0:02

Hello and welcome to Noon Conference hosted

0:03

by MRI Online. Noon Conference was created when

0:06

the pandemic hit as a way to connect to the global

0:08

radiology community through free live educational

0:11

conferences that are accessible for all.

0:14

It has become an amazing weekly opportunity to

0:16

learn alongside radiologists from around the world.

0:18

And we encourage you to ask questions and share

0:20

ideas to help the community learn and grow.

0:23

You can access the recording of today's

0:25

conference and previous Noon Conferences

0:27

by creating a free MRI Online account.

0:29

The link will be provided in the chat box.

0:31

You can also sign up for a free trial of MRI

0:33

Online Premium Membership to get access to

0:35

hundreds of case-based microlearning courses

0:38

across all key radiology subspecialties.

0:41

Learn more at mrionline.com.

0:43

Today we're honored to welcome Dr. Alka Singhal for

0:46

a lecture on the role of Doppler ultrasound in

0:49

liver cirrhosis and portal hypertension. Dr. Singhal

0:54

has over 28 years of global radiology

0:56

experience and has worked and trained

0:57

in Sydney, Australia, and the U.S.

1:00

She has various publications and presentations in

1:03

national and international journals and conferences

1:05

to her credit. She has authored several

1:07

chapters on thyroid and parathyroid in leading

1:10

textbooks, and she is the Associate Editor

1:12

of Indian Journal of Radiology and Imaging.

1:15

At the end of the lecture, join Dr. Singhal

1:17

on a Q and A session where she will address

1:19

any questions you may have on today's topic.

1:21

Please remember to use the Q and A feature

1:23

to submit your questions so we can get to

1:24

as many as we can before our time is up.

1:27

With that being said, we are

1:28

ready to begin today's lecture.

1:30

Dr. Singhal, please take it from here.

1:32

Thank you so much.

1:33

The role of Doppler ultrasound in

1:35

liver cirrhosis and portal hypertension.

1:37

So it definitely includes our

1:41

ultrasound that comes prior to Doppler and

1:44

the elastography that comes prior to Doppler,

1:48

and then we move on to Doppler.

1:50

So we will run through the basics like how

1:52

we go about the spectrum of the disease,

1:56

beginning from what we commonly see.

1:58

Fatty liver.

1:59

Fatty liver, fatty liver.

2:00

That's what we've been used to

2:02

report all throughout our lives.

2:04

And then when do we begin to

2:06

see the subtle coarseness?

2:08

That's when we have to detect the early

2:10

chronic liver disease and give an early

2:12

diagnosis and then follow it up further.

2:15

And of course, in advanced liver cirrhosis, then the role

2:19

of portal hypertension and all the various things

2:21

that we have to talk, let's look at as it begins.

2:26

So commonly we assume that...

2:29

Taking a case scenario of an adult

2:31

cirrhosis or a fatty liver disease.

2:35

However, there is a big spectrum when we

2:37

discuss pediatric population versus, uh,

2:41

the, uh, the, uh, prevalent incidence in

2:44

the etiology in various parts of the world

2:47

vary, right?

2:48

So coming to fatty liver disease where the normal

2:51

liver is replaced by more than 5% to 6% of

2:54

fat, the fatty liver disease, accumulation of

2:57

fat causes inflammation, cell death and scarring,

3:00

and the condition called steatohepatitis. It's

3:02

too much of fat accumulating in the liver cells.

3:05

And of course, over a period of time, it leads

3:08

to fibrosis, and then fibrosis is like the

3:12

beginning of the irreversible changes, and then

3:15

it, of course, leads to liver cirrhosis, failure. And then, of course,

3:17

that kind of failure is a fertile soil for hepatic

3:23

malignancies, other lesions.

3:26

So that's the whole spectrum.

3:27

So we need to understand, we need to, we need to

3:30

give advice and management in very early stages,

3:34

right? Now, major causes of fatty liver disease,

3:38

of course, the commonest is alcohol due to excessive

3:41

alcohol intake because when it metabolizes,

3:44

it's converted into fat and stored over there.

3:47

And of course, non-alcoholic disease due to high

3:50

cholesterol and diabetes being one of the most

3:53

important factors that contribute to the same.

3:56

And of course, infections in Asia.

4:00

Of course, it's one of the common

4:02

challenges at the moment, and which leads to

4:04

significant cases of chronic liver disease.

4:08

So in cases of infection, the common are

4:11

the hepatitis B, the hepatitis C, and of

4:14

course the other common causes are alcohol.

4:16

Then non-alcoholic, which includes all

4:18

the various metabolic and other causes,

4:21

and then drugs and autoimmune liver.

4:24

Now, what is the challenge?

4:26

When do we think we are in the fat liver disease?

4:29

When do we think we're heading towards

4:31

the diverse cirrhosis and torture?

4:33

Hypertension, it's a spectrum.

4:36

It is a progressive, deteriorating kind

4:38

of a spectrum, and the symptoms kind of

4:41

overlap, so it's a real challenge for us.

4:44

We, as imaging professionals in ultrasound,

4:47

we're in a position to suggest what's going on.

4:51

So that's why our work is very important because

4:55

as we all look, symptoms of fatty liver or

4:59

chronic liver disease, they overlap and both can

5:01

be weakness, appetite, nausea, weight loss, and

5:04

other jaundice and other episodes.

5:07

So we need to develop tools to be able to do

5:11

early diagnosis by imaging non-invasive tools.

5:15

Liver biopsy, of course, is a gold standard to

5:17

diagnose chronic liver disease or liver cirrhosis.

5:20

However, it's an invasive procedure at

5:24

the end of the day because there could

5:27

be sampling errors, it could be hemorrhage, and

5:29

there's a marginal small risk of any complications.

5:32

Right.

5:33

And basically our imaging ultrasound is this.

5:37

So we have a tool — from our grayscale

5:41

imaging to understand the subtle coarseness.

5:44

And the subtle coarseness is actually, you

5:47

know, we are used to the routine 2 to 4

5:49

megahertz per transducer, but do switch

5:53

over to highest frequency transducer, especially

5:56

if you are doing a pediatric population

5:58

or whenever you have a lean patient.

6:01

You can really see the marginal capsular

6:03

irregularities, even on grayscale before ELA.

6:08

You can have a diagnosis as to

6:10

what we are looking at, right?

6:12

So of course next is the—

6:14

the shear wave elastography imaging.

6:18

So what do we do here?

6:21

So we analyze the tissue. The ultrasound

6:26

beam goes through a centimeter cube, a volume

6:30

of tissue, and then it evaluates the

6:33

stiffness based on the speed it reached.

6:35

The sound wave goes through it, because as we

6:39

know, we read in physics — solids, liquids, gases —

6:42

solids are the fastest sound speed, liquids

6:45

a bit slower, and the gas is a bit more slower.

6:49

So the more stiff the tissue, the higher

6:52

the velocity. That concept we are trying to

6:55

use by the application of the sound beam to

6:58

get the velocity and understand what's the

7:01

stiffness of the tissue that we're dealing with.

7:04

So it's a sort of a palpation

7:07

with the ultrasound probe, right?

7:09

We are not getting inside the body. However, the sound

7:13

beam — we're trying to palpate inside our body, right?

7:17

It hits the liver tissue and provides a

7:20

quantitative measurement of the liver stiffness.

7:23

And what we do is the movement of the liver

7:26

tip by the ultrasound wave is

7:29

measured and we get a velocity measurement.

7:34

So what is it that it gives us?

7:36

Information and the stiffness of the tissue

7:38

is in the size assessment of the lesion.

7:40

Because sometimes the lesion could be more

7:43

than what you can appreciate on grayscale.

7:45

There could be some more fibrous

7:46

strands that are going beyond.

7:48

So when you put another tool, a graphic

7:51

tool, you can see that actually the actual

7:54

extent of the lesion is way more than that.

7:57

Alright.

7:58

And of course there's got

8:03

a lot of many other applications as well.

8:09

It's very simple. Now it's available in most ultrasound

8:13

equipment — most high-end ultrasound equipment.

8:16

And it's just a very short learning curve if you call

8:20

your application specialist to train you to do it.

8:24

And I use this tool even when I'm doing

8:26

a routine whole abdominal scan. The liver —

8:29

whenever I feel it's marginally coarse,

8:31

I use this as an adjunct to give further

8:34

valuable information, even if

8:36

I'm not doing a complete study.

8:39

So the principle and how to

8:40

interpret — we'll look at it.

8:44

We compare with the gold standard,

8:46

which is the system. And there are

8:49

papers by various machine manufacturers

8:51

which are available on the net.

8:53

What's the scoring system?

8:55

It is used to assess the extent of inflammation

8:59

and fibrosis based on the liver biopsy.

9:03

And you have scores from zero to four.

9:05

So fibrosis score F0 is no fibrosis, F1 is

9:09

portal fibrosis without intersept involvement,

9:12

F2 is with septal involvement, and

9:16

F4 is frank cirrhosis.

9:18

And depending upon the activity, we have

9:21

scores of A0, A1, A2, and A3.

9:24

Now here in ultrasound, we are going to measure

9:27

the stiffness with the software, which is

9:30

integrated along with the ultrasound machine.

9:34

Okay?

9:35

Right, so,

9:40

so what are we going to do?

9:41

What happens is we,

9:43

we send out a short-duration pulse.

9:47

And it causes a minute displacement

9:52

of the tissue, and that is measured and

9:55

documented and processed and recorded, right?

9:58

So that short area that is insonated by the

10:02

ultrasound machine that we are recording

10:03

is called the ROI or the region of—

10:07

Now our role is to remember where to place that

10:11

ROI — region of interest — so that we get the most

10:14

appropriate region that we are desiring to read.

10:18

Right?

10:19

So let's look at it.

10:20

Where do we place that?

10:23

So the pulse is going to go,

10:27

so we record the wave speed.

10:32

At present, give the readings either

10:34

in m/s or in the kPa.

10:37

The kPa is the value which the gastroenterologists

10:41

are used to because

10:45

that's the way the FibroScan reads.

10:48

So conventionally, since FibroScan's been more

10:51

popular — has been here with us for a longer

10:55

period than the advent of the ultrasound-based ELA,

10:59

so we try and give the reading in both

11:03

the measurements so that it is easily

11:06

interpreted by the treating physician.

11:09

Okay.

11:10

Alright.

11:11

So what is the patient position, of course?

11:15

We place the patient in supine or

11:17

in the lateral decubitus position,

11:19

and with the arm in maximum abduction, the

11:22

transducer is located in the intercostal space on the right.

11:27

Now.

11:28

How do we do it?

11:30

So, of course, the patient is fasting.

11:32

This dorsal decubitus position, the right arm is elevated.

11:36

And of course, we do not apply too much pressure.

11:38

We use a resting respiratory position.

11:42

ROI is placed beneath the Glisson’s capsule about

11:45

1.5 to 2 centimeters below, to avoid the

11:49

reverberation and increase in subcapsular stiffness.

11:52

And of course, we avoid larger vessels.

11:56

And why do we prefer the right lobe? To avoid

11:59

the cardiac pulsations from the left lobe.

12:03

So this is how we place the area of interest — the ROI —

12:07

and we sample not too close to the capsule, not near

12:12

any of the portal vein or the hepatic veins,

12:15

not near the GB, so that we don't have any dilution

12:20

of the effect that we are trying to ascertain.

12:23

Right.

12:24

And we perform 10 valid measurements at an average

12:28

depth of between 2.5 centimeters to 5.5 centimeters.

12:33

And the machine calculates a median value for

12:36

us, which we understand and interpret

12:40

as per the manufacturer's guidelines.

12:44

So we try and keep the standard deviation as low and

12:47

IQR low, and accordingly, various manufacturers have

12:53

given their own interpretation as to what velocity

12:56

range falls under which corresponding threshold category.

13:02

That way we help

13:04

understand the elastography. Just

13:06

a little word about FibroScan.

13:09

That's not a guided procedure,

13:11

that's a blanket procedure.

13:13

And we need a different size of transducer probe

13:16

depending upon the pediatric or adult population.

13:19

And of course, when there's ascites or any focal

13:22

hepatic lesion, it is a challenge to do that.

13:26

So the advantages of ultrasound-based elastography:

13:29

we can do it in cases of patients with ascites,

13:32

we can do it in post-op patients, narrow

13:34

intercostal spaces, and it requires lesser training.

13:39

And of course, we can do it in children,

13:42

and we record the typical appearances.

13:45

I remember I was talking about

13:47

the very early cirrhosis.

13:48

Sometimes if you can just appreciate this irregularity

13:52

even of the capsule, even a marginal irregularity,

13:55

even or not being beam-formed imaging suspect,

14:01

worsening of the ion — suspect early cirrhotic

14:04

changes — and suggest further imaging, elastography,

14:08

or a TRAC-CE CT or any other stiffness

14:12

measurement tool to alert the patient.

14:15

So see, you see this kind of a wavy outline of the

14:18

capsule, and of course the parenchyma does look

14:22

coarse. There’s relative hypertrophy

14:24

of the left lobe that we can see.

14:26

The caudate lobe appears enlarged.

14:28

We're looking at chronic liver disease, and of

14:32

course when there is a focal hepatic lesion, this

14:35

is a case that came to us to assess what is the

14:39

status of the remainder of the liver parenchyma.

14:42

Okay, so said a lot about liver ELA.

14:46

So we assess the stiffness.

14:49

We have to move to the next topic for today.

14:54

Topic for today.

14:55

Once we've assessed that yes, there is

14:57

a chronic liver disease, now what next?

15:01

Where are we in the disease process?

15:05

How much are the secondary changes — the portal

15:07

hypertension, and then all the altered pathophysiology —

15:12

the ductal physiology — that we need to evaluate?

15:16

That's the next thing that we need to do.

15:18

So what is portal hypertension?

15:20

Portal hypertension represents increased

15:24

hydrostatic pressure within the portal

15:27

vein and distributaries, and it's defined as

15:29

increased pressure gradient between the

15:31

portal vein and the hepatic veins of the IVC.

15:34

So the portal pressure normally

15:35

is mean 8 millimeters

15:36

mercury. Portal flow is

15:38

1,000 to 1,200 milliliters per—

15:43

also.

15:44

So when the venous pressure is more than 5

15:47

millimeters mercury, that's when we think it's

15:50

portal hypertension. But we actually don't

15:52

put in a vessel in our measuring instrument.

15:56

There, we ascertain by various other

16:00

means.

16:01

Now, portal hypertension—

16:05

the portal hypertension can have causes, which

16:08

can be suprahepatic, hepatic, or post-hepatic.

16:13

Now suprahepatic causes could be

16:17

situations which all cause conditions in

16:20

the liver, like cardiac disease, hepatic

16:23

vein etiology, inferior vena cava thrombosis, or webs.

16:27

This outflow obstruction — hepatic vein thrombosis

16:30

or Budd–Chiari syndrome — has multiple etiologies but

16:33

generally is related to a hypercoagulable state

16:36

and is often treated with anticoagulation.

16:39

Liver fibrosis can result from hepatic disease,

16:42

and cirrhosis can develop later in the—

16:45

so these are the— the commonest is the

16:48

hepatic causes: all the fatty liver disease.

16:51

And when the basic liver cell morphology

16:54

is altered, all those causes fall

16:57

into the category of hepatic liver disease.

17:00

Right?

17:01

Cirrhosis is the most common hepatic

17:04

cause of portal hypertension, and chronic hepatitis C

17:09

is the most common cause of cirrhosis, right?

17:12

Others are alcohol-induced, and less common are

17:16

all the metabolic disorders — hemochromatosis, alpha-1

17:20

antitrypsin deficiency — and drug-induced. And portal hypertension is

17:24

considered an advanced complication of cirrhosis.

17:27

And when you actually see signs of portal

17:32

hypertension, it's kind of a decompensated cirrhosis.

17:35

So basically a nodular outline of the contour,

17:38

and irregularity of the capsule — that we

17:41

can appreciate very well on ultrasound imaging.

17:45

Use the highest frequency transducer

17:48

to get the required depth of imaging to

17:50

follow the golden rule of ultrasound.

17:52

That's really, really rewarding.

17:55

Okay, so coming to the infrahepatic

17:57

causes — the alterations of the

18:01

portal venous blood flow can also lead

18:03

to portal hypertension, such as abnormalities of

18:07

the splenic vasculature. Splenic vein and

18:09

portal vein thrombosis are the common causes.

18:13

So this is just a table that is

18:15

summing up what we just discussed.

18:18

It's static — prothrombosis or compression. Intrahepatic —

18:22

the liver parenchymal disease — fibrosis, and due

18:26

to various causes. And post-sinusoidal — cirrhosis,

18:30

hepatic, and right heart failure and hyperflow such as a

18:37

fistula.

18:40

So what all do we see in portal hypertension?

18:43

It's a clinical spectrum of multiple systems getting

18:48

affected, and we have findings in multiple systems.

18:53

We see gastric varices, we see esophageal varices, we

18:56

see portal hypertensive gastropathy, splenomegaly,

19:00

ascites, hepatic hydrothorax, hepatic encephalopathy,

19:05

hepatorenal syndrome, hepatopulmonary syndrome,

19:09

pulmonary hypertension, cirrhotic cardiomyopathy.

19:12

All of these are actually predominantly

19:16

a result of activation of all the bypass

19:20

channels to support the circulation.

19:24

Let's understand what happens.

19:25

So, what are our goals of diagnostic studies?

19:29

What are we aiming to do?

19:31

Understand the extent first —

19:34

whether it is a disease, yes or no.

19:38

Whether there is any obstruction

19:41

to the flow, and if yes, at what level?

19:43

Acute? Chronic? Are there any portosystemic collaterals —

19:48

intra-abdominal or on the anterior abdominal

19:51

wall that you'll see? And the direction of the

19:54

flow — is it headed towards the liver?

19:58

Is it hepatopetal — toward the liver?

20:00

Or kind of a mixed pattern, and

20:03

presence of thrombosis, if any?

20:04

And of course, if there are any ILLs or

20:07

any heterogeneous lesions in the liver

20:09

parenchyma — any malignancy that has developed —

20:11

of course, we are looking for those and

20:14

any other pathology that we can find.

20:17

Right. So like we discussed, evaluation of the abdomen,

20:21

the liver, gallbladder, and abdominal viscera —

20:25

we prefer to do it in the fasting status, but of

20:28

course, in cases of stat orders, we have to give a

20:31

report as per the case and report whatever limited

20:35

study you are able to do depending on what the

20:37

clinician is requesting you to do at that time.

20:41

Okay.

20:41

So of course supine position — and position

20:44

will keep on changing during the examination

20:46

to see the area of ROI in the best possible

20:50

elevated position with minimal depth of

20:54

penetration. Post-respiratory effort is needed.

20:58

Patients sometimes are very drowsy.

21:00

They look unwell, they have a lot of effusion — it

21:03

can get very challenging for them to hold breath.

21:07

There’s large-volume ascites, and

21:09

again, it's very challenging.

21:11

We have to scan

21:13

despite all these challenges. That’s our role.

21:16

Right.

21:17

So let's look at it.

21:19

So what do we see? The normal anatomy — where is it?

21:25

Where do we see it’s formed? Behind the

21:27

head of the pancreas at the level of L2 vertebra. How?

21:32

By the confluence of splenic vein

21:34

and the superior mesenteric vein.

21:38

Okay.

21:39

Right.

21:39

So we have the splenic vein and

21:41

the mesenteric vein — the confluence.

21:44

And that forms the portal vein,

21:46

that ascends to the porta hepatis.

21:47

Right.

21:49

So we may see tortuous splenic

21:55

vein and we see this kind of appearance, right?

21:59

And just to understand the vascular

22:01

anatomy — because this is very important —

22:05

to understand the collateral flow as well.

22:07

The portal vein normally supplies 70% of the blood flow

22:11

to the liver and only 40% of the liver's oxygen supply.

22:15

The remainder of the blood comes from the hepatic artery, and

22:18

the blood from both of these mixes in the sinusoids.

22:22

So it’s important to understand that

22:25

the liver does have a dual blood supply from

22:28

both the portal and the systemic circulation.

22:32

So once the portal vein ascends to the porta, it

22:35

branches into the right

22:37

and the left portal veins intrahepatically.

22:40

It has an intrahepatic, intrasegmental

22:44

course, and the left portal vein supplies segments

22:48

2, 3, and 4 — may receive branches

22:51

from both the right and the left portal vein.

22:53

The portal vein then terminates into the sinusoids.

22:59

Right portal vein supplies segments 5 and 8, and

23:02

the left portal vein supplies segments 6 and 7.

23:07

So accordingly, we have to understand the anatomy.

23:13

That is very important when you're trying to

23:15

localize a lesion — whether it's going for an

23:18

RFA or a surgery or any other follow-up.

23:24

And whether you're dealing with the routine anatomy

23:27

or a variation — that you have to also understand.

23:32

What's the dimension of the normal portal vein?

23:35

Length is about 6 to 8 centimeters.

23:37

Caliber varies from 13 to 16 mm.

23:41

Age-related variation is there.

23:43

We add a millimeter for every 10 years, and then

23:47

after 60 years, increases during deep inspiration.

23:52

And where do we measure? At the

23:54

crossing of the hepatic artery. Right?

23:58

So that's the portal vein.

24:01

And we measure at the crossing

24:03

of the hepatic artery. Right?

24:06

So we have formulas for the

24:10

flow volume calculation, which is

24:13

however in-built into our machines.

24:16

And we follow the guidelines as per the manufacturers

24:21

to calculate the portal flow volume based

24:27

on the peak velocity measurements that we do

24:30

and the

24:34

diameter of the portal vein that we

24:35

measure. And we get those values. Right?

24:40

We can also know that normal portal vein may have a

24:43

slight undulating and phasic pattern that we can

24:46

appreciate. And often, we can also record pulsatility indexes,

24:52

however, we are not using that as a routine.

24:55

What's the normal portal vein velocity?

24:58

So the normal portal venous pressure is 5 to

25:00

10 mmHg, and the velocity that

25:03

we record on ultrasound is normally between 16

25:07

to 40, or maybe even 50, centimeters per second.

25:12

A reduced velocity is an indicator

25:16

of portal hypertension, but

25:19

normal velocity does not exclude portal hypertension.

25:25

The flow volume, the range is between 500 or 600 to 1,200.

25:32

And varies between 14 to 20% with posture, exercise,

25:37

and diet. And the splenic vein and the SMV

25:42

also we must look at, because often you can

25:44

have a thrombus sitting there, which can

25:47

be overlooked, and only when we suspect the

25:50

pathology, then only we can advise for

25:52

further imaging, even for CT or any other imaging.

25:56

So do look at the splenic vein diameter,

25:59

the mesenteric vein diameter, and document

26:03

those. Same coming to the hepatic veins.

26:06

So we know normally there are three which enter the

26:10

IVC about two centimeters caudal to the right atrium,

26:12

and they divide the liver into the segments.

26:16

The middle and the left hepatic veins may

26:19

form a common trunk and drain into the IVC.

26:25

Normally the veins show a triphasic flow, and

26:29

the flow below the baseline peaks twice,

26:32

corresponding with the movements of the tricuspid

26:35

valve. And transient flow reversal or peak above

26:38

the baseline corresponds to the atrial contraction.

26:43

So these

26:44

two correspond with the ECG tracing as well.

26:50

So that's about the hepatic veins.

26:54

Now,

26:55

so how do we scan the liver?

26:58

So one word is lawnmower technique.

27:00

So we are basically trying to see that we

27:02

actually scan every millimeter of the hepatic

27:06

parenchyma, because it is voluminous. It's one

27:09

of the largest organs in the body, right?

27:12

And the lesions can be small. They

27:14

can be subcentimeter, they can be 5, 8, 9, 10.

27:20

I mean, ultrasound actually is capable

27:22

of detecting lesions which are five

27:26

mm, or like small lesions as well.

27:30

So unless we are very thorough and we make sure we

27:34

are scanning each and every region of the parenchyma

27:37

of the hepatic parenchyma, then we can do a thorough job of

27:41

actually ensuring the whole hepatic parenchyma is free of any SOL.

27:48

Or you can also follow the vasculature — trace

27:52

the portal vein or hepatic veins — and look at all the

27:56

draining segments one by one. Whichever way you adopt,

28:00

we have to be very, very thorough in our scanning

28:03

and understand the variations of the vasculature

28:07

anatomy. That will support us in evaluating. Coming next

28:14

to the artery.

28:17

So,

28:19

it arises from the—

28:24

the main hepatic artery divides into the

28:25

right and left hepatic arteries.

28:28

And the normal diameter is about 5 millimeters.

28:30

I don't think it would reach even 5 millimeters.

28:32

And it's actually very much dilated and

28:36

prominent in cases of chronic liver disease.

28:39

And it’s red in traditional color Doppler

28:42

because the way you have the transducer,

28:44

the flow is going towards the liver.

28:46

So it’ll have a traditional — and it's the

28:48

same direction as the portal vein normally, because

28:50

they're both taking the blood into the liver.

28:54

And it does have a lighter color as compared

28:57

to the portal vein, normally speaking, because

28:59

the velocities are much higher here. The higher

29:02

velocities are in the upper part of the spectrum.

29:04

The lower velocities are the orange —

29:06

they are in the lower part of the spectrum.

29:09

So that’s how we have a coarse heterogeneous parenchyma.

29:13

You can see the portal vein and very dilated, prominent

29:17

hepatic artery here, which is well demonstrated on

29:21

the panel. Here again, you can see the dilated hepatic—

29:29

very well appreciated all in the

29:31

cases of chronic liver disease.

29:33

Right, now how do we do Doppler?

29:36

Of course, we will first get a nice grayscale image.

29:39

We’ll put the color, and of course, there’s a little

29:41

bit of aliasing happening there, and we put our—

29:46

the cursor where you think the hepatic artery is,

29:49

and you will be able to identify with a little

29:52

difference in the color or kind of — and then you record.

29:58

It has a low-resistance diastolic flow, and

30:01

you record the peak systolic velocity, the

30:03

end diastolic velocity to calculate the RI or the PI,

30:07

and then you do calculate the S/D ratio as well.

30:12

So coming to the flow in the vein —

30:17

so anatomical variations are there.

30:20

So generally, the normal values, just to sum up:

30:23

hepatic veins — triphasic flow, portal vein — about

30:27

1,200, and hepatic artery — about 400 mL per minute.

30:30

And pressure is about

30:32

100 mmHg.

30:34

And that's the normal scenario. Right, now coming

30:38

to the challenges that we have to diagnose. Right?

30:42

So you can have obstructive or increased

30:46

post-venous resistance, or a hyperkinetic

30:48

situation where you have splenomegaly, AVM,

30:51

fistulas, or you can have the post-hepatic

30:55

situation — the Budd–Chiari kind of a scenario. Right?

30:59

What all do we need to do?

31:01

We look, need to look at establish

31:03

the cause of portal hypertension.

31:05

We need to evaluate the status of liver and

31:08

being per, if there is any focal lesion, we

31:11

need to see the diameter, direction of flow,

31:13

velocity of flow, and the collaterals and com—

31:17

Other complications.

31:19

What all are we going to do?

31:20

We are going to do in gray scale and P—

31:22

Doppler—portal and splenic vein size, portal

31:25

vein shape, respiratory variation, dilatation

31:28

of splenic vein, loss of pha variation.

31:31

We're gonna look for thrombus.

31:33

We're gonna look at the hepatic artery.

31:35

We look for the coronary vein.

31:38

We look at the direction of flow, and we

31:40

look for the presence of collaterals, right?

31:44

So this is just, as we know, the data of

31:47

India is, uh, cirrhosis is less, but in the

31:50

Western world, cirrhosis is a leading cause.

31:53

Now what are the findings?

31:55

Uh, got eight findings that we, that

31:58

are the key findings that you'll see

32:00

in earliest chronic liver disease.

32:02

You have a volume redistribution.

32:04

What's the earliest findings?

32:06

If anybody was to ask me is that I see

32:07

the caudate enlargement even before

32:10

I see the capsular irregularity.

32:12

Sometimes I feel why is the

32:14

caudate lobe looking prominent?

32:16

And I really evaluate the

32:17

capsule very, very carefully.

32:19

And I see subtle margin

32:22

irregularity, and I look at the post.

32:25

It's like a—you have to, you have to, uh,

32:30

be aware of it, and you have to be looking

32:33

for it so that you actually make a diagnosis.

32:36

So liver can be enlarged in early stages.

32:40

It may not be short and shrunken, like you said.

32:43

It can be acute or chronic.

32:45

So if you see in a window where it's chronic, but it's

32:48

gone into fulminant hepatic failure or something,

32:50

you can actually see the liver is enlarged.

32:52

So size really is not, uh, like a definite criteria.

32:57

So liver may be enlarged.

32:59

However, there is a relative enlargement of

33:02

the caudate lobe, left lobe, or both in comparison

33:08

with the right lobe, with concomitant

33:11

atrophy of the segments of the right lobe.

33:14

Right?

33:15

So enlarged caudate lobe, relative enlargement

33:18

of left lobe and tiny right lobe, enlarged

33:20

left lobe, separated by the main lobar fissure.

33:23

These are early pointers towards the chronic liver

33:27

disease, and we all need to be aware of it, right?

33:31

For example, here you see the—

33:33

left lobe puts a little bit.

33:37

You see what's more than prominent and enlarged.

33:41

And of course, we do have the

33:43

dilated coronary vein as well.

33:45

So we take a section immediately below the vein.

33:50

We draw line one, a para line through the right

33:55

lateral border of the falciform vein, and a PH line

33:59

to the left lateral border of the caudate lobe.

34:02

And line three is line orthogonal

34:04

to lines one and two, and—

34:07

We measure the right lobe

34:09

length on the line three, and—

34:11

We measure the caudate lobe and we get the

34:14

ratio, the caudate-to-right lobe ratio, C-slash—

34:21

It's better to do it on a CT, but yes,

34:24

you can do it on ultrasound as well.

34:26

Caudate lobe and the right lobe.

34:29

So this ratio, when normal, is less than 0.6.

34:35

0.6 to 0.65 is borderline. More than 0.65—

34:38

When the caudate is enlarging, it's

34:41

likely to be cirrhosis. When it's more

34:44

than 0.73—99% likelihood to be cirrhosis.

34:50

Okay.

34:50

Alright, so we have this

34:54

picture of enlarged left lobe.

34:57

Uh, we have a thrombus here, probably also in the

35:00

portal vein, and we have very poor hepatic perfusion there.

35:07

So we, again, we have a nicely visualized

35:10

portal vein, hepatic artery, proper hepatic

35:13

artery, and capsular irregularity.

35:16

And of course, coarse hepatic parenchyma, thickened

35:19

interlobular septal walls that we can appreciate.

35:23

So again, we have altered

35:25

echo texture and subtle hypoechoic nodules.

35:30

These could be regenerative nodules.

35:33

Then this nodular surface, this is a very important

35:37

area that you need to look at—the capsule.

35:39

And of course, any focal lesion—you have

35:43

to keep, uh, be aware and look for them.

35:48

Ascitic fluid gives a very nice natural contrast

35:52

for us to appreciate the surface nodularity.

35:55

And of course, also the, uh, very nice

35:58

contrast to look at the nodules as well.

36:03

So you can have dysplastic nodules,

36:05

you can have regenerative nodules.

36:08

And basically, final answer was given by the,

36:11

uh, further cross-sectional dynamic imaging.

36:15

So.

36:16

Ultrasound will give subtle nodules.

36:18

The characterization is, however, uh, beyond

36:22

the relevance of ultrasound for the moment.

36:24

So you, of course, unless you see some obvious

36:28

heterogeneous solid lesion, which is, uh, showing

36:32

capsular bulge, heterogeneous vascularity.

36:35

So we are looking at an obvious SOL,

36:37

obviously, most likelihood it's a HCC—

36:41

hepatocellular carcinoma in this case.

36:44

Now, coming next, looking at the spleen,

36:47

of course we will measure the size, which

36:49

is usually enlarged, and we measure it in

36:52

the mid-spleen at the level of the hilum.

36:55

So you must be seeing the hilum.

36:57

So normally it's less than 13 centimeters, and

37:03

that's the measurement that we usually refer to.

37:07

And of course, you can just get an idea

37:10

that, that that's a kidney, normal kidney.

37:12

And of course, you can see a lot of

37:14

collaterals as well, splenic enlargement.

37:19

And also clinical picture is affected by

37:22

hypersplenism and other pathophysiologists.

37:27

Another complication is peritoneal fluid or ascites,

37:31

which leaks across the hepatic sinusoidal epithelium

37:36

due to the high hepatic sinusoidal pressure.

37:39

So the fluid across the endothelium is normally

37:42

controlled by the oncotic pressure gradient.

37:44

So the intra-abdominal fluid is normally absorbed

37:48

by the peritoneum, but in this case it's just,

37:52

uh, it's one of the markers of compensated

37:55

or decompensated, uh, chronic liver disease.

37:59

And, uh, we have to sometimes—

38:03

distend abdomen and just ascitic fluid and

38:06

you have differential diagnosis of TB, losses, or

38:09

various other, uh, reasons when, unless there are

38:14

classic features on ultrasound imaging or pointing

38:18

towards the diagnosis, we still have to be open

38:21

to all the other possibilities of the causes.

38:26

So, which could be—so ascites due to portal

38:29

hypertension or due to non-portal hypertension.

38:32

So these could be due to cirrhosis or cardiac

38:34

disease or tumors, or hepatic failure, or thrombosis,

38:37

or commonest non-cirrhotic cause could

38:42

be tuberculosis or pancreatic, uh, disorder,

38:46

or carcinomatosis, or nephrotic syndrome, or

38:50

lymphatic obstruction, or any other metastasis,

38:53

or any other systemic disorder anywhere, right?

38:58

So.

39:00

Another less frequent complication is a

39:02

spontaneous bacterial peritonitis, which is

39:06

due to the development of inflammation and—

39:11

coming to the Doppler assessment.

39:13

So we have to detect the flow, the direction,

39:16

and type of flow like we discussed.

39:19

So what happens in chronic liver disease,

39:21

the portal vein size neither increases.

39:24

However, the velocity is still

39:26

falling, right? In advance,

39:29

the opening of the portal rales may decrease,

39:31

the decreased mean velocity of portal

39:36

vein—less than 16 centimeters per second.

39:38

However, that is, score less than 12 centimeters

39:41

per second is of portal hypertension.

39:44

And of course, you would see increased

39:46

portosystemic collateral flow or fistulas, right?

39:50

So you can see a dilated coronary

39:53

vein.

39:54

You can see the low PSV.

39:58

Right, and you can see the volume is also

40:03

reduced, kind of 493.

40:06

So roughly around less than 500 ml per minute.

40:10

This is demo case the same.

40:13

So, and the direction—you can see

40:16

it towards the liver, or helical, or

40:19

reversing as well.

40:21

You can see "hepatofugal" or reversing as well,

40:27

right?

40:29

So you can see there's a different direction of the

40:31

hepatic, uh, artery and the portal

40:34

vein suggesting hepatofugal flow

40:37

in the—

40:40

vessel.

40:41

Right?

40:44

So what is the next complication that you're going

40:48

to look out for is a IVC thrombosis.

40:51

This is very interesting because this is one

40:53

of the diagnoses which is often missed on

40:56

ultrasound imaging. And why is it missed?

40:59

Because many a times, even on a whole abdominal

41:02

scan, we have the capacity to diagnose thrombosis

41:08

even though a Doppler has not been requested.

41:11

Because in any and every case of chronic liver

41:16

disease, I always put on the color Doppler to

41:19

see if the portal is filling well everywhere.

41:22

Is there any good effect?

41:24

Because if thrombus is fresh, it is almost iso.

41:38

Okay, indirect signs of HCC.

41:41

What are the indirect signs?

41:42

You can see maybe umbilical formation, maybe lots of

41:46

collaterals on the GB wall and lots of other collaterals and

41:50

various other features that suggest that there is

41:54

an alternate route of circulating being developed.

41:57

Why?

41:58

Because maybe the primary route of circulation

42:01

or the portal vein is impacted somewhere.

42:05

So look out for those cues and then you will

42:08

be a great, uh, ultrasound professional giving.

42:12

Great.

42:14

Alright, so portal vein is usually—

42:22

However, recent thrombus may be hypoechoic or anechoic,

42:25

and on color Doppler, you can evaluate that

42:29

and see hypoechoic echoes in the lumen—echoes in the

42:32

lumen—and you can see large hypoechoic echoes and

42:36

heterogeneous echoes in the lumen. You can see very

42:39

large hypoechoic echoes and umbilical formation around.

42:45

If it's like completely thrombosed and lost,

42:48

then you can have numerous tortuous vessels at

42:51

the porta trying to support the circulation.

42:56

Of course,

42:56

we see prominent hepatic artery, which has been

42:58

dilated, tortuous, giving like corkscrew appearance.

43:04

That's the kind of appearance that you can see.

43:06

So you have a dilated tortuous hepatic artery

43:09

that is there in chronic liver disease,

43:12

and we have increased PSV, and

43:20

you can see—

43:23

How much of portal vein, uh, how

43:27

much of hepatic artery is happening?

43:30

A lot of it, right?

43:32

So—

43:35

Ultrasound signs of significant, uh, clinically

43:38

significant portal hypertension: of course, a portal

43:41

vein, reduced portal vein velocity, increased congestion

43:44

in its splenic vein and dilated hepatic venous stopped

43:47

pattern, increased intraparenchymal hepatic artery

43:51

impedance, right?

43:53

So with that, you'll see multiple collaterals.

43:59

So presence of the collaterals is clearly

44:01

indication that portal hypertension is there.

44:06

And there are various sites that we look at.

44:09

So ultrasound is good to see 65 to 90% of

44:16

the portal collaterals. Where do we look for them?

44:21

We look at the GE junction. We look at the

44:24

rectum, uh, they're in the lower

44:27

rectum, in the retroperitoneum and around them.

44:30

Like us, we see the caput medusae in the anterior wall.

44:35

So see here we have lots of,

44:37

uh, renal varices.

44:43

So significant amount of renal

44:47

renal collaterals we can see.

44:53

So we can—

44:58

Right.

45:00

Now.

45:01

So the next area that I wanted you

45:03

to see was the paraesophageal collaterals that we

45:06

have at the GE or gastroesophageal junction.

45:09

So we have the left lobe of the liver.

45:11

That's where we have the GE junction.

45:13

So you'll see lots of collaterals in that area.

45:15

You can see paraesophageal, gastroesophageal, splenorenal

45:19

collaterals, and you can see, uh, splenic retroperitoneal

45:24

equates in the posterior aspect of the spleen.

45:30

You can see the cavernous transformation of the portal vein,

45:34

which is like a tortuous network

45:37

of vessels that you can see.

45:41

You can see collaterals around the gall

45:43

bladder, which is like this here, where you

45:47

can see variceal channels along the gallbladder.

45:49

It is a GB varix that you can see on 3D here.

45:56

Vein—so acute and chronic CLD may not

45:59

have those classical, classic features.

46:01

The liver may be enlarged. However, you can

46:06

appreciate maybe subtle coarseness, but it may or

46:09

may not be there and, uh, could be due to Budd–Chiari

46:14

or other causes that you have to see.

46:21

We have, we have enlarged liver.

46:23

It looks a little bit coarse.

46:25

We have GB wall edema. We have vessels. We have, so

46:33

complete scan—we have a little bit of wall thickness.

46:40

And here again, we're trying to see what was enlarged.

46:46

Right.

46:50

Okay.

46:51

So.

46:53

Now coming to the

46:53

hepatic veins and the TIPS shunt that we create.

46:56

So you will image all the hepatic veins.

46:59

That brings us to the question and

47:01

the diagnosis of particular syndrome.

47:03

So normally, we should be able to

47:05

see the hepatic veins very well like this.

47:09

If we don't see—aha, like this very well-visualized

47:13

hepatic veins and their confluence into the IVC—

47:17

you don't see a picture like this.

47:18

I'm repeating this again—

47:20

Think Budd–Chiari or any other abnormality.

47:25

So when you see this is probably the IVC, but

47:29

you see rather where the hepatic veins could have

47:34

been, I'd rather seen some echogenic threads.

47:38

So that's like hepatic veins are

47:41

blocked by fibrosis or thrombosis, right?

47:44

That's when you begin to suspect.

47:46

Fibrosis is a long list of, uh—

47:49

Pathology and things.

47:51

So just again, a recap of the normal,

47:53

this is how we see the hepatic veins, and

47:57

this is the Doppler of the hepatic veins.

47:58

But you have specific signs when you

48:02

see the hepatic veins as fibrosed, thrombosed,

48:05

or suggestive signs are of course all

48:08

the alternative routes of circulation.

48:11

We have those collaterals, and that has formed.

48:14

So the specific—so you see there is

48:17

specific rocket—so we don't see the—we

48:20

see the vein, but we don't see the vein.

48:23

We see—we don't see the vein there.

48:25

Right.

48:26

This is kind of a—all these findings, fibrotic, yeah.

48:35

Okay, so how many veins for a diagnosis?

48:39

So I think any supports the diagnosis. Three types

48:42

of Budd–Chiari syndrome based on the level of obstruction:

48:47

Obstruction of IVC with or without secondary

48:50

hepatic vein obstruction. 2. Obstruction of hepatic

48:53

veins. 3. Obstruction of small centrilobular veins,

48:56

considered the same as veno-occlusive diseases.

49:00

So depending upon the levels, you can have the

49:02

different scenarios, and accordingly, depending upon

49:07

the scenario of BCS—acute, subacute or chronic—you

49:10

will have the different timelines and symptomatology.

49:14

So why is the timely diagnosis of BCS important?

49:17

Of course, we can prevent liver cirrhosis,

49:20

we can manage, we can, uh—we can salvage the

49:24

circulation and save the liver parenchyma.

49:27

So it's very, very important whenever you

49:29

are doing any liver scan, and if you don't see

49:32

hepatic veins, you have to document that.

49:37

And that's a B-mode diagnosis that does not

49:40

require a request for a color Doppler. We

49:43

can diagnose it on B-mode imaging, right?

49:46

Of course, clinical signs are likely, and various

49:51

other features are there that we all know.

49:55

So most important is to be aware of

49:58

the appearance of the hepatic veins and

50:04

evaluate the straight veins.

50:06

That kind of an appearance—that's

50:08

like an easy diagnosis on ultrasound.

50:13

So normal vein, and then you have the

50:15

echogenic material in the hepatic vein.

50:19

Alright, so again, you have these

50:21

other collaterals—hepatic collaterals.

50:24

These are the attempt to rescue the circulation.

50:29

So again, you have those collateral circulation that

50:31

is developing—subcapsular collaterals and other pathways—to

50:35

salvage the hepatic parenchyma.

50:38

In cases of blockage of the vein, the distal

50:42

end of the vein, you have overt venous collaterals

50:45

and all the other collateral formation, right?

50:50

So again here, you can see there's a

50:53

bare narrowing, and then you see

50:55

there's a comma-shaped vein that you

50:57

can see, and there's an obstruction there.

51:00

Again, thread-like veins here.

51:03

Shunt. So we'll come to the shunt.

51:10

Uh, diameter.

51:11

Of course, we have to look.

51:13

That's another point.

51:14

You can see the caudate lobe and the vein.

51:17

When it's dilated, it is again

51:19

suggesting a

51:24

diagnosis of chronic liver disease.

51:28

So time is 10:24.

51:30

So other complications can be hepatic

51:33

artery aneurysm—so vascular lesions.

51:36

So let's come to TIPS shunt.

51:38

So we are trying to bypass the liver.

51:41

So we have created a shunt between the IVC and the

51:45

portal vein, and we have to evaluate this shunt.

51:50

We look, look at this shunt for the patency. So

51:53

whenever we get a patient for Doppler, we look

51:55

at the shunt for the patency and flow, and the

51:58

volume flow of the TIPS shunt that we have to do.

52:02

So it's very—it's easy.

52:07

And like we record the

52:09

measurements of the portal vein,

52:10

we have to record the measurements of this as well.

52:14

And I think these are just some

52:16

cases of collaterals in the wall.

52:20

We have large number of collaterals—that's

52:22

on B-mode, and that's on power Doppler imaging.

52:26

Uh, more collaterals.

52:27

More collaterals.

52:28

And that's again, some spotters with collaterals.

52:34

And again, lots of collaterals there.

52:41

Okay.

52:41

It's a multiple—

52:43

heterogeneous SOL in the

52:46

liver, like neoplastic lesions.

52:49

So we are, again, that's another

52:51

lesion there, another lesion there.

52:55

So the complications are, uh, of

52:58

course we use CEUS is mainly for—

53:03

Oh, this thing.

53:04

So then we have pediatric biliary system, but I

53:07

think I'll just skip the pediatric biliary system.

53:11

And that's a long chapter

53:13

again, so thank you very much.

53:16

So in conclusion, this was just a

53:19

spotter, so I'll just come back to that.

53:22

So again, we have the confluence,

53:24

and then what do we see here?

53:26

So this has a thrombotic occlusion of main

53:29

portal vein and the splenic vein, and there's

53:32

numerous collaterals being developed there.

53:35

So thank you everyone for your great, uh,

53:39

for your joining in and for your listening.

53:42

And thank you to all the 133 participants.

53:46

Thank you so much, and I am happy to take the

53:50

questions if need.

53:52

So let's have a look at those.

53:59

So even look at the questions.

54:01

Yes.

54:02

The first—

54:02

question is how to defer from renal from hepatic?

54:07

So in hepatic, we are, uh, uh, measuring

54:11

the liver, uh, span in the midline.

54:15

Uh, so thank you so much.

54:18

So that's the basically and, uh,

54:21

beyond 150 millimeters for an adult,

54:25

we take that as an enlargement.

54:28

So how do you measure spleen on CT to say that?

54:31

Is there splenomegaly?

54:33

I think renal chord axis,

54:34

that's how you would measure.

54:36

But, uh, we are doing ultrasound.

54:37

Again, we'll use it from the portal, and we have

54:40

to make sure that we are seeing the, uh, the

54:44

hilum because that will ensure that you are in

54:47

the correct plane when you are measuring it.

54:50

That's the most important thing.

54:54

So next is, well, how do you mean measuring

54:57

portal vein and where it crosses hepatic artery?

54:59

Yeah, because portal vein is a long vessel.

55:02

So we've just developed, uh,

55:04

we have developed a landmark.

55:06

So, uh, where the portal vein, CBD, hepatic artery—

55:11

so we have that confluence when they're crossing.

55:13

That's the, that's what the literature says, with

55:16

the crossing over of the hepatic artery that

55:18

when it's crossing over from, uh, the side. So

55:23

I mean, this is in pre, but of course in post

55:28

and anastomotic or post-liver transplant

55:31

patients, you would measure it pre-anastomosis,

55:35

at anastomosis, and post-anastomosis.

55:38

That's a different scenario.

55:39

But for the pre, and of course, if you see any focal

55:43

uh, dilatation, then you will measure that as well.

55:47

And I would usually also include the

55:49

widest measurement of the portal vein.

55:53

Okay, thanks.

55:54

Next, the best liver span measurement on CT.

55:57

So most questions are coming from CT.

55:59

So again, it would be, uh,

56:01

the axis and the axial plane.

56:05

What's the meaning of monophasic

56:07

flow in the hepatic vein?

56:08

So the normal flow, as we saw, was triphasic.

56:11

So you have three, three waves—two waves below

56:14

the baseline, below the baseline, and one above.

56:18

So many a times, we see post-liver transplant

56:21

patients, we see a monophasic flow.

56:24

So often the, um, the variations

56:30

in the waves are not seen.

56:31

So you just see one, one kind of a

56:34

phase in either one direction.

56:36

That's what's monophasic.

56:38

When you see the two kinds of

56:39

flow, then it's biphasic flow.

56:44

How to measure liver and spleen properly?

56:47

Again, it is, of course, a matter of

56:49

practice, but for liver, I would follow

56:52

the mid, mid, uh, mid-axillary line.

56:57

So the cranio-caudal span.

56:59

So of course, you take it from the

57:02

anterior surface and you go down to the

57:06

segment seven and eight to the diaphragm.

57:09

You take the longest span that you can measure, and,

57:13

uh, along the axis of the, uh, right kidney—basically

57:20

the cranio-caudal, uh, the extent that you can get.

57:24

And similarly, for the spleen, I would

57:27

take the portal width included. That

57:31

will give the most, uh, valuable information.

57:36

Does FibroScan occur on ultrasound or MRI machines?

57:40

Is it MRI? No, FibroScan is something—it's

57:45

an equipment that the gastroenterologists use.

57:48

It's neither an ultrasound nor an

57:50

MRI, nor is it MRI Elastography.

57:53

It's just FibroScan.

57:54

So they again have a, a, a, a transducer kind of

57:59

a probe, which is an, uh, which is a wave kind

58:03

of pattern, but they don't have a screen to

58:06

see it as to where they are putting the probe.

58:09

But they place the probe in the intercostal

58:12

space, and then they get the reading, uh,

58:16

based on the pulses that have gone through.

58:19

They measure the stiffness of

58:20

the liver, and it's displayed.

58:22

It's not a targeted scan, it's like a blind

58:26

procedure where you put something on the liver, and

58:28

you just get the stiffness of the parenchyma, and

58:31

it's just displayed in KPA reading on the screen.

58:38

But that's the course.

58:40

Is the spleen volume more accurate than

58:42

the splenic length? Clinically, volume, uh, is

58:46

a, uh—for ultrasound, I have not used it.

58:49

I use the spleen length, and my clinicians

58:52

and all are happy with the spleen length, and

58:54

they use that as a, uh, as a guide to the

58:58

disease progression or improvement as well.

59:02

Thank you.

59:03

Can we see monophasic flow in hepatic vein in BCS?

59:07

Yes, of course you can, because all the basic

59:09

physiology is altered, so it can be from both.

59:12

So in early cases, of course, like that's often a

59:16

precursor that instead of triphasic waveform,

59:19

now the waveforms become biphasic,

59:21

now the waveforms become monophasic.

59:23

So that's kind of suggesting that the events are

59:26

getting—going towards a sluggish circulation or going

59:30

towards an impacted circulation or no flow at all.

59:34

Right.

59:35

So yes, you can see a monophasic flow in hepatic BCS.

59:40

So what's the best scanning technique for the

59:43

caudate-right lobe ratio? Like I discussed, I

59:46

think we discussed all that in detail in the scan.

59:50

Thank you.

59:51

So is Doppler gold standard for portal hypertension?

59:55

I mean for the flow dynamics, we need

59:58

Doppler, because Doppler is something

60:01

we do not have a CT or MRI to replace.

60:04

How much blood is actually

60:06

flowing within a blood vessel?

60:08

That is a tool which can only be answered by Doppler.

60:11

So that's why Doppler is unique.

60:14

What Doppler information can

60:15

provide, no other tool can provide.

60:18

So Doppler to get the flow dynamics.

60:25

Uh, of the, uh, patency and the amount of

60:29

blood that is flowing across any vessel.

60:32

The Doppler is the thing, and of course, uh, I

60:35

mean to understand the cirrhosis, the stiffness,

60:39

and, uh, various other diameters, uh, of the

60:43

caudate lobe and relative volume distribution.

60:45

Of course, CT is very helpful as well, because it'll

60:49

also assess lots of other things, and it'll evaluate

60:52

all the blood vessels, which are often hard to reach.

60:55

And ultrasound imaging, you can have challenges

60:58

depending on the patient body habitus, preparation,

61:01

breath-holding, various other challenges.

61:03

So CT is very helpful, but to

61:06

get the flow—let's stop there.

61:09

What is the helical flow in portal vein?

61:11

Any significance?

61:12

Um, so helical flow in portal vein—

61:16

we see in cases because many times,

61:19

normally the flow is hepatopetal, towards

61:22

the liver, but sometimes you can get

61:24

the yin-yang kind of a phenomenon.

61:26

So that means it's just showing

61:28

that there's a transiently increased

61:29

resistance towards the liver, or—

61:33

there's too much high resistance

61:34

to the flow towards the liver.

61:36

So it's reversing. So it means it's

61:38

a process in evolution before it

61:40

probably becomes like a reversal flow.

61:44

So it's like, it's like another marker.

61:46

It can be transient, it can be there.

61:48

So it's another level of progression

61:51

of the disease that you see.

61:54

Okay.

61:54

So that's what—it’s what's the best scanning

61:56

technique for C/R ratio with ultrasound?

62:00

So again, we discussed that in detail.

62:03

And can you have loss of triphasic

62:07

flow in physiologic conditions?

62:11

I haven't seen—normally, I mean, cardiac congestion or

62:14

cardiac failure or any other causes can lead to that

62:19

if there is, uh, back pressure changes or something.

62:24

But physiologic conditions—normally

62:27

speaking—the waveform is triphasic. So you

62:30

don't see it unless it's just transient.

62:32

And if you see the patient again after some

62:34

time, it may be okay. But I haven't seen,

62:37

normally you can have like bi- to triphasic,

62:41

but it would suggest there is some pathology.

62:46

Does liver size change with habitus?

62:51

Uh, or if beyond 15.5 in normal-looking build

62:55

patient, liver size changes with the habitus of the patient.

63:00

Uh.

63:02

We haven't, uh, used that as a criteria

63:04

because, uh, we use the adults as a 15 or 15.5.

63:10

We do give some consideration unless if you

63:12

see anything like out of the, maybe the fifth

63:16

or the 95th centile for the body mass index.

63:19

But generally speaking, we haven't done that.

63:23

Is ultrasound elastography

63:25

more accurate than FibroScan?

63:26

I'm a, I'm a user of ultrasound imaging and I would

63:30

say ultrasound elastography is the preferred modality over

63:33

FibroScan because of course we are doing targeted,

63:38

and I did have requests—there were cases where

63:42

there was a lesion in the liver and we want to assess

63:44

in the back, which is excluded on the hepatic.

63:49

So FibroScan is—

63:53

We don't know if there's any

63:55

rib or any calcification.

63:57

Sometimes there can be some benign

63:58

calcification in the area, or there

64:00

can be some SOL or any other lesions.

64:03

So I think ultrasound elastography is the way to go.

64:07

And FibroScan offers only reading of diffuse

64:10

liver disease and can't comment on HCC.

64:16

Right.

64:16

I mean that's why, because if there is

64:18

any focal lesion or focal pathology,

64:21

ultrasound-guided GRE is the preferred modality.

64:25

Yes.

64:25

Okay.

64:27

If the patient is doing well, Valsalva of—

64:33

For what?

64:34

FibroScan is a—

64:36

gentle breath-holding.

64:37

So we are not doing SVA or FibroScan.

64:40

Is that for hepatic veins or—

64:43

Pertaining to?

64:48

We normally see—

64:49

triphasic, we don't use the Valsalva

64:51

maneuver for hepatic Doppler evaluation.

64:53

So that's, uh, never been a part of the

64:56

protocol or scanning that I've read anywhere.

64:59

So just a gentle breath-holding or a

65:02

maybe deep breath-holding if required.

65:05

That's what's, uh, helpful in supporting.

65:09

All right.

65:09

I think you—all the questions.

65:12

Thank you so much.

65:13

Thank you.

65:14

Thank you everybody for your questions.

65:16

It made it really interesting and interactive.

65:18

Thank you.

65:20

Dr. Sal, thank you so much for your

65:21

lecture today, and thanks to all for your

65:23

participation in our noon conference.

65:25

A reminder that you can access the recording of

65:27

today's conference and all our other previous noon

65:30

conferences by creating a free MRI Online account.

65:33

If you'd like to access our full library of case-based

65:36

topics with unlimited CME, you can sign up for a

65:38

free seven-day trial of our premium membership.

65:41

Be sure to join us next week on Thursday, October 20th,

65:44

at 12:00 PM Eastern Time for a lecture with Dr. James

65:47

Ola on the overview of ultrasound-guided biopsies.

65:51

You can register for this lecture at MRIOnline.com

65:54

and follow us on social media for updates

65:56

and reminders on upcoming noon conferences.

65:58

Thanks again and have a wonderful day.