist,

55:09

whether it's something that they want to go in

55:11

and try to fetch a stone for.

55:14

Uh, I guess it depends on whether they think

55:15

that the patient might improve, uh,

55:18

after, um, retrieving a, a, a stone from the, the duct

55:22

of a pancreat of a, of a pancreatic duct

55:24

and somebody with chronic pancreatitis, uh,

55:27

I've seen it be left behind in many, many cases.

55:30

I'm not sure if it's because, um,

55:32

there may not be significant, uh,

55:34

pancreatic exocrine function left, but, um,

55:37

but that's, it's definitely finding, I I will mention

55:39

to the, um, two our refers.

55:42

Whether it gets intervened upon

55:44

or not is, um, is another question,

55:47

but it's not typically something I see with a,

55:49

a pancreatic mass, a pancreatic mass, if it's associated

55:52

with ductal dilatation should look more like, uh, extrinsic,

55:55

uh, impression upon the duct.

55:57

And, uh, oftentimes more often than not,

55:59

I will not see the duct at the level of the mass.

56:02

So there's a finding called a, um, a duct penetration sign

56:05

that's been described where, um,

56:08

focal pancreatitis may narrow the, uh,

56:11

the traversing pancreatic duct.

56:13

But oftentimes on those thin cut TT weight images,

56:16

you may still see a trace of the pancreatic doctor, uh,

56:20

penetrating through the area of inflammation.

56:23

Whereas a pancreatic, uh, uh, a mass like an adenocarcinoma,

56:28

uh, often will, oftentimes will completely occlude the duct

56:31

with smooth upstream pancreatic ductal dilatation,

56:35

which is a different appearance than you typically see

56:37

with the dilated duct that you see

56:39

with in chronic pancreatitis.

56:40

So in chronic pancreatitis, you've got inflammation,

56:43

recurrent inflammation throughout the pancreas or fibrosis

56:47

or whatever the, um, the etiology of

56:48

that chronic pancreatitis is,

56:50

and it affects a duct in multiple locations.

56:53

So you get that beaded appearance rather than the smooth

56:56

upstream ductal delete that, that, uh, you'll see from a,

57:00

a single point of obstruction downstream, uh, from the duct.

57:05

And then, um, next question is the side effects

57:08

of secretin injection for MRCP.

57:10

I think the, the main one that, uh, that,

57:13

and the reason why we inject very slowly is

57:15

that it can cause nausea.

57:17

Um, we don't do a huge amount of them, so I have, I'm not,

57:21

uh, I don't, I don't often, uh, see what the, um,

57:25

other side effects for secretine injection might be,

57:27

but it is definitely a, a medication that's used, um,

57:31

relatively routinely in some, uh, ERCPs.

57:34

So it's, um, it's definitely a, a, a medication

57:37

that's relatively safe otherwise to give.

57:40

And then, um, somebody asked about

57:44

duodenal pan pancreatitis.

57:45

Certainly, uh, I, I can include that in a future lecture.

57:48

I should have, uh, remembered to put a slide in on that.

57:50

But, um, duodenal pancreatitis

57:53

or also known as a groove pancreatitis is, um, pancreatitis.

57:58

It's a, it's a form of mostly chronic pancreatitis

58:00

that occurs between the pancreatic head

58:03

and the, um, c-suite of the duodenum.

58:06

So it's often, uh, manifests as, um,

58:10

pancreatitis inflammatory changes in

58:12

that pancreatic duodenal groove

58:15

and, uh, is highly associated with, uh,

58:17

small pseudo sys in that location.

58:19

So it's got that characteristic appearance, uh, which, uh,

58:24

I, I, I'll show in a feature version of the talk.

58:27

Um, let's see. Next questions

58:34

somebody ask about, uh, pancreatic calcifications.

58:36

Could this be the only feature of chronic pancreatitis?

58:39

I think it can be, um, don't always see dilated, um,

58:42

docs in these cases, but typically pancreatic

58:45

calcifications, um, especially, uh,

58:47

when they're in multiple locations

58:48

and the pancreas are associated with, um,

58:50

with chronic pancreatitis.

58:54

Um, any tips for differentiating focal chronic pancreatitis

58:59

on a DC and dual energy ct?

59:03

Uh, good questions.

59:04

I'm not familiar with using, using a DC maps to, to

59:10

evaluate chronic pancreatitis.

59:12

Um, we do have a lot of dual energy CT at my institution.

59:16

Uh, I think the, the main feature, the main use that I use

59:19

for dual energy CT is on just looking there

59:23

or better accentuating the enhancement pattern

59:25

of the pancreas, particularly on the low, uh, KEV images

59:29

or on the iodine maps.

59:31

Um, uh, I think it also is a great way

59:34

to look at the vessels, um, especially the arteries

59:37

and veins, um, making sure that they're patent, uh,

59:40

in the setting of pan of, um, pancreatitis.

59:43

I'm not sure if I use dual energy

59:47

much in the evaluation of chronic pancreatitis.

59:53

And then somebody else was asking about severity

59:55

indices and grading systems.

59:57

There definitely are some systems out there.

60:00

I I don't tend to use them,

60:01

but there are multiple grading systems out there, uh,

60:05

which you can, uh, Google yourself.

60:08

Um, the next question is,

60:12

do pseudocyst communicate with a duct like an IPMN?

60:14

And the answer is yes. Um, when you see a cystic finding,

60:20

communicate with the duct, that narrows your differential

60:23

down to two possibilities.

60:25

One is, uh, an intraductal pap neoplasm,

60:28

and the other, the other is pseudocyst.

60:30

So, um, in those cases, the differentiation

60:34

can be made based off whether the patient is presenting

60:37

with pancreatitis or not.

60:38

But in the absence of, of that kind of a history, uh,

60:42

these are the ones where at least one follow-up is warranted

60:45

because a pseudocyst should change over time

60:48

or resolve, uh, in, in most cases,

60:51

whereas an IPMN will persist or maybe slowly enlarge.

60:56

So, um, so yes, both can communicate with the duct.

61:01

Next question.

61:06

So if you're unsure if an underlying pancreatic lesion is a

61:10

pseudo lesion from pancreatitis.

61:13

Um, when is the optimal imaging follow-up?

61:17

Uh, I'm not sure if there, if I'm aware of the exact, uh,

61:23

best time interval, basically.

61:25

Uh, uh, if, if it's acute pancreatitis,

61:29

I would follow up maybe in, I don't know, three,

61:32

three months maybe, or maybe

61:33

following resolution of symptoms.

61:35

Uh, I'm not, some kind of a follow-up would be,

61:38

um, would be good.

61:40

I'd have to there, there you could look at the, um,

61:45

there are some papers out there that will describe

61:47

what the imaging follow-up time interval is.

61:49

But, um, some, uh, reasonable amount

61:51

of time would be, uh, would be good.

61:53

I don't exactly know what the, the best timing is.

61:55

Usually I leave that up to the gastroenterologist to, uh,

61:58

to decide, uh, an optimal time interval.

62:00

But, uh, in the absence of, uh, of an opinion from them,

62:04

I would say within three months.

62:06

And then, um,

62:13

the next question has to do with hepatocellular carcinoma,

62:15

which is not relevant to this talk.

62:17

And then last question is, uh, relevance

62:21

of 40 flow MRI in assessing

62:23

vessels of the pancreatic region?

62:24

That's an interesting, uh, question.

62:26

I have seen some 40 flow papers out there looking at, um,

62:30

uh, mesenteric and, and, uh, portal venous flow.

62:34

Uh, it's definitely something

62:36

that I've seen done in research.

62:37

I don't know of many places using 40 flow

62:42

to look at the flow patterns.

62:45

Uh, and especially for pancreatitis.

62:47

Usually it's more for evaluation for portal hypertension,

62:50

but, um, but 40 flow is not, uh, in our, um,

62:54

routine clinical armamentarium for pancreatic imaging.

63:00

And then one last question here is,

63:02

in the pseudo aneurysm case, how can you differentiate

63:06

hemorrhagic pancreatitis without contrast?

63:12

So hemorrhagic pancreatitis on MRI, you can make that

63:16

diagnosis without contrast.

63:17

On the T one fat saturated image, we use M Dixon.

63:20

There's a whole bunch of other, um,

63:22

pulse sequences out there, like vibe and uh, and,

63:26

and, uh, lava and whatnot.

63:28

But basically you're looking

63:29

for persistent intrinsic T one hyperintensity, um,

63:34

greater than that of the normal pancreatic parenchyma.

63:37

And in those cases, especially if they're associated

63:39

with areas of T two signal heterogeneity, you can, um, um,

63:44

raise a suspicion for hemorrhage.

63:46

Um, in those cases, in fact, it's a, it's a diagnosis

63:49

that I, that I, uh, get more suspicious

63:52

of on the pre contrast images rather

63:54

than the post contrast images.

63:55

The post contrast images can often mask the findings

63:58

of hemorrhage because the, the other structures

64:02

around there, including the pancreatic

64:03

parenchyma enhanced as well.

64:05

So it's definitely something I see more easily on the, um,

64:08

the pre contrast images.

64:11

Alright. And then the, the last question, another, uh,

64:16

last minute question here is, um, important sequences

64:19

for complicated pancreatitis

64:23

or, uh, yeah com uh, uh, I'm gonna interpret that

64:26

as complex pancreatitis.

64:29

So you wanna look at all the pulse sequences, I'm assuming,

64:32

um, complicated pancreatitis,

64:34

you mean necrotizing pancreatitis

64:36

or pancreatitis with adjacent fluid collections?

64:39

Uh, basically it'd be, uh, looking at the,

64:44

i I look at the T two weight images for fluid collections.

64:47

Um, looking for organized fluid collections, uh, especially,

64:52

uh, the presence of pseudocysts

64:54

or walldorf necrosis to differentiate

64:57

walldorf necrosis from pseudocyst.

64:59

I look at how complex the collections are as well as

65:01

what parts of the pancreas are involved.

65:03

Uh, if you see, if I see fat content like, um,

65:07

peric pancreatic necrosis, um, the fat content within some

65:11

of these complex collections would tip you off to the,

65:14

the presence of per per pancreatic necrosis rather

65:17

than a pseudocyst.

65:19

'cause a pseudocyst shouldn't contain fat.

65:21

Um, other findings I'd be looking for would be the presence

65:24

of, um, gas on T one weighted in

65:27

and out phase, um, gradient echo pulse sequences.

65:30

So if you see bubbles that look like they're blooming or,

65:32

or looking more T two dark on the endphase muc compared

65:35

to the out phase images, that would be the MR findings

65:38

for, for gas content.

65:40

Although definitely it would be easier

65:42

to see on a CT scan than an MRI.

65:45

And then otherwise just looking at the multi-phase post

65:48

contrast images for, um, for the enhancement pattern

65:51

of the pancreas itself.

65:53

So I think that was our whirlwind of, um, of questions.

65:58

I think you got 'em all. Yeah, that was like 15

66:02

Rapid fire. Yeah.

66:04

Well, thank you so much for your lecture

66:06

and yeah, for answering all those questions.

66:07

We so appreciated you being here today. Oh,

66:09

My pleasure. Thank you very

66:10

much for the invitation.

66:12

Absolutely. And thanks to everyone else

66:14

for participating in this NOOM conference

66:16

and asking such great questions.

66:18

Be sure to join us next week, Thursday,

66:20

March 13th at 12:00 PM Eastern, where Dr.

66:23

Myan Ho will deliver a lecture entitled,

66:25

A Practical Approach to Neonatal Brain Imaging.

66:28

You can register for that@mrionline.com

66:30

and follow us on social media

66:32

for updates on future NOOM conferences.

66:34

Thanks again for learning with us and have a great day.