ª Springer Science+Business Media, LLC 2017 Abdom Radiol (2018) 43:2037–2051
Abdominal Published online: 17 November 2017
Radiology
Congestive hepatopathy
Michael L. Wells, Sudhakar K. Venkatesh
Department of Radiology, Mayo Clinic College of Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
Abstract
Passive hepatic congestion may result from a variety of
distinct cardiovascular conditions. Injury to the liver
caused by congestion is often asymptomatic and may not
be recognized clinically. Diagnosis of congestive hep-
atopathy is important as it has the potential to cause
complications including hepatic fibrosis and develop-
ment of benign and malignant liver masses. This review
will summarize the pathophysiologic mechanisms of
congestive hepatopathy and provide both description
and examples of its multimodality imaging findings.
Examples of alternative disease which may have a similar
imaging appearance will be provided. Knowledge
regarding the characteristic imaging findings of conges-
tive hepatopathy will allow for its accurate identification.
Reviewing both the benefits and limitations of imaging
performed to evaluate congestive hepatopathy and its
complications will help to avoid pitfalls and enable rec-
ommendation of appropriate next steps in diagnostic
evaluation.
Key words: Passive congestion—Cardiac
failure—Cardiac cirrhosis—CT—MRI—FNH-like
nodules
Congestive hepatopathy (CH) refers to liver injury in-
duced by impaired hepatic venous outflow. There are
many types of pathology which may slow venous outflow
resulting in parenchymal congestion. CH most com-
monly refers to parenchymal congestion which is the
result of cardiac disease, but it may also be the result of
abnormalities of the inferior vena cava (IVC) or hepatic
veins [1–3].
Any cause of right-sided cardiac failure may result in
elevated central and hepatic venous pressure. Common
conditions include tricuspid regurgitation or stenosis,
cardiomyopathy, constrictive pericarditis, cor pul-
monale, and left heart failure. Surgical alterations to the
Correspondence to: Michael L. Wells; email: wells.michael@mayo.edu
https://doi.org/10.1007/s00261-017-1387-x
hepatic veins, IVC or heart can also result in impaired
hepatic venous outflow. Patients with congenital cardiac
anomalies who have undergone surgical palliation with
the Fontan procedure are at particular risk for chronic
passive hepatic congestion [4]. In these patients, the
pulmonary bed is passively perfused via systemic pul-
monary venous return. Over time, the pulmonary vas-
cular resistance increases and cardiac output declines
resulting in severe hepatic congestion. Extrinsic com-
pression upon or primary disease of the suprahepatic
vena cava or hepatic veins (such as Budd-Chiari syn-
drome), result in impaired hepatic venous outflow and
hepatic congestion.
Heart disease causing elevated central venous pres-
sure is frequently associated with poor cardiac output
and decreased hepatic perfusion. Because of this, liver
injury due to CH frequently occurs in combination with
liver injury due to ischemia [5]. The combination of
congestive and ischemic liver injury is frequently
encountered in conditions such as constrictive peri-
carditis, congestive heart failure, and surgical palliation
of congenital cardiac anomalies.
Histological changes
Congestive hepatopathy results in macroscopic and
microscopic changes within the liver parenchyma [1, 6–
10]. Elevated venous pressure causes dilation of lobular
hepatic veins and the hepatic sinusoids. In passive con-
gestion due to cardiac disease, the degree of sinusoidal
dilation is correlated with the degree of venous pressure
elevation [11]. Fluid and hemorrhage becomes extra-
vasated into the perisinusoidal space of Disse. Local
steatotic change and atrophy within zone 3 of the hepatic
acinus (centrilobular parenchyma located adjacent to
central hepatic veins) occurs due to hepatocyte injury.
Persistent or severe injury results in perisinusoidal and
perivenular deposition of fibrotic tissue. Over time,
fibrosis within zone 3 of the hepatic acinus may progress
to form bridging fibrosis between hepatic veins [12]. This
is in contrast to the typical pattern of fibrosis seen in
conditions such as alcoholic cirrhosis or hepatitis C, in
which bridging fibrosis occurs between portal triads. The
2038
pattern of fibrosis seen in CH is referred to as ‘‘reverse
lobulation’’ and specific histologic staging systems of
fibrosis for CH have been proposed [13]. In patients with
chronic heart disease, the degree of fibrosis is positively
correlated with central venous pressures and right heart
chamber dilation [13]. The degree of hepatic fibrosis
found at pathology varies between patients with similar
degrees of cardiac decompensation and in between dif-
ferent spatial regions of the liver [1, 10, 14]. Fibrosis
deposition is likely related to local thrombotic events
within sinusoids and veins caused by static blood flow,
and the variation in locations of thrombosis may explain
the heterogeneity of fibrosis deposition. At gross
pathologic evaluation, the hemosiderosis due to extra-
vasated red blood cells surrounding the hepatic veins and
sinusoids can be seen as reddening of the hepatic par-
enchyma. The reddened areas surround normal or stea-
totic hepatic parenchyma creating a characteristic
appearance termed the ‘‘nutmeg liver’’ [9].
Fig. 1. 63 year old male with carcinoid heart disease
resulting in severe tricuspid regurgitation and severe pul-
monary valve regurgitation. A, B Radiographs of the chest
demonstrate a prominent right atrium (A, arrow), right
ventricle (B, arrow), and IVC (B, arrowhead). C Axial CT
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
Arterialized large regenerative nodules or focal
nodular hyperplasia (FNH) are often found in chroni-
cally congested livers [2, 5, 15]. A region of parenchyma
with compromised hepatic venous outflow and secon-
darily impaired portal venous inflow may become reliant
on arterial supply to maintain parenchymal perfusion.
Nodular regeneration of hepatocytes within arterially
supplied regions of the liver may result in formation of
these nodules in the congested liver [2]. Chronic liver
injury resulting in fibrosis and cirrhosis leads to in-
creased risk of developing hepatocellular carcinoma
(HCC) [16]. The incidence of carcinoma development in
the setting of cardiac cirrhosis is unknown.
Presentation and clinical evaluation
Patients with CH are most often asymptomatic with re-
spect to their liver disease. Uncommonly, a patient with
hepatic congestion may present with mild jaundice, as-
cites, or right upper quadrant pain due to liver expansion
[1]. The clinical presentation is typically dominated by
image shows a dilated right atrium (arrow) and small peri-
cardial and right pleural effusions (arrowheads). D–F Patient
underwent replacement of the tricuspid and pulmonary
valves with resolution of the abnormalities described in
images A–C.
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
symptoms of cardiac failure. The presence of a cardiac
disease known to result in elevated central venous pres-
sure is the typical indication for clinical evaluation of
passive congestion.
Diagnosis of hepatic congestion requires exclusion of
other causes of liver injury in those patients with risk
factors (e.g. Hepatitis C, drug use, etc.) [17]. Systemic
disease such as amyloidosis or hemochromatosis may
simultaneously result in heart failure and liver disease.
Liver biopsy performed for the diagnosis of CH is gen-
erally unnecessary, and is only required in equivocal or
complicated cases.
Hepatomegaly and hepatojugular reflux may be de-
tected at physical exam [1, 17]. Splenomegaly is uncom-
mon and is generally related to central venous pressure
being transmitted through dilated hepatic sinusoids to
the portal venous system [11]. The transhepatic pressure
gradient in CH is usually normal [11]. Portosystemic
varices are correspondingly uncommon due to lack of a
pressure gradient stimulating their formation. If varices
are present, it suggests that the liver is fibrotic with an
elevated transhepatic pressure gradient [18].
Laboratory abnormalities in chronic CH are most
commonly represented by a mild hyperbilirubinemia,
which may be found in up to 70% of patients [6]. Serum
Fig. 2. Ultrasound findings of CH. A Example of a normal
spectral hepatic venous waveform. Normal respiratory varia-
tion in the waveform over time is demonstrated in this
example. B Example of normal doppler portal vein waveform.
C–F 41 year old female with severe tricuspid regurgitation.
C Ventricular contraction forces blood through the incompe-
tent tricuspid valve resulting in retrograde flow during systole
‘‘s’’. The result is a biphasic waveform with antegrade flow
2039
bilirubin levels have been shown to correlate with right
atrial pressures; the total bilirubin rarely exceeds 3 mg/dL
[1, 9]. Serum aspartate amino transferase (AST) levels may
be mildly elevated (2–3 times normal) [1]. In acute cardiac
decompensation, the AST levels may be markedly elevated
reflecting acute liver injury. In these cases, the cause of
AST elevation is likely related to ischemic injury and the
AST levels correlate with the extent of zone 3 hepatocyte
necrosis [1, 11]. Liver synthetic function is typically pre-
served in CH [1]. Mild hypoalbuminemia may be present
(rarely less than 2.5 g/dL) and related to nutritional defi-
ciency, edema, or protein losing enteropathy [1, 9]. Brain
natriuretic peptide levels are typically elevated.
Ascites may be present in patients with CH. Analysis
of the ascetic fluid is helpful as the combined findings of
high protein content > 2.5 g/dL (thought to be due to
rupture of hepatic lymphatics), serum to ascites albumin
gradient ‡ 1.1, and elevated lactate dehydrogenase levels
and red blood cell count are unique and helpful to the
diagnosis [19].
Treatment
Symptoms and complications from CH are uncommon.
Even the presence of cardiac cirrhosis rarely results in
seen only in diastole ‘‘d’’. D Marked abnormal variation in
portal vein velocity with periods of retrograde flow resulting in
a ‘‘to and fro’’ waveform. E Elevated central venous pressures
result in abnormal dilation of the right hepatic vein (arrow).
F Coarsened echotexture of the hepatic parenchyma may be
related to a combination of edema and fibrosis. Also note the
presence of ascites.
2040
Fig. 3. A, B 47 year old male with constrictive pericarditis.
CT demonstrates typical findings of cirrhosis including a
nodular liver, splenomegaly and ascites. Portosystemic
shunts were notably absent in this patient due to the lack of a
portal to systemic pressure gradient. Pressures measured at
cardiac catheterization demonstrated a marked elevation in
right atrial pressure of 28 mmHg, while the transhepatic
pressure gradient was normal at 2 mmHg. C, D 33 year old
serious complications such as variceal bleeding [9]. In
most cases, the patient’s prognosis is determined by the
presence of underlying cardiac or vascular disease.
Treatment is focused on managing the underlying cause
of CH. In patients with symptoms from hepatic con-
gestion due to heart failure, diuretics may be judiciously
used to treat jaundice and ascites, knowing that in pa-
tients with poor cardiac function this may result in
ischemia [20]. In patients with Budd-Chiari syndrome,
treatment may involve endovascular or surgical inter-
vention to restore hepatic venous drainage or palliate
portal hypertension, possibly in combination with anti-
coagulation therapy [21].
Radiologic evaluation
Radiographic
Radiographs have a limited role in the evaluation of CH.
Chest radiographs may demonstrate cardiac chamber
enlargement reflecting heart failure, pulmonary artery
enlargement due to cor pulmonale, or pericardial calci-
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
female who underwent the Fontan operation for palliation of
tricuspid and pulmonary atresia. MRI demonstrates a mildly
nodular liver with altered parenchymal perfusion, and sple-
nomegaly. A large splenorenal portosystemic shunt (D, ar-
rows) was present suggesting elevated transhepatic pressure
gradient. Patient subsequently underwent cardiac catheteri-
zation which demonstrated abnormal transhepatic pressure
gradients measuring up to 7 mmHg.
fications in constrictive pericarditis (Fig. 1). The vena
cava and azygos veins may be engorged.
Ultrasound
Ultrasound evaluation of the hepatic vasculature may be
valuable in the setting of CH. Hepatic vein dilation can
be measured at grayscale ultrasound (Fig. 2). Henriksson
found the normal right hepatic vein diameter to be
5.6–6.2 mm and it increased to 8.8 mm in the presence of
CHF and 13.3 mm in the presence of CHF with pleural
effusion [22]. In right-sided heart failure normal respi-
ratory variation in venous diameter may be lost [23].
The normal hepatic venous waveform is referred to as
a ‘‘triphasic’’ pattern but is made up of four identifiable
waves; two antegrade pulsations and two retrograde
pulsations (Fig. 2) [24–26]. The normal pattern consists
of two antegrade waves which occur during ventricular
systole ‘‘s’’ and ventricular filling ‘‘d’’, and two retro-
grade waves which occur during atrial contraction ‘‘a’’
and from atrial overfilling at the end of systole ‘‘v’’ (note
that the normal v wave may be represented by a period of
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
Fig. 4. A, B Patient with congestive hepatopathy and peri-
portal edema. Portal venous phase CT image demonstrates
peripheral perfusion irregularity (A, arrows) and periportal low
attenuation (A, arrowheads). A T2 weighted MRI image from
the same patient shows corresponding periportal high T2
signal (B, arrowheads). C, D Additional patient with conges-
relatively slower antegrade flow rather than true retro-
grade flow). In the setting of tricuspid regurgitation, the
normal antegrade pulsation during systole may be
diminished or reversed. In constrictive pericarditis an
extra retrograde hepatic venous wave (‘‘C’’ wave) may be
seen during the end of diastole as atrial expansion is
abruptly limited by the noncompliant pericardium [24].
The normal portal venous waveforms show mild velocity
variation due to respiratory and cardiac pulsations. In
congestive hepatopathy due to tricuspid regurgitation,
right-sided heart pressures are transmitted through the
2041
tive hepatopathy. Periportal lymphedema represented by low
attenuation on a late arterial phase CT (C, arrowheads) re-
sults in contrast retention and periportal high signal (D,
arrowheads) on a delayed phase MRI image. The appearance
at delayed phase MRI may be mistaken for portal vein luminal
thrombus.
dilated sinusoids to the portal vein resulting in the
abnormally increased temporal variation.
In chronic hepatic congestion in which cardiac cir-
rhosis is present, stiffening of the parenchyma sur-
rounding the hepatic veins may dampen waveforms
[24]. In the presence of edema or fibrosis the accom-
panying gray scale ultrasound images may show the
hepatic parenchyma to be abnormally echogenic. In-
creased echogenicity and the decreased penetration of
sound waves may also be found if hepatic steatosis is
present.
2042
Fig. 5. 48 year old female with CH due to ischemic heart dis-
ease. A, B Late arterial phase CT images demonstrate reflux of
contrast into the hepatic veins (A, arrows). In the late arterial
phase, the liver is relatively homogenous with only mild de-
Fig. 6. MRI findings of hepatic congestion in a 20 year old
female who had undergone the Fontan procedure for pallia-
tion of complex congenital heart disease. A T2 weighted fast
spine echo (FSE) MRI demonstrates high signal in the
periphery of the liver (arrows), representative of edema or
fibrosis. B, C Corresponding DWI (C) and ADC (D) images
show high signal on DWI without low signal on the ADC map.
The findings represent T2 shine through and correspond with
high signal found on the T2 FSE image. D, E Late arterial
phase and delayed phase images enhanced with extracellular
CT and MRI
The kinetics of IV contrast enhancement are typically
abnormal in CH. In the setting of right heart failure, an
IV contrast bolus injection injected into the upper
extremities may transiently reflux into the hepatic veins
[27, 28]. Stasis within the hepatic veins due to congestion
leads to decreased portal venous flow. Decreased portal
venous flow combined with poor cardiac output results
in abnormally delayed bolus arrival to the liver and slow
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
creased early enhancement of the liver periphery (B, arrows). C A
delayed phase image acquired 120 s after injection clearly
demonstrates abnormal parenchymal enhancement with reticu-
lar regions of low attenuation (arrows) in the periphery of the liver.
contrast show reticular regions of poor enhancement in the
late arterial phase (D, arrows) which correspond with high T2
signal images on T2 FSE image. The abnormal regions of
enhancement become indistinct on the delayed phase (E).
F Hepatobiliary phase image from MRI exam performed with
hepatocyte specific contrast agent clearly shows reticular re-
gions of poor contrast uptake in the periphery of the liver
(arrows). These findings correspond with abnormalities
demonstrated on the remaining sequences and may repre-
sent poor hepatocyte function or fibrosis.
transit through the parenchyma [29]. Obtaining an
abnormally early phase of enhancement despite use of
standard contrast bolus timing (e.g., obtaining a late
arterial phase of enhancement when using standard
portal venous timing) suggests slow systemic circulation.
The hepatic veins and IVC are typically dilated and
these are readily identified at CT or MRI, as with
ultrasound. In severe cases, atypical hepatic venous to
hepatic venous shunts may form [12]. Portosystemic
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
shunts are frequently absent even in the presence of both
hepatic anatomic findings of cirrhosis and findings sug-
gesting portal hypertension such as splenomegaly and
ascites [1, 30, 31]. The presence of portosystemic shunts
implies the presence of cirrhosis and an elevated tran-
shepatic pressure gradient (Fig. 3) [18]. Engorgement of
the perivascular lymphatics is seen at CT in MRI as
periportal edema (Fig. 4) [27]. The regions of edema are
seen extending completely around the portal tracts.
Extracellular contrast media may diffuse into the peri-
portal lymphatic space in the delayed phase, creating a
ring of enhancement which may be mistaken for a
luminal thrombus [27].
Imaging of the hepatic parenchyma with CT and
MRI demonstrates several parenchymal and perfusional
abnormalities which are highly suggestive of CH (Figs. 5,
6) [27, 28, 32]. The abnormal parenchymal findings are
characteristically most pronounced at the periphery of
the liver with the parenchyma near the hilum also being
involved in more severe disease [18]. At non-contrast
enhanced CT, reticular regions of low attenuation related
to edema and fibrosis are seen which are most prominent
adjacent to the hepatic veins [28]. Non-contrast enhanced
MRI may show peripheral distribution of edema within
the parenchyma, visible as generalized increased signal
Fig. 7. Patient who had undergone the Fontan procedure for
palliation of congenital heart disease. A, B T2 FSE (A) and
portal venous phase (A) enhanced MRI show typical conven-
tional imaging findings of CH with peripheral high T2 signal (A,
arrows) and reticular regions of poor enhancement (B, arrows).
C MR elastogram demonstrates abnormally increased liver
stiffness in the periphery of the liver (arrows; color scale is in
units of kilopascal). The regions of increased stiffness corre-
spond to the abnormal conventional imaging findings on T2
2043
on the T2-weighted and diffusion-weighted sequences
(related to T2 shine through effect). Similar to CT,
perivenous reticular regions of edema or fibrosis are
evident at MRI as high signal on T2 weighted and low
signal on T1 weighted images. At both CT and MRI,
these regions become more conspicuous after intra-
venous (IV) contrast enhancement, and are generally best
seen at the portal venous phase of enhancement [12].
Imaging with hepatocyte specific contrast media in the
hepatobiliary phase may also clearly demonstrate these
parenchymal abnormalities by showing peripheral retic-
ular regions of poor uptake. Liver injury resulting in
steatosis may be evident on in-and-opposed phase or
Dixon based MRI sequences.
Elastography
Passive hepatic congestion can increase the liver
parenchymal stiffness [33]. This increase in stiffness
maybe detected at either ultrasound or MR based elas-
tography. Prior studies have shown correlation between
liver stiffness and clinical improvement of heart failure
after administration of diuretics, pericardiectomy, or
cardiac valve replacement [33–37]. Prior study in Fontan
patients has shown correlation between stiffness and
weighted and contrast enhanced imaging. D, E 11 year old
patient who had undergone the Fontan procedure for palliation
of hypoplastic left heart. T2 FSE image shows slightly increased
signal in the periphery of the liver (D, arrows). Elastogram
shows marked abnormal stiffness (E), primarily in the periphery
of the liver. Liver biopsy was performed which showed con-
gestive findings including sinusoidal dilation with only slight
fibrosis present. The marked elevated liver stiffness is pre-
sumed to be primarily due to parenchymal congestion.
2044
Fig. 8. 55 year old male presenting with constrictive peri-
carditis. A Chest radiograph shows calcified pericardium (ar-
rows). B Cardiac MRI shows thickening of the pericardium
(arrow) and demonstrated physiologic findings of interven-
tricular dependence (not shown). C Hepatic venous spectral
waveforms show an abnormal C-wave related to reversal of
flow caused by early arrest of atrial expansion by the non-
many clinical and laboratory parameters including
pressure in the Fontan circuit, and liver fibrosis scoring
[38]. CH and liver fibrosis may both increase liver stiff-
ness, likely in an additive fashion. At this time, elastog-
raphy methods cannot reliably distinguish the
contributing components of congestion and fibrosis to
liver stiffness.
MR elastography has the benefit of displaying three-
dimensional elastogram maps of parenchymal stiffness.
Elastogram maps show that in congestion the
parenchymal stiffness is heterogeneous, with the regions
of greatest stiffness occurring along the periphery of the
liver (Figs. 7, 8) [12, 39]. These regions of greatest stiff-
ness correspond with the anatomic abnormalities visible
at CT and MRI. The pattern of stiffness within the liver
may represent a helpful clue to the diagnosis of CH.
Imaging of complications
Congestive hepatopathy may lead to liver fibrosis, gen-
eration of benign regenerative nodules or FNH-like le-
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
compliant pericardium. Spectral waveforms also show
abnormally low antegrade velocity in systole ‘‘s’’ when com-
pared to diastole ‘‘d’’ which is a finding also found in other
causes of right-sided heart failure. D Conventional MRI ima-
ges of the liver were normal. E Elastography further suggests
the presence of CH by demonstrating elevated liver stiffness
isolated to the liver periphery.
sions, and HCC [9, 15, 38]. Differentiating liver fibrosis
from parenchymal congestion is difficult with imaging.
Both fibrosis and edema are visible as high T2 and low
T1 signal at conventional MRI and low attenuation on
CT, and at Elastography both fibrosis and congestion
may result in abnormally increased liver stiffness. Liver
biopsy may ultimately be needed to differentiate between
parenchymal congestion and fibrosis but fortunately this
is rarely a clinical necessity. In cases of advanced fibrosis
or cirrhosis, the liver imaging findings of CH may
resemble other advanced chronic liver diseases. In these
cases, clinical history will be helpful to correctly diagnose
CH, but in difficult cases biopsy may be needed to ex-
clude other chronic liver disease.
Benign regenerative nodules or FNH-like masses
occurring in the congested liver most commonly
demonstrate typical benign imaging findings [15]. Benign
nodules tend to have characteristic imaging and patho-
logical findings of FNH, but are referred to as ‘‘FNH-
like’’ due to the presence of abnormal background liver
parenchyma. The imaging features of these nodules in-
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
Fig. 9. 34 year old female with chronic CH after the Fontan
procedure. A Late arterial phase CT demonstrates a hyper-
enhancing hepatic mass (arrow) with background parenchy-
mal perfusion abnormality characteristic of CH. B Mass fades
to isoattenuation on portal venous phase CT. C T2 FSE MRI
shows peripheral T2 hyperintensity of the liver parenchyma
(arrowheads) related to CH. The hepatic mass is T2 hy-
clude a well-circumscribed, homogeneous nodule with
late arterial hyperenhancement which fades to isointen-
sity/Isoattenuation on delayed phase imaging (Fig. 9). At
MRI, these nodules are iso to mildly T1 hypointense, iso
to mildly T2 hyperintense, and tend not to restrict dif-
fusion. These nodules retain hepatobiliary contrast agent
in the hepatobiliary phase. The background parenchymal
abnormalities found in CH may result in a benign nodule
having an atypical appearance [15]. Abnormally in-
creased T2 signal in the background liver has the
potential to make these nodules appear hypointense on
2045
pointense relative to the background parenchyma (arrow).
D Hepatobiliary phase MRI demonstrates homogenous
retention of hepatobiliary contrast agent within the hepatic
mass (arrow). Multiple hepatic masses in this patient had
similar imaging findings and were unchanged in size over
31 months of imaging follow up.
T2 weighted imaging. The expanded extracellular space
within the liver has the potential to cause increased
parenchymal contrast retention in the delayed phase. The
abnormally increased background parenchymal
enhancement in the delayed phase may cause benign
nodules to have a washout appearance, which could be
mistaken for carcinoma [15].
Patients with passive hepatic congestion may develop
HCC [15, 16]. This has been best documented in patients
with chronic passive hepatic congestion due to the
Fontan procedure. In these patients HCC presents as a
2046 M. L. Wells, S. K. Venkatesh: Congestive hepatopathy

heterogeneous, rapidly enlarging mass. Findings char-

acteristic of hepatocellular malignancy such as venous
invasion, lymphadenopathy or metastases may also be
present. Clinically, serum alpha-fetoprotein levels are
frequently elevated. Differentiating HCC from an FNH-
like nodule may occasionally present a diagnostic di-
lemma and biopsy may be required for accurate diag-
nosis.

Variation of imaging findings based

on the anatomic location of pathology
Congestive hepatopathy may result from impairment of
central venous blood flow at the level of the heart, hep-
atic outflow at the level of the hepatic veins or IVC, or
obstruction may occur within the liver due to occlusion
of the hepatic sinusoids and terminal hepatic venules
[sinusoidal obstruction syndrome (SOS)]. When CH oc-
curs due to SOS (also known as veno-occlusive disease),
imaging abnormalities are typically limited to the hepatic
parenchyma [40]. If the obstruction is caused by throm-
bosis of the larger hepatic veins as in Budd-Chiari syn-
drome, the hepatic parenchymal abnormalities may spare
the central liver due to the preserved venous drainage
through the caudate veins. In this case the thrombosed
hepatic veins are diminutive and have no significant
enhancement. If the level of obstruction occurs at the
heart, cardiac enlargement or pericardial thicken-
ing/calcification may be seen. Passive congestion due to
cardiac pathology leads to dilation of the IVC and hep-
atic veins in addition to the hepatic parenchymal
abnormalities. Abnormalities of contrast bolus kinetics
due to poor cardiac function may also be present such as
reflux into the hepatic veins and slow bolus transit.

Sinusoidal obstruction syndrome

Sinusoidal obstruction syndrome results from primary
injury to the sinusoidal epithelial cells, often associated
with bone marrow transplantation or use of oxaliplatin
chemotherapy [3, 41]. Gaps form in the epithelial wall
allowing accumulation of red blood cells and other
material within the space of Disse. Subsequent sloughing
of epithelial cells results in embolic occlusion of the
downstream terminal venules and post-sinusoidal Fig. 10. 70 year old patient treated with a chemotherapy
obstruction. Varying amounts of centrilobular conges- regimen which included oxaliplatin for metastatic colonic
tion and perivenular fibrosis may be seen at pathology adenocarcinoma. When compared with pretreatment CT scan
depending on the acute or chronic stage of the disease. (A), post-treatment T2 FSE MRI (B) shows new splenome-
At hepatobiliary phase imaging with hepatocyte specific galy and ascites. Hepatobiliary phase imaging with hepato-
cyte specific contrast agent demonstrates poor parenchymal
contrast agent, the liver may show peripheral regions of
retention of contrast agent throughout the liver, with a small
reticular hypointensity which appears similar to that seen region of normal uptake in the central liver. Findings are
in other causes of CH (Fig. 10) [40]. Progressive consistent with chemotherapy induced sinusoidal obstruction
enlargement of the spleen caused by portal hypertension syndrome.
may also be present.
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
Fig. 11. A–E 24 year old female with Budd-Chiari Syn-
drome. A Portal venous phase CT image demonstrates poor
peripheral perfusion with reticular regions of low attenuation
(arrows). Hypertrophy of the caudate lobe with normal
central parenchymal enhancement facilitated by persistent
patency of the caudate veins (arrowhead). B Hepatic veins
are diminutive without identifiable enhancement (arrows).
C Patient developed multiple intrahepatic venous collaterals
(arrows) which are characteristic of chronic Budd-Chiari
syndrome. D Late arterial phase image shows numerous
hyperenhancing regenerative nodules (arrows) which are a
common finding in chronic Budd-Chiari syndrome. E Patient
was treated with a portocaval shunt. Portal venogram shows
2047
irregularity of the intrahepatic portal branches with devel-
opment of numerous small collateral veins. Reflux of con-
trast is seen entering the IVC across the portocaval shunt
(arrow). F Hepatic venogram from a 47 year old male with
Budd-Chiari shows irregularity and diminished caliber of the
right hepatic vein due to prior thrombosis and recanaliza-
tion. G, H CH due to extrinsic compression of the supra-
hepatic IVC and right atrium in a 60 year old female with
metastatic leiomyosarcoma. Axial CT image demonstrates
peripheral hepatic perfusional findings of CH (G, arrows).
Coronal CT shows a large cystic mass deviating and com-
pressing the suprahepatic IVC (H, arrows) and mediastinal
structures.
2048
Fig. 12. Acute hepatic congestion. A, B 30 year old female
being evaluated for routine follow up of crohn’s disease.
Periportal edema (arrows) and peripheral hepatic perfusion
irregularity (arrowheads) was new from prior exams. Patient
had received an IV infusion of 2 L normal saline shortly prior
to the CT exam for clinically suspected dehydration. C–
E 47 year old male presenting to the emergency room after
his motor vehicle collided with a tree. Portal venous phase CT
Budd-chiari syndrome
Budd-Chiari Syndrome may be caused by hepatic vein
obstruction due to internal thrombosis or web, or due to
extrinsic compression [21]. Acute presentations can be
associated with fulminant liver failure, but most patients
present with chronic disease. Typical parenchymal con-
gestive findings are found in the distribution of the oc-
cluded vein or veins. The occluded hepatic veins
themselves may be diminutive in size and not well seen.
In most cases the IVC remains patent, and preserved
venous drainage of the caudate and liver hilum into the
IVC may result in characteristic hypertrophy of the
central liver (Fig. 11) [28]. The spared central liver par-
enchyma tends to enhance to a greater degree in the early
phases of IV contrast administration, followed by
washout in the delayed phase. The finding of intrahepatic
collateral vessels is suggestive of Budd-Chiari syndrome
[28]. Chronically elevated portal pressure may result in
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
scan shows poor perfusion in the periphery of the liver (C,
arrows) and reflux of injected contrast bolus into the hepatic
veins (D, arrow). Patient was found to have an inferior ST
elevated myocardial infarction and subsequently underwent
right coronary artery thrombectomy with stent placement.
Follow up CT scan (E) shows resolution of the hepatic per-
fusion abnormalities.
splenomegaly, the formation of portosystemic shunts
and ascites.
Acute vs. chronic congestion
Findings of passive hepatic congestion suggest a signifi-
cant underlying cardiovascular abnormality. It is
important to remember that the imaging findings of
congestion may occur acutely and due to benign causes.
Resuscitative fluid administration may raise central ve-
nous pressures, and in the emergency setting this fre-
quently results in findings of passive hepatic congestion
including venous expansion and periportal edema [42–
44]. A fluid bolus such as that administered along with a
medication infusion may create a surprisingly large
amount of periportal edema and parenchymal enhance-
ment abnormality (Fig. 12). Interpreting the significance
of the imaging findings of CH requires access to an
accurate medical history.
M. L. Wells, S. K. Venkatesh: Congestive hepatopathy
Fig. 13. Acute hepatitis. A, B 41 year old female presenting
to emergency department with confusion. CT demonstrates
hepatomegaly, extensive periportal edema (arrows) and mild
peripheral perfusion irregularity (B, arrowhead). Patient had
taken an overdose of acetaminophen and subsequently
developed fulminant liver failure requiring liver transplant. C,
Simulators
Several diseases of the liver may appear similar to CH. In
general, these conditions are easily distinguished from
CH by close examination of the imaging findings and
verification of the patient’s medical history.
Acute hepatitis
Inflammation caused by acute hepatitis due to a variety
of causes (viral, drug induced, etc.) may result in hep-
atomegaly, periportal edema, gallbladder wall thicken-
ing, perihepatic fat stranding, and ascites (Fig. 13) [45,
46]. The parenchyma of these patients may also
2049
D) 21 year old female presenting to the emergency room with
abrupt onset of abdominal pain. CT demonstrates hep-
atomegaly and periportal edema (arrows). Patient was diag-
nosed with viral hepatitis and symptoms resolved with
conservative management.
demonstrate transient heterogeneous enhancement [47].
These patients are frequently present in the acute care
setting where IV fluids may have been administered. The
combined effects of parenchymal inflammation and in-
creased systemic fluid volume may appear similar to CH.
Hepatic infarcts
Small portal emboli typically create wedge shaped re-
gions of poor perfusion in the periphery of the liver [28].
Large infarcts or solitary infarcts are easily distinguished
from the reticular perivenous perfusion abnormalities
found in CH. Multifocal small infarcts have the potential
2050
to create diagnostic uncertainty; however, additional
findings such as slow contrast bolus transit and hepatic
venous dilation are absent. Clinical history and review of
previous imaging will be useful to differentiate from CH.
Primary sclerosing cholangitis (PSC)
Early PSC and small duct PSC present with liver disease
and no visible stricturing of the biliary tree on cross-
sectional imaging. In these patients, parenchymal imag-
ing abnormalities representing regions of fibrosis, atro-
phy, and edema can be found primarily in the periphery
of the liver [48]. In PSC, the peripheral parenchymal
abnormalities tend to be larger and more confluent than
those seen in CH. At MR Elastography, the periphery of
the liver tends to have the greatest stiffness early in the
disease process [39, 49]. These findings may be confused
for CH which should be distinguished by the clinical and
laboratory assessment. In addition, patients with pri-
mary sclerosing cholangitis often have elevated serum
alkaline phosphatase suggesting cholestasis which is ab-
sent in CH.
Conclusion
Congestive hepatopathy is a clinically important entity
which may go unrecognized. Radiologists can add clini-
cally valuable information by identifying the character-
istic imaging abnormalities of CH and suggesting the
diagnosis. While other liver disease may simulate CH at
imaging, correlation of the imaging findings with clinical
history will facilitate accurate diagnosis in most cases.
While the imaging findings of CH are well established on
conventional imaging, new imaging methods such as
elastography have potential to improve the existing
radiologic and clinical evaluation of this condition.
Compliance with ethical standards
Conflict of interest Michael Wells and Sudhakar Venkatesh declare no
conflict of interest.
Ethical approval This is a review article only. This article does not
contain any studies with human participants or animals performed by
any of the authors.
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