Ultrasound1 Robert
A. Lee,
MD
Figure 1. Transverse oval, sharply marginated, I = inferior vena cava.
#{149} I
William
Cbarboneau,
MD
sonogram of the liver (a) isoechoic mass (arrow)
and magnified US view of the left lobe (b) with an echogenic central scar (arrowheads)
HISTORY
U
A 24-year-old
woman
pain underwent trasonography
(CT)
, and
with
vague
scintigraphy
(Figs
ul-
1-3).
The US images demonstrated a 6-cm, sharply marginated, isoechoic mass in the lateral segment of the left lobe of the liver. The mass had a homogeneous architecture except for an echogenic band running through its middlc portion, which is consistent with a central scar (Fig 1). CT scans obtained before the administra-
Index
terms:
RadloGraphics I From the sembly. CRSNA,
954
U
Liver, 1990; Department
Received 1990
RadioGrapbics
and
focal
nodular
hyperplasia,
l0954-956 of Diagnostic
Radiology,
accepted
March
U
23,
1990.
Lee and
76 1 .3 1 1 4 #{149} Liver
neoplasms,
Mayo
First
Address
Clinic,
200 reprint
Charboneau
a 6-cm A
aorta,
=
.
FINDINGS
U
.
tion of contrast material showed the mass to be hypoattenuated, well circumscribed, and homogeneous (Fig 2a) During the arterial phase of dynamic CT scanning, the mass was inhomogeneous and hyperattenuated (Fig 2b). On slightly delayed scans, the mass was isoattenuated relative to the normal hepatic parenchyma (Fig 2c). Scintigraphy of the liven was performed with technctium-99m sulfur colloid. Planar images (Fig 3a) and axial single photon emission computed tomographic (SPECT) images (Fig 3b) were obtained and demonstrated a large mass with mildly increased uptake in the left lobe of the liven.
abdominal
diagnostic imaging with (US), computed tomography
show
St. SW,
requests
diagnosis Rochester,
MN 55905.
From
the
1989
RNSA
scientific
as-
toJ.W.C.
Volume
10
Number
5
a.
b. Figure 2. (a) Nonenhanced CT scan demonstrates an oval, wcll-marginatcd, hypoattenuated mass (arrows) in the lateral segment of the left lobe. (b) Dynamic CT scan obtained during artenial phase shows heterogeneous, hypcrattcnuated pattern of enhancement (arrowheads) (c) Dclayed CT scan shows the mass to be homogeneously isoattenuated relative to liver (arrows). .
C.
a. Figure creased
September
1990
3. Planar Tc-99m sulfur-colloid liver scan (a) and axial SPECT uptake in the mass located in the left lobe (arrows) S = spleen, .
Lee and
image *
Charboneau
=
(b) demonstrate gallbladder.
U
slightly
RadioGrapbics
in-
U
955
DIAGNOSIS: the liven. U
Focal
nodular
hyperplasia
of
DISCUSSION
Focal nodular hyperplasia is a benign hepatic tumor composed of nodules of hepatocytes and Kupffcr cells separated by fibrous septa. Characteristically, there is a central stellate scar of connective tissue with septa radiating toward the periphery. Bile duct proliferation occurs within the fibrous septa or between hepatocytes. Portal tniads and central veins are absent (1). Focal nodular hyperplasia occurs most frequently in the 3rd to 5th decades of life, with a 2 : 1 female preponderance. Patients with these tumors are usually asymptomatic and have normal liver function (1). The diagnosis of focal nodular hyperplasia may require correlation of findings from 5evenal different radiologic studies. On US scans, the tumors are usually homogeneous and well marginated. The echogenicity of the tumors is variable, with isoechoic and hypoechoic lesions being the most common, as reported by Welch et al (2) On CT scans obtained without contrast enhancement, focal nodular hyperplasia is usually hypoattenuated and homogeneous. After the intravenous administration of contrast material, the tumor usually becomes either hyperattenuated or isoattenuated, depending on the rate of contrast material injection and the time delaybefore scanning (2,3). The central scar is usually not seen on cither CT or US scans (2) In addition, central scarring is not specific for focal nodular hyperplasia. Scarring can also be seen in fibrolamellar hepatocellular carcinoma, hemangioma, and hepatic adenoma after hemorrhage or necrosis (3 ,4) Therefore, correlation of
ful in making the diagnosis. Since significant numbers of Kupffer cells are normally present in focal nodular hyperplasia, uptake equal to or greater than that in normal liven parenchyma can occur. In a review of the literature by Rogers et al (5), 58% of the cases of focal nodular hyperplasia showed uptake equal to that of normal parenchyma, 7% showed hyperconcentration of Tc-99m sulfun colloid, and were relatively photopenic. No other hepatic masses usually contam sufficient Kupffen cells to cause normal or increased uptake (5) However, rare instances of focally increased uptake due to hemangioma, hepatoblastoma, liver herniation, and hepatocellular carcinoma have been reported (1). 35%
.
U REFERENCES 1 . Friedman A, Fishman
cal disease. the liver, Baltimore: 2
.
biliary tract, pancreas, Williams & Wilkins,
T, Sheedy
P, et al.
Fo-
A, ed. Radiology
P, Johnson
of
and spleen. 1987; 183-
CM, et al.
Focal
nodular hyperplasia and hepatic adenoma: comparison of angiography, CT, US, and tigraphy. Radiology 1985; 156:593-595.
.
.
188. Welch
E, Radecki
In: Friedman
3
.
4
.
5
.
Matheu D, Bruncton C, Vasilc N. Hepatic
J, Drouillard adenomas
scm-
J, Pointrcau and focal
nodular hypcrplasia: dynamic CT study. Radiology 1986; 160:53-58. Friedman A, Lichtcnstein J, Goodman Z, Fishman E, Siegelman 5, Dachman A. Fibrolamellan hepatocellular carcinoma. Radiology 1985; 157:583-587. Rogers J, Mack L, Freeny P, Johnson M, Sones
P.
Hepatic
focal
nodular
graphy, CT, sonography, AJR 1981; 137:983-990.
hypcrplasia: and
anglo-
scintigraphy.
.
US and
CT
sulfur-colloid
956
U
RadioGrapbics
findings
liven
with
scans
U
those
from
is sometimes
Lee and
Tc-99m
help-
Charboneau
Volume
10
Number
5