Doppler sonography of the liver is an important noninvasive means of investigating the hepatic vascular system and determining vessel patency and flow direction. In this article, the authors review the anatomy of the portal venous system and the hepatic artery, and describe Doppler imaging appearances of their abnormalities.
Doppler sonography of the liver is an important noninvasive
means of investigating the hepatic vascular system and determining
vessel patency and flow direction.
The hepatic vasculature can be assessed by both pulsed Doppler
and color flow Doppler sonography. Pulsed Doppler allows assessment
of the presence, direction, and velocity of blood flow within a
selected sample volume. For velocity measurements, pulsed Doppler
signals should be obtained from an angle of insonation of less then
60° so that errors in velocity calculation can be minimized. At
times this may prove difficult, and hepatic vessels may need to be
visualized from several approaches during the examination. Pulsed
Doppler measurements are time consuming, as all areas of interest
must be sampled individually and successively. Color Doppler
provides a more rapid assessment of the presence, direction, and
pattern of blood flow and may facilitate the detection of vessels
that can be missed with gray-scale or pulsed Doppler
Portal venous system
-The splenic and superior mesenteric veins join at the level of the
pancreatic neck to form the portal vein. This vein courses in the
hepatoduodenal ligament and bifurcates at the porta hepatis into
right and left branches, which supply the right and left hepatic
The portal vein and its major branches are easily visualized
using a right oblique intercostal approach. The extrahepatic portal
vein also can be easily visualized using a subcostal, anterior
abdominal approach (figure 1). Because of a thick investment of
collagenous tissue, portal veins have highly echogenic walls. The
portal vein is seen in about 97% of normal patients; failure to
visualize it can suggest the presence of pathology, such as
Doppler flow signature
-Portal veins exhibit continuous low velocity flow which undulates
slightly in response to respiration. Portal venous flow varies
considerably with posture, exercise, and dietary state.2,3 Flow is
normally directed in a hepatopetal direction (figure 1).
Abnormalities of the portal venous system
Portal venous hypertension
-Portal hypertension develops when hepatopetal flow within the
portal venous system is impeded. Cirrhosis and congestive heart
failure account for the majority of cases of portal hypertension in
the western world; other causes include hepatic vein occlusion,
portal vein occlusion, and schistosomiasis.
Although the absolute documentation of portal hypertension
requires an invasive procedure such as arteriography, Doppler
sonography plays a useful role as a noninvasive method of assessing
the portal venous system.
Initial studies suggested that portal vein dilatation may be a
predictor of portal hypertension, but this measurement has been
demonstrated to have a low sensitivity in detecting portal
hypertension,4,5 as portal vein diameter is highly variable and can
be affected by factors such as phase of respiration, ingestion of
food, exercise, and by the presence of portosystemic collaterals.
Sensitivity is increased by evaluating the response of the splenic
or superior mesenteric veins to respiratory maneuvers.4
The measurement of decreased portal vein velocity by duplex
sonography also has been used as a predictor of portal
hypertension, but again, normal portal vein velocity is extremely
variable and can be affected by many factors unassociated with
portal hypertension. A "congestive index" has been shown to have a
positive correlation with directly measured portal venous pressure;
it is calculated from the ratio between the cross-sectional area
(cm2) and the blood flow velocity (cm/sec) of the portal vein.6 In
normal individuals, this ratio should not exceed 0.7.
It is the identification of the reversal of portal venous flow
or of collaterals that most successfully allows the sonographic
diagnosis of portal hypertension, as well as the detection of
secondary findings such as splenomegaly and ascites. Sonography is
reported to visualize 65 to 90% of portosystemic collaterals. The
most common collateral pathway is the coronary gastroesophageal
route, which is present in 80 to 90% of patients.7,8 The coronary
vein is best seen on a longitudinal scan just medial to where the
splenic vein joins the superior mesenteric vein. A dilated coronary
vein (> 0.7 cm) is associated with severe portal
A patent paraumbilical vein which demonstrates hepatofugal flow
also is an important predictor of portal hypertension (figures 2A
and 2B). Although slow hepatofugal venous flow (25 cm/sec) may be
detected in the ligamentum teres fissure in healthy subjects,
hepatofugal flow with a velocity greater than 5 cm/sec or flow that
is visualized with color Doppler sonography continuing anterior to
the liver's surface is highly specific for the presence of portal
hypertension.10 Other important portosystemic collaterals which may
be detected by color Doppler include splenorenal, gastrorenal, and
Portal vein thrombosis
As mentioned above, failure to visualize the main portal vein
raises the suspicion of portal vein thrombosis. Portal vein
thrombosis is associated with neoplasia, especially hepatocellular
carcinoma, hypercoagulable states, and intraperitoneal inflammatory
processes such as pancreatitis. In many cases, an underlying cause
is not found.
Color Doppler sonography provides a rapid, noninvasive means of
identifying portal vein thrombosis. It has been demonstrated to
have high negative predictive value (0.98), so that a normal
finding on color Doppler imaging virtually excludes the
diagnosis.11 Although echogenic material may be seen within the
portal vein lumen on gray scale sonography (figure 3), recently
formed clot may be almost anechoic and may be overlooked unless
color Doppler imaging is employed.12
In the color Doppler evaluation of suspected portal vein
thrombosis, machine settings which maximize sensitivity to low flow
and low wall-filter settings should be employed. Patients should be
scanned during quiet respiration because the Valsalva maneuver,
which occurs during breath holding, may abolish low flow
entirely.13 Eating increases portal venous flow, and if portal flow
is absent, postprandial scanning should be considered.13
Following acute portal vein thrombosis, the thrombus may resolve
or the portal vein may undergo fibrosis. Chronic portal vein
thrombosis may lead to "cavernous transformation" of the portal
vein. In this condition, a single portal vein is not visualized,
but multiple serpiginous vessels are seen in the region of the
porta hepatitis (figure 4C) and can be identified as hepatopetal
collaterals by using color (figures 4A and 4B) and pulsed Doppler
(figure 4C) techniques.14
Congestive heart failure
-Several studies15,16 have demonstrated that increased pulsatility
of the portal venous Doppler signal may be seen in patients with
congestive cardiac failure. A similar finding may be seen in severe
Transjugular intrahepatic portosystemic shunt (TIPS)-The
transjugular placement of an intrahepatic shunt between the hepatic
and portal veins is a relatively new nonsurgical treatment for
complications of portal hypertension, including variceal bleeding
and refractory ascites. Dysfunction of the shunt, either by
occlusion or stenosis, occurs in up to 30% of patients within 6
Early detection of shunt dysfunction and prompt intervention are
important to maintain patency and to prevent recurrent variceal
bleeding. In patent, well-functioning stents, high velocity blood
flow with peak velocities frequently greater than l00 cm/sec second
can be seen.18 In stent stenosis, low velocity blood flow of 60
cm/sec or less may be detected within the entire stent, or there
may be low velocity flow with focal velocity elevation at the
site of stenosis.18 Other changes in hepatic hemodynamics, such
as interval change in direction of intrahepatic portal venous flow
from hepatofugal to hepatopetal, interval change to hepatofugal
flow in portosystemic collateral veins,19 or an interval decrease
in stent blood flow velocity, also are suggestive of stent
-In the normal liver, 70% of the blood supply is derived from the
portal vein; the hepatic artery provides the remaining 30%. The
common hepatic artery typically is a branch of the celiac axis, but
anatomical variations are common and are seen in up to 45% of
patients. One common anomaly is the origin of the right hepatic
artery from the superior mesenteric artery, as seen in
approximately 11% of patients. The left hepatic artery also may
have an anomalous origin, usually from the left gastric artery
(10%).20 At the porta hepatis, the hepatic artery usually lies
anteromedial to the portal vein (figure 5). If the artery is seen
dorsal to the portal vein, an anomalous origin should be
Doppler flow signature
-The hepatic artery and its tributaries demonstrate a low
resistance arterial signal with a broad systolic peak and a large
amount of forward flow during diastole.
Abnormalities of hepatic arterial flow
-Increased hepatic arterial flow is seen in severe portal
hypertension.21 In portal hypertension, as portal venous flow to
the liver decreases, arterial flow increases,22 and the hepatic
arterial system becomes more conspicuous, with vessels becoming
larger in diameter and demonstrating higher velocity flow than
normal hepatic arteries.21 "Corkscrew" arteries also have been
demonstrated sonographically in patients with severe portal
hypertension. These enlarged, torturous arteries appear similar to
those frequently noted angiographically in patients with
Vascular liver tumors
-Arterial enlargement also may be seen occasionally in vascular
liver tumors such as focal nodular hyperplasia and hepatocellular
Hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber
disease)-This autosomal dominant condition is characterized by
telangiectases, arteriovenous fistulas, and aneurysms which involve
the skin, mucosa, and the blood vessels of the lung, liver, and
central nervous system.24 Sonography in patients with hereditary
hemorrhagic telangiectasia should demonstrate enlarged torturous
extra- and intrahepatic arteries with high velocity arterial
flow.25,26 Large arteriovenous fistulas within the liver and
"arterialization" of hepatic venous flow in the presence of these
large AV fistulas also can be visible on sonography.
-In most adults, three main hepatic veins (right, middle, and left)
drain the liver (figure 6), with the middle and left veins merging
just prior to their entry into the IVC.27 Variations in the
branching of the hepatic veins and accessory hepatic veins are,
however, relatively common. An inferior hepatic vein which drains
the right hepatic lobe (segment VI), directly into the IVC is seen
in 10% of patients and can sometimes be visualized on
Doppler flow signature
-The hepatic veins demonstrate a complex triphasic Doppler waveform
(figure 7) which is seen in all central systemic veins and is
caused by fluctuation in right atrial pressure during the cardiac
cycle. The hepatic veins have two periods of forward flow during
the cardiac cycle, corresponding to the two phases of right atrial
filling.13 A short-lived period of flow reversal is seen with right
Abnormalities of the hepatic veins
Hepatic venous obstruction, Budd-Chiari syndrome and
hepatic venoocclusive disease
-Budd-Chiari syndrome is a rare disorder resulting from occlusion
of the hepatic venous system. The occlusion may be located at any
level, from the hepatic venules to the inferior vena cava;
occlusion at the venule level that is classically seen after bone
marrow transplantation is sometimes known as hepatic venoocclusive
Hepatic venous occlusion results in a classic triad of clinical
symptoms: hepatomegaly, ascites, and abdominal pain. Budd-Chiari
syndrome has been associated with polycythemia rubra vera, chronic
leukemia, use of oral contraceptives, neoplasms, pregnancy, and
congenital obstructing venous webs, but the exact cause cannot be
determined in approximately two-thirds of cases.28
Although inferior vena cavography and hepatic venography remain
the gold standard for investigating patients with Budd-Chiari
syndrome, the use of color Doppler sonography as a screening tool
has been advocated more recently, because it is a noninvasive,
relatively inexpensive, and readily available technique.29,30 A
positive correlation has been demonstrated with findings at
In acute Budd-Chiari syndrome, the liver is invariably enlarged
and frequently inhomogeneous. There may be atrophy of the right
lobe of the liver, hypertrophy of the lateral segment of the left
lobe, and enlargement of the vena cava.32 If the hepatic veins are
visualized by real-time sonography, thickened walls, areas of
stenosis, irregularity, or proximal dilatation may be identified.33
Hepatomegaly, however, will often compress these vessels and render
them invisible to real-time examination. In this situation, color
Doppler can be used, as it allows visualization of compressed but
patent hepatic veins so that the diagnosis of Budd-Chiari syndrome
can be excluded.
The middle and left hepatic veins are best scanned in the
transverse plane at the level of the xiphoid process because at
this angle, the veins are oriented nearly parallel to the Doppler
beam. For the same reason, a lateral intercostal approach is used
to evaluate the right hepatic vein. Three hepatic veins must be
found to exclude the diagnosis because involvement may be
segmental. In Budd-Chiari syndrome, Doppler signals from the IVC
and/or hepatic veins change from the normal phasic flow to absent,
reversed, turbulent, or continuous flow due to interference of
blood flow from these veins to the right atrium. Portal vein blood
flow also may be affected and is characteristically either slowed
Soon after an acute thrombotic episode, intrahepatic collateral
pathways develop, many of which are unique to Budd-Chiari syndrome
and provide a definite diagnosis on color Doppler imaging. A
"bicolored" hepatic vein is said to be pathognomic, indicating a
Sonography in Budd-Chiari syndrome has several limitations.
Direct visualization of a hepatic vein web is difficult and
venography may be needed in this situation, with possible treatment
by balloon angioplasty.34 Involvement of the inferior vena cava
also may be underestimated.31
Chronic liver disease
-Liver parenchymal disease impairs the compliance of the hepatic
veins, decreasing and flattening phasic oscillations. Flattening of
phasic oscillations within the hepatic venous system is seen in 50
to 75% of patients with cirrhosis.35,36
Cardiac failure and tricuspid regurgitation-In right heart
failure, increased systolic venous pressure causes the hepatic
veins to dilate considerably. Normally, hepatic venous flow is
directed towards the inferior vena cava, whereas in tricuspid
regurgitation, a pronounced systolic reversal of hepatic venous
blood flow is seen.
Doppler sonography provides an accurate, noninvasive method of
assessing the hepatic vascular system, decreasing the need for
hepatic angiography. Pulsed Doppler sonography allows the
determination of flow direction and velocity within a selected
sample volume, but is time-consuming and unable to provide a global
visual display of Doppler information. Color Doppler sonography, on
the other hand, provides a more rapid method of visually assessing
the presence, direction, and pattern of blood flow within the
liver. These two methods are complementary in the investigation of
numerous hepatic vascular abnormalities, such as Budd-Chiari
syndrome, portal hypertension, and vascular liver tumors. The use
of Doppler sonography in the assessment of patients following
surgery or after the TIPS procedure is also invaluable. AR
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Dr. Belcher is with the Imaging Department at Medway NHS Trust
in Gillingham, Kent, United Kingdom. Dr. Beidle is with the
Department of Radiology at Louisiana State University Medical
Center in New Orleans.