The Value of Doppler in Abdominal Sonography - SD

Introduction

Hello, I'm Dr. Beatrice Mado.
I'm at the University of Miami where I am an associate professor of clinical radiology
and my lecture will be on the value of doppler
and abdominal sonography,
the value of doppler and abdominal sonography.
These will be individual cases
that I've collected over the years that
demonstrate the value of doppler and color.

Case Number One

Doppler case number one is of a patient who has undergone a
nephrectomy and now is found to have liver mass.
The liver mass was seen on ct
and then the patient was brought to ultrasound for
the evaluation because there was a suspicion
that the mass may be of vascular nature.
We can see that there is an une coic
lesion in segment three.
Yet despite its une coic appearance,
it's arguable if there is acoustic enhancement.
So the absence of the acoustic enhancement, which could
lead us to think this is a cyst,
makes us then further evaluate this with color doppler.
And in fact, this is very rewarding
because this is not a cyst.
This represents a vascular lesion in segment three,
and we can see even some
of its additional components, a large draining vein.
So an arteriovenous malformation that on CT was considered as a possibility.
But the fact that renal cell carcinomas are known
to have vascular metastasis led us
to further evaluate this finding with ultrasound,
a very rewarding diagnosis
of a simple arteriovenous malformation of the liver.

Other Examples

Other examples that I've collected over the years here,
this patient is seen to have at the very
anterior margin of segment two, a vascular
area in her liver.
Patient returns for additional evaluation years later,
and the sonographer is surveying the same area,
yet she only used a five megahertz transducer.
And except for a slight bulge to the contour of the liver,
we're not really showing the vascular malformation
that is known to be present.
When we switch to a higher frequency transducer,
a 10 megahertz linear array,
we can now discern on gray scale the presence of the mass
color, the upper displays to great detail, the
nature of the mass, the presence of multiple
vascular channels, somewhat disorganized, that composed this
isolated hepatic arterial venous malformation.
Sampling with spectral doppler demonstrates is no low
resistance flow pattern, typical of vessels that have
very elastic walls
because they are composing and arterial venous malformation.
So low resistivity indices in these vascular malformation.
So isolated hepatic arteriovenous malformation

Case Number Two

case number two is also a very rewarding
case for sonography.
The patient had undergone a recent abdominal ct,
which was read as normal.
We were asked to survey the patient
because of additional concerns by the clinicians,
and we can see that there are tubular structures
within the hepatic parenchyma that do not correspond to any
of our normal vascular hepatic structures.
Note also that some of these become quite large
towards the hepatic periphery.
This is the gallbladder.
So these large tubular structures throughout the hepatic
parenchyma made us further evaluate this finding.
And we also noted that there was a disproportionate
larger caliber to the middle hepatic vein relative
to the right and left hepatic veins.
Color doppler displays to great detail the presence of
multiple vascular malformations throughout the hepatic
parenchyma, corresponding to the une coic tubular structures
that were seen by gray scale.
And these vascular malformations were the reason why there
was such a tremendous volume of
blood egressing out of the middle hepatic vein,
which caused it to be quite large.
As we surveyed the port of Hepa, we were surprised.
This is our second case of this entity, to find the typical,
the characteristic finding in this population.
This finding is a hypertrophy HEPA card noted
that this HEPA card is
larger than the portal vein, which is seen here.
This hypertrophy heico is the hallmark of this condition.
We're talking about Oslo Weber Redu
and its findings in the liver parenchyma.
So we have here CT study, which was, as I said, interpreted
as being normal, but upon re retrospective review,
it was not normal.
This large vessel at the porta heus is the hepatic artery.
While this vessel further into the porta, HEPA
represents the portal vein.
In the normal setting,
the hepa artery average is six millimeters
and the portal vein, as we know, 12 millimeters or less.
So this hypertrophy hepa artery is very characteristic
of Oslo Weber randu
because of the shunts, there is a steel
from the aorta preferentially
through the hepatic parenchyma due to these multiple
arterial venous or arterial portal vascular malformations.
For comparison, you can see on the CT
that the hepatic artery equals
or is even a little bit larger than the main portal vein.
Throughout the hepatic parenchyma, we had multiple small
vascular malformations
that you can appreciate here in segment four B.
And some of these extend to the hepatic surface,
capsular surface, and the more typical appearance
of the peripheral arteriovenous malformations, which are the
atic versions, the small areas that are known
to exist throughout the hepatic parenchyma in this entity.
Again, these are little magnetic
areas throughout the substance of the liver corresponding
to these vascular malformations.
And again, the discrepancy
of the middle hepatic vein being larger than the
right or the left.
Due to most of these vascular malformation
draining via the middle hepatic vein, autosomal
dominant Oslo Weber randu occurs in families.
It is also known as hemorrhagic hereditary injects.
The hepatic disease demonstrates widened
and tortuous hepatic arteries.
There can be either arterial venous
or arterial portal fistulas, both intra
or extrahepatic, as well as multiple small tele
areas in the he hepatic parenchyma Oslo.
Weber Randu is a connective tissue proliferation
that results eventually in fibrosis and cirrhosis.
The patients may experience high cardiac output due
to these shunts, and eventually these patients will
develop portal hypertension.
Hepatic involvement varies from eight to 37%.
Most of these are asymptomatic except when they have
reached perhaps the sixth decade when they can become
symptomatic due to cardiac failure.
Secondary to these intra hepatic shunts
Doppler findings, A hepatic artery
that is greater than 10 millimeters is the hallmark,
and we should then seek shunts within the liver
because this is considered a hypertrophy hepatic.
So either isolated shunt or these related to Oslo Wedu.

Second Case of Oslo Wedu

This is a second case of Oslo Wedu.
He has a known a Weber randu.
He has experienced multiple bouts of epistaxis,
which we know is the manifestation most commonly
associated with this entity.
He comes from the Basque region of Spain
where several family members have been documented,
and his physician wanted
to know if we could just assess the caliber
of his hepatic artery to see if he happens to have
hepatic involvement.
This is the great scale study of this patient,
and you can see that the hepatic artery is not markedly
increased in size.
The portal vein is seen posterior to it
and on color doppler perhaps mildly hyper purified
above the six millimeter value,
but not significantly enlarged yet.
He did not have intra hepatic shunts
that we could identify at the time of surveillance.
So Oslo Weber du
with multiple hepatic arter venous malformations.

Case Number Three

Case number three is also very rewarding.
This child was only seven
years old when he had
to undergo an MRI study due to seizures.
He had a behavior of restlessness, which
was very difficult to handle by his parents.
The MRI study demonstrated high signal intensities
In the global poly die, and these were bilaterally
and nearly symmetric.
These are known to occur when there is a liver dysfunction
to the point where manganese
and magnesium deposit in the global globus palai.
So because of this finding, it was recommended that liver disease be excluded on this patient.
The initial sonogram was aimed at assessing for biliary atresia
and they did document the presence
of a well-developed gallbladder
and those signs of liver dysfunction.
The liver appeared normal.
The restlessness of the child was an issue, so we asked
that the mother sent the child for a meal,
and when the child returned, he was more cooperative.
At this point, we did a very detailed surveillance
of the liver and noted that
we could not identify the intra hepatic portal branches.
Instead, what we saw were linear echogenic areas
where the intra hepatic portal veins
should have been present.
So the absence of the intra hepatic portal veins led us to
seek what could be happening to flow from the portal system from the gut,
from the splenic vein into the liver.
And as we sought to explain the finding, we realized
that we could see a portion
of the extra hepatic portal vein,
but it's direction was towards the
inferior vena cava rather than towards the portal hepatis.
So on color doppler, you can see the anomalous direction.
The main portal vein achieves towards the inferior vena cava
rather that than into the int hepatic region.
So this anomalous communication of the portal vein
with the intra hepatic segment of the IVC was due
to a congenital portal cavo shunt
in gray scale, you can see that the portal vein
has an aneurysmal component
and at which point it has an anomalous course
and anastomosis with the intra hepatic inferior vena cava.
So this is a congenital portal c shunt
displayed here in color Doppler very elegantly.
When we sampled with spectral Doppler,
the flow was very chaotic
because we had this aneurysmal component
and we had spectral waveforms that were a combination
of the portal venous components in parts
of the cable flow,
so very turbulent flow through this extra hepatic
portal cable shunt.
This congenital portal cable shunt was described
by Abernathy in 1793.
The fact that the child had these high signal intensity
areas in the global PDI
and li high levels of serum ammonia was
resulting in him having seizures
because he really had bouts of hepatic encephalopathy.
This finding of deposition of magnesium
and manganese in the global PDI can be found in patients
with liver dysfunction is very prevalent in alcoholics
or in patients on parental nutrition.
Our case reflects absence of the normal metabolic pathways
for the clearance of these metals.
Due to the presence of this portal cable shunt,
The ABER anatomy malformation has two versions.
Type one has absence of the intrahepatic portal.
Veins flow is redirected into the IVC
and this can be isolated,
but in females unfortunately they have
associated anomalies.
They have polys, pia, biliary atresia, and liver tumors.
Type two is just an extra hepatic connection
between the main portal vein and the retro hepatic IBC.
This is the type we have in our patient.
It occurs in males without associated anomalies.
The theology of the ABER anatomy malformation is thought
to be excessive evolution
of the per intestinal villin venous loop
or total failure of the villin veins
to establish anastomosis
with the hepatic sinusoids or hepatic veins.
Additional intrahepatic portal systemic shunts have been
classified and according to par
type one would be a single large tube that connects
with the right portal vein with the inferior n cava.
Type two would be peripheral shunts within a
single hepatic segment.
And type three portal systemic shunts through an aneurysm
type four, multiple communications between peripheral portal
and systemic veins.
So this was a case of congenital portal.
Cable shunt also termed ABER anatomy malformation.
The child was sent for a hepatic transplant
because long term he would have high risks
of developing hepatocellular carcinomas.

Case Number Four

Case number four is an elderly female
with congestive heart failure.
Gray scale sonography of the liver demonstrates very
engorged hepatic veins due to her longstanding
congestive heart failure.
As we evaluate these hepatic veins in more detail, we
identify aneurysmal dilatation
of the right hepatic vein in an anomalous communication
with the middle hepatic vein.
This is described in association with chronic
significant tricuspid regurgitation, which this patient had
on power doppler.
We can see very well the aneurysmal dilatation
of the right hepatic vein
and its anomalous communication with a middle hepatic vein.
Spectral doppler demonstrates typical wave forms
of the hepatic vein, an accentuated flow
during atrial systole due to the regurgitation
from the tricuspid regurgitation down the hepatic veins,
intra hepatic venous collateral secondary to chronic
tricuspid regurgitation.
This was described by Middleton
using color doppler just similar to the case we have,
and this is thought to be secondary
to hepatic venous congestion.

Case Number Five

Case number five is a patient suspected
of having cholangiocarcinoma.
The patient was to undergo liver biopsy prior
to coming to sonography.
The patient had undergone a CT which we display here
we're on the early arterial phase.
We can see the cortical enhancement of the kidneys
and hepatic enhancement hepatic artery enhancement
and multiple low attenuating areas in the hepatic parenchyma
of variable shapes associated ascites
Portal hypertension and enlarged spleen is seen.
We can also note that there are some areas
of peripheral enhancement relative
to these low attenuating areas in the liver.
Note that segments two and three are very large.
So is the caudate lobe consistent
with her portal Hypertension an MR had also been done
and again, on the early phases of gadolinium infusion,
multiple low signal intensity areas were seen in the liver,
but we could not convince ourselves that they corresponded
to any type of pattern that we could accept
as being diagnostic for any entity.
So at this time we were a little concerned
because some of the findings suggested dilated biliary segments
and we noted on delay the studies that there were areas
of retention near the port of Hepa.
So for this reason, we were considering
as a possibility underlying cholangiocarcinoma.
When we studied the patient with gray scale,
We noted that in the enlarged segments two
and three, there were very unusual patterns of decreased echogenicity surrounding the portal vein venous regions.
And as we used colored the upper, we could see numerous
shunts within the hepatic parenchyma.
And as we survey the livering greater detail,
these shunts were present also in the right hepatic lobe.
These shunts were associated with ascites
and as we saw, the patient had cirrhotic features
and had portal hypertension again
throughout the hepatic parenchyma, multiple shunts
that we could identify unequivocally
with colored doper.
Since we do not have to time ourselves with the infusion
of contrast, like CT and MR have to do so.
The presence of the shunts could not be documented on either
CT or MR convincingly,
but could be unequivocally diagnosed on color doppler.
Some of these shots extended
beyond the hepatic capsule as you can see here.
Upon retrospective review of her Mrs
and cts, we realized that what we were dealing
with was Bud Chiari.
We could never identify the intra hepatic segment
of the portal vein or the hepatic veins.
So this patient had been suspected
of having cholangiocarcinoma,
but we could eventually realized that portions
of her int hepatic cava were thrombosis,
especially at the confluence with the hepatic veins.
And we could also identify the dilated aous vein
due to the lack of egress of blood out
of the liver via the cava and hepatic veins.
So this is the shunts associated with Bud Chiari
that on ct.
And Mr, because we had not carried the study to the very
late phases of contrast, we could not determine
that they were due to venous shunts in the liver
and not liver masses.

Case Number Six

Case number six, a patient with liver disease.
And now we're looking at the pancreas.
And on gray scale we can identify the region
of the pancreas,
but instead of seeing the normal gland,
what we're seeing are tubular structures that are une coic
serpiginous that would make us concerned
for vascular channels.
Indeed putting color doppler, we identify multiple
vascular channels in the expected location
of the pancreatic gland ct.
On the early arterial phase,
we can see cortical enhancements.
So we're very early in the bolus.
The hepatic artery is here,
but we can see numerous vascular channels in the region
of the pancreatic gland.
In fact, on this lower image,
we can very clearly identify these vascular channels
that superimpose the region of the pancreas.
And as we follow the portal heus,
we can see the hepatic artery of normal caliber.
And yet in the region of the portal veins,
we have very dilated structures
that are not the normal portal veins.
So what we're looking at are varicosities in the region
of the pancreas, secondary to a cavernous transformation
of the portal vein.
Another finding that substantiates the presence
of portal vein thrombosis is the presence of
peric cystic varis.
You can see them against the lateral wall
of the gallbladder.
So the cavernous transformation has resulted in numerous
dilated channels in the region of the pancreas.
And notice that we also do not identify the splenic vein,
which has also undergone thrombosis.
And perhaps this is the reason why the cavernoma extends
to incorporate portions of the pancreatic gland.
Now, if we had image this patient on a very delayed CT
like we see here when the kidneys are already filtering the
iodine, we would've failed to recognize these varicosities.
Obviously. Now with these faster scanners, we take advantage
of boluses during the arterial phase
and also portal venous phase.
Now a combined set of images showing you the CT findings
in comparison with the color Doppler findings,
which are quite comparative.
So portal and splenic vein thrombosis result in cavernous
transformation and pancreatic varicosities due
to the cavernoma extending to the region of the pancreas.
The presence of associated splenic vein thrombosis explains
the reasons why the patient developed
pancreatic varicosities.

Case Number Seven

Case number seven is a 58-year-old female with hematuria.
The study was performed in the emergency room,
an expiratory urogram.
The patient had no history of trauma,
but the urology resident told me
that he could feel a pulsatile mass in her right flank.
Note that the left kidney has already begun
to clear the iodine
and there's a normal collecting system on the left yet
where we expect the right kidney to be located.
We have an enlarged kidney that has not
yet filtered contrast.
And on a more delayed set of images, we do see
hydronephrosis of the left kidney of the right kidney,
sorry, a CT was performed because of the clinical suspicion
that something was very unusual
because a pulsatile mass could be felt On this patient's
flank, the patient denied trauma.
The only finding
or symptoms she had of recent was
that she could no longer use her usual clothing pieces
because her girth abdominal girth had increased.
So we initially interpreted the findings related
to the right kidney as those of a renal cell carcinoma
with probably venous involvement
of the inferior vena cava
'cause the inferior vena cava was quite large.
However, because of the pulsatile nature of this process, the urology resident asked could we further evaluate this patient.
And we of course had already given iodine
so we couldn't repeat the ct.
We brought the patient to ultrasound.
Gray scale demonstrates a tubular structure that extends
beyond the contours of the patient.
Red kidney, A small area of calcification
with ring down artifact is identified.
And when we evaluated the patient with color doppler,
we realized this represented
a renal arterial venous malformation.
Now, in earlier days,
artery venous malformation were confused for hydronephrosis
of the kidney because they simulated the cystic areas
in the region of the sinus.
But you can see here color the upper gives us disadvantage
of unequivocally documenting the presence
of this arteriovenous malformation.
The patient was then evaluated with angiography
for the possibility of coil embolizing,
this larger arterial venous malformation.
However, the caliber of the renal artery supplying this
arterial venous malformation exceeded the size
of the coils available at that time.
The risk was that the coil could migrate
into this vascular malformation or into other channels
and then embolize.
So instead of undergoing coil mobilization,
the patient underwent a nephrectomy.
So here's a composite showing this renal arterial venous
malformation most likely congenital
because there was no previous history of biopsy or trauma.
The gray scale study, which we reviewed, the color doppler,
the ct, which shows enhancement
to the same degree as vascular structures
of these areas in the liver, in the kidney.
So the hypertrophy hepa is seen by arteriography
and the inability
to coil embolize this arterio venous malformation.
The classification of a renal arteriovenous malformation
depend on their location and extent.
Some peripheral arteriovenous malformation are near
the CAE system.
They're called central when they're near the renal pelvis,
extensive if they extend from the caly calyx
to the renal pelvis,
they're called aneurysmal artery malformation.
If there's a single feeding artery
and a single draining vein, they're referred to
as anters if there's a single feeding artery
and multiple draining veins.
Andoid, arterial venous malformation when there are multiple
feeding arteries in multiple draining veins.

Case Number Eight

Case number eight is a patient with right flank pain.
The patient undergoes ultrasound evaluation
and using color doppler.
We note the normal vascular structures
that are portrayed in red and blue.
Yet if we analyze this image, there is a
another interesting finding.
We have a group of echos
that are trailing are becoming less in width.
They have a mosaic of colors
and this is due to the presence of a calculus.
Here we see in gray scale that same area
with an associated acoustic shadow
and taking advantage of color doppler.
We can identify renal calculi better
by using color doppler to demonstrate the twinkle artifact.
This is due to the multiple reverberations of the signal
as it bounces from the front to the back, front to the back
of this calculus.
So taking advantage of color the upper
to identify renal calculi is a very significant contribution
of sonography.
Now what about this case?
We're looking at the left kidney
and we see mosaics of color throughout the region
of the left kidney.
Is this an arteriovenous malformation
or what could be happening
while in fact this is a large calcification
and what we were looking at is a twinkle artifact.
Notice the cluster of calculi in this kidney,
and this was not an arteriovenous malformation.
We see the cortex well enhanced.
This was just a cluster of cal calcifications.
So the twinkle artifact is useful
to identify renal calculi in the kidney.

Case Number Nine

Case number nine is an abdominal sonogram
and this is of a left kidney.
And as we look at the left kidney, we see a nice
homogeneous renal cortex
and we can identify the medullary pyramids.
Yet we see similar to the renal cortex area that protrudes into the region
of the renal sinus.
So what could this be?
And we can see that it communicates
with the renal cortic cortex,
but extends a little bit
more medial towards the sinus region.
It's very important to recognize this finding
because it's a variant of normal
and if you put color you can see that it,
it does not cause any displacement of the renal vessels.
The renal vessels come out
of this region without any mass effect
and their normal arterial flow
can be demonstrated on spectral dopper.
This is a column of ton.
The iso echoic nature relative to the renal cortex of this
column is key.
In arriving at the diagnosis of this normal variant
of the kidney, this results from the invagination
of the renal cortex towards the renal sinus region.

Case Number 10

Case number 10 is an abdominal sonogram.
And now we're looking at the
segment six of the liver in the right kidney.
And as we analyze the kidney,
we again can find the normal architecture
of the renal cortex in medullary regions.
But don't stop there. Look at the sinus of the kidney.
And as we analyze the renal sinus,
we now see a hypoechoic mass within the renal sinus
and this mass is rather homogeneous
and there is, there are small cysts in the renal cortex,
so we should not be distracted by the cyst
because the most significant finding
is this mass In the renal sinus it measured 2.9
by 1.8 centimeters.
And on colored doppler we could not demonstrate flow within
the mass, but the mass was unequivocally solid
and additional evaluation led us
to recognize further the small cyst adjacent to the mass.
But patient was sent
for additional evaluation on non-contrast ct.
The mass is iso dense
to the renal parenchyma.
Note the presence of the small cyst adjacent to the mass
on arterial phase ct.
We see the normal renal cortex
and medullary pyramids, yet the region
of the mass does not enhance
and does not demonstrate the normal architecture of the
renal cortex.
So we don't have the enhancement.
If this was a column of ton,
we should have seen the normal enhancement of the cortex.
So here's the cyst
and as we carry the study further onto later phases
of contrast delivery,
the mass exhibited then a very heterogeneous enhancement.
The normal renal parenchyma is in the nephro grand phase,
yet the mass is heterogeneous
with the multiple areas of enhancement.
Notice the phase
of contrast here is already the excretory phase,
so a mass in the renal sinus region.
And here's the cyst and the mass.
This is biopsy proven oncocytoma.
Now oncocytoma do have a central scar which we may
or may not appreciate.
This happened to be a rather small oncocytoma,
so this is a biopsy proven
and I think the patient has already
undergone additional surgical management.

Case Number 11

Case number 11, this patient has been hypertensive
since age 33.
She had undergone evaluation at that early age,
but no findings could explain her hypertension.
She had undergone a CT study at the time
of complete evaluation.
She now presents with gross hematuria.
This is a CT obtained in the emergency room
and notice that the right kidney is already
excreting contrast.
The left kidney is retaining contrast.
There has been intervention by the urologist
who placed a stent and who could not visualize
on endoscopy the cause of this massive bleeding.
The patient was undergoing well, we had just had the other case of renal arteriovenous malformation.
So he asked could we evaluate the patient with sonography and colored daper to see if she had any cause
for a bleeding in her left kidney.
So we see here the clot filled the renal pelvis
with the stent and the delayed nephro due
to the obstructive changes secondary to the hemorrhage.
Now in retrospect, we're looking at the sinus region
of the lower pole of this patient's left kidney.
Now I magnified this area so
that we could appreciate this serpiginous areas in the sinus
of this left kidney,
an astute sonographer had documented the findings
but on colored doper
and in retrospect I collected the gray scale feature
so we could look at it in a more detailed fashion.
So on power doppler we see the normal architectural arrangements of the vascular structures
of the right kidney, the normal kidney.
And yet when we looked at the left kidney there were
clusters of vascular channels in the lower pole.
And these are related
to a small arterial venous malformation in the lower pole
of this left kidney.
The patient, as we mentioned, had undergone previous
complete evaluation because of her hypertension.
That could not be explained.
However, in those days,
CT was rather limited.
The slower nature of the scanners would not allow us to identify some
of these arteriovenous malformation
because we would image too late
to note the presence of these vascular channels.
But on spectral doper, I just wanted to show you
that the inelasticity of these vessels
that compose the arterial venous malformation
results in very low resistance, chaotic
flow patterns because of the
flabby nature of the arterial walls.
So here's the normal right kidney, the focal area
of a cluster of vessel secondary
to the arteriovenous malformation in the lower pole
and the spectral doppler
with the very low resistant resistance waveform.
Arteriography did demonstrate a ser
arteriovenous malformation multiple feeding arteries
and multiple draining veins that is termed ser notice
that the main renal artery supplies the superior portions
of the arterial venous malformation,
but an accessory renal artery supplies the lower portion
of this arterial venous malformation.
Well, consideration was given to coil embolization
but it had to be done with super selective technique.
The concern was if they embolized the lower component
of this arturian malformation, could they compromise flow
to the renal pelvis and proximal ureter.
So the patient underwent selective co embolization
successfully completely occluding the entire tear
of in formation and her renal vascular hypertension
was then corrected.
So this was a surfside renal A VM, which was the cause
for longstanding renal vascular hypertension in this
42-year-old female.

Case Number 12

Case number 12 is a 33-year-old male
in renal failure referred for renal biopsy.
We by now had experience
with two ous male formations
and we were considering arter malformation when our sonographer pointed out that
what appeared to be a simple cyst adjacent
to the right kidney in fact had
vascular channels leading to it.
So it was not a cyst.
And these vascular channels had very low resistivity
to flow suggesting
that this was again another arterial venous malformation.
We suggested that the patient undergo Mr
because the patient was in renal failure and the Mr.
Arteriography graphy was completely normal,
surprising all of us.
There was no findings to suggest the right
arterial venous male formation,
but my astute colleague decided to
repeat the MR and bring the patient
but image during the venous phase of contrast
and it wa was apparent then
that the patient had caval interruption
with aus discontinuation that led back into the left atrium.
There was never a identifiable
if you've vena cava through the liver.
And so these renal veins
were constituting this channel of vessels.
We saw PHA led to the right kidney,
so all the renal venous C grass took place
through this convoluted varis along the upper pole
of the right kidney.
So cable interruption with Aus continuation
and large supra renal varis.

Case Number 13

Case number 13 is a 13-year-old male with hyper hypertension
and we look at his right kidney
which appears relatively normal,
but his left kidney is grossly abnormal.
We're unable to identify the sinus region of the kidney,
the renal cortex and medullary pyramids
because he was hypertensive, we had
to do further surveillance for explanation which could be due to a renal cause
for his hypertension.
So the central region
of the left kidney was grossly abnormal.
We could never identify medullary pyramids, renal cortex
or renal pelvis vessels could be seen
coursing through this anomalous area in the kidney,
but we needed to have further evaluation
and we opted to have CT studies done on the child.
As we were looking at his renal arteries,
we identified normal velocities in his main renal artery
that was 99.6 centimeters per second.
So we still didn't have a good explanation for what was
that area that had an abnormal echo texture in
his left kidney.
So here's the left renal artery in its mid portion
has a normal appearance.
The renal vein was patent and it was also normal.
His right kidney had a normal distribution
of intrarenal vessels with arties
and veins readily perceptible.
And the right renal hilum was normal with the renal artery
of normal caliber in the draining vein.
The right renal already had a velocity
of 70 centimeters per second also in the normal range.
So as we did his ct we realized
that the left kidney was very abnormal in appearance
with a central area of enhancement corresponding to the renal cortex.
But there was also a low attenuation area,
partially calcified in the posterior aspect
of this left mid kidney, which we felt was probably an area where this patients
left kidney had been traumatized
and had healed in an anomalous fashion
and had resulted in a partially calcified renal hematoma.
So we thought maybe he had sustained a partial fracture
during the trauma
and had not realized that this had happened
and was now with the ischemic changes of his left kidney
and resulting renal vascular hypertension.
This is another patient with a similar situation.
She has a calcified subcapsular renal
hematoma and as we know page kidneys are associated
with renal vascular hypertension.
So this patient has unequivocally a subcapsular
calcified renal hematoma
and resultant renal vascular hypertension.

Case Number 14

This is a patient case number 14 pregnant
with left flank pain.
We can see an early pregnancy, 26-year-old female,
obese
with left flank pain and was taught to have pyelonephritis.
The kidney was seen to be engorged enlarged
and peri renal fluid could be identified.
This kidney measured 14.3 centimeters.
So what would be the differential diagnosis
of unilateral renal enlargement?
Well, we excluded hydronephrosis
and we excluded masses, so possibilities
to be considered compensatory hypertrophy,
but she had a normal right kidney, a duplicated
system of this kidney.
We could not identify that pilo renal vein thrombosis
or acute renal infarction.
So the patient was brought back
and evaluation with color Doppler demonstrated a patent
renal artery yet adjacent to the renal artery.
We could never identify flow in the renal vein.
Here we can see the renal artery of normal caliber
but adjacent to it we should have seen the renal vein
and we did not appreciate flow in the renal vein.
So this patient was pregnant and had renal vein thrombosis.
She was subsequent diagnosed
with thrombophilic condition.
This is another example of renal vein thrombosis noted.
Notice the irregularity of the margins of the renal vein due
to the presence of thrombus.
This is that same patient when he was more acutely ill.
Can see the entire renal vein is thromboses.
It was distended, measured 13 millimeters
and he also had associated
inferior vena cava thrombus.
So the second patient
with renal vein thrombosis is this younger male
that we're discussing now.
So extension
of the renal vein thrombus into the inferior vena cava
and he had glomerulonephritis had undergone a CT
and we could see the enlarged left renal vein
due to the underlying nephropathy that he was presently
being worked up for.
So renal and inferior cava thrombosis.

Case Number 15

This patient is evaluated prior
to cardiac transplantation
and we tell the cardiologist taking care of the patient
that she has a very echogenic mass in her right kidney,
a very large mass
and that we were concerned for an angiomyolipoma.
You can see the nature of the angio, my lipoma, some
distortion of the sound beam loss of the back wall
because of the fatty nature of the lesion.
And as we know, the average speed
of sound transmission in our systems is
1,540 meters per second, which is the average speed
of sound in our tissues.
Yet adipose tissues have a slower speed
of sound transmission average is
1,450 meters a second.
This slower transmission through fat results in an apparent
delay of returning signals that cause fatty masses to appear larger than their true size.
Here's the CT on that same patient that is about
to receive a cardiac transplant.
You can see the low attenuation nature
of the mass, it's quite large.
There are some intrinsic areas
that are higher in attenuation
and this is the angiomyolipoma.
Well, the patient underwent cardiac transplant
and then subsequent to the transplantation, she was placed on Coumadin
and she experienced severe right flank pain
and we were asked to reassess the angiomyolipoma
and of course the anticoagulation
resulted in hemorrhage into this angiomyolipoma.
These masses are known to have small aneurysms
and again, they're walls anters components within an angio.
My lipoma has these vessels that are very flabby and cannot sustain a lot of changes in pressure
and can bleed very readily.
And the present recommendation is four
centimeters or greater.
These angio my lipoma should be selectively embolized
to prevent a catastrophic event.
So here is the angiomyolipoma following its intrinsic
hemorrhage due to anticoagulation therapy.
You can see on the CT similar findings.
It now has changed its characteristics
with some residual low attenuation areas,
but higher attenuation areas composed now the mass due
to the presence of associated hemorrhage.
So we know that these elastin poor vascular structures in angio
lipomas can sustain spontaneous hemorrhage.
In our case, the hemorrhage was triggered
by the anticoagulation.
So we now know that lesions
that exceed four centimeters are best embolized.
So renal angio, my lipoma with bleeding case number 15
and last case of my series is of a patient
that has right flank pain on gray scale.
We would have called this a normal kidney, which we did.
Yet the clinician was astute
because the patient was experiencing a lot of discomfort
and he opted for a ct.
Notice that the kidney size is also preserved 12.9
by 4.7 and yet on ct
this kidney is completely infarcted.
So a global infarction of the right kidney has occurred.
Now infarcts early on may not alter the texture of the region of interest.
So I caution you if the patient is symptomatic enough
that either you put color, make sure the vessels are patent,
which we didn't do at that time, so we didn't quite achieve the best diagnosis on the patient.
So this is a global renal in fart, not
perceptible on gray scale alone.

Conclusion

So again, the value
of color doppler in abdominal sonography is a very
important component of our evaluation of patients
with conditions that vary from kidneys, liver,
spleen, anywhere where vascular evaluation can result in the correct diagnosis.
Thank you very much.