AJR 2002; 179:81-85
© American Roentgen Ray Society
Hemodynamic Characterization of Focal Nodular Hyperplasia Using Three-Dimensional Volume-Rendered Multidetector CT Angiography
Giuseppe Brancatelli1,2,
Michael P. Federle1,
Sanjeev Katyal1 and
Vibhu Kapoor1
1 Department of Radiology, Division of Abdominal Imaging, University of
Pittsburgh Medical Center, 200 Lothrop St., Pittsburgh, PA 15213.
2 Present address: Department of Radiology, University of Palermo, Italy.
Received December 13, 2000;
accepted after revision January 15, 2002.
Address correspondence to M. P. Federle.
Abstract
OBJECTIVE. The goal of this study was to show the ability of
three-dimensional multidetector CT angiography to display the
angioarchitecture of focal nodular hyperplasia.
CONCLUSION. CT angiography with volume rendering shows the anomalous
feeding artery and hepatic draining veins that are characteristic of focal
nodular hyperplasia. These features may be helpful in distinguishing focal
nodular hyperplasia from other lesions.
Introduction
Because helical CT scanning of the abdomen during a rapid bolus injection
of contrast medium has become standard practice, hypervascular hepatic lesions
are recognized frequently. Although the possibility of a hypervascular primary
or metastatic hepatic neoplasm must be considered, many of these lesions prove
to be focal nodular hyperplasia. Focal nodular hyperplasia is a benign
neoplasm that is present in 3-5% of the general population and seems to
develop as a hyperplastic response to a localized vascular abnormality
[1]. Because focal nodular
hyperplasia is rarely symptomatic and has no malignant potential,
differentiation from other hypervascular hepatic masses is important.
Improvements in CT and MR imaging have allowed accurate diagnosis of focal
nodular hyperplasia in many cases, although many patients still undergo
multiple imaging studies, percutaneous biopsy, and even surgery because the
radiologists failed to make a confident diagnosis. Focal nodular hyperplasia
lesions are usually nearly isoattenuating to the liver on unenhanced, portal
venous phase, and delayedenhanced CT scans and are homogeneously
hyperattenuating on arterial phase CT scans. A central fibrous scar is highly
characteristic, but it is identified in only 50% of cases
[2].
The angioarchitecture and pathophysiology of focal nodular hyperplasia have
been studied extensively by pathologists and hepatologists and have been found
to differ substantially from the angioarchitecture of hepatocellular carcinoma
and other malignant hepatic neoplasms
[1]. Focal nodular hyperplasia
is supplied by an enlarged anomalous hepatic artery; its venous drainage is
always into the hepatic veins
[1]. Conversely, the efferent
vessels in hepatocellular carcinoma are almost exclusively drained into the
portal vein system [3]. Several
investigators have concluded that unequivocal visualization of hepatic venous
drainage from a hypervascular hepatic mass would be useful in diagnosing focal
nodular hyperplasia
[3,4,5].
Although multiphasic thin-section helical CT often shows blood vessels
within or surrounding hypervascular liver masses, it is often difficult to
recognize the origin and path of vessels on a series of transverse CT scans.
The purpose of this article is to show the ability of three-dimensional (3D)
multidetector CT angiography using volume rendering to display the
hemodynamics and angioarchitecture of focal nodular hyperplasia, features that
should prove useful in distinguishing the lesions from malignant masses.
Subjects and Methods
Between July 1999 and October 2000, four women (age range, 37-45 years;
mean age, 42 years) who were being evaluated for a known or suspected hepatic
tumor had a hypervascular liver lesion found on helical CT that was
subsequently proven to be focal nodular hyperplasia. The liver lesion was
first detected on CT, which was requested to evaluate abdominal pain
(n = 3) or possible metastatic breast carcinoma (n = 1).
None of the patients had cirrhosis or viral hepatitis. Proof of focal nodular
hyperplasia was by liver resection (n = 1), focal uptake of
99mTc diethyl-iminodiacetic acid (n = 1), and the stable
size of the lesion for 1 and 4 years (n = 2). The CT protocol was
designed to allow optimal characterization of the hypervascular liver lesion
on transverse and 3D volume-rendered images. All CT examinations were
performed on a Lightspeed QX/i scanner (General Electric Medical Systems,
Milwaukee, WI). After a series of unenhanced 7-mm sections through the liver,
all patients received IV contrast medium ([ioversol] Optiray 350;
Mallinckrodt, St. Louis, MO) at a rate of 5 mL/sec and a volume of 125 mL.
Arterial dominant phase images were initiated at a time determined by contrast
bolustracking software to coincide with peak aortic enhancement with a scan
delay of 13-25 sec. Portal venous dominant phase imaging was initiated 40 sec
after the initiation of the arterial phase images (range, 53-65 sec).
For the arterial phase images, we used a collimator width of 1.25 mm and a
table speed of 7.5 mm per rotation (high-speed mode; pitch, 6). For the portal
venous phase, we used a collimator width of 2.5 mm and a table speed of 15.0
mm per rotation.
Three-dimensional volume-rendered reconstructions were performed using a
free-standing workstation (Advantage Windows; General Electric Medical
Systems). All reconstructions were performed by a radiologist experienced in
3D postprocessing techniques, and each procedure required approximately 20
min. Volumes of interest were selected manually from the axial source images
to include only the aorta, celiac axis, hepatic artery, draining veins, and
lesion. CT angiograms were then reconstructed using the volume-rendering
algorithm with lower thresholds of 70-140 H. Display parameters including
width, level, opacity, and brightness were chosen subjectively. The
volume-rendered images were obtained in projections selected to best depict
the course of the hepatic vasculature. Standard projections performed in all
cases included right anterior, oblique, inferior, posterior, and lateral
projections.
The reconstructed axial images and the 3D volume-rendered reconstructions
were reviewed by two radiologists, and the arterial supply and venous drainage
to and from the lesion were recorded as part of the official CT report.
Results
A single focal nodular hyperplasia lesion was found in three patients, and
two lesions were found in a fourth patient. The lesions ranged in diameter
from 1 to 9 cm. All lesions were hypo- to isoattenuating on unenhanced CT. All
lesions appeared homogeneously and brightly enhancing on the arterial dominant
phase, and all were isoattenuating on the portal venous dominant phase (Figs.
1A,1B,1C
and
2A,2B,2C,2D).
One patient underwent 6-min delayed scanning, with the lesion remaining
isoattenuating to the liver. A central scar was shown in two lesions, and it
was isoattenuating to the surrounding focal nodular hyperplasia on unenhanced
images and hypoattenuating on both arterial and portal venous phases. The scar
was hyperattenuating to the liver and the focal nodular hyperplasia on delayed
scans in one patient.

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Fig. 1A. 39-year-old woman with focal nodular hyperplasia. Early
hepatic arterial phase transverse CT scan (20-sec delay) shows large
homogeneously and brightly enhancing mass (solid straight arrow) with
central scar (open arrow). Blood vessels (curved arrows) are
evident within mass and on its surface, but their origin and course are
difficult to determine.
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Fig. 1B. 39-year-old woman with focal nodular hyperplasia. Portal
venous phase transverse CT scan (70-sec delay) reveals blood vessels
(arrows), probably veins, within mass and on its surface. Mass is
nearly isoattenuating to liver.
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Fig. 1C. 39-year-old woman with focal nodular hyperplasia.
Volume-rendered CT angiogram (20-sec delay) shows focal nodular hyperplasia
(FNH) lesion supplied by anomalous artery (a a) arising from hepatic artery
(HA). Lesion is drained by two hepatic vein tributaries (HV).
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Fig. 2A. 45-year-old woman with focal nodular hyperplasia. Early
arterial phase transverse CT scan (13-sec delay) shows lesion (straight
arrow) is brightly and homogeneously enhancing. Blood vessels (curved
arrow) are noted on surface of mass.
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Fig. 2B. 45-year-old woman with focal nodular hyperplasia. Portal
venous phase CT scan (60-sec delay) shows mass almost isoattenuating to liver
with hypoattenuating central scar (open arrow). Large blood vessels
(solid arrows) are noted.
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Fig. 2C. 45-year-old woman with focal nodular hyperplasia.
Volume-rendered CT angiogram (13-sec delay) shows multiple branches of
anomalous artery (a a) spread over lesionlike spider legs. HA = hepatic
artery, FNH = focal nodular hyperplasia.
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Fig. 2D. 45-year-old woman with focal nodular hyperplasia.
Volume-rendered CT angiogram (60-sec delay) shows that multiple draining veins
(arrows) coalesce to drain into right hepatic vein (RHV) and inferior
vena cava (IVC).
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In the arterial phase, one or more anomalous feeding arteries to each
lesion were identified (Figs.
1A,1B,1C
and
2A,2B,2C,2D).
The arteries branched into a spiderlike series of vessels on the surface of
the focal nodular hyperplasia (Fig.
2A,2B,2C,2D);
the course of the vessels within the focal nodular hyperplasia could not be
visualized on the volume-rendered images. Anomalous draining veins were
identified that could be followed into or toward larger hepatic veins and not
into portal vein branches (Fig.
2A,2B,2C,2D).
In the patient with the smaller lesions, an anomalous draining vein could not
be identified (Fig. 3).

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Fig. 3. 43-year-old woman with focal nodular hyperplasia.
Volume-rendered CT angiogram (20-sec delay) shows large focal nodular
hyperplasia lesion (FNH) supplied by multiple branches of anomalous artery (a
a) arising from hepatic artery (HA). Small lesion (FNH) is supplied by single
artery.
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For comparison, we illustrate the portal venous drainage of hepatocellular
carcinoma (Fig.
4A,4B).

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Fig. 4B. 70-year-old woman with cirrhosis and hepatocellular
carcinoma. Maximum-intensity-projection off-axial CT scan shows two enhancing
vessels (straight arrows) at periphery of mass draining lesion and
joining right branch of portal vein (curved arrow). On biopsy, mass
was well-differentiated hepatocellular carcinoma.
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Discussion
Multiphasic multidetector CT allows greater spatial and temporal or
hemodynamic characterization than conventional or single-detector helical CT,
which can result in a more confident and specific diagnosis of focal hepatic
lesions. Many of these features, such as uniform hypervascularity and a
central scar, are evident on transverse CT sections and have been reported to
result in a more frequent and confident diagnosis of focal nodular hyperplasia
[6]. The ability to acquire a
volume of CT data with near-isotropic voxels (the same in the x, y,
and z planes) offers further possibilities to characterize the shape
and hemodynamics of focal liver masses. Graphics workstations and software
packages are now affordable accessories to multidetector CT scanners and have
become more user-friendly for radiologists and technologists.
The relatively minor alterations of our standard biphasic CT liver protocol
and the moderate amount of time necessary to perform the 3D reconstructions
provided unique insights into the angioarchitecture of focal nodular
hyperplasia in these four patients. Prior attempts to study the hemodynamics
of focal nodular hyperplasia have been quite invasive and labor-intensive.
Transcatheter angiography was more widely used in the past to detect and
characterize liver tumors, but few cases of focal nodular hyperplasia were
studied and were generally characterized merely as hypervascular masses
supplied by an enlarged anomalous artery
[7]. Miyayama et al.
[8] coupled hepatic
arteriography with single-level dynamic CT and showed arteries and veins in or
near the central stellate scar and at the junction of the focal nodular
hyperplasia and normal liver tissue. They noted that blood (contrast media)
occasionally drained from the focal nodular hyperplasia nodule into
surrounding hepatic sinusoids producing an enhanced capsulelike rim. Their CT
technique did not allow depiction of the shape or number of focal nodular
hyperplasia lesions or the pattern of feeding or draining vessels beyond the
focal nodular hyperplasia.
Fukukura et al. [3] studied
29 surgically resected focal nodular hyperplasia lesions and three autopsy
specimens with angiography; in the autopsy cases, they studied the injection
of colored gelatin into the hepatic artery and portal vein. They concluded
that focal nodular hyperplasia is supplied by an anomalous enlarged hepatic
artery and is neither supplied nor drained by the portal vein. Rather, venous
drainage of focal nodular hyperplasia was exclusively into the hepatic vein
branches [3]. Conversely,
several investigators have studied the vascular supply and drainage of
hepatocellular carcinoma in great detail and have found that hepatocellular
carcinoma is supplied almost exclusively by the hepatic artery and is drained
almost always into the portal vein
[4,
9,
10]. Okuda et al.
[11] showed some drainage into
hepatic veins in only 1.8% of hepatocellular carcinoma.
Wanless et al. [1], who have
written most extensively on the pathophysiology of hypervascular liver masses,
have conducted detailed studies on the morphometry of these lesions. They
report that focal nodular hyperplasia is supplied by an anomalous artery,
larger than expected for its hepatic location, that branches into a spiderlike
structure on or within the focal nodular hyperplasia lesion. They further
report that the artery is not accompanied by a portal vein branch and that
focal nodular hyperplasia drains directly to hepatic veins or first through
enlarged sinusoids near its periphery
[1].
These and other investigators
[3] have concluded that the
visualization of these vascular features should prove useful in distinguishing
focal nodular hyperplasia from other hepatic masses including hepatocellular
carcinoma. We believe the CT angiographic techniques that we have reported
accomplish this goal and do so noninvasively and relatively inexpensively.
The CT angiograms provided by volume-rendered 3D modeling showed the size,
number, and angioarchitecture of focal nodular hyperplasia in each of our four
patients. The images showed the characteristic enlarged anomalous feeding
arteries, the spiderlike branching on the surface of the focal nodular
hyperplasia, and the hepatic venous drainage (Figs.
1A,1B,1C
and
2A,2B,2C,2D).
The portal vein supplied neither inflow nor drainage of the focal nodular
hyperplasia in our cases.
Another potential benefit of the 3D display of hepatic vasculature provided
by CT angiography is in planning for embolization or ligation of vessels for
the rare symptomatic cases of focal nodular hyperplasia
[12].
Our study has some limitations. The detection of draining veins was not
possible for the smallest of the lesions shown. From our knowledge, based on
our prior surgical and gross pathologic studies, the depiction of hepatic
venous drainage (for focal nodular hyperplasia) or portal venous drainage (for
hepatocellular carcinoma) should be a reliable criterion. Nevertheless, our
study size is small, and a study of a larger group of patients may be
warranted. We conclude that 3D CT angiography can provide useful information
in cases of suspected focal nodular hyperplasia that may allow a more
confident diagnosis and treatment in some cases.
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