Springer Science+Business Media, LLC 2017 Abdom Radiol (2017)

Abdominal DOI: 10.1007/s00261-017-1351-9

Radiology

Hepatic morphology abnormalities: beyond

cirrhosis
Giuseppe Mamone ,1 Kelvin Cortis,2 Aquilina Sarah,2 Settimo Caruso,1
Roberto Miraglia1
1
Radiology Unit, Diagnostic and Therapeutic Services, IRCCS ISMETT (Mediterranean Institute for Transplantation and
Advanced Specialized Therapies), via Tricomi 5, 90127 Palermo, Italy
2
Department of Radiology, Mater Dei Hospital, Msida, Malta

Abstract
The diagnosis of cirrhosis can be reached on the basis of
established hepatic morphological changes. However,
some other conditions can mimic cirrhosis. The aim of
this pictorial essay is to review the CT and MRI
appearances of hepatic morphology abnormalities in the
cirrhotic liver and other diseases, describing pathologic
conditions that can mimic cirrhosis, with useful tips for
the differential diagnosis. Mimickers of cirrhosis include
congenital hepatic brosis, Caroli disease, BuddChiari
Syndrome, hepatoportal sclerosis, cavernous transfor-
mation of the portal vein, pseudocirrhosis from meta-
static disease, acute liver failure, post-therapeutic
morphologic changes in the liver, and infective condi-
tions including schistosomiasis and oriental cholangio-
hepatitis. Recognizing the hepatic morphological
changes in images can help radiologists to diagnose cir-
rhosis and other diseases in early stages.
Key words: Morphological abnormalitiesLiver
CirrhosisMimickers of cirrhosisMagnetic
resonanceComputed tomography
Hepatic morphological abnormalities are seen commonly
on CT or MRI performed in patients with chronic liver
disease. Cirrhosis is the most common chronic liver disease
but certain other liver diseases may present with a pseu-
docirrhotic appearance on imaging and require different
management. The goal of this pictorial essay is to famil-
iarize radiologists with the most common imaging features
seen in cirrhosis and to provide some diagnostic cues
essential in differentiating cirrhosis from other non-cir-
rhotic liver conditions that can mimic cirrhosis (Table 1).
Correspondence to: Giuseppe Mamone; email: gmamone@ismett.edu
Cirrhosis
Cirrhosis is the end-result of chronic diffuse liver disease
from various etiologies. The most common causes are
hepatitis B and C viral infection, chronic alcoholism,
biliary diseases and non-alcoholic fatty liver disease.
Cirrhosis is pathologically characterized by distortion of
hepatic architecture due to extensive hepatic brosis and
nodular regeneration. The main role of the radiologist is
that of evaluating changes in liver morphology and to
identify the various manifestations of portal hyperten-
sion. There are various imaging criteria for the diagnosis
of cirrhosis, including:
morphologic changes in the liver: irregular hepatic
margins, atrophy of the posterior segments of the right
liver lobe and medial segments of the left liver lobe,
hypertrophy of the lateral segments of the left liver
lobe and caudate lobe, increased caudate/right lobe
ratio, increased periportal fat (enlarged hilar space),
expansion of the gallbladder fossa, posterior notch
sign, confluent hepatic fibrosis;
signs of portal hypertension: esophageal and parae-
sophageal varices, gastric fundal varices, recanaliza-
tion of the paraumbilical veins with abdominal wall
collaterals (caput medusae), splenorenal and gastrore-
nal shunts, portosystemic shunting through the hem-
orrhoidal veins, retroperitoneal collaterals (Retzius
veins), and ascites, amongst others.
Irregular hepatic margins
The margins of the liver are normally smooth, but cir-
rhosis often renders them nodular due to the existence of
numerous regeneration nodules [1]. At an early stage of
cirrhosis, the liver may appear normal on cross sectional
imaging. With disease progression, irregular hepatic
 G. Mamone et al.: Hepatic morphology abnormalities

Table 1. Summary table of key findings for the hepatic morphological abnormalities
Findings CIRR CHF CD BCS HS CAV PSEUD ALF PTC SCHIS OC

Irregular hepatic margins + + + +

Hypertrophy of S1 + + + + +
Hypertrophy of S2S3 + + +
Atrophy of S4 + +
Normal sized or hypertrophy of S4 + +
Atrophy of right liver + + +
Peripheral atrophy +
Segmental atrophy + +
Segmental hypertrophy +
Caudate/right lobe ratio +
Expanded gallbladder fossa +
Enlarged hilar periportal space +
Notch sign +
Focal confluent fibrosis +
Signs of portal hypertension + + + + + + + + + + +
Vascular abnormalities + + + +
Regenerative nodules + +
Association with other diseases +
Biliary cystic dilatations + +
Biliary calculi or sludge + +
Central dot sign +
Secondary biliary cirrhosis +
Decreased peripheral enhanc. +
Stronger central enhanc. +
Multiple regenerative nodules +
Perfusion disorders + +
Metastases after chemotherapy +
Fatty enlarged liver +
Subcapsular/periportal wedge-shaped hypo-enhancing regions +
Egg-shell urothelial calcification +
Multiple biliary strictures +
Hepatic peripheral calcification +

CIRR, cirrhosis; CHF, congenital hepatic fibrosis; CD, Caroli disease; BCS, BuddChiari syndrome; HS, hepatoportal sclerosis; CAV, caver-
nomatosis; PSEUD, pseudocirrhosis; ALF, acute liver failure; PTC, post-therapeutic changes; SCHIS, schistosomiasis; OC, oriental cholangio-
hepatitis

Fig. 1. CT images show irregular hepatic margins in a cirrhotic patient.

margins are observed (Fig. 1). The appearance of the
margins of the liver depend on the size of the underlying
regenerative nodules. Margins that are smooth or de-
formed by multiple small nodules are typical in micron-
odular cirrhosis (regenerative nodules < 3 mm). Grossly
lobular margins suggest macronodular cirrhosis (regen-
erative nodules > 3 mm). Lobular liver margins are
found more frequently in patients with primary scleros-
ing cholangitis.
G. Mamone et al.: Hepatic morphology abnormalities
Regional changes (hypertrophy/atrophy)
Regional changes in hepatic morphology typically seen in
advanced cirrhosis are segmental hypertrophy involving
the caudate lobe and the segments (II, III) of the left lobe
and segmental atrophy affecting both the posterior seg-
ments (VI, VII) of the right lobe and the fourth segment
[2] (Fig. 2). Alteration of blood flow is the likely expla-
nation for these morphologic abnormalities.
Caudate/right lobe ratio
Caudate lobe hypertrophy is the most characteristic
morphologic feature of liver cirrhosis (Fig. 3). A ratio of
transverse caudate lobe width to right lobe width greater
than or equal to 0.65, using the main portal vein bifur-
Fig. 2. Typical changes in hepatic morphology in cirrhosis
with atrophy affecting both the right lobe and the fourth seg-
ment (red circle), and hypertrophy involving the caudate lobe
and the left lobe, showed on portal venous phase MR.
Fig. 3. Portal venous phase MR images show the increased caudate/right lobe ratio in cirrhotic patient proposed by Harbin
(A) and Awaya (B).
cation as a landmark between the two lobes, constitutes a
positive indicator for the diagnosis of cirrhosis with high
level of accuracy [3]. A modified caudate lobe width to
right lobe width ratio, using the bifurcation of the right
portal vein instead of the main portal vein to set the
lateral boundary, has been proposed by Awaya [4]. In
fact, the authors have noted that the hypertrophied
caudate lobe extended beyond the main portal vein
bifurcation. A ratio greater than 0.90 suggested a diag-
nosis of cirrhosis.
Expanded gallbladder fossa sign
Normally, the gallbladder is located on the visceral sur-
face of the liver in a fossa between the right hepatic lobe
and the medial segment of the left hepatic lobe. The
pericholecystic space is often enlarged in patients with
cirrhosis due to the presence of fat, with a resultant
expanded gallbladder fossa sign [5]. This sign is con-
sidered present if there is enlargement of the perichole-
cystic space and the space is bound laterally by the edge
of the right hepatic lobe and medially by the edge of the
segments II and III without the IVth segment (Fig. 4).
The expanded gallbladder fossa sign in cirrhotic livers
may depend on four factors: (a) atrophy of the IVth
segment, (b) hypertrophy of the caudate lobe, (c) atrophy
of the right hepatic lobe (mainly the anterior segment)
and (d) enlargement of the lateral segment of the left
hepatic lobe especially in the cephalocaudal direction.
Enlarged hilar periportal space
In the normal physiological state, the anterior space of
the right portal vein (hilar periportal space) is narrow,
containing minimal fatty tissue. In patients with early
cirrhosis, the hilar periportal space is enlarged given the
presence of periportal fat, which might be a consequence
 G. Mamone et al.: Hepatic morphology abnormalities

Fig. 4. Portal venous phase MR images exhibit a normal gallbladder fossa in healthy patient (A) and an expanded gallbladder
fossa sign (white arrows) in patient with cirrhosis (B).

Fig. 5. MR and CT imaging showing, respectively, a normal hilar periportal space in healthy patient (A) and an enlarged hilar
periportal space (red lines) in patients with early cirrhosis (B).

of atrophy of the medial segment of the left hepatic lobe
[6] (Fig. 5). The exact mechanism of atrophy of the IVth
segment is not understood fully. However, the most
likely cause of this atrophy may be portal venous
hypoperfusion based on anatomical variations in blood
supply to this segment. A cutoff value of 10 mm (defined
as a distance between the right portal vein and the pos-
terior edge of segment IV) had a sensitivity of 93%, a
specificity of 92%, an accuracy of 92% and a positive
predictive value of 91% for a diagnosis of early cirrhosis.
Notch sign
In the normal liver, the right posteromedial capsular
surface is concave due to the right renal impression. In
cirrhosis, the notch sign is a sharp indentation in the
right medial posterior liver surface and it probably cor-
responds to the functional boundary between the
hypertrophied caudate lobe and the atrophied right
posterior segment of the liver [7] (Fig. 6).
Focal conuent brosis
Focal conuent brosis is observed as a wedge-shaped
region located in the subcapsular portion of segment
IV, V, or VIII, with associated capsular retraction [8
10] (Fig. 7). In those rare cases in which the lesion
shows enhancement in arterial phase, it may be mis-
taken for hepatocellular carcinoma. Delayed, persistent
contrast enhancement, however, is typically observed
with the use of extracellular MRI contrast agents, and
is due to the retention of contrast by the fibrotic tis-
sue. This feature, along with the characteristic capsular
retraction and typical location and shape help to dis-
tinguish confluent fibrosis from hepatocellular carci-
noma.
G. Mamone et al.: Hepatic morphology abnormalities

Fig. 6. CT image exhibits that in normal liver, the right medial posterior liver surface is concave due to the right renal
impression (A). In cirrhotic liver, the notch sign (white arrow) is a sharp indentation in the right medial posterior liver surface (B).

Fig. 7. MR appearance of focal confluent fibrosis observed circle). Typically it doesnt show enhancement on arterial
on T2-w (A), arterial phase (B), and late phase (C). Notice the phase and exhibits delayed persistent contrast enhancement
wedge morphology with associated capsular retraction (red on late phases (white arrows).

Signs of portal hypertension temic collateral vessels (signs of portal hypertension)

include:
In chronic liver disease, progressive hepatic brosis leads
to increased vascular resistance at the sinusoidal level Esophageal and paraesophageal varices, gastric fundal
with portal hypertension and related complications such varices, coronary vein;
as ascites and the development of engorged and tortuous splenorenal shunt, gastrorenal shunt, perigastric, and
portosystemic collateral vessels (Figs. 8, 9, 10, 11). In perisplenic collaterals;
portal hypertension, the hepatopetal blood flow is re- paraumbilical veins, abdominal wall collaterals (caput
routed away from the liver through collateral pathways medusae);
to low-pressure systemic vessels. Among these collateral omental and mesenteric varices;
pathways, esophageal varices are the most important diaphragmatic and pericardiacophrenic veins;
clinically because they are a frequent source of gas- hemorrhoidal veins;
trointestinal bleeding. Information about other collateral retroperitoneal-paravertebral collaterals (veins of Ret-
pathways is also relevant, especially when interventional zius);
procedures or surgery is contemplated, because inad- mesenteric edema with resultant portal hypertensive
vertent disruption of these veins can cause significant enteropathy;
bleeding with potentially fatal consequences. Portosys- splenomegaly and ascites.

Fig. 8. CT images show esophageal and paraesophageal varices (A), coronary vein (B), splenorenal shunt and perisplenic
collaterals (C), and gastric fundus varices and gastrorenal shunt (D).
Congenital hepatic fibrosis
Congenital hepatic brosis is a developmental disorder
and part of the spectrum of hepatic ductal plate mal-
formations. This condition is characterized histologically
by a variable degree of periportal brosis and irregularly
shaped proliferating bile ducts. 50% of patients with
congenital hepatic brosis have one or more associated
congenital abnormalities of the biliary tree (Caroli dis-
ease, biliary hamartomas, choledochal cysts), as all these
conditions belong to the same spectrum of ductal plate
malformations. Moreover, there is an association with
congenital renal abnormalities (polycystic renal disease,
parenchymal calcications, parenchymal atrophy, and
medullary sponge kidney disease). CT and MR ndings
in congenital hepatic brosis [11, 12] are shown on
Fig. 12. Hypertrophy of the left lateral segments and
caudate lobe, normal sized or hypertrophy of left medial
segment (IV) and atrophy of the right lobe are typical
findings.
Atrophy of the right lobe and hypertrophy of the left
lateral segment and caudate lobe are common both in
patients with congenital hepatic brosis and in those with
advanced viral or alcoholic cirrhosis; however, the
G. Mamone et al.: Hepatic morphology abnormalities
medial segment (IV) is normal in size or enlarged, a
morphologic nding that may be useful in distinguishing
congenital hepatic brosis from conventional cirrhosis.
Vascular abnormalities are described such as enlarged
hepatic artery or a tangle of abnormally numerous
arterial vessels at the liver hilum, and portal vein
thrombosis with or without cavernomatosis. Large
regenerative nodules can be present with the following
features: range 530 mm, multiple lesions, homoge-
neously hyperattenuating on hepatic arterial and portal
venous phase. They can be viewed as a response to a
focal loss of portal perfusion and hyperarterialization.
Signs of portal hypertension are common with varices,
splenorenal shunt, splenomegaly and ascites.
Caroli disease
Caroli disease is also a ductal plate malformations and is
characterized by multifocal segmental dilatation of the
large intrahepatic bile ducts, which retain their commu-
nication with the biliary tree. Two types of Caroli disease
are described in the literature: Caroli disease proper
(pure form), which is caused by arrested remodeling of
the ductal plates of the larger intrahepatic ducts, and
G. Mamone et al.: Hepatic morphology abnormalities
Fig. 9. CT and MR images show paraumbilical vein (A), splenomegaly and ascites (B), and abdominal wall collaterals or caput
medusae (C,D).
Caroli syndrome (i.e., Caroli disease with congenital
hepatic brosis), in which the arrest of remodeling occurs
both in the early period of bile duct embryogenesis and
later during the development of the more peripheral
biliary ramications. Caroli disease typically manifests
with saccular or fusiform cystic dilatations of the intra-
hepatic bile ducts of up to 5 cm in diameter, often con-
taining calculi or sludge [12, 13] (Fig. 13). Contrast-
enhanced CT or gadolinium-enhanced MR imaging of
the liver often shows fibrovascular bundles with strong
contrast enhancement within dilated cystic intrahepatic
ducts. This finding called central dot sign corresponds
to vascular branches (arterial and portal vein branches)
protruding into the lumen of a dilated bile duct. MR
cholangiography is capable of noninvasively demon-
strating the communication between the cystic dilata-
tions and the biliary tree, thus helping rule out conditions
such as polycystic liver disease and biliary hamartomas.
Complications in Caroli disease are mostly due to bile
stagnation, which leads to cholangitis, stone formation
(predominantly bilirubin), jaundice, and liver abscesses.
In Caroli syndrome, cystic biliary dilatation along with
congenital hepatic fibrosis, portal hypertension, and
hematemesis due to ruptured esophageal varices are
more likely to be seen at presentation than are cholan-
gitis or jaundice. Secondary biliary cirrhosis can occur
due to biliary obstruction. Malignancy has been de-
scribed as a complication; cholangiocarcinomas have
been reported, with a prevalence of 7%.
BuddChiari syndrome
The term BuddChiari syndrome is applied to the clinical
manifestations of hepatic venous outow obstruction at
any level from the small hepatic veins to the junction of
the inferior vena cava and the right atrium regardless of
the cause of obstruction. Presentation varies depending
on the chronicity of the disease (acute, subacute, or
chronic) [14]. BuddChiari syndrome can be classified
into primary or secondary.
Acute BuddChiari syndrome
A diffusely enlarged liver with normal morphology is
seen at this stage, with occlusion of the hepatic veins with
ascites and splenomegaly are the typical finding. The liver
exhibits patchy, decreased peripheral enhancement caused
by portal and sinusoidal stasis and stronger enhancement

Fig. 10. CT and MR imaging of mesenteric varices (A), hemorrhoidal veins (B), mesenteric edema (C), and omental varices (D).
of the central portion of the liver parenchyma. MR ima-
ges obtained with T2-weighted sequences usually show
heterogeneously increased signal intensity in the periph-
eral portion of the liver. The caudate lobe exhibits nor-
mal or increased enhancement.
Subacute or chronic BuddChiari syndrome
The inferior vena cava can be compressed by the en-
larged caudate lobe. The morphologic changes in the
liver are the result of the type of venous involvement,
and portosystemic and intrahepatic collateral vessels are
often found. The diameter of the hepatic artery is usu-
ally enlarged compared with that of the splenic artery.
Portal vein thrombosis can develop. Chronic Budd
Chiari syndrome is also characterized by the develop-
ment of multiple regenerative nodules, which can be
viewed as a response to a focal loss of portal perfusion
and hyperarterialization. These nodules are hypervas-
cular on arterial phase images without wash-out; this
feature distinguishes them from hepatocellular carci-
G. Mamone et al.: Hepatic morphology abnormalities
noma. The above mentioned findings are showed on
Fig. 14.
Hepatoportal sclerosis
Hepatoportal sclerosis (HS), also known as idiopathic
portal hypertension or obliterative portal venopathy, is
one of the diseases that most closely mimics cirrhosis
(Fig. 15) because portal hypertension is a key finding
and in advanced cases and the morphological changes of
the liver are indistinguishable from those of cirrhosis [15,
16]. The primary lesions of HS are in the portal tracts,
which show varying degrees of thrombosis, fibrosis, and
sclerosis of portal vein branches. This disease also in-
cludes a spectrum of entities, such as nodular regenera-
tive hyperplasia. Most patients manifest morphologic
changes in the liver and in 25% of the cases they are
similar to those observed in cirrhosis (atrophy of right
lobe and segment IV and hypertrophy of caudate lobe and
left lobe). Certain findings help differentiate obliterative
portal venopathy and cirrhosis: intra- or extrahepatic
portal vein anomalies (complete or partial thrombosis,
G. Mamone et al.: Hepatic morphology abnormalities

Fig. 11. CT MIP and VR reconstruction images demonstrating mesenteric-caval shunt (A), Retzius veins (B), diaphragmatic
vein (C), and pericardiacophrenic vein (D).

Fig. 12. Axial CT and MRI images showing hepatic mor- the hypertrophy of the left lobe and the atrophy of the right liver
phology abnormalities in some cases of congenital hepatic lobe, the coronary vein (arrow) and the association with Caroli
fibrosis. Notice the enlargement of the forth segment (red lines), disease and medullary sponge kidneys (white circles).
 G. Mamone et al.: Hepatic morphology abnormalities

Fig. 13. CT and MRI images showing hepatic morphology arrows), in a patients with Carolis disease. The first row of
changes and multifocal large cystic dilatations of segmental images shows coexistence of multiple stones (red arrows)
intrahepatic bile ducts with the classic central dot sign (white inside the cystic dilatations.

Fig. 14. MR images show the typical findings of BuddChiari artery (yellow arrowhead), hypervascular regenerative nodules
syndrome: occlusion of the hepatic veins (red arrows), central (white arrowhead), presence of intrahepatic venous shunt (red
liver enhancement (red line), changes in hepatic morphology arrowhead), and signs of portal hypertension (splenomegaly
with caudate lobe enlargement (yellow line), enlarged hepatic and caput medusae: red asterisk and white arrow).
G. Mamone et al.: Hepatic morphology abnormalities
Fig. 15. Hepatoportal sclerosis with resultant non-cirrhotic
portal hypertension signs as coronary vein (red arrow), eso-
phageal varices (white arrowhead), and splenomegaly (red
Fig. 16. Axial contrast-enhanced CT images demonstrat-
ing cavernous transformation of the portal vein at the liver
hilum (arrows), atrophy of the left lateral segments (II and
stenosis or lack of visibility, and mural calcifications) are
mainly observed in patients with obliterative portal
venopathy (71%), whereas a nodular liver surface is rarely
found. Nodular regenerative hyperplasia (RNH) is a
common histologic finding in patients with HS. These
lesions are known to be a response to hemodynamic
disturbances from decreased portal venous inflow and
increased arterial inflow. Other liver nodules are rarely
described; only few cases of hepatocellular carcinoma in
patients with HS have been reported. An enlarged hepatic
artery or several arteries at the hilum were identified in
45% of patients. The parenchyma can be heterogeneous
with perfusion disorders.
asterisk). Hypertrophy of the left liver lobe and the segment IV
is seen (yellow line), in the absence of capsular nodularity.
Notice the enlargement of the hepatic artery (white arrow).
III), hypertrophy of the fourth segment, and caudate lobe
(central hypertrophy), without nodularity of the hepatic
margins.
Signs of portal hypertension were seen at diagnosis at
CT o MR in nearly all patients with HS.
Cavernous transformation
of the portal vein
Cavernous transformation of the portal vein occurs in a
proportion of patients with portal vein thrombosis. This
is manifested as formation of extensive pericholedochal
collaterals that attempt to preserve hepatopetal ow
(from the splanchnic veins to the intrahepatic portal
veins). These collaterals are formed from the parachole-
dochal and epicholedochal plexi of Petren and Saint,

Fig. 17. Elderly lady with a history of metastatic breast
cancer treated with multiple chemotherapeutic agents. Axial
and coronal contrast-enhanced CT images demonstrating an
irregular, nodular liver contour with capsular retraction, seg-
mental atrophy. No secondary signs of portal hypertension
are demonstrated in this case.
Fig. 18. Axial CT images demonstrating 3 cases of acute
liver failure. The first case shows a normal liver morphol-
ogy with splenomegaly and ascites. The second case
G. Mamone et al.: Hepatic morphology abnormalities
respectively, which dilate in an attempt to bypass the
thrombosed portal vein.
Atrophy of the right liver, hypertrophy of the caudate
lobe, and signs of portal hypertension are confusing and
can mimic cirrhosis [17, 18] (Fig. 16). However, the at-
rophy-hypertrophy complex is different from cirrhosis
because hypertrophy is central (segment 4 and the cau-
date lobe) as a result of maintained portal inflow and
peripheral atrophy (right liver and left liver lobe).
Moreover, nodularity of the hepatic contour is usually not
present. Imaging features also include direct signs of
complete portal vein obstruction with lack of enhance-
ment of the main portal vein and venous collaterals in the
porta hepatis (cavernoma) on contrast-enhanced CT and
MR images.
Pseudocirrhosis
Diffuse morphologic changes of the liver may also be
found in patients with liver metastases (in particular
hepatic metastatic disease from breast cancer), especially
after chemotherapy [19, 20]. This condition is called
hepar lobatum or more recently pseudocirrhosis.
While it was initially described almost exclusively in
patients with liver metastases from breast cancer, pseu-
docirrhosis has now been observed in patients with eso-
phageal cancer, pancreatic cancer, thyroid cancer, and
colorectal cancer. The pathophysiologic mechanism has
not yet been elucidated. It could be due to tumor
shrinkage and subsequent severe desmoplastic fibrosis
around the liver metastases and/or nodular regenerative
shows a fatty enlarged liver with regular margins. The third
case shows a liver with irregular margins and ascites,
simulating cirrhosis.
G. Mamone et al.: Hepatic morphology abnormalities
Fig. 19. MR image demonstrating hepatic morphology
changes after partial right hepatic resection, with compen-
satory hypertrophy of the left lobe (A). CT images show
Fig. 20. Axial CT image of the liver shows multiple periph-
eral subcapsular and periportal wedge-shaped hypo-en-
hancing regions (white arrows) in association with capsular
retraction, in patient with schistosomiasis. Axial image from a
non-contrast CT shows a calculus in the distal right ureter and
egg-shell urothelial calcification in the ureters and the urinary
bladder (red arrows).
hyperplasia in response to chemotherapy. Interestingly, it
is often observed in patients with a major morphologic
response to chemotherapy. Imaging findings include
hypertrophy of the left lobe and atrophy of the right lobe, after
embolization with coils (arrows) of the right portal branches, in
patient with cholangiocarcinoma (B).
segmental atrophy with frequent enlargement of the cau-
date lobe and nodular liver surface related to multifocal
capsular retraction (Fig. 17). The key to the diagnosis is a
clinical history and normal liver imaging results at prior
examinations. These patients had various degrees of liver
contour abnormalities, from limited retraction to diffuse
nodularity. Moreover, 9% of these patients developed
portal hypertension. These changes may develop rapidly
after a median follow-up of 15 months. Radiologists
should be aware of this entity and of the potential
implicationsanticancer therapy should be modified and
sometimes interrupted in these patients. The imaging
findings in pseudocirrhosis have been shown to com-
pletely resolve in some patients.
Acute liver failure
Acute liver failure, a very severe disease with a high risk
of spontaneous mortality, is characterized by the onset of
hepatic encephalopathy from severe acute liver injury in
the absence of pre-existing liver disease. The prognosis
has dramatically changed with orthotopic liver trans-
plantation, so it is crucial to assess the absence of chronic
liver disease in these patients. Percutaneous liver biopsy
is often contraindicated as these patients commonly have
impaired coagulation. In patients with acute liver failure,
the liver morphology is normal or is possible to see an
enlarged fatty liver. Portal hypertension is seen in most
patients with acute liver injury, and ascites is common.
Occasionally, imaging findings can mimic cirrhosis [21,
22] (Fig. 18)., In fact, liver atrophy and liver surface
nodularity (up to 43%) can be seen in these patients
especially in those who have been ill for more than
7 days. This is thought to be due to confluent regenera-
tive nodules and massive necrosis. Indeed, both radiol-
ogists and hepatologists should be aware of this and be
careful not to misdiagnose cirrhosis because patients
with acute liver failure can receive higher priority on
transplantation waiting lists. On the other hand, incor-

Fig. 21. Non-contrast CT image (A) shows diffuse saccular
biliary dilatation and intraductal calculi (white arrow) with
peripheral calcification in patient with oriental cholangiohep-
atitis. Similar findings are seen on a selected axial T2
rect prioritization (listing a patient as having fulminant
hepatic failure whose explant is shown to have underly-
ing cirrhosis) can have serious consequences. The clinical
background, a negative hepatitis B or C virus serology,
or no history of alcohol abuse favors a diagnosis of acute
liver failure.
Post-therapeutic morphologic
changes
Morphologic changes may also be induced in the liver by
the treatment of liver tumors [23, 24]. Indeed, hypertro-
phy of the remnant liver segments is seen after major liver
resection (resection of at least three liver segments).
Nonsurgical liver-directed therapy can also cause mor-
phologic changes (Fig. 19).
In particular, selective intraarterial radiation
therapy (also known as radioembolization) and
portal vein embolization can result in signicant
changes with marked atrophy of the treated liver and
hypertrophy of the contralateral lobe. These tech-
niques are used for the treatment of hepatocellular
carcinoma, cholangiocarcinoma, and liver metas-
tases.
The increase in size in the nontreated liver regions
may increase resectability as future liver remnant liver
volume is increased, so these techniques can be used as a
bridge to major resection, stimulating hypertrophy in the
contralateral lobe.
G. Mamone et al.: Hepatic morphology abnormalities
weighted MRI image (B). MRCP (C) shows the extent of bil-
iary tree involvement with intra and extrahepatic biliary
dilatation, and multiple strictures (red arrows) mostly involving
the first and second order bile ducts.
Signs of portal hypertension with splenomegaly are
found in some patients.
It is easy for radiologists and clinicians to recognize
this entity based on the patients history.
Infective diseases
Parasitic infections can result in hepatic morphological
changes; these include schistosomiasis and oriental
cholangiohepatitis [25].
Schistosomiasis is an infection of trematodes, Schisto-
soma, causing periportal fibrosis, and liver cirrhosis due to
deposition of eggs in the small portal venules. Hepatos-
plenomegaly, liver cirrhosis, portal hypertension, and
gastroesophageal varices are commonly associated.
Imaging findings of the liver are multiple peripheral sub-
capsular and periportal wedge-shaped hypo-enhancing re-
gions in association with capsular retraction (Fig. 20);
these findings are in keeping with periportal and
parenchymal fibrosis. These fibrotic bands occur sec-
ondary to embolisation of schistosome eggs from the
mesenteric vein into the portal vein radicles, with a resul-
tant granulomatous inflammatory response, that leads to
fibrosis and, in certain instances, presinusoidal portal
hypertension. Egg-shell urothelial calcification may be
noted throughout the ureters and the urinary bladder.
Oriental cholangiohepatitis (OCH), also called recur-
rent pyogenic cholangitis, is secondary to Clonorchis
sinensis infection and it is characterized by intrahepatic
G. Mamone et al.: Hepatic morphology abnormalities
duct calculi, strictures, and recurrent infections. It is seen
almost exclusively in South East Asia. Cirrhosis with
portal hypertension may occur as a long-term compli-
cation of OCH and it may be complicated by hepato-
cellular carcinoma. Cholangiocarcinoma complicates
about 5% cases of OCH. Imaging features of the liver are
diffuse saccular biliary dilatation with intraductal calculi,
peripheral calcification, and multiple strictures mostly
involving the first and second order bile ducts (Fig. 21).
Conclusion
Interpretation of morphological hepatic alterations can
provide vital clues towards establishing a differential
diagnosis in patients with chronic liver disease. Cirrhosis
is the most common chronic liver disease but certain
other liver diseases may have a pseudocirrhotic appear-
ance on imaging and require different management.
Hepatic morphology abnormalities are commonly seen
on CT and MRI; although these ndings are not specic,
a knowledge of the possible aetiological factors may
facilitate recognition of the underlying diagnosis.
Compliance with ethical standards
Financial support We declare no financial support.
Conflict of interest We declare no conflict of interest.
Institutional review board statement and informed consent
statement The Institutional Research Review Board reviewed and
approved this article, with waiver of the informed consent; a written
informed consent to the MR and CT procedures was obtained after a
full explanation of the purpose and nature of the procedure.
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