Hepatic doppler

Indications
• Evaluation of parenchymal liver disease (most common )
• Patency and the direction of portal venous flow in patients
with cirrhosis or chronic hepatitis.
• Budd–chiari syndrome(impaired hepatic venous outflow)
• Bone marrow transplantation(veno-occlusive disease).
• Hepatic transplantation(identify vascular complications)
• Assess the patency and functionality of TIPS
• Other uses:
 characterization of liver masses and
 assessment of portal flow prior to interventions such
as hepatic artery embolization
Technique

• Fast for at least 6 h prior to the examination,

as food intake can affect portal venous flow,
and bowel gas can obscure extrahepatic vessel
analysis.
• Transducers are 4 or 6 MHz curved array or 4
MHz phased array.
• Occasionally, a lower frequency transducer is
needed for improved depth of penetration of
the ultrasound beam
• Visualization of the main and right portal veins and
right hepatic vein is usually best achieved with the
patient in the left posterior oblique or left lateral
decubitus position using an intercostal window.
• The left portal vein and middle and left hepatic veins
are best seen with the patient supine through a
subcostal approach.
• When a high left lobe is present, an intercostal window
may be better.
• Pulsed Doppler waveforms are obtained with
optimized scanning parameters
• In patients in whom Doppler ultrasound is being performed
for hepatitis or cirrhosis, velocities and therefore angle
correction are not typically needed.
• When velocities are used to determine the patency of
vascular structures (i.e. TIPS), angle correction (<60) is
needed.
• The hepatic veins are sampled near the confluence with the
inferior vena cava (IVC), and spectral waveforms are
recorded.
• Waveforms of the main, right, and left portal veins are
obtained
• Care should be taken to avoid sampling during deep
inspiration or expiration because of the effect of these
maneuvers on the waveform pattern
Portal vein
• Two import considerations:
1. Physiologic flow should always be antegrade/hepatopetal
(which is toward the transducer).
2. Hepatic venous pulsatility (due to atrial systole) is
partially transmitted to the portal veins through the
hepatic sinusoids, which accounts for the cardiac
variability seen in this waveform.
• The normal portal venous waveform should gently
undulate and always remain above the baseline
• Flow velocity in this vessel is relatively low (16–40 cm/sec)
compared to hepatic artery.
• The degree of undulation is highly variable but may be
quantified with a PI.
It is important to note that the PI calculation for the portal vein is different from that for
the hepatic arteries (arterial PI = (V1–V2)/Vmean). In the portal veins, the PI is calculated as
V2/V1, with V1 normally being greater than 0.5.
Another point worth emphasizing is that lower calculated PIs correspond to higher
pulsatility.
Abnormal (pathologic) portal venous flow

1. Increased pulsatility (pulsatile waveform)

2. Slow portal venous flow
3. Hepatofugal (retrograde) flow
4. Absent (aphasic) portal venous flow
 Increased pulsatility
• Pulsatile portal venous flow occurs when there is a large difference
between flow velocity at peak systole and at end diastole.
• A pulsatility ratio >0.54 is found in over 90% of normal individuals.
• Anything that abnormally transmits pressure to the sinusoids will
result in a pulsatile portal venous waveform. Hepatic venous side
 Tricuspid regurgitation
 Right-sided CHF
Arterial side
 Arteriovenous shunting (in  pulsatility
severe cirrhosis)
 Arteriovenous fistulas (in
hereditary hemorrhagic
telangiectasia)
Tricuspid regurgitation and a marked pulsatile flow of
the portal vein
Caveat
• Recently, even marked
pulsatile hepatopetal flow
of the portal vein has
been described,
particularly in thin
subjects with an inverse
correlation to body mass .
• Decreased pulsatility has
been observed when the
patient is sitting and
during deep inspiration,
and in obese subjects
Doppler ultrasound of the portal vein with
marked pulsatile modulation of the portal flow
in a thin, healthy adult.
Slow portal venous flow

• Abnormally slow flow occurs when back pressure limits

forward velocity.
• Slow flow is diagnostic for portal hypertension, which
is diagnosed when peak velocity is less than 16 cm/sec.
• Portal hypertension is caused by cirrhosis in the vast
majority of cases; however, the exhaustive list of
causes is generally divided into prehepatic (eg, portal
vein thrombosis), intrahepatic (eg, cirrhosis from any
cause), and posthepatic (right-sided heart failure,
tricuspid regurgitation, Budd-Chiari syndrome) causes.
Slow flow
Hepatofugal (retrograde) flow

• Hepatofugal flow occurs when back pressure

exceeds forward pressure, with flow subsequently
reversing direction. This results in a waveform that
is below the baseline.
• As with slow flow, this finding is diagnostic for
portal hypertension from whatever cause.
FINDINGS THAT ARE DIAGNOSTIC FOR PORTAL HYPERTENSION
• Low portal venous velocity (<16 cm/sec)
• Hepatofugal portal venous flow
• Portosystemic shunts (including a recanalized umbilical vein)
• Dilated portal vein
* Splenomegaly and ascites are nonspecific
Hepatofugal (retrograde) flow
Absent (aphasic) portal venous flow
• Absent flow in the portal vein may be due to stagnant
flow (portal hypertension) or occlusive disease, usually
caused by bland or malignant thrombosis.
• Absent portal venous flow is the sine qua non of
occlusive portal vein thrombosis.
• Not all cases of absent flow represent occlusive
disease. In severe portal hypertension, there is a
period of time during the disease course when flow is
neither hepatopetal nor hepatofugal, but stagnant.
This results in absent portal venous flow (appreciable
at Doppler US) and puts the patient at increased risk
for portal vein thrombosis.
Absent (aphasic) portal venous flow

Causes of Absent Portal Venous Flow

• Stagnant flow (severe portal hypertension)
• Portal vein thrombosis (bland thrombus)
• Tumor invasion
 Bland and malignant thrombus

MALIGNANT THROMBUS
• Often seen as dilation of portal vein
 Diameter > 23mm
• Intrathrombus neovascularity
 Pulsatile flow on Doppler US (Arterial
enhancement on CT)
• “Thread and streak sign”
 Multiple enhancing intraluminal
smaller vessels that can be seen at
arterial phase imaging
• Contiguity to tumor
 Often with direct invasion

*Cavernous transformation tends to be a marker for bland thrombus, since these

collateral vessels usually take a long time (months to years) to develop
 Hepatic artery
• The flow is antegrade
throughout the entire cardiac
cycle and is displayed above the
baseline.
• Because the liver requires
continuous blood flow, the
hepatic artery is a low-
resistance vessel, with an
expected RI ranging from 0.55
to 0.7.
• In summary, the hepatic arterial
waveform is normally pulsatile
with low resistance.
• Liver disease may manifest in
the hepatic artery as
abnormally elevated (RI >0.7) or
decreased (RI <0.55) resistance
 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
 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)

Arcuate ligament syndrome

Hepatic Veins

• First, the bulk of hepatic venous flow is

antegrade. Although there are moments of
retrograde flow, the 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.
• Second, pressure changes in the right atrium will
be transmitted directly to the hepatic veins.
a wave  atrial contraction (end
diastole).
S wave decreasing right atrial pressure
due to the downward motion of the AV
septum ( midsystole).
v wave  right atrial pressure resulting
from continued systemic venous return
against the still-closed tricuspid valve
(end of systole).
D wave  rapid early diastolic right
ventricular filling.
 Increased pulsatility (pulsatile waveform)

• Dramatic fluctuations between TR

abnormally tall retrograde waves and
abnormally deep antegrade waves.

Right-sided CHF
• Decreased phasicity (decreased pulsatility)
and spectral broadening

• Absent (aphasic) hepatic venous flow.

(diagnostic for venous outflow obstruction -
Budd-Chiari syndrome).
Transjugular Intrahepatic Portosystemic Shunts

• TIPS are most commonly used for the treatment of

severe portal hypertension with refractory variceal
bleeding or ascites. Other indications include
hepatorenal syndrome, hepatic hydrothorax, and
hepatic vein occlusion (Budd-Chiari syndrome).
• Doppler US has a long track record of reliably helping
detect TIPS malfunction.
• The key to successful TIPS evaluation lies in knowing
the most common anatomic positions of these shunts
and how shunt placement affects blood flow.
AWAY TOWARDS
• A standard TIPS examination is used to sample (a) the three
parts of the shunt; (b) any intervening hepatic vein
segment; and (c) the main, right, and left portal veins.
• Shunt malfunction is the result of narrowing or occlusion
caused by intimal hyperplasia or in situ thrombosis.
Stenosis, or occlusion, can occur anywhere within the stent;
however, it most commonly occurs in the cephalic portion.

TIPS
occlusion
Signs of TIPS Malfunction
DIRECT EVIDENCE
• Shunt velocity <90 cm/sec or
≥190 cm/sec
• Temporal increase or decrease
in shunt velocity >50 cm/sec

INDIRECT EVIDENCE
• Main portal venous velocity
<30 cm/sec
• Collateral vessels (recurrent,
new, or increased)
• Ascites (recurrent, new, or
increased)
• Right-left portal venous flow
reversal (ie, hepatofugal to
hepatopetal)
thank you
Q&A

1. Indications of hepatic doppler

2. Normal flow pattern in portal vein
3. Abnormal flow patterns in portal vein and
their significance
4. Normal hepatic artery waveform and its
variation
5. Evaluation of hepatic veins by doppler
6. Imaging findings in TIPS malfunction