AJR 2004; 183:1595-1601
© American Roentgen Ray Society
CT and MRI of Cirrhosis and its Mimics
Ankur A. Gupta1,
Danny C. Kim,
Glenn A. Krinsky and
Vivian S. Lee
1 All authors: Department of Radiology, New York University Medical Center, 530
First Ave., New York, NY 10016.
Received March 3, 2004;
accepted after revision June 2, 2004.
Address correspondence to V. S. Lee
(vivian.lee{at}med.nyu.edu).
Introduction
Cirrhosis is among the leading causes of death in the western world.
Cirrhosis and its associated complications have characteristic appearances on
CT and MRI that are briefly reviewed. A variety of other disease entities can
mimic cirrhosis. These are discussed and differentiating features
emphasized.
Cirrhosis
Cirrhosis is most commonly caused by chronic hepatitis infection or alcohol
abuse, although a number of other diseases causing hepatic injury can lead to
cirrhosis. It is pathologically defined by three main characteristics:
fibrosis, nodular transformation, and distortion of hepatic architecture.
Subtle morphologic changes of the liver may be among the earliest detectable
with imaging including enlargement of the hilar periportal space, enlargement
of the major interlobar fissure, and expansion of pericholecystic space or
gallbladder fossa. Typically, the anterior segment of the right lobe and
medial segment of the left lobe atrophy, whereas the caudate lobe and left
lateral segment hypertrophy
[1].
The nodular changes in cirrhosis yield characteristic radiologic findings
(Fig. 1A,
1B,
1C). The nodularity is best
seen affecting the liver margin, especially on the left lateral segment.
Micronodular cirrhosis, common in alcoholic liver disease, gives rise to a
fine cobblestone appearance resulting from nodules typically smaller than 3
mm. A grossly nodular liver margin with 3- to 15-mm regenerative nodules is
characteristic of macronodular cirrhosis, more commonly associated with viral
hepatitis.
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Fig. 1A. —33-year-old man with viral cirrhosis. Axial breath-hold
gradient-echo T1-weighted MR image shows diffuse nodules with distinct larger
nodules that are hyperintense to background parenchyma (arrows).
Patient also had evidence of portal hypertension: splenomegaly and esophageal
varices (not shown).
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Fig. 1B. —33-year-old man with viral cirrhosis. Axial breath-hold
T2-weighted turbo STIR MR image shows larger nodules (arrows) are
hypointense. Linear areas of fibrosis (arrowheads) are present.
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Fig. 1C. —33-year-old man with viral cirrhosis. Axial breath-hold
contrast-enhanced fat-suppressed 3D MR image obtained in portal venous phase
shows nodules are now slightly hyperintense to background parenchyma
(arrows). Arterial phase MR images (not shown) failed to show
enhancement of nodules, consistent with diagnosis of either large regenerative
or dysplastic nodules.
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Other changes in cirrhosis include diffuse heterogeneity of the organ on CT
and T1- and T2-weighted MRI. Fibrosis is the predominant cause for hepatic
heterogeneity and appears high in signal intensity on T2-weighted MRI
[1] (Fig.
1A,
1B,
1C). Also, sequelae of portal
hypertension commonly are found and include esophageal varices, ascites,
splenomegaly, hepatofugal portal venous flow, enlargement and tortuosity of
the hepatic artery, and portosystemic vascular shunts. The most significant
complication of cirrhosis is hepatocellular carcinoma (Fig.
2A,
2B). Distinction of benign
regenerative from premalignant dysplastic nodules can be challenging on both
CT and MRI when primarily relying on arterial phase contrast enhancement for
diagnosis. Both regenerative and dysplastic nodules may show homogeneous
hyperenhancement and mimic hepatocellular carcinoma. On MRI, regenerative
nodules appear hypointense on T2-weighted spin-echo images and isointense on
T1-weighted images, although less frequently they can be hypo- or hyperintense
on T1-weighted images. Most dysplastic nodules are not visualized on CT or
MRI. They may appear hyperintense on T1-weighted imaging, but this does not
distinguish them from regenerative nodules.
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Fig. 2A. —53-year-old woman with cirrhosis and hepatocellular
carcinoma. Axial breath-hold T2-weighted turbo STIR MR image shows enlargement
of caudate (arrows). Hepatocellular carcinoma is visible as mildly
hyperintense mass in right lobe (arrowhead).
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Fig. 2B. —53-year-old woman with cirrhosis and hepatocellular
carcinoma. Axial breath-hold contrast-enhanced fat-suppressed 3D MR image
obtained in hepatic arterial dominant phase shows enhancement of
hepatocellular carcinoma (arrowhead).
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Pseudocirrhosis
In patients with cancer metastases to the liver, treatment with
chemotherapy can result in areas of retracted tumor tissue and scarring.
Between areas of scarring, the liver parenchyma is regenerative. This entity
is referred to as pseudocirrhosis because it resembles macronodular cirrhosis.
Common imaging findings include a lobular margin, volume loss caudate
hypertrophy, and portal hypertension and can be observed within a few weeks or
months after therapy [2,
3] (Figs.
3A,
3B,
3C and
4A,
4B,
4C,
4D). Unlike cirrhosis, at
pathology patients do not have bridging portal fibrosis, but can manifest
nodular regenerative hyperplasia. Frequently, patients have a residual tumor
that is difficult to detect given the morphologic abnormalities. The findings
of pseudocirrhosis typically have been described in chemotherapy-treated
patients with metastatic disease in the liver. However, these changes also can
occur without coexistent liver disease, secondary to the hepatotoxic effects
of chemotherapy [3].
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Fig. 3B. —74-year-old woman with metastatic B-cell lymphoma. Axial
portal venous phase CT scan obtained 5 months after chemotherapy with Cytoxan
(cyclophosphamide, Bristol-Myers Squibb), Adriamycin (doxorubicin
hydrochloride, Pharmacia), and vincristine shows near-complete resolution of
previously seen masses but new appearance of volume loss and nodularity of
contour, mimicking cirrhosis.
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Fig. 3C. —74-year-old woman with metastatic B-cell lymphoma. Axial
breath-hold contrast-enhanced fat-suppressed 3D MR image obtained in portal
venous phase shows lobulated contour and areas of linear enhancing fibrosis
(arrows), mimicking cirrhosis.
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Fig. 4C. —51-year-old woman with metastatic breast carcinoma. Axial
breath-hold gradient-echo T1-weighted MR image obtained 7 months after
chemotherapy shows marked regression of masses with morphologic changes
including lobular contour (arrows) and areas of capsular retraction,
mimicking cirrhosis.
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Metastatic Disease
Typically, hepatic metastases appear on MRI as focal lesions that are
hypointense on T1-weighted images and hyperintense on T2-weighted images.
Contrast-enhanced MR images may show peripheral rim enhancement with the
"peripheral washout" sign in the delayed enhancement phases, where
the peripheral rim is hypointense relative to the center of the lesion
[4]. In the setting of
diffusely infiltrative metastatic disease with an associated desmoplastic
reaction, the liver can appear cirrhotic. Without focal lesions, imaging
studies may fail to detect metastases
[4]. Diffuse metastatic
involvement of the liver giving rise to a cirrhotic appearance has been
reported most commonly with breast cancer, although melanoma also has been
reported. Findings include nodular margins, decreased volume, and enlargement
of the caudate lobe [5] (Fig.
5A,
5B). In addition, patients may
present with signs of portal hypertension, including splenomegaly and varices.
Pathologic evaluation of the liver does not show cirrhosis and instead shows
dense areas of fibrosis and diffusely abnormal liver architecture
[4]. Unlike patients with
pseudocirrhosis, the parenchyma is diffusely replaced with viable tumor, with
little healthy liver tissue
[5].
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Fig. 5A. —70-year-old woman with metastatic breast carcinoma. Axial
breath-hold T2-weighted turbo STIR MR image shows lobular contour
(arrows) and innumerable hyperintense metastases
(arrowheads). Morphology of liver resembles that seen in cirrhosis.
Note marked decreased signal intensity of spleen.
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Fig. 5B. —70-year-old woman with metastatic breast carcinoma. Axial
breath-hold contrast-enhanced fat-suppressed 3D MR image obtained in hepatic
arterial dominant phase shows innumerable enhancing liver metastases
(arrowheads) and bone metastasis (arrow).
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Hepatic Necrosis and Regeneration After Fulminant Hepatitis
Fulminant hepatitis is characterized clinically by acute severe impairment
of liver function resulting in hepatic coma within 8 weeks. It usually is
associated with large areas of hepatic necrosis along with inflammation and
hemorrhage [6]. If patients
survive, necrotic areas shrink because of replacement by scarring and
fibrosis, and regenerating nodules appear within weeks (Fig.
6A,
6B). These nodules distort the
liver margin, yielding an appearance of macronodular cirrhosis. Areas of
regenerating liver appear as hypervascular masses on contrast-enhanced
imaging, mimicking hepatocellular carcinoma. The combination of nodularity,
fibrosis, and segmental volume changes may make distinguishing hepatic
necrosis from cirrhosis difficult; however, one clue may be that in hepatic
necrosis, vessels may traverse necrotic lesions without displacement
[6] (Fig.
7A,
7B,
7C). Intraoperatively,
differentiation of hepatic necrosis with regeneration from true cirrhosis is
readily made by palpation; the former results in a soft, pliable liver whereas
the cirrhotic liver is firm.
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Fig. 6A. —59-year-old woman with subacute hepatic necrosis of unknown
cause. Axial breath-hold gradient-echo T1-weighted MR image shows lobular
contour (small arrows) and fibrosis (large arrow), mimicking
cirrhosis.
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Fig. 6B. —59-year-old woman with subacute hepatic necrosis of unknown
cause. Axial breath-hold T2-weighted turbo STIR MR image shows fibrosis is
hyperintense with respect to background hepatic parenchyma
(arrow).
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Fig. 7A. —37-year-old man with fulminant hepatic necrosis secondary to
drug toxicity. Axial breath-hold T2-weighted turbo STIR MR image shows
lobulated contour (arrows) and hyperintense nodule
(arrowhead) that could be confused with hepatocellular carcinoma in
setting of cirrhosis. Marked ascites is present.
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Fig. 7B. —37-year-old man with fulminant hepatic necrosis secondary to
drug toxicity. Axial breath-hold contrast-enhanced fat-suppressed 3D MR image
obtained in hepatic arterial dominant phase shows relative increased
enhancement of posterior right lobe that could be confused with hepatocellular
carcinoma. However, note healthy arteries (arrows) traversing
region.
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Fig. 7C. —37-year-old man with fulminant hepatic necrosis secondary to
drug toxicity. Axial breath-hold contrast-enhanced fat-suppressed 3D MR image
obtained in portal venous phase shows decreased enhancement of areas of
presumed necrosis (arrows). No corresponding areas of focal fat or
sparing were seen on opposed phase MRI (not shown).
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Nodular Regenerative Hyperplasia or Hepatoportal Sclerosis
Noncirrhotic intrahepatic portal hypertension is a nonspecific term that
encompasses a spectrum of disease processes including nodular regenerative
hyperplasia, periportal fibrosis, and hepatoportal sclerosis
[7]. Nodular regenerative
hyperplasia is described histopathologically as regenerative nodules with
little or no hepatic fibrosis and largely healthy hepatic architecture (Fig.
8A,
8B,
8C). Without obvious clinical
manifestations of portal hypertension, the diagnosis usually is detected on
liver biopsy specimens. Periportal fibrosis refers to fibrous enlargement of
the portal tracts with or without extending fibrous septa. Hepatoportal
sclerosis describes a pathologic diagnosis of intimal fibrous thickening of
the portal vein. Each of these processes can occur in tandem and can imitate
cirrhosis on CT and MRI [7,
8]. Imaging may show
heterogeneous hepatic parenchyma, nodular transformation, fibrosis, and
sequelae of portal hypertension (Fig.
8A,
8B,
8C). The nodules in nodular
regenerative hyperplasia may be hypo-, iso-, or hyperintense on T1- and
T2-weighted images, respectively, and may show a peripheral ring of
enhancement, or a halo sign, on T2-weighted imaging, imitating metastatic
tumor or regenerative nodules
[8].
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Fig. 8B. —42-year-old woman with nodular regenerative hyperplasia.
Axial breath-hold T2-weighted turbo STIR MR image shows lobulation and linear
high-signal-intensity areas of fibrosis (arrows).
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Fig. 8C. —42-year-old woman with nodular regenerative hyperplasia.
Axial breath-hold contrast-enhanced fat-suppressed 3D MR image obtained in
equilibrium phase also shows lobulation and enhancing fibrosis
(arrows).
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Conclusion
MRI and CT of the liver are widely used tools for the evaluation of
cirrhosis and its related complications. Among disease entities that can mimic
cirrhosis are chemotherapy-induced cirrhosis (with and without the presence of
metastases), diffuse hepatic metastases, massive hepatic necrosis with
regeneration, and hepatoportal sclerosis or nodular regenerative hyperplasia.
These disease processes should be considered in the differential diagnosis of
a cirrhotic-appearing liver on CT and MRI, particularly in the absence of a
cause for cirrhosis.
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Introduction
Cirrhosis
