AJR 2003; 180:1583-1591
© American Roentgen Ray Society
Imaging and Intervention in the Hepatic Veins
Terry S. Desser1,
Daniel Y. Sze and
R. Brooke Jeffrey
1 All authors: Department of Radiology, Stanford University School of Medicine,
Mail Code 5621, 300 Pasteur Dr., Stanford, CA 94305.
Received September 9, 2002;
accepted after revision November 6, 2002.
Address correspondence to T. S. Desser.
Introduction
Compared with the portal veins, the hepatic veins have received less
attention in the radiology literature. Therefore, radiologists may not be as
familiar with hepatic vein abnormalities. As the population of patients who
are imaged for liver disease in our institution continues to grow, we are
encountering hepatic vein disorders more frequently in a variety of clinical
settings. In this article, we review the cross-sectional imaging features of
normal hepatic veins and describe a number of abnormal processes that may
alter their appearance. Because sonography is widely used to screen for
vascular abnormalities of the liver, we emphasize this technique for imaging
of the hepatic veins. Interventional techniques that have proven useful in the
treatment of hepatic vein disorders are also
presented.
Normal Hepatic Veins
Anatomy
Although the liver has a dual blood supply, the hepatic veins provide the
sole route of egress for blood exiting the liver. The segmental anatomy of the
liver as defined by the French surgeon Claude Couinaud
[1] divides the liver into
eight segments, with portal vein branches at the center and hepatic veins at
the periphery. The right, middle, and left hepatic veins enter the
retrohepatic inferior vena cava just before it traverses the diaphragm,
approximately 2 cm caudad to the right atrium and eustachian valve. The right
hepatic vein enters the inferior vena cava separately, but the middle hepatic
vein and the left hepatic vein may share a common trunk in 65–85% of
patients [2]. Besides the three
major hepatic veins, additional small accessory or short hepatic veins from
the pericaval liver segments drain directly into the inferior vena cava caudad
to its junction with the major veins
[3]. These accessory veins are
usually associated with the right lobe or caudate lobe and may occasionally be
up to 1 cm in diameter (Fig.
1). Common anatomic variants include an accessory inferior right
hepatic vein that drains Couinaud segment VI and a middle right hepatic vein
that drains segment V. In one study, these variants were seen in 18% and 5.5%
of patients, respectively [2].
The inferior right hepatic vein may be identified running parallel and deep to
the posterior division of the right portal vein
[4]
(Fig. 2). Both the major and
accessory hepatic veins exit the liver in its bare area, where the veins are
surrounded by loose areolar tissue before joining the inferior vena cava.
Anatomic variations in venous drainage are particularly important in
surgical planning of right lobe living donor transplantation, an increasingly
common procedure in the treatment of end-stage liver disease
[5]. If the main right hepatic
vein is small, portions of the right lobe may be drained by the middle hepatic
vein or an inferior right hepatic vein, and viability of the graft will depend
on preservation of this venous drainage. Some centers therefore routinely use
intraoperative Doppler sonography for assessing venous drainage of the split
liver graft.
Unlike the portal veins, whose walls are echogenic over a wide range of
insonation angles, the walls of the hepatic vein are echogenic only with
perpendicular beam incidence. This is due to differences in the orientation of
connective tissue fibers in the vessel walls, which are parallel and tightly
packed in the hepatic veins but only loosely arrayed in a variety of
directions along the portal veins
[6].
Physiology
The hepatic veins are central veins whose flow pattern reflects the
pressure variations within the right atrium during the cardiac cycle
(Fig. 3). Normally, free
communication exists between the hepatic veins and the right atrium, and
hepatic venous flow is triphasic. There is a low-velocity phase of retrograde
flow during right atrial contraction (the a wave). Two higher
velocity phases of hepatofugal flow follow, the first during right ventricular
systole after closure of the tricuspid valve, and the second during right
ventricular diastole. These represent periods of declining right atrial
pressure. Between these two phases of forward flow, preceding the opening of
the tricuspid valve, the atrial pressure rises briefly (the v wave).
This rise in atrial pressure interrupts the two periods of forward flow and
may produce a short second period of hepatic venous flow reversal, even in
healthy patients. V wave flow reversal is almost always smaller than
the a wave flow reversal
[7,
8,
9].
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Fig. 3. —Schematic representation shows temporal events of cardiac
cycle (EKG) and their relationship to central venous pressure (CVP) tracing
and hepatic venous (HV) velocity waveform. Opening and closing of tricuspid
valve are indicated.
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Systolic forward flow velocities depend on atrial relaxation, motion of the
tricuspid annulus toward the cardiac apex, and static right atrial pressure.
High right atrial pressures reduce the gradient between this chamber and the
hepatic veins and thereby decrease the velocity and quantity (estimated with
flow-velocity integrals) of systolic forward flow. Hepatic venous velocity
waveforms can thus be used to estimate right atrial pressure
[9].
Spectral Doppler sonography readily shows the normal triphasic hepatic
venous waveform (Fig. 4). To
minimize the effect of the adjacent inferior vena cava, one should place the
Doppler sonography sample volume 3–6 cm from the vessel outlet.
We ask patients to suspend respiration but not to deeply inhale or exhale
because these maneuvers alter venous pressures and consequently the hepatic
venous waveform [10].
Likewise, the Valsalva maneuver raises intrathoracic pressure and alters the
hepatic venous waveform, often rendering it monophasic
[7]. Because hepatic blood flow
increases in the postprandial state, patients should be examined when
fasting.
Hepatic venous pulsatility may disappear during pregnancy and may remain
abnormal even beyond 8 weeks postpartum
[11]. Hepatic venous waveforms
in pregnant patients may be dampened or monophasic even before 20 weeks'
gestation, and most patients (80%) have flat waveforms in the final 10 weeks
of pregnancy [12]. The precise
cause of these changes in pregnancy is unknown, although the altered cardiac
output seen in pregnancy coupled with the pressure effects of the enlarged
uterus may play a role [11].
Therefore, caution should be exercised when diagnosing suspected hepatic
venous abnormalities in pregnant patients.
Abnormal Flow Patterns
A variety of abnormal processes both intrinsic and extrinsic to the liver
may alter flow patterns in the hepatic veins. Abnormal flow may occur in the
hepatic veins if there is abnormal communication between the hepatic veins and
other hepatic vessels, right heart pressures are elevated, transmission of the
right atrial pressure pattern is impeded because of venous outflow
obstruction, or infiltration and altered compliance of the hepatic parenchyma
result in dampening of hepatic venous flow patterns. Examples of each of these
abnormal flow patterns are discussed in the following sections.
Intrahepatic Vascular Shunts and Vascular Malformations
Although they may mimic complex cysts or tortuous vessels on gray-scale
sonography, vascular malformations are readily identified with color and power
Doppler sonography.
Shunts between the hepatic arteries and the hepatic veins are rare but may
occur in cavernous lymphangiomatosis or in Rendu-Osler-Weber syndrome
[13]. More commonly,
arteriosystemic shunts occur in the setting of hepatocellular carcinoma with
hepatic venous invasion [14].
They may also develop after liver biopsy or with penetrating trauma.
Color Doppler sonography may reveal dilated and tortuous hepatic arteries
and aliasing at the junction with the draining hepatic vein. The hepatic veins
may show abnormal color-flow patterns, and spectral tracings typically show
arterialization. Although arterioportal shunts are the most typical vascular
communications associated with hepatocellular carcinoma, identification of
hepatic artery-to-hepatic vein shunt should also prompt a search for an
underlying neoplasm.
Portosystemic venovenous shunts are more common and may also be congenital
or acquired. Congenital shunts are rare
(Fig. 5). They are thought to
occur either by persistence of connections among tributaries of the vitelline
vein (the precursor of the portal and hepatic veins and portions of the
inferior vena cava [13]) or by
rupture of a portal vein aneurysm into the hepatic vein
[14]. By contrast, acquired
shunts are common because they occur as sequelae of cirrhosis. These shunts
provide collateral pathways for venous drainage of the liver in the setting of
portal hypertension. Although the most commonly identified portosystemic
shunts are extrahepatic, large intrahepatic portosystemic collaterals may be
identified in the subcapsular area of the liver or may drain directly into the
inferior vena cava [14].
Spectral tracings typically show turbulent waveforms with large shunts or
high-velocity flow in smaller shunts.
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Fig. 5. —84-year-old woman referred for evaluation of lower extremity
edema. Contrast-enhanced portal venous phase CT scan shows portal
vein–hepatic vein shunt. Hepatic vein tributary (white arrow)
connects to left portal vein (arrowhead) via small vascular
malformation (black arrow).
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Hepatic venovenous shunts are most commonly identified in the setting of
venous outflow obstruction and are discussed in the next section.
Right Heart Failure
When the volume of venous blood return exceeds the capacity of the right
heart, central venous pressure rises, and the inferior vena cava and hepatic
veins dilate [15]. Gray-scale
sonography shows marked increase in the diameter of the inferior vena cava and
the hepatic veins. Congestion in the hepatic sinusoids leads to compression,
atrophy, and necrosis of centrilobular hepatocytes, first producing fatty
infiltration and, when chronic, fibrosis (i.e., cirrhosis). The perisinusoidal
fibrosis seen in cardiac cirrhosis results in decreased hepatic compliance,
and hepatic venous waveforms may change from triphasic to monophasic. Forward
flow velocities in the hepatic veins are typically slowed because of a lowered
pressure gradient with the right atrium. Alternatively, if tricuspid
regurgitation is present, hepatic venous pulsatility may increase, and hepatic
venous flow during right ventricular systole may decrease or even reverse
[15]. Hepatic venous flow
patterns may also be abnormal in constrictive pericarditis
[16]. Portal venous waveforms
may be abnormal as well, changing from monophasic to pulsatile flow.
CT scans in patients with passive congestion may show reticulated or
mottled enhancement of the hepatic parenchyma, the pattern typical of venous
outflow obstruction described at greater length in the next section
[15]
(Fig. 6). The hepatic veins and
the inferior vena cava may be distended, and there may be reflux of contrast
material into the hepatic veins if tricuspid regurgitation is present.
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Fig. 6. —42-year-old woman with suspected intraabdominal abscess.
Contrast-enhanced portal venous phase CT scan shows reticular or mosaic
perfusion of liver similar to pattern in Budd-Chiari syndrome. At autopsy,
patient had severe ischemic cardiomyopathy and hepatic congestion.
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Venous Obstruction
Obstruction of hepatic venous outflow results in the clinical phenomenon
known as Budd-Chiari syndrome, consisting of congestive hepatomegaly,
abdominal pain (from hepatic capsular distention), and ascites. Budd-Chiari
syndrome is also a rare but important cause of portal hypertension. The
original reports by Budd and Chiari described thrombosis of the major hepatic
veins, in some cases also of the suprahepatic inferior vena cava
[17]. Later reviews of
patients with impairment of hepatic venous outflow included cases of both
suprahepatic inferior vena cava obstruction and hepatic vein thrombosis, and
the term Budd-Chiari syndrome came to be applied to both entities. Recently,
however, one authority suggested that obstructions of both the inferior vena
cava and the hepatic vein should be considered as separate entities
[17]. Nevertheless, hepatic
venous obstruction and congestion can be a reversible cause of inferior vena
cava obstruction.
Thrombosis is by far the leading cause of obstruction of the major hepatic
veins. In the intrahepatic inferior vena cava, obstruction may also be caused
by a membrane or web. These webs were originally thought to be congenital in
origin, but evidence now suggests that they are actually sequelae of
thrombosis [17]. One authority
now prefers the term "obliterative hepatocavopathy" rather than
"membranous obstruction of the inferior vena cava." Symptomatic
hepatic vein thrombosis is almost always due to an underlying
myelopro-liferative disorder, hypercoagulable state, or other predisposing
factors such as the use of oral contraceptives
[18]. Hepatic vein thrombosis
may also be due to infection, tumor invasion, or sequelae of trauma (Figs.
7 and
8). In contrast, obliterative
hepatocavopathy is most often idiopathic but may be associated with increased
risk of hepatocellular carcinoma.
An increasingly important cause of hepatic venous outflow obstruction is
venous anastomotic stricture in patients who have undergone liver
transplantation. Newer liver transplantation techniques such as living related
donor liver transplantation (split liver transplantation) and orthotopic liver
transplantation with piggyback anastomosis may increase the risk of hepatic
venous anastomotic stricture
[19,
20]. Torsion of the right
liver graft and hypertrophy of the graft with compression of the inferior vena
cava are other reported causes of venous outflow obstruction in this patient
population [21,
22].
Budd-Chiari syndrome can be diagnosed on color Doppler sonography when
color flow is absent in the main hepatic veins
[23,
24]. Duplex Doppler sonography
can be used to confirm absence of flow when findings on color Doppler
sonography are suggestive of venous occlusion. Color-flow Doppler sonography
may also reveal intrahepatic venovenous collaterals that provide alternative
pathways for venous return to the right heart when the inferior vena cava or
the hepatic veins are obstructed
[25,
26] (Figs.
9A,
9B). One common collateral
pathway connects intrahepatic venous collaterals to systemic venous pathways
via subcapsular veins and may be identified on the surface of the liver
[25]. Alternatively, blood may
be shunted away from an obstructed hepatic vein and toward a patent one,
producing a pattern of bicolored hepatic veins (two adjoining hepatic veins
with flow in opposite directions on color Doppler sonography). Venous
obstruction elevates sinusoidal pressure, causing portal hypertension and
conversion of the portal vein to an outflow tract.
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Fig. 9B. —40-year-old woman with Budd-Chiari syndrome. CT scan obtained
at same level as A shows characteristic appearance of Budd-Chiari
syndrome, with increased central hepatic enhancement and decreased enhancement
of liver periphery.
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Gray-scale sonography in Budd-Chiari syndrome may show low-level echogenic
material within the normally sonolucent lumen of the hepatic vein. However,
even if the hepatic veins appear patent on gray-scale and color Doppler
sonography, spectral tracings should be obtained. Absence of phasicity
(monophasic flow) in the hepatic venous waveform may indicate the presence of
a hepatic venous anastomotic stricture and a hemodynamically significant
obstruction of venous outflow
[19,
20]. Decrease in hepatic
venous peak velocity to less than 10 cm/sec may also occur
[20]
(Figs. 10A,10B,10C,10D).
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Fig. 10A. —60-year-old man with liver dysfunction after orthotopic liver
transplantation 2 years earlier. Duplex sonogram of right hepatic vein shows
low-velocity undulating monophasic waveform suggestive of venous outflow
obstruction.
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Fig. 10B. —60-year-old man with liver dysfunction after orthotopic liver
transplantation 2 years earlier. Percutaneous transhepatic venogram shows near
occlusion at anastomosis, with stasis of flow. Pressure gradient was 14 mm
Hg.
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Fig. 10D. —60-year-old man with liver dysfunction after orthotopic liver
transplantation 2 years earlier. Final venogram obtained after stent placement
shows rapid passage of contrast material from hepatic vein into inferior vena
cava and right atrium.
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Contrast-enhanced CT and MR imaging in Budd-Chiari syndrome may show
non-visualization of the major hepatic veins and a mosaic heterogenous
perfusion pattern diffusely involving the liver
[27]
(Fig. 11). Although the
classic finding is preserved enhancement in the central pericaval portion of
the liver because of preservation of venous drainage of the caudate lobe, in
practice, enhancement patterns will depend on the relative degree of
obstruction of the various draining veins
[28]. When Budd-Chiari
syndrome is caused by thrombosis of the major hepatic veins, compensatory
hypertrophy of the caudate lobe will usually occur as a result of venous
drainage directly into the inferior vena cava. The enlarged caudate lobe may
cause compression of the inferior vena cava. Prominent collaterals, typically
the ascending lumbar, azygos, and hemiazygos veins, may be seen in patients
with Budd-Chiari syndrome because of obstruction of the intrahepatic inferior
vena cava. Intrahepatic collaterals may also be identified (Figs.
12A,
12B). Enlargement of the
normally small accessory hepatic veins may also occur.
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Fig. 11. —45-year-old woman with ulcerative proctitis and Budd-Chiari
syndrome. Contrast-enhanced CT scan shows heterogeneous hepatic enhancement,
with relatively increased enhancement in pericaval region. Transjugular
intrahepatic portosystemic shunt (arrow) was placed from stump of
right hepatic vein to right portal vein for treatment of portal
hypertension.
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Fig. 12A. —20-year-old man with Budd-Chiari syndrome with portosystemic
collaterals. Contrast-enhanced portal venous phase CT scan obtained at dome of
liver shows thrombosed hepatic veins (arrows). Esophageal varices
(arrowhead) are present.
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Fig. 12B. —20-year-old man with Budd-Chiari syndrome with portosystemic
collaterals. Portal venous phase CT scan obtained inferior to A shows
pericaval intrahepatic collaterals (white arrow) and dilated
paraumbilical vein (black arrow).
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Regardless of the cause, prolonged obstruction of venous outflow leads to
hepatic congestion with ensuing loss of hepatocytes. If elevated pressure
continues, fibrosis will occur, with development of cirrhosis and hyperplastic
nodules. Large hyperplastic nodules may be seen in patients with Budd-Chiari
syndrome and should not be mistaken for hepatocellular carcinoma
[29].
Budd-Chiari syndrome may be fulminant with rapidly progressive liver
failure (uncommon) or acute or subacute, with abdominal pain, ascites,
hepatomegaly, and renal failure developing over a week or two. Most common is
the chronic form of Budd-Chiari syndrome, with ascites developing over 2
months or more. In subacute and chronic Budd-Chiari syndrome, complications of
portal hypertension determine prognosis and are fatal in more than 50% of
patients within 2 years [30].
Although Budd-Chiari syndrome leads to portal hypertension, it is the culprit
in only a small minority of portal hypertension cases, approximately 2% in
some recent series [30,
31].
Interventional radiologic techniques such as placement of transjugular
intrahepatic portosystemic shunts have produced good outcomes in patients with
Budd-Chiari syndrome complicated by portal hypertension
[30]. If feasible, angioplasty
and stenting of hepatic venous obstruction
[32] or of segmental stenosis
of the inferior vena cava [33]
have proven useful, whereas thrombolysis has proven effective in treatment of
acute thrombosis [31,
34]. Frequently, resolution of
hepatic venous outflow obstruction allows spontaneous restoration of inferior
vena cava flow and luminal diameter.
Venoocclusive Disease and Sinusoidal Obstruction Syndrome
Vascular obstruction may also occur in the liver at the microscopic level.
Commonly termed "venoocclusive disease," microscopic obstruction
is due to marked fibrosis in hepatic sinusoids produced by a toxic insult to
endothelial cells and may not necessarily involve the hepatic venules
[35]. Damaged endothelial
cells swell, slough, and embolize distally, causing microvascular obstruction.
Consequently, the term "sinusoidal obstruction syndrome" is now
preferred by several authors
[35]. Although the clinical
picture of sinusoidal obstruction syndrome—hepatomegaly, ascites, and
jaundice—may be indistinguishable from Budd-Chiari syndrome and
macroscopic vascular obstruction, the cause of sinusoidal obstruction syndrome
and its patient populations are different. First described in South African
patients who had ingested herbal teas or foods containing pyrrolizidine
alkaloids, sinusoidal obstruction syndrome in Western countries is almost
always seen in association with chemotherapy conditioning regimens for bone
marrow transplantation, particularly those containing cyclophosphamide or
busulfan.
Sonographic and CT findings in sinusoidal obstruction syndrome may be
similar to those of Budd-Chiari syndrome, with hepatomegaly and ascites. In
sinusoidal obstruction syndrome, the venous flow may appear attenuated (Figs.
13A,
13B), but unlike Budd-Chiari
syndrome, the major hepatic veins may appear patent. Sinusoidal fibrosis may
lead to portal vein thrombosis or portal flow reversal evident on color
Doppler sonography. Acutely, reversal of portal venous flow may represent the
only pathway of venous drainage in these patients. Sonography is also useful
to exclude other potential causes of hepatomegaly and jaundice in this patient
population, such as biliary tract disease or infiltrative tumor.
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Fig. 13A. —23-year-old woman with acute myelogenous leukemia and
sinusoidal obstruction syndrome (hepatic venoocclusive disease) after bone
marrow transplantation. Duplex Doppler sonogram shows low-velocity monophasic
flow in middle hepatic vein.
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Fig. 13B. —23-year-old woman with acute myelogenous leukemia and
sinusoidal obstruction syndrome (hepatic venoocclusive disease) after bone
marrow transplantation. Contrast-enhanced CT scan shows heterogeneous hepatic
enhancement and low attenuation adjacent to patent right hepatic vein and
inferior vena cava, presumably representing lymphedema.
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Most patients with sinusoidal obstruction syndrome recover spontaneously
with supportive treatment of fluid and respiratory status, but severe cases
are commonly fatal. Interventional radiologists may be called on to perform
wedged hepatic pressures or transvenous liver biopsy for diagnosis of this
entity because this technique is safer than percutaneous biopsy in patients
with thrombocytopenia. Tissue plasminogen activator and anticoagulation have
been investigated but proved effective in less than one third of patients with
sinusoidal obstruction syndrome and not useful at all in patients with
associated renal or pulmonary failure. Placement of a transjugular
intrahepatic portosystemic shunt may be useful for reduction of portal venous
pressure and for reduction of ascites, but some authors suggest that these
shunts have no effect on outcome in this entity
[35].
Parenchymal Diseases
Dampening of the normal triphasic waveform may occur when diffuse liver
disease alters the elasticity and vascular resistance of the liver. Cirrhosis
may produce a pattern of pseudoportal flow—that is, monophasic turbulent
flat flow in the hepatic veins
[36,
37,
38,
39,
40].
In studies of patients with chronic hepatitis, abnormal hepatic venous
waveforms were shown to correlate histologically with cirrhosis, fibrosis, and
steatosis, although not with periportal inflammation or necrosis
[38]. Alterations of hepatic
venous flow in this population included loss of the brief period of flow
reversal leading to a biphasic waveform or a completely flat (monophasic)
waveform. Monophasic hepatic venous flow has never been seen in healthy
control subjects [36,
37]. Abnormal hepatic venous
waveforms correlate with the severity of cirrhosis, as measured by the
Child-Pugh score [36,
37,
41].
Focal hepatic masses that compress adjacent hepatic veins may also cause
flattening of the hepatic venous waveform. Even benign masses such as focal
nodular hyperplasia may produce sufficient local mass effect to dampen the
hepatic venous waveforms (Figs.
14A,
14B).
Hepatic Venous Injuries
Injuries of the retrohepatic inferior vena cava and the major hepatic veins
after blunt trauma are associated with high mortality rates, ranging from 50%
to 80% in some series. Death usually results from exsanguination during
surgical attempts at control, exposure, and repair of hemorrhage from these
largely inaccessible structures located within the bare area of the liver. In
potentially lethal injuries—that is, those associated with free
bleeding—there is disruption of surrounding tissues capable of
tamponading the hemorrhage. Such surrounding structures include the liver
parenchyma (for intrahepatic venous lacerations) and the retrohepatic areolar
tissue, suspensory ligaments, and diaphragm (for extrahepatic venous injuries)
[42].
High-grade liver lacerations may damage the major hepatic veins in the
parenchyma or may avulse them at their extrahepatic portions. The most common
major hepatic venous injuries involve the intraparenchymal segments and are
produced by damage to the central posterior portion of the liver—the
liver dome. Massive hemorrhage can occur when the surrounding containing
structures—liver parenchyma and capsule, ligaments, and
diaphragm—have been disrupted. Although these injuries can extend
centrally to involve portal vein or hepatic artery branches, it is thought
that hepatic veins are more prone to injury because they are less well
supported by connective tissue. On CT and sonography, injury of the hepatic
veins or the retrohepatic inferior vena cava should be suspected when a deep
laceration involves the dome of the liver and blood is present in the bare
area of the liver.
Treatment of major hepatic venous injuries has evolved from a strategy of
attempted direct surgical repair to one of tamponading with packing, either
with gauze or omentum [42].
Tamponading and containment strategies have reduced mortality substantially
compared with surgical repair. Recently, however, interventional radiologic
techniques have proven useful in cases of packing failures. Transvenous
stenting of a retrohepatic inferior vena cava tear at its junction with the
right hepatic vein in a patient with repeated intraoperative packing failures
has been reported in the literature
[43]. This technique may prove
increasingly important in the years to come.
Conclusion
Obstruction of the hepatic veins may produce profound liver dysfunction.
Alternatively, sonographic abnormalities of the hepatic veins may reflect
underlying focal or diffuse hepatic disease. In patients who are not pregnant,
loss of the normal triphasic waveform in the hepatic veins indicates an
abnormality either in venous outflow or in hepatic compliance. Attention to
the Doppler sonographic signature of the hepatic veins may provide critical
evidence of underlying abnormality in the liver. Color Doppler sonography may
reveal vascular occlusions or altered venous pathways that may be invisible on
gray-scale sonography alone. Findings on CT may suggest the diagnosis of
hepatic venous outflow obstruction if the hepatic veins are not visualized or
perfusion is heterogeneous, and CT may show complications such as large
hyperplastic nodules and collateral venous pathways. Interventional radiologic
techniques, particularly the placement of hepatic venous or inferior vena cava
stents or transjugular intrahepatic portosystemic shunts, may reduce morbidity
in patients with venous outflow disorders stemming from hepatic congestion and
ensuing portal hypertension.
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Introduction
Normal Hepatic Veins
