AJR 2000; 174:705-712
© American Roentgen Ray Society
CT of Focal Nodular Hyperplasia of the Liver
Stephanie K. Carlson1,
C. Daniel Johnson,
Claire E. Bender and
Timothy J. Welch
1
All authors: Department of Diagnostic Radiology, Mayo Clinic and Mayo
Foundation, 200 First St., S.W., Rochester, MN 55905.
Received June 28, 1999;
accepted after revision August 9, 1999.
Presented at the annual meeting of the American Roentgen Ray Society, New
Orleans, May 1999.
Address correspondence to S. K. Carlson.
Introduction
Focal nodular hyperplasia of the liver is a benign vascular neoplasm that
can occur in men and women of any age but is most often found in young women
[1]. Focal nodular hyperplasia
is typically an incidental discovery during radiologic imaging performed for
other reasons. Although considered a rare neoplasm, focal nodular hyperplasia
is the second most common benign liver tumor after hemangioma
[2] and has a reported
frequency of 3% in adults [3].
With the increasing use and improvement of fast scanning techniques, focal
nodular hyperplasia is being detected more often. These lesions, particularly
in patients with a known malignancy, pose a diagnostic dilemma. Familiarity
with the spectrum of CT findings of focal nodular hyperplasia is important so
that accurate and efficient diagnoses are made. Such familiarity may help to
avoid unnecessary testing, expense, concern, biopsy, or surgery.
Methods
We performed a retrospective review of 45 consecutive patients with focal
nodular hyperplasia. All patients underwent contrast-enhanced CT at our
institution between January 1990 and January 1999. Proof of diagnosis included
percutaneous biopsy (16 patients), surgical biopsy or resection (five
patients), further confirmatory imaging (Tc—sulfur colloid radionuclide
scanning, MR imaging, or sonography), and clinical follow-up documenting
lesion stability for a minimum of 2 years (24 patients). Lesions were analyzed
for unenhanced attenuation, calcification, dynamic enhancement pattern,
peripheral vascularity, and the presence and enhancement pattern of a central
scar. The study was approved by the institutional review board.
Demographics
Thirty-seven females and eight males were included in our study (age range,
15-75 years; mean, 41 years). Thirty-seven (82%) of 45 patients were
asymptomatic. Of these patients, two had palpable masses. The remaining eight
patients complained of mild intermittent right upper quadrant pain. Tumor size
ranged from 1.5 to 11.0 cm (mean, 4.7 cm).
Tumor Biology
The microscopic and gross pathologic features of focal nodular hyperplasia
are important because they explain the CT features of this tumor. Focal
nodular hyperplasia is believed to originate in utero as an arteriovenous
malformation in the liver. The localized enriched blood supply stimulates the
growth of normal hepatic elements. Focal nodular hyperplasia is a lobulated
well-circumscribed tumorlike hypervascular solid mass histologically
characterized by a proliferation of hepatocytes, bile ductules, Kupffer's
cells, and blood vessels arranged in an abnormal pattern
[4]. The multiple nodules of
hyperplastic hepatocytes are divided by fibrous septa that may or may not
radiate from a central fibrous scar (Fig.
1). These lesions are unencapsulated, and compression fibrosis of
the adjacent liver is rare. Bile ductules and abnormally enlarged arterial
vessels are prominent throughout the scar and septa that extend from the
central portion of the lesion to the periphery
(Fig. 2). These vessels explain
the marked arterial blush seen on angiography
(Fig. 3).
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Fig. 1. —35-year-old woman with focal nodular hyperplasia. Cut section shows
lobulated nodular hepatic parenchyma with variable congestion and septate
fibrosis radiating from white central stellate scar.
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Fig. 2. —42-year-old woman with focal nodular hyperplasia. Photomicrograph
shows stellate scar with radiating fibrous septa (arrows). Multiple
enlarged vessels (arrowheads) course through central scar and extend
along septa to periphery. Note ductular proliferation at periphery of septa.
Involved hepatic parenchyma have vaguely nodular architecture.
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Fig. 3. —36-year-old woman with focal nodular hyperplasia. Selective hepatic
arteriogram shows hypervascular mass (short arrows) with dense
homogeneous stain on arterial phase imaging. Mass is centrally supplied by
enlarged right hepatic artery (long arrow). Note vessels radiating in
spoke-wheel pattern from periphery to center of tumor.
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Unenhanced Imaging
Most focal nodular hyperplasias are isodense or slightly hypodense to the
liver on unenhanced CT. When isodense to the liver, the lesions may be
detectable only because of mass effect (Fig.
4A,4B),
or the presence of a low-attenuation central scar, or they may be invisible
(Fig.
5A,5B).
In our series, unenhanced images were obtained for 33 patients. The tumors
were hypodense to the liver in 14 patients (42%), isodense in 16 patients
(48%), and hyperdense in three patients (9%) (all lesions were found in
diffusely fatty infiltrated livers). Nine patients (27%) had visible
low-attenuation central scars. Typically, focal nodular hyperplasias are well
circumscribed and rarely contain calcification. In our study, all tumors were
well circumscribed and calcification was seen in one patient (two flecks of
calcification in the central portion of the tumor).
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Fig. 4A. —39-year-old asymptomatic woman with incidentally discovered focal
nodular hyperplasia in left hepatic lobe. Unenhanced CT scan shows large mass
(arrows) involving entire medial segment of left lobe. Mass is
slightly hypodense to liver.
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Fig. 4B. —39-year-old asymptomatic woman with incidentally discovered focal
nodular hyperplasia in left hepatic lobe. Portal venous phase CT scan shows
homogeneously enhancing mass that is isodense to liver. In certain patients,
lesions that are isoattenuating to liver on unenhanced or portal venous phase
CT may be detectable only because of mass effect.
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Fig. 5B. —47-year-old asymptomatic woman with 2-cm focal nodular hyperplasia
in right hepatic lobe. Arterial phase CT scan at same level as A shows
small early homogeneously enhancing mass (arrow) consistent with
focal nodular hyperplasia. Such stealth lesions are often invisible on
unenhanced CT and may be detectable only during arterial-dominant phase of
contrast enhancement.
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Contrast-Enhanced Imaging
Technique
The ideal technique for the CT evaluation of suspected focal nodular
hyperplasia is a biphasic helical examination with images obtained during the
arterial and portal venous phases. Delayed scans (2-5 min after contrast
injection) may display delayed fill-in of a central scar or a capsulelike rim
of retained contrast material. If adenoma or hepatocellular carcinoma is
suspected (pain, signs of hemorrhage, history of liver disease), unenhanced
images are beneficial to reveal hemorrhage, intratumoral fat, and
calcification. Such features are not typical of focal nodular hyperplasia.
Tumoral Enhancement
The typical contrast enhancement pattern of focal nodular hyperplasia is
diffuse immediate homogeneous hyperdense enhancement on early phases (arterial
and early portal venous) with rapid washout of contrast material becoming
isodense to the liver on late portal venous and delayed images (Figs.
5A,5B,6A,6B,7A,7B,7C,8).
This pattern was noted in 40 tumors (89%). Homogeneous enhancement is caused
by the uniform internal architecture of the tumor. Intratumoral necrosis and
hemorrhage are rare findings. The dynamic enhancement pattern is caused by the
rich arterial blood supply and large draining veins and sinusoids in the
periphery of the tumor. These veins and sinusoids allow rapid washin and
washout phases during contrast-enhanced CT.
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Fig. 6A. —29-year-old asymptomatic woman with biopsy-proven focal nodular
hyperplasia. Late arterial phase (A) and portal venous phase (B)
CT scans show small well-circumscribed rapidly and homogeneously enhancing
mass in dome of liver. Note rapid washout of tumoral contrast enhancement.
Images were obtained 35 sec apart.
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Fig. 6B. —29-year-old asymptomatic woman with biopsy-proven focal nodular
hyperplasia. Late arterial phase (A) and portal venous phase (B)
CT scans show small well-circumscribed rapidly and homogeneously enhancing
mass in dome of liver. Note rapid washout of tumoral contrast enhancement.
Images were obtained 35 sec apart.
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Fig. 7A. —30-year-old asymptomatic man with incidentally discovered focal
nodular hyperplasia in left hepatic lobe. Arterial phase CT scan shows 2-cm
hypervascular well-circumscribed homogeneously enhancing mass (arrow)
in lateral segment of left hepatic lobe anteriorly.
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Fig. 7B. —30-year-old asymptomatic man with incidentally discovered focal
nodular hyperplasia in left hepatic lobe. Portal venous phase CT scan shows
continued increased attenuation of mass relative to liver.
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Fig. 7C. —30-year-old asymptomatic man with incidentally discovered focal
nodular hyperplasia in left hepatic lobe. Delayed CT scan (approximately 2 min
after IV contrast material injection) shows progressive washout of contrast
material from mass (which remains minimally hyperdense to liver). Immediate
marked homogeneous transient enhancement with rapid washout after bolus
injection is characteristic of focal nodular hyperplasia.
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Fig. 8. —68-year-old man with biopsy-proven focal nodular hyperplasia and
history of transitional cell carcinoma of bladder. Late arterial phase CT scan
shows well-circumscribed hypervascular homogeneously enhancing mass in dome of
liver. Note enlarged peripheral vessels (arrows). Findings are
typical of focal nodular hyperplasia.
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Peripheral Vascularity
On late portal venous and delayed images, peripheral vascularity that may
mimic capsular enhancement is often seen surrounding focal nodular
hyperplasias (Figs.
9A,9B,9C,9D,10,11).
This finding corresponds to enlarged vessels or sinusoids in the periphery of
the tumor. These large peripheral draining vessels have been documented on
color Doppler sonography [5].
Usually, these vessels appear as an incomplete rim of blood density contrast
around the focal mass. The capsules associated with hepatocellular carcinoma
and adenoma are enhancing true fibrous capsules that often completely
encompass the mass. Peripheral rimlike vascularity was seen in 17 (38%) of 45
patients and was thin and incomplete in nearly all patients.
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Fig. 9A —30-year-old asymptomatic woman. Early (A) and late (B)
arterial phase CT scans (at two different levels) show typical focal nodular
hyperplasia. Note enlarged feeding artery (straight arrow),
low-attenuation scar (curved arrow, B), and multiple areas of
peripheral vascularity (arrowheads) that correspond to enlarged
tumoral vessels or sinusoids.
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Fig. 9B. —30-year-old asymptomatic woman. Early (A) and late (B)
arterial phase CT scans (at two different levels) show typical focal nodular
hyperplasia. Note enlarged feeding artery (straight arrow),
low-attenuation scar (curved arrow, B), and multiple areas of
peripheral vascularity (arrowheads) that correspond to enlarged
tumoral vessels or sinusoids.
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Fig. 9C —30-year-old asymptomatic woman. Portal venous phase CT scans (at
same levels as A and B, respectively) show rapid washout of
contrast material because of arteriovenous shunting. Note persistent rim of
peripheral vascularity.
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Fig. 9D. —30-year-old asymptomatic woman. Portal venous phase CT scans (at
same levels as A and B, respectively) show rapid washout of
contrast material because of arteriovenous shunting. Note persistent rim of
peripheral vascularity.
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Fig. 10. —39-year-old woman with biopsy-proven focal nodular hyperplasia.
Delayed CT scan shows capsulelike peripheral vascularity (arrows).
Central portion of tumor is homogeneous and isodense to liver. Peripheral
vascular channels may be only clue to presence of focal nodular hyperplasia on
portal venous phase and delayed CT images.
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Fig. 11. —33-year-old woman with histologically proven focal nodular
hyperplasia. Late arterial phase CT scan shows large well-circumscribed
homogeneously enhancing mass that is hyperdense to liver. Note classic
low-attenuation central scar and areas of peripheral vascularity
(arrowheads).
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Enlarged Feeding Artery
Focal nodular hyperplasia is thought to be a hyperplastic hepatocellular
response to increased arterial perfusion from an underlying congenital
vascular malformation [4].
Angiographically, these tumors are supplied by an abnormally enlarged hepatic
artery. This anomalous artery can often be identified if images are obtained
during the arterial phase of contrast enhancement (Figs.
8,
9A,9B,9C,9D,
and
12A,12B).
In our series, arterial phase images were obtained in eight patients, and an
enlarged feeding artery was revealed in five patients (63%).
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Fig. 12A. —39-year-old woman with mild intermittent right upper quadrant pain
and multiple sites of biopsy-proven focal nodular hyperplasia. Arterial phase
CT scan shows enlarged feeding artery (arrowhead) and focal nodular
hyperplasia in right hepatic lobe. Note second focal nodular hyperplasia with
low-attenuation central scar in left lobe (arrow).
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Fig. 12B. —39-year-old woman with mild intermittent right upper quadrant pain
and multiple sites of biopsy-proven focal nodular hyperplasia. Early portal
venous phase CT scan (at slightly higher level than A) shows
well-circumscribed mass that is slightly hyperdense to liver with central
low-attenuation scar. Note that rapid washout of enlarged feeding artery is no
longer visible. Third biopsy-proven focal nodular hyperplasia with
low-attenuation central scar and septa involves lateral segment of left lobe
(arrow). Low-attenuation radiating septa that course from central
scar peripherally are helpful secondary findings of focal nodular
hyperplasia.
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Scars and Septa
A central scar is histologically present in almost all patients with focal
nodular hyperplasia; however, scars are visualized on CT in only one third of
patients [6,
7]. Scars are hypodense to the
liver on unenhanced and early contrast-enhanced images. An enhancing vessel
may be seen in the scar on arterial phase imaging, representing the
intratumoral portion of the feeding artery. Gradual fill-in of the scar is
identified on portal venous and delayed images because of diffusion of
contrast material into the myxomatous stroma. The slowly enhancing scar may
then appear isodense to the surrounding tumor or may appear hyperdense in
relation to the surrounding tissue (Figs.
11,12A,12B,13A,13B,14).
In our study, scars were visualized in 27 patients (60%). All scars were
hypodense relative to the liver on arterial and portal venous phase images.
Delayed scans were obtained in only 17 patients with scars. On delayed images,
scars were isodense to liver in 12 patients (71%), hyperdense in three
patients (18%), and hypodense in two patients (12%).
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Fig. 13A. —50-year-old asymptomatic woman with focal nodular hyperplasia.
Portal venous phase CT scan shows large mass in posterior segment of right
hepatic lobe (arrows). Mass is slightly hyperdense compared with
normal liver and is homogeneously enhancing except for low-attenuation central
scar.
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Fig. 13B. —50-year-old asymptomatic woman with focal nodular hyperplasia.
Delayed CT scan (3 min after IV contrast material injection) shows mass that
is isoattentuating to liver. Note enhancement of scar with small portion of
scar remaining hypodense to liver (arrowhead).
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Fig. 14. —58-year-old asymptomatic woman with biopsy-proven focal nodular
hyperplasia in dome of liver. Arterial phase CT scan shows focal nodular
hyperplasia (arrow) with early homogeneous enhancement and
low-attenuation central scar.
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Occasionally, contrast-enhanced images reveal hypoenhancing radiating
fibrous septa. These septa usually divide the tumor into sections because they
radiate from the central scar toward the periphery. This finding can be a
helpful secondary sign of focal nodular hyperplasia (Fig.
12A,12B);
it was observed in five (11%) of our 45 patients.
Multiplicity
Multiple focal nodular hyperplasias occur in about 20% of patients
[8,
9]. Our series supports this
statistic. Multiple lesions were seen in 10 (22%) of our 45 patients (Fig.
12A,12B).
Atypical Examples of Focal Nodular Hyperplasia
In our study, five (11%) of 45 patients had atypical imaging features.
Atypical features included heterogeneous enhancement (two patients), a
capsulelike rim of low attenuation (two patients), and hypoattenuation
relative to the liver after IV contrast enhancement (one patient). Similar
atypical features have been reported in other published series
[10]. Patients with these
lesions require further examination (such as scintigraphy using
Tc—sulfur colloid, MR imaging, or percutaneous biopsy) to confirm the
diagnosis of focal nodular hyperplasia. Biopsy should include samples of the
fibrous scar because diagnostic bile ductules may be found only in this region
of the tumor.
Differential Diagnosis
Major differential considerations in the diagnosis of focal nodular
hyperplasia are hepatocellular adenoma, hepatocellular carcinoma (particularly
fibrolamellar hepatocellular carcinoma), and hypervascular hepatic metastases.
The distinction between these tumors is critical to ensure proper treatment.
Often these lesions have specific characteristics that can aid in the
diagnosis (Figs.
15,16,17).
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Fig. 15. —22-year-old woman with known fibrolamellar hepatocellular carcinoma.
Portal venous phase CT scan shows large lesion involving lateral segment of
left hepatic lobe (arrowheads) that contains low-attenuation central
scar (arrow). Heterogeneous mosaic perfusion and hyperenhancing true
capsule are worrisome features for hepatocellular carcinoma and should prompt
further evaluation. Central scars may also be seen, although less commonly, in
adenomas and cavernous hemangiomas. Peripheral low-attenuation changes should
be considered atypical in patients with suspected focal nodular
hyperplasia.
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Fig. 16. —50-year-old man with known hepatocellular carcinoma. Portal venous
phase CT scan shows large heterogeneously enhancing mass in right hepatic
lobe. Note well-defined thick hyperenhancing capsule (arrows)
surrounding lesion. Hepatocellular carcinomas have true capsules, and when
seen on imaging, capsules can be helpful in confirming diagnosis. True
capsules are also seen in adenomas and differ from capsulelike rim of
peripheral vascularity sometimes seen in focal nodular hyperplasia, which is
usually thinner and discontinuous and represents enlarged peripheral tumoral
vessels.
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Fig. 17. —48-year-old woman with hypervascular hepatic metastases
(neuroendocrine primary tumor). Arterial phase CT scan shows multiple
hyperenhancing masses in liver. Slow washout, heterogeneous or ring
enhancement, adjacent low-attenuation edema, and multiplicity are features
suggestive of malignancy. Hypervascular masses in patients with known
hypervascular primary tumors should be regarded as metastasis until proven
otherwise.
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Conclusion
Typical imaging features of focal nodular hyperplasia include diffuse
homogeneous hyperdense enhancement during the early phases (arterial and early
portal venous phases) of contrast-enhanced CT with progressive or rapid
washout of contrast material. The lesion often appears isodense to the liver
during and after the portal venous phase of contrast enhancement. Findings of
a central scar, low-attenuation radiating septa, and thin, incomplete
capsulelike peripheral vascularity are helpful secondary features.
Because focal nodular hyperplasia is usually encountered incidentally
during the search for other abnormalities, radiologists should be aware of the
appearances of focal nodular hyperplasia so that the diagnosis can be made
regardless of the phase of contrast enhancement. In most patients, an accurate
diagnosis can be made on CT without the need for additional imaging
studies.
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