European Journal of Radiology 61 (2007) 5769

Cirrhosis: CT and MR imaging evaluation

Giuseppe Brancatelli
a,b,c,
, Michael P. Federle
c
, Roberta Ambrosini
d
,
Roberto Lagalla
b
, Alessandro Carriero
d
, Massimo Midiri
b
, Val erie Vilgrain
e
a
Sezione di Radiologia, Ospedale Specializzato in Gastroenterologia, Saverio de BellisIRCCS, 70013 Castellana Grotte (Bari), Italy
b
Sezione di Scienze Radiologiche, Dipartimento di Biotecnologie Mediche e Medicina Legale,
Universit ` a di Palermo, Via del Vespro 127, 90127 Palermo, Italy
c
Department of Radiology, University of Pittsburgh Medical Center, 200 Lothrop Street, 15213 Pittsburgh, PA, USA
d
Department of Diagnostic and Interventional Radiology, Maggiore della Carit ` a University Hospital,
A.Avogadro Eastern Piemonte University, Corso Mazzini 18, Novara, Italy
e
Service de Radiologie, Hopital Beaujon, 100 Boulevard du General Leclerc, 92118 Clichy, France
Received 7 July 2006; accepted 2 November 2006
Abstract
In this article, we present the CT and MR imaging characteristics of the cirrhotic liver. We describe the altered liver morphology in different
forms of viral, alcoholic and autoimmune end-stage liver disease. We present the spectrum of imaging ndings in portal hypertension, such as
splenomegaly, ascites and varices. We describe the patchy and lacelike patterns of brosis, along with the focal conuent form. The process of
hepatocarcinogenesis is detailed, from regenerative to dysplastic nodules to overt hepatocellular carcinoma. Different types of non-neoplastic focal
liver lesions occurring in the cirrhotic liver are discussed, including arterially enhancing nodules, hemangiomas and peribiliary cysts. We show
different conditions causing liver morphology changes that can mimic cirrhosis, such as congenital hepatic brosis, pseudo-cirrhosis due to
breast metastases treated with chemotherapy, Budd-Chiari syndrome, sarcoidosis and cavernous transformation of the portal vein.
2006 Elsevier Ireland Ltd. All rights reserved.
Keywords: Liver; Cirrhosis; Computed tomography; Magnetic resonance imaging
1. Introduction
Cirrhosis is the nal result of chronic damage to the liver from
various etiologies, characterized by parenchymal injury lead-
ing to extensive brosis and nodular regeneration. The result is
a diffuse disorganization of hepatic morphology with progres-
sive loss of liver function. Although the mortality rate has been
reduced by about 30% in the last few decades, within the Euro-
peanUnioncirrhosis is still one of the leadingcauses of deathand
serious morbidity. Cirrhosis is most commonly the result of hep-
atitis Band Cvirus infection or chronic alcoholism; other causes
are biliary, cryptogenic and metabolic. Usual clinical manifes-
tations result from portal hypertension, portosystemic shunting
and hepatic insufciency. Common complications are ascites,
gastrointestinal bleeding, encephalopathy and coagulopathy.

Corresponding author at: Via Villaermosa 29, 90139 Palermo, Italy.

Tel.: +39 3291828155; fax: +39 0916552325.
E-mail address: gbranca@yahoo.com (G. Brancatelli).
In this review, we present the CT and MR imaging ndings
in the cirrhotic liver.
2. Liver morphology
At an early stage of cirrhosis, the liver may appear normal on
cross sectional imaging. With disease progression, heterogene-
ity of liver parenchyma and surface nodularity are observed.
Caudate lobe hypertrophy is the most characteristic morpho-
logic feature of liver cirrhosis (Fig. 1). A ratio of transverse
caudate lobe width to right lobe width greater than or equal
to 0.65 constitutes a positive indicator for the diagnosis of
cirrhosis with high level of accuracy [1]. A modied caudate
lobe width to right lobe width ratio, using the right portal vein
instead of the main portal vein to set the lateral boundary has
recently been proposed [2]. Other regional changes in hepatic
morphology typically seen in advanced cirrhosis are segmental
hypertrophy involving the lateral segments (II, III) of the left
lobe (Fig. 2), and segmental atrophy affecting both the posterior
0720-048X/$ see front matter 2006 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ejrad.2006.11.003
58 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
Fig. 1. Typical cirrhotic morphology at MR imaging. Transverse T2-weighted
fat-suppressed turbo spin-echo MR image (A) shows enlarged caudate lobe,
mildly lobulated liver margins (arrowheads) and regions of high attenuation
(arrow) of hepatic parenchyma caused by patchy brosis. Gadolinium-enhanced
T1-weighted fat-suppressed gradient-echo MRimage (B) obtained during portal
venous phase shows inhomogeneous liver enhancement and caudate to right lobe
ratio of 1.80.
segments (VI, VII) of the right lobe and medial segment (IV) of
the left lobe [3] (Fig. 2). Alteration of blood ow is the likely
explanation for these morphologic abnormalities. Enlargement
of hilar periportal space, the notch-sign [4] (Fig. 2), an expanded
gallbladder fossa (Fig. 2) [5] and generalized widening of
the interlobar ssures are also considered typical ndings of
cirrhosis.
Primary sclerosing cholangitis and primary biliary cirrhosis
have some distinctive features in comparison to other types of
cirrhosis. In primary sclerosing cholangitis induced end-stage
cirrhosis, pseudotumoral enlargement of the caudate lobe is
Fig. 2. Typical cirrhotic morphology at CT. Portal venous phase CT scan shows
an enlarged left lateral lobe and caudate lobe (C), an enlarged gallbladder fossa
with the gallbladder (g) herniated toward the anterior abdominal wall, marked
atrophy of the medial segment of the left hepatic lobe (arrowheads) and of the
right posterior hepatic lobe (arrow), and presence of right posterior hepatic notch
(asterisk).
observed in virtually all patients, along with atrophy of the
peripheral hepatic segments resulting in a lobulated liver contour
(Fig. 3Aand B). Concomitant multiple irregular strictures of the
intra- and extrahepatic bile ducts are also observed (Fig. 3C) [6].
Primary biliary cirrhosis typically produces early signs of portal
hypertension while the liver is enlarged, along with prominent
lacelike brosis, regenerative nodules, and lymphadenopathy
(Fig. 4) [7]. Late-stage primary biliary cirrhosis results in mor-
phologic changes including a shrunken, brotic liver, that is
indistinguishable from other etiologies.
3. Portal hypertension and mesenteric edema
In chronic liver disease, progressive hepatic brosis leads
to increased vascular resistance at the level of the hepatic
sinusoids. The increased pressure gradient is dened as por-
tal hypertension, and causes complications such as ascites and
the development of engorged and tortuous collateral vessels
that typically develop at the lower end of the esophagus (Figs.
3C and 5A) and at the gastric fundus (hypertensive gastropa-
thy) (Fig. 5B) [8]. The paraumbilical veins (Fig. 5C) and the
left gastric vein, both draining into the portal vein, also reopen
to form portosystemic shunts. Other shunts between the por-
tal and the systemic circulation include splenorenal collaterals
(Fig. 5B), hemorrhoidal veins, abdominal wall (Fig. 5D) and
retroperitoneal collaterals.
Increased venous pressure is also responsible for the promi-
nent mesenteric edema and stranding occurring in 86% of
patients with cirrhosis [9]. It can occur in mild, moderate or
severe formwith pseudonodules surrounding mesenteric vessels
and mimicking enlarged lymph nodes (Fig. 6).
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 59
Fig. 3. Primary sclerosing cholangitis at CT. (A) Nonenhanced CT shows severe lobulation (arrows) of the hepatic contour and compensatory hypertrophy of the
caudate lobe (arrowheads). The peripheral areas of the liver are hypodense due to atrophy. The phenomenon of segmental hyperplasia associated with atrophy of
other parts of the liver is known as the atrophyhypertrophy complex. (B) In the portal venous phase, the attenuation difference between the caudate and the liver is
lost. (C) Portal venous phase CT scan in a different patient with primary sclerosing cholangitis shows irregular dilatation of the intra-hepatic bile ducts (arrowheads).
Note esophageal varices (arrow) due to portal hypertension.
Fig. 4. Primary biliary cirrhosis at CT. (A) Transverse nonenhanced CT scan (narrow window setting) shows lacelike pattern of low-attenuating brosis surrounding
subcentimeter regenerative nodules that are hyperattenuating to normal liver or spleen. (B) On portal venous phase CT scan obtained at the same level as A,
regenerative nodules are not easily recognized. Splenomegaly and enlarged porta hepatis and portacaval lymph nodes (arrows) are also noted.
4. Fibrosis
Fibrosis is an inherent part of hepatic cirrhosis, and is typi-
cally detected as patchy brosis (Fig. 1A), as a lacelike pattern,
or as a conuent mass. The lacelike type of brosis is best
described as thin or thick bands that surround regenerative
nodules. This pattern is best visualized on nonenhanced CT
(Fig. 4A), and is usually not well visualized on portal venous
phase images (Fig. 4B) [10]. It is seen in about one-third of
patients with primary biliary cirrhosis [7], regardless of stage.
60 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
Fig. 5. Axial (A), multiplanar reformatted in the coronal plane (B), axial maximum intensity projection (C) and sagittal maximum intensity projection (D) contrast-
enhanced CT images show different examples of collateral vessels developing in end-stage chronic liver disease due to severe portal hypertension. Part (A) shows
dilated and tortuous esophageal varices (arrow); part (B) shows varices in the gastric fundus (arrow) and a splenorenal shunt (double arrows); part Cshows recanalized
parumbilical vein (arrow), and part D shows abdominal wall collaterals (arrowheads).
Focal conuent brosis is observed in end-stage liver disease
and is usually a wedge-shaped lesion located in the subcapsu-
lar portion of segment IV, V or VIII, with associated capsular
retraction [11,12] (Fig. 7). In those rare cases in which the lesion
shows enhancement on arterial dominant phase, it may be mis-
taken for hepatocellular carcinoma. Delayed, persistent contrast
enhancement, however, is typically observed, and is due to the
retention of contrast by the brotic tissue (Fig. 7D). This fea-
ture, along with the characteristic capsular retraction and typical
location and shape help to distinguish conuent brosis from
hepatocellular carcinoma.
5. Regenerative nodules
In the cirrhotic liver, regenerative nodules are macronodular
(9 mm), as usually seen in chronic hepatitis B, or micronodular
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 61
Fig. 6. Mesenteric edema in cirrhosis. Contrast-enhanced CT scan shows
increased attenuation of the fat (arrows) around the mesenteric vessels due to
congestion and edema caused by portal hypertension. Mesenteric edema in this
case mimics the appearance of lymph-nodes.
(39 mm), as seen in other causes of cirrhosis. Most regenera-
tive nodules are difcult to detect at CT or MR because they
are too small or are too similar to surrounding liver parenchyma
[13]. Computed tomography detects regenerative nodules when
they are surrounded by hypodense brotic bands on nonen-
hanced CT (Fig. 4A) or when they accumulate iron (siderotic
nodules) [14]. Siderotic regenerative nodules are typically
hyperattenuating to liver on nonenhanced CT and are isoatten-
uating to liver, and therefore difcult to detect, after contrast
injection.
MR imaging demonstrates regenerative nodules with greater
sensitivity than any other imaging modality. They usually appear
isointense (Fig. 8A) to hypointense on T2-weighted MR images
relative to the surrounding inammatory brous septa and isoin-
tense (Fig. 8B) to hyperintense relative to background liver
parenchyma on T1-weighted sequences [13]. The accumulation
of iron within regenerative nodules may cause hypointensity
on T2-weighted images (Fig. 9A) because of magnetic eld
inhomogeneities, and marked hypointensity on T1-weighted
gradient-Echo MR images (Fig. 9B), usually best visualized
using TEs greater than 10 ms. Due to their portal venous supply,
regenerative nodules usually enhance to the same degree than
the background liver.
6. Dysplastic nodules
Dysplastic nodules are regenerative nodules containing atyp-
ical cells without denite histological signs of malignancy, and
Fig. 7. Cirrhosis and focal conuent brosis at MR imaging. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows focal conuent brosis
lesion (arrows) in segment four as an area of moderate to high intensity in comparison to background liver. T1-weighted gradient-echo fat-suppressed MR image (B)
shows lowintensity of focal conuent brosis lesion (arrow). Note adjacent retraction (arrowhead) of liver capsule. Gadolinium-enhanced T1-weighted fat-suppressed
gradient-echo MRimage obtained during arterial dominant phase (C) shows no apparent enhancement of focal conuent brosis lesion. On equilibrium-phase (5 min)
gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image (D), focal conuent brosis lesion shows delayed enhancement (arrow) due to presence
of brotic tissue.
62 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
Fig. 8. Cirrhosis and multiple regenerative nodules at MR imaging. Transverse T1-weighted gradient-echo MR image (A) shows multiple subcentimeter isointense
nodules (arrows), surrounded by diffuse lacework of low-intensity brosis. On transverse T2-weighted fat-suppressed turbo spin-echo MR image (B), nodules
(arrows) are still isointense and surrounded by thick hyperintense septa of lacelike brosis. Arterial dominant phase (not shown) failed to show enhancement of
nodules, consistent with diagnosis of regenerative nodules.
Fig. 9. Cirrhosis and siderotic regenerative nodules at MRimaging. Transverse T2-weighted fat-suppressed turbo spin-echo MRimage (A) shows multiple hypointense
nodules (arrowheads). On transverse T1-weighted gradient-echo breath-hold MR image (B), nodules are hypointense.
Fig. 10. Cirrhosis and dysplastic nodule at MR imaging. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (a) shows irregular liver margins,
perihepatic ascites (a) and 1 cm hypointense mass (arrow). On transverse T1-weighted gradient-echo breath-hold MR image (b), the mass is hyperintense (arrow).
Arterial dominant phase (not shown) failed to show enhancement of nodule.
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 63
Fig. 11. Cirrhosis and typical hepatocellular carcinoma at MR imaging. Transverse T2-weighted half-Fourier acquired single-shot turbo spin-echo MR image (A)
shows 2 cmmildly hyperintense lesion (arrow) in right hepatic lobe. On T1-weighted gradient-echo MRimage (B), lesion is hypointense in comparison to background
liver. Gadolinium-enhanced T1-weighted gradient-echo MR image obtained during arterial dominant phase (C) shows marked enhancement of lesion (arrow) with
central hypointense area due to necrosis. On gadolinium-enhanced T1-weighted gradient-echo MR image obtained during portal venous phase (D), lesion becomes
hypointense to surrounding parenchyma. Note hyperintense capsule (arrowhead) surrounding lesion.
64 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
Fig. 12. Cirrhosis and large hepatocellular carcinoma with mosaic appearance at MR imaging. Transverse T2-weighted fat-suppressed turbo spin-echo MR image
(A) shows large tumor (arrows) in right lobe of the liver that is slightly hyperintense to surrounding nontumorous parenchyma and heterogeneous due to presence of
some hypointense areas. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image obtained during arterial dominant phase (B) shows that only
peripheral portion of tumor enhances (arrow), while remaining part is hypointense. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image
obtained during portal venous phase (C) shows washout of tumor portion that enhanced in arterial dominant phase. The brotic capsule (arrows) surrounding lesion
is well seen because of contrast retention. Mosaic appearance is caused by areas of different intensity level and results from peculiar growth pattern of hepatocellular
carcinoma, which contain small viable nodules with interspersed areas of necrosis, brosis, and cystic or fatty degeneration. Capsule and mosaic pattern are seen
more frequently with increasing tumor diameter.
Fig. 13. Cirrhosis and benign arterially enhancing nodule at CT. (A) Arterial dominant phase CT scan of the liver shows small enhancing lesion (arrows). (B) On
portal venous phase CT scan obtained at same level as A, lesions are minimally hyperattenuating to isoattenuating compared to surrounding liver.
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 65
are considered an intermediate, premalignant step along the
hepatocarcinogenesis process. Malignant transformation within
a dysplastic nodule has been identied as early as 4 months
after the rst detection of the dysplastic nodule [15]. Dysplastic
nodules are found in 1525% of cirrhotic livers at the time of
transplantation and are subclassied on the basis of the degree
of cellular abnormalities: low-grade (containing hepatocytes
with mild atypia) and high-grade (when the degree of atypia
is moderate, but insufcient for the diagnosis of malignancy)
[16].
As with regenerative nodules, dysplastic nodules receive pre-
dominantly portal venous ow, and do not usually demonstrate
bright enhancement on arterial phase CT or MRI. Therefore,
marked arterial phase enhancement should suggest hepato-
cellular carcinoma rather than dysplastic nodule, but there is
much overlap in imaging features between regenerative nod-
ules, dysplastic nodules and well-differentiated hepatocellular
carcinoma. Dysplastic nodules typically appear hypointense
to the background liver parenchyma on T2-weighted images
(Fig. 10a), and show hyperintensity on T1-weighted images
(Fig. 10b), quite in contrast to typical ndings for hepatocel-
lular carcinoma. Arterial phase enhancement should suggest
development of a focus of hepatocellular carcinoma within a
Fig. 14. Transient hepatic attenuation difference due to portal vein thrombosis
in cirrhosis at CT. (A) Arterial dominant phase CT scan shows hyperattenu-
ation of the right lobe of the liver (arrowheads) in comparison to normal left
liver due to thrombosis of the anterior branch of the right portal vein (arrow)
and increased arterial ow. (B) Delayed phase contrast-enhanced transverse CT
scan demonstrates isoattenuation of right liver to the normal parenchyma. Note
splenomegaly.
high-grade dysplastic nodule, the so-called nodule within a
nodule appearance on MR imaging [17].
Dysplastic nodules are detected and characterized better by
MR than by CT; however, accurate diagnosis may be made in
only about 15% of cases [18].
7. Hepatocellular carcinoma
Hepatocellular carcinoma typically occurs within the cir-
rhotic liver. As the degree of (de-differentiation) malignancy
increases, portal blood supply decreases, whereas nontriadal
arteries (i.e., unaccompanied by portal venules and biliary ducts)
develop to feed the nodules. The presence of early arterial
enhancement with rapid washout during the portal venous phase
should be regarded as highly suspicious for the presence of
hepatocellular carcinoma. Characteristically, hepatocellular car-
cinoma is hypoattenuating to liver on unenhanced CT, and
Fig. 15. Cirrhosis and multiple hemangiomas at MR imaging. Transverse
T2-weighted fat-suppressed turbo spin-echo MR image (A) shows two heman-
giomas (arrows) as strongly hyperintense in comparison to liver parenchyma.
(B) Transverse T2-weighted fat-suppressed turbo spin-echo MR image through
the same level obtained 2 years later. The cavernous hemangioma in the right
lobe is much smaller (arrow), while the cavernous hemangioma in the left lobe
is no longer visible.
66 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
manifests as a heterogeneous, moderately enhancing lesion dur-
ing the arterial phase, with washout on portal venous and delayed
phase [19,20]. Similar features are evident on MR imaging,
and hepatocellular carcinoma is usually hypointense to liver on
T1-weighted imaging and hyperintense on T2-weighted imag-
ing (Fig. 11) [21]. Other useful characteristics of hepatocellular
carcinoma are heterogeneity, mosaic appearance (Fig. 12), mul-
tiplicity, encapsulation (Figs. 11D and 12C), and portovenous
or hepatovenous invasion.
Both CT and MR are quite accurate in diagnosis of hepato-
cellular carcinoma nodule 2 cm in diameter [18,22]. Smaller
lesions are more challenging, but these are the goal of surveil-
lance programs in which patients with cirrhosis have imaging
evaluation at intervals of 612 months or less [23,24]. Accu-
rate detection of small hepatocellular carcinomas is especially
important because it offers the chance of curative therapy by per-
cutaneous ablation, surgical resection and liver transplantation.
In patients with hepatocellular carcinoma, an expert panel
fromthe EuropeanAssociationfor the Studyof the Liver (EASL)
distinguishes between lesions measuring less than 2 cm and
those with larger diameters [25]. According to their guidelines,
imaging detection of a liver nodule 2.0 cm or smaller should
always be conrmed with needle biopsy, and in case of negative
result, should be subjected to an increase in the frequency of US
surveillance. For a mass greater than 2.0 cm, the coincident nd-
ings of characteristic arterial vascularization that is seen on at
least two imaging techniques (e.g., multiphasic CT and MRI),
or hypervascularity in one imaging technique associated with
wash out in the portal venous and/or delayed phase may be used
to condently establish the diagnosis without biopsy [26].
Distinction among regenerating nodules, dysplastic nodules,
and hepatocellular carcinoma with varying degrees of differen-
tiation requires an assessment of the hemodynamic nature of
the mass. In evaluation of the cirrhotic liver, whether by CT or
Fig. 16. Cirrhosis and peribiliary cysts at MR imaging. Transverse T2-weighted half-Fourier acquired single-shot turbo spin-echo MR image (A) shows organized
cluster of high-intensity cysts (arrows) close to each other in left liver lobe. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image (B) obtained
during portal venous phase shows collection of discrete low intensity cysts (arrows) close to each other, separated by thin walls and lying along enhancing left portal
vein. Thick slab MR cholangiography (C) shows multiple peribiliary cysts at hepatic hilum and in left liver lobe. Note other single high intensity areas (arrowheads)
in right liver lobe, likely representing biliary hamartomas.
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 67
MR, it is essential to obtain multiple phases of imaging before
and during the rapid (>4 ml/s) IV administration of contrast
medium. Unenhanced images are followed by dynamic acqui-
sition of images during the arterial, and portal venous phases
of enhancement. With MR, we add an equilibrium or delayed
phase acquisition as well [27].
8. Arterially enhancing nodules and perfusion
anomalies
With the increasing use of thin section CT and MR imaging
and the rapid bolus injection of contrast, small enhancing nod-
ules and perfusion anomalies are increasingly being observed in
the cirrhotic liver [28,29]. Both nodules and perfusion anomalies
are likely due to intrahepatic shunts between a hepatic arterial
branch and the portal venous system. These pseudolesions may
simulate a hypervascular hepatic lesion on the arterial dominant
phase, and are not detectable on portal venous and delayed phase
(Fig. 13). Lack of growth, or even disappearance on subsequent
imaging is the key to diagnosis of these vascular entities. Perfu-
sion anomalies can also result from occlusion of a portal venous
branch with compensatory increased arterial ow causing arte-
rial phase hyperenhancement (Fig. 14) [30]. These perfusion
pseudolesions can usually be distinguished from tumor by their
peripheral location, wedge shape, lack of mass effect, and isoat-
tenuation with liver on all other phases. Conversely, spherical
shape or central location are features that may require close
imaging follow-up (e.g., 46 months) to exclude malignancy.
9. Hemangiomas
In the cirrhotic liver, hemangiomas are more difcult to rec-
ognize radiologically and pathologically. Progressive brosis
alters the blood supply of the liver and causes loss of some
identifying characteristics of hemangiomas, such as nodular
peripheral enhancement and isoattenuation to blood vessels.
Usually, however, the characteristic feature of high signal
intensity on heavily T2-weighted images remains, helping to
distinguish hemangioma from hepatocellular lesions. Fibrosis
also causes progressive diminution in size, ultimately result-
ing in obliteration of the hemangioma (Fig. 15) [31]. In some
instances, capsular retraction develops over those hemangiomas
that regress in size.
10. Peribiliary cysts
Peribiliary cysts are cystic lesions typically found on both
sides of the intrahepatic portal venous branches. These lesions
may have variable size and morphology: linear and conuent
tube-like aspect, coursing adjacent to right or left portal vein,
simulating dilated bile ducts, or linear cluster (string of beads)
of cysts, with a prominent involvement of the left-sided intra-
hepatic ducts. They represent cystic dilatation of the extramural
glands in the periductal connective tissue, and may increase in
size and number as the cirrhosis progresses. Peribiliary cysts
show the same imaging ndings as simple cysts, i.e., low atten-
uation at CT, lowsignal intensity on T1-weighted MRsequences
and high signal on heavily T2-weighted MR sequences, with no
contrast enhancement [32] (Fig. 16).
11. Diseases that mimic cirrhosis
Several disease processes may result in distorted hepatic mor-
phology that might be misinterpreted as cirrhosis on imaging.
In congenital hepatic brosis, the liver generally shows vari-
able segmental hypertrophy or atrophy, with caudate lobe and
left lateral segment enlargement andright lobe atrophyobserved.
Fig. 17. Congenital hepatic brosis at CT. CT scan obtained during the portal
venous phase in a 16-year-old male with congenital hepatic brosis shows an
enlarged liver. An abnormal network of small vessels representing a collateral
circulation is seen running parallel to the intrahepatic portal veins (arrow). This
network likely represent an hypertrophied peribiliary vascular plexus due to
presinusoidal portal hypertension. Note splenomegaly.
Fig. 18. Pseudocirrhosis at CT. Portal venous phase CT scan in a woman with
metastatic breast carcinoma tothe liver. The liver shows nodular contours (arrow-
head) and a pseudocirrhotic appearance. There is subtle capsular retraction
adjacent to some of the lesions (arrow).
68 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769
However, as opposed to cirrhosis, the left medial segment is of
normal size or enlarged (Fig. 17). This morphologic nding has
beenconsidereduseful indistinguishingpatients withcongenital
hepatic brosis from those with cirrhosis [33,34].
Patients with liver metastases from breast carcinoma treated
with chemotherapy often develop retraction of the capsular sur-
face with segmental volume loss, lobular hepatic contour and
enlargement of the caudate lobe, a patternthat has beendescribed
as pseudo-cirrhosis (Fig. 18) [35].
Budd-Chiari syndrome is characterized by hypertrophy of the
caudate lobe and variable atrophy/hypertrophy of the remaining
portions of the liver, along with heterogeneous liver enhance-
ment, ascites andsplenomegaly. Sometimes, large hypervascular
regenerative nodules can be mistaken for hepatocellular carci-
noma (Fig. 19) [3638].
Sarcoidosis is a multisystem granulomatous disease that
affects the liver in 2479% of patients, and may result in hep-
atic injury that simulates or causes cirrhosis. Multifocal nodular
hypoenhancing lesions in the liver (and spleen) are typical nd-
Fig. 19. Chronic Budd-Chiari syndrome and large regenerative nodules at MR
imaging. T1-weighted gradient-echo MR image obtained during arterial dom-
inant phase (A) and portal venous phase (B) shows an enlarged caudate lobe
and several nodules with marked enhancement (arrows). Nodules showed low
signal intensity on T2-weighted images (not shown) and high signal intensity on
unenhanced T1-weighted images. Lack of washout on portal venous phase and
the appearance of these nodules on T2- and unenhanced T1-weighted images
are opposite to what is expected for hepatocellular carcinoma. Note transjugular
intrahepatic portosystemic shunt (arrowhead), ascites and splenomegaly.
Fig. 20. Sarcoidosis at CT. Portal venous phase CT scan in a patient with sar-
coidosis shows enlarged left lobe and small right lobe, as typically seen in
cirrhosis. Splenomegaly and periaortic and hilar adenopathy also noted.
Fig. 21. Liver morphology changes in a patient with cavernous transformation
of the portal vein at CT. Portal venous phase CT scan performed 3 months after
occurrence of portal vein thrombosis shows hypertrophy of the caudate lobe and
relative atrophy of the peripheral portions of the liver.
ings, but widened ssures, splenomegaly and upper abdominal
lymphadenopathy are features seen in cirrhosis and hepatic sar-
coidosis, requiring liver biopsy for further evaluation (Fig. 20)
[39].
In those patients with cavernous transformation of the portal
vein, serial cross sectional studies have demonstrated hyper-
trophy of the central zones of the liver (segment 1 and 4) and
hypotrophy of the left and right lobes due to the portal hypop-
erfusion of these peripheral areas (Fig. 21) [40].
12. Summary
Both CT and MR provide valuable insights into the extent of
hepatic injury from cirrhosis and complications including por-
G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 69
tal hypertension. Distinction among small hepatic focal lesions
remains challenging, while both CT and MR are quite accu-
rate in detection and characterization of larger (>2 cm) lesions,
including hepatocellular carcinoma. Attention to scan technique
is key, including the use of multiphasic imaging with a rapid IV
bolus of contrast medium.
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