Liver Doppler made simple JC

JSS Medical College, Mysuru
Doppler US of the Liver Made Simple
Dean Alexander McNaughton, MD • Monzer M. Abu-Yousef, MD
Doppler
Authors:
Journal:
Presenter
Dr.Vishwanath Patil
PG Resident
Moderator
Dr. Geetha M J
Assistant Professor
RSNA, PUBLISHED ON FEB 201 1

Introduction
• Normal and abnormal waveforms for each of the major hepatic vessels
(hepatic artery, hepatic vein, and portal vein) has “signature” appearance.
• Every disease process that affects the liver has its own characteristic effect
therefore, affects the waveforms for the three major hepatic vessels in a unique
way .

What are we going discuss?
• Terminologies.
• Basic concepts of flow dynamics.
• Normal waveforms.
• Abnormal waveforms.
• Brief US findings at transjugular intrahepatic
portosystemic shunt (TIPS).

Terminology and Flow Concepts
• Ideally, the sample volume should be placed in
the midportion of the lumen.
• Doppler angle (Θ)—the angle between the
actual Doppler beam and the Doppler
interrogation line.

Terminology and Flow Concepts
• V = (DF)(C) /2(Ft)(cosΘ)
• where C = the speed of sound in tissue (1.54
m/ sec),
ΔF=Doppler frequency shift, and Ft=transducer
frequency.
• As Θ increases from 0° to 60°, cosΘ decreases
from 1 to 0.5; however, as Θ increases from
60° to 90°, cosΘ decreases from 0.5 to 0 .

Waveform Features and Information
• DIRECTION- Above the baseline or below.
• VELOCITY -distance from the baseline at any
given point .
• ACCELERATION- slope of the curve (ie, rate of
change in velocity) .
• INFLECTION POINTS -changes in acceleration
and these generate characteristic audible
sound.

Flow Direction
• The first is to describe flow with respect to the
circulatory system.
• Antegrade refers to flow in the forward direction with
respect to its expected direction in the circulatory system.
• Eg: Antegrade flow moves away from the heart in the
systemic arteries and toward the heart in the systemic veins.
• However, antegrade flow may be either toward or away from the transducer,
depending on the spatial relationship of the transducer to the vessels.
• Antegrade flow may be displayed above or below the baseline, depending on
the vessel being interrogated.

Flow Direction
• Retrograde refers to flow in the reverse direction with respect to its
expected direction in the circulatory system.
• Eg: Severe portal hypertension, in which portal venous flow reverses direction
(hepatofugal flow).

Phasicity versus Phase Quantification
• Phasic is another word for cyclic.
• Its absence or presence (and degree) may be qualified.
• A phase is a stage, or portion, of a phasic process.
• The number of phases may be quantified.
• Aphasic: Absolutely no flow
(ie, no velocity),there is no phase.
• Nonphasic: There is flow (ie, velocity)
but no velocity or acceleration
changes are present, the waveform is flat.

• PHASIC: Mild undulation (shallow slopes and a small vertical range between
inflections), as in normal veins.
• PULSATILE: Marked undulation (steep slopes and a wide vertical range between
inflections), as in normal arteries.

• D.A.M. prefers: Discrete flow components in either direction (ie,
portions on either side of The baseline).
• M.M.A.Y. prefers : Interprets a phase as each unique inflection point on the
waveform during one cycle .“Biphasic” if two sounds are heard during each
cycle and as “Triphasic” if three sounds are heard.

Unidirectional versus Bidirectional
• Vessels with flow in only one direction (whether antegrade or retrograde)
can be said to have unidirectional flow, which can only be monophasic .
• Vessels that have flow in two directions said to have bidirectional flow.

Inflection Quantification
• Aninflectional: Waveforms without inflection
• Maximum number of inflections per cardiac cycle—are tetrainflectional.

Arterial Resistance.
• Resistance, or impedance to flow, may be described empirically or quantitatively .
• If the lowest point (trough) of the waveform at end diastole is high, there is
relatively more flow during diastole, a finding that indicates a low-resistance
vessel.
• If the trough is low, there is relatively less flow during diastole, a finding that
indicates a high-resistance vessel .
• The most frequently used index in the hepatic arteries is the RI .
• Low-resistance arteries normally have an RI of 0.55–0.7

Arterial Resistance
Low-Resistance Arteries (Normal RI = 0.55–0.7)
• Internal carotid arteries
• Hepatic arteries :However, wider normal ranges of 0.55–0.81 .
• Renal arteries
• Testicular arteries
• High-resistance arteries physiologically have an RI greater than 0.7 .
High-Resistance Arteries (Normal RI >0.7)
• External carotid arteries
• Extremity arteries (eg, external iliac arteries, axillary arteries)
• Fasting mesenteric arteries (superior and inferior mesenteric arteries)

Arterial Resistance
• A high RI is not specific for liver disease; therefore, it is less meaningful as
an isolated finding than is a low RI.
• An RI that is too high may be the result of the postprandial state,
advanced patient age, or diffuse distal microvascular disease, which has a
wide variety of causes including chronic liver disease due to cirrhosis or
chronic hepatitis.
• An RI that is too low may be the result of proximal stenosis or distal
vascular shunting (arteriovenous or arterioportal fistulas), as seen in
severe cirrhosis; trauma (including iatrogenic injury); or Osler-Weber-
Rendu syndrome.

Flow Patterns and Waveform Findings
• Plug flow is the ultimate large vessel effect, being described only in the
thoracic aorta
• “Drag effect “ -The wall exerts a “drag” effect on the moving blood, so that
the velocity at the periphery of the lumen is lower than at the center .
• Smaller vessels with laminar flow, the drag effect is
more significant, with a wider range of velocities from
the center to the periphery.
• Turbulent flow represents disorganized
flow, with pockets of flow moving at different
velocities and in different directions.

Flow Patterns and Waveform Findings
• Spectral broadening is seen when the waveform is no longer traceable
with a pencil or marker. In other words, the spectral window starts to fill
in.
• Causes of Spectral Broadening
– Artificial
• Large sample volume
• High gain
– Physiologic
• Normal small vessels (hepatic arteries)
• Normal turbulence (bifurcations)
– Pathologic
• Compressed vessels (eg, hepatic veins in cirrhosis)
• Turbulent flow (poststenotic flow)

Waveform Nomenclature

Stenosis Flow Dynamics
• UPSTREAM : Refers to blood that has not yet passed a reference point .
• DOWNSTREAM : Refers to blood that has already passed the reference
point.

• upstream stenosis : transducer is sampling flow velocities
from blood that has previously passed through the stenotic
portion of a vessel.
• Transducer is actually downstream.
• Downstream stenosis : transducer is sampling flow velocities
from blood that has not yet passed through the stenosis

Signs of stenosis
• Direct signs are those found at the stenosis.
• Indirect signs are those found upstream or downstream from
the stenosis.

• Tardus-parvus is most commonly applied in cases of aortic stenosis and
renal artery stenosis.
• However, this finding may be observed in the post stenotic downstream
portion of any vascular territory.
• A tardus-parvus waveform can be objectively confirmed on the basis of
calculations such as acceleration values (normal, >5 m/sec2), time to peak (normal,
<70 msec), and RI.
• It should be remembered that this finding is not specific for downstream stenosis,
since diffuse microvascular disease, among other entities, can also increase
resistance.

Liver Doppler Waveforms
• The characteristic waveform signature, which correlates with the unique flow
pattern of the vessel is dictated by,
1. Anatomic position of the vessel in the circulatory system (systemic arterial side,
systemic venous side, or portal venous position)
2. Cyclic pressure variations generated by cardiac activity.

Hepatic Arteries
• Pulsatile.
• Its peak height corresponds to peak systolic velocity (V1).
• Trough corresponds to end-diastolic velocity (V2).
• Antegrade throughout the entire cardiac cycle.
• Displayed above the baseline.
• Hepatic artery is a low-resistance vessel.
• RI ranging from 0.55 to 0.7.

Hepatic Arteries
1. Causes of Elevated Hepatic Arterial Resistance (RI >0.7)
• Pathologic (microvascular compression or disease)
• Chronic hepatocellular disease (including cirrhosis)
• Hepatic venous congestion
• Acute congestion diffuse peripheral vasoconstriction
• Chronic congestion fibrosis with diffuse peripheral
compression (cardiac cirrhosis)
• Transplant rejection (any stage)
• Any other disease that causes diffuse compression or
narrowing of peripheral arterioles
• Physiologic
• Postprandial state
• Advanced patient age

Hepatic Arteries
2 .Causes of Decreased Hepatic Arterial Resistance (RI <0.55)
• Proximal arterial narrowing
• Transplant stenosis (anastomosis)
• Atherosclerotic disease (celiac or hepatic)
• Arcuate ligament syndrome (relatively less common than transplant stenosis
or atherosclerotic disease)
• Distal (peripheral) vascular shunts (arteriovenous or arterioportal fistulas)
• Cirrhosis with portal hypertension
• Posttraumatic or iatrogenic causes
• Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)
*Hepatic arterial RI is not useful for diagnosing cirrhosis or predicting
its severity

Hepatic Veins
• Difficult to understand than the hepatic arterial waveform, owing to its
many components generated by complex alternating antegrade-
retrograde pressure or flow variations, which are in turn created by
pressure variations related to the cardiac cycle .
• Pressure changes in the right atrium will be transmitted directly to the
hepatic veins.
• Majority of blood flow must be antegrade to get back to the heart.
• Antegrade flow is away from the liver and toward the heart thus, it will
also be away from the transducer and, therefore, displayed below the
baseline

Hepatic Veins
• “a” wave is the first wave encountered on the waveform.
• It is generated by increased right atrial pressure resulting from atrial contraction.
• The a wave is an upward-pointing wave with a peak that corresponds to maximal
retrograde flow .
• S wave correlates with peak negative pressure created
by the downward motion of the atrioventricular
septum during early to midsystole.
• v wave correlates with opening of the
tricuspid valve, which marks the transition
from systole to diastole.
• The peak of this wave may cross above the baseline
(retrograde flow) or may stay below the baseline
(ie, remain antegrade)

Hepatic Veins
• D wave correlate.s with rapid early diastolic right ventricular filling.
• Overall W shape of the hepatic venous waveform is produced.
• However, it is important to remember that physiologic flow in the hepatic veins is
hepatofugal (ie, away from the liver and toward the heart).
• In summary, the hepatic venous waveform
is normally phasic and predominantly antegrade.

Abnormal (pathologic) hepatic venous flow
1. Increased pulsatility (pulsatile waveform).
waveform with dramatic fluctuations between abnormally tall retrograde
waves and abnormally deep antegrade waves .
TWO CONDITIONS
1. Tricuspid regurgitation
2. Right-sided heart failure without tricuspid regurgitation .

Whats abnormal?

Tricuspid regurgitation
A- v wave is very tall, and the S. wave is not as deep as the D wave .
Severe Tricuspid regurgitation - S wave will no longer dip below the baseline, and there will
be one large retrograde a-S-v complex, .or “reversed S wave”

Right-sided CHF without tricuspid regurgitation
• The a wave is very tall.
• Normal relationship between the S and D waves is
maintained (S [systole] is deeper than D [diastole]).

Decreased phasicity (decreased pulsatility) and spectral
broadening.
• Both result from hepatic vein compression.
• waveform is affected not only by the cardiac cycle, but also by
respiratory variation.
• The ideal time to acquire the spectral waveform is during a
small (incomplete) inspiratory breath hold.
• Both result from hepatic vein compression.
• Decreased venous compliance is seen as a waveform with a
proportional loss of phasicity.
• As long as the a wave remains above the baseline, there is
normal phasicity .

Decreased phasicity (decreased pulsatility) and spectral broadening.
• Causes of Decreased Hepatic Venous Phasicity
• Cirrhosis
• Hepatic vein thrombosis (Budd-Chiari syndrome)
• Hepatic veno-occlusive disease
• Hepatic venous outflow obstruction from any cause

Degrees of severity of decreased phasicity in the hepatic vein by
Farrant and Meire
• position of the a wave relative to the
baseline and peak negative S wave
excursion.
Moderately decreased phasicity :peak of
the a wave is at least halfway between
the baseline and the peak negative
excursion of the waveform.

Decreased phasicity in the hepatic vein
• Absent (aphasic) hepatic venous flow : Diagnostic for venous
outflow obstruction (Budd-Chiari syndrome)
• This syndrome may also manifest as
(a) incomplete obstruction, which may have a spectral waveform
with decreased phasicity (eg, nonphasicity)
(b) increased flow velocities and turbulence at the level of
stenosis.
Strong association of portal vein thrombosis with Budd-Chiari
syndrome (25%) .

The characteristic color Doppler US
in Budd-Chiari syndrome
• Bicolored, curving hepatic venous collateral vessels.
• The two colors are generated by the different drainage pathways in these
collateral vessels, since they transmit blood to any other patent vein,
whether systemic or portal.
• if there is a malignant thrombus, intratumoral color signals may be
appreciated.
• Spectral Doppler US of bland thrombus will show no appreciable
waveform other than noise .

The characteristic color Doppler US
in Budd-Chiari syndrome
1. Gray-scale of hepatic venous confluence shows
complete absence of the right hepatic vein
with obliteration of the lumen of a common
trunk for the middle and left hepatic veins.
2. Color Doppler image shows that blood flow in
the middle hepatic vein (blue) is normally
directed toward the inferior vena cava. As the
trunk is obliterated, all the blood is flowing out
of the left hepatic vein (red), which is
abnormal.

Portal Veins
• First, physiologic flow should always be antegrade.
• Creates a waveform that is above the baseline.
• Hepatic venous pulsatility is partially transmitted to the portal veins
through the hepatic sinusoids, which accounts for the cardiac variability.
• Flow velocity in this vessel is relatively low (16–40 cm/sec).
• It is important to note that the PI
calculation for the portal vein is different
PI is calculated as V2/V1,
• PI should be greater than 0.5 .
• Another point worth emphasizing is
that lower calculated PIs correspond to
higher pulsatility.

Portal Veins
• Portal vein is the only vessel in which the terms hepatopetal
(physiologic) or hepatofugal (pathologic) are used to describe
flow direction.
•

Abnormal (pathologic) portal venous flow
• Four ways.
1. Increased pulsatility (pulsatile waveform).
2. Slow portal venous flow.
3. Hepatofugal (retrograde) flow .
4. Absent (aphasic) portal venous flow.

1.Increased pulsatility (pulsatile waveform)
• Hepatic sinusoids connect the portal veins with the hepatic arteries and
veins.
• Anything that abnormally transmits pressure to the sinusoids will result in
a pulsatile portal venous waveform.
• Causes of Pulsatile Portal Venous Waveform
1. Tricuspid regurgitation
2. Right-sided CHF
3. Cirrhosis with vascular arterioportal shunting
4. Hereditary hemorrhagic telangiectasia–arteriovenous fistulas

2.Slow portal venous flow
• Abnormally slow flow occurs when back pressure limits forward velocity .
• Findings That Are Diagnostic for Portal Hypertension
1. Low portal venous velocity (<16 cm/sec)
2. Hepatofugal portal venous flow -specific
3. Portosystemic shunts (including a recanalized umbilical vein) -specific
4. Dilated portal vein
Splenomegaly and ascites are nonspecific.

3. Hepatofugal (retrograde) flow
• Hepatofugal flow occurs when back pressure exceeds forward pressure
reversing direction .
• This results in a waveform that is below the baseline.
•

Absent (aphasic) portal venous flow
• Occlusive disease, usually caused by bland or malignant thrombosis.
• In Severe portal hypertension, there is a period of time during the disease course
when flow is neither hepatopetal nor hepatofugal, but stagnant ,this puts the
patient at increased risk for portal vein thrombosis.
• Benign from malignant portal vein thrombosis is a regular task for radiologists.
Malignant thrombosis -Thrombus echogenicity, portal vein enlargement on gray-scale
US
However, tumor thrombus can be seen in the setting of a normal-sized portal vein,
and bland thrombus.
• Most reliable distinguishing gray-scale US feature of malignant thrombus
is the combination of an echogenic filling defect + adjacent liver mass.

Specific sign of tumor thrombus
• Some cases of malignant thrombosis, there may be color
signals within the thrombus.
• This has been referred to as the “thread and streak sign” at
both CT angiography and color Doppler US
• Color Doppler US of the main PV, Rt. and Lt. PV branches
revealed; Rt. and Lt. PV thrombus, with intrathrombus
pulsatile flow (arterial waveforms) denoting
neovascularity of the thrombus, suggesting malignant
nature of the thrombus

Bland thrombus
• Cavernous transformation tends to be a marker for bland thrombus .
• These collateral vessels usually take a long time .
• When patients have tumor thrombus, they usually do not live long enough
for this development to occur.

Transjugular Intrahepatic Portosystemic Shunts
• TIPS are most commonly used for the treatment of severe portal
hypertension with refractory variceal bleeding or ascites.
• Doppler US has a long track record of reliably helping detect TIPS
malfunction.
• cephalic end of the shunt is most commonly located immediate to the
connection of the right hepatic vein with the IVC,
• Caudal end is located in the right portal vein.

TIPS
1. Shunt is best seen in the long view.
2. Normal flow starts toward the transducer (red, above the baseline) in the caudal
portion of the shunt
3. Then moves away from the transducer (blue, below the baseline) in the cephalic
part.

TIPS
• segment of the portal vein between the caudal portion of the TIPS and the portal
bifurcation will have hepatopetal flow.
• Normal flow in the cephalic (left) and caudal (right) parts of
the TIPS.

Standard TIPS examination
• Standard TIPS examination is used to sample
(a) The three parts of the shunt -Direct evidence is obtained by imaging
the consequences of failure at the site of disease.
b) Any intervening hepatic vein segment
(c) The main, right, and left portal veins- for indirect evidence of
failure .

Standard TIPS examination
• Impossible to draw a meaningful conclusion from a TIPS examination
without comparing velocities and flow directions to those from prior
examinations.
• First baseline examination should be performed
1. < 1 week of initial placement for Wallstents (Boston Scientific, Natick, Mass),
2. <1 month after initial placement for covered stents.
• Performed 1 month after stent placement is because the polytetrafluoroethylene
graft lining contains a small amount of air, which eventually reabsorbs but also
generates US artifact soon after placement.
• Further surveillance includes examination 3 months after the baseline
examination, with an additional examination every 6 months thereafter.

Normally functioning TIPS
• a) On a spectral Doppler US image, the
color Doppler image shows the cephalic end
of a TIPS in blue
• b) Spectral Doppler image shows the caudal
end of the TIPS in red.
• (c) On a spectral Doppler US image of the
right portal vein, the waveform is below the
baseline. Flow within the vein is
hepatofugal .
• (d) Spectral Doppler US image shows the
main portal vein in red and a waveform
above the baseline.

Shunt malfunction
• Narrowing or occlusion caused by intimal hyperplasia or in
situ thrombosis.
• It most commonly occurs in the cephalic portion.
• Occlusion is the easiest type of failure to detect, since it
manifests as absent flow at color Doppler US and has an
aphasic spectral waveform.

TIPS malfunction Signs
• These signs include an abnormally high (>190 cm/sec) or abnormally low
(<90 cm/sec) velocity within the shunt .
• Abnormal change in velocity (increase or decrease >50 cm/sec) compared
with the prior examination.
• Intrahepatic portal venous flow that was hepatofugal on the prior ex
amination and has changed to hepatopetal flow.

TIPS malfunction Signs
• Low velocity (<30 cm/sec) in the main portal vein.
• The development or recurrence of collateral vessels such as a recanalized
umbilical vein, also suggest failure.

Conclusions
• Pathologic conditions such as portal hypertension, right-sided heart
failure, and tricuspid regurgitation have characteristic effects on Doppler
waveforms .
• Doppler US remains the “workhorse” modality for the evaluation of TIPS
patency .

References
• Abu-Yousef MM. Normal and respiratory variations of the hepatic and portal venous duplex
Doppler waveforms with simultaneous electrocardiographic correlation. J Ultrasound Med
1992;11(6):263–268.
• 2. Abu-Yousef MM. Duplex Doppler sonography of the hepatic vein in tricuspid regurgitation.
AJR Am J Roentgenol 1991;156(1):79–83.

Liver Doppler made simple JC

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