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461303

JDMXXX10.1177/8756479312461303Journ

al of Diagnostic Medical SonographyMcCann and Penny

Case Studies

Focal Nodular Hyperplasia:


Case Study, Imaging, and Treatment

Journal of Diagnostic Medical Sonography


29(1) 1723
The Author(s) 2013
Reprints and permission: http://www.
sagepub.com/journalsPermissions.nav
DOI: 10.1177/8756479312461303
http://jdms.sagepub.com

Chelsey N. McCann, RT(R), RDMS1, and


Steven M. Penny, BS, RT(R), RDMS2

Abstract
Focal nodular hyperplasia (FNH) is the second most common benign hepatic mass. The primary purpose of this article
is to provide a relevant case study and offer a review of the recent literature related to FNH with a discussion of
both the clinical and imaging findings of this classically benign hepatic lesion. Although magnetic resonance imaging is
considered the gold standard of FNH imaging, the sonographic and computed tomography appearance also is offered in
this article. Furthermore, contrast-enhanced ultrasound, which boasts a 96% success rate at differentiating FNH from
other hepatic tumors, is analyzed.The historical treatment options, including medical and possible surgical intervention,
are provided as well. Last, this article offers an analysis of the prognosis for the patient diagnosed with FNH.
Keywords
focal nodular hyperplasia, sonography, central stellate scar, liver lesions, benign hepatic mass, contrast-enhanced
ultrasound

The case study provided in this article confirms the need


for both clinical and imaging follow-up of pathology discovered during either a routine sonographic examination
or, in this case, during educational training. Although the
sonographic appearances of benign hepatic lesions often
overlap, it is imperative for the sonographer to understand the etiology of these benign lesions. Sonographers
should also have a comprehensive understanding of valuable clinical history information that can assist an interpreting physician to make a proper diagnosis.

Case Presentation
A young white woman in her early 20s entered the sonography program and was offered an educational assignment that included the sonographic evaluation of her liver.
Incidentally, during a practice scanning laboratory session, a liver mass was recognized using an ATL HDI 5000
(Philips/ATL, Philips Healthcare, Andover, Massachusetts)
C5-2 transducer. The lesion was well marginated, hyperechoic, and positioned adjacent to the inferior vena cava
within the right lobe of the liver (Figures 1 and 2). The
mass did appear to distort the hepatic architecture in a
manner that was inconsistent with a cavernous hemangioma. Color Doppler revealed blood flow around and
within the mass, thus providing another sonographic
feature that was thought to be less likely indicative of a

Figure 1. Longitudinal sonographic image of the liver showing


a hyperechoic mass (between calipers) adjacent to the inferior
vena cava.

Raleigh Radiology Cary, NC


Johnston Community College, Smithfield, NC, USA

Corresponding Author:
Steven M. Penny, BS, RT(R), RDMS, Johnston Community College
Imaging, PO Box 2350, Smithfield, NC 27577, USA
Email: smpenny@johnstoncc.edu

18

Figure 2. Transverse sonographic image of the liver


demonstrating the location of the incidentally discovered
tumor (between calipers).

Journal of Diagnostic Medical Sonography 29(1)

Figure 4. The mass (between calipers) was again


demonstrated on this longitudinal image taken during the
follow-up sonogram.

Figure 3. Color Doppler analysis of the lesion revealed flow


both within and around the mass.

cavernous hemangioma (Figure 3). The student denied the


use of oral contraceptives, and she was nulliparious and
asymptomatic. She also denied having weight loss or any
history of abdominal pain or surgery. She was referred to
her primary care physician for clinical evaluation.
Her physician performed a physical examination of
the abdomen and stated that the liver did not feel
enlarged upon palpation. The physician ordered a right
upper quadrant sonogram and blood work, including an
analysis of liver function. The blood work revealed a
slightly elevated bilirubin level, with all other laboratory values unremarkable. An elevation in bilirubin levels could indicate a biliary obstruction, anemia,
cirrhosis, or one of several other clinically noticeable
abnormalities.

Figure 5. Color Doppler imaging showed the presence of


vasculature within the central portion of the mass (white
arrow), suggesting the presence of a central scar that
contained a prominent vessel.

A complete sonographic examination of the right upper


quadrant was performed using a GE-Logiq 7 (General
Electric Medical Systems, Milwaukee, Wisconsin) curvilinear 3.5-MHz abdominal transducer. A well-defined
hyperechoic lesion was visualized in the right posterior
lobe of the liver measuring 4.4 3.8 3.6 cm (Figure 4).
Color Doppler demonstrated blood flow both around and
within the central portion of the mass (Figure 5). Pulsedwave Doppler of the portal vein confirmed hepatopedal
flow, and the main portal vein measured 14 mm in the
anteroposterior dimension. No biliary ductal dilatation
was noted. The right kidney, inferior vena cava, pancreas,

19

McCann and Penny

Figure 6. Magnetic resonance image of focal nodular


hyperplasia (between white arrows) without contrast. The
liver lesion was seen as a solitary mass that initially had
the same appearance as the surrounding parenchyma on
precontrast images.

Figure 7. Magnetic resonance image of focal nodular


hyperplasia (between black arrows) with contrast. On this
image, the mass appears brighter than the liver.

and gallbladder all appeared unremarkable. The patient


was referred for magnetic resonance imaging (MRI) of
the abdomen.
MRI was performed with and without contrast. After
routine noncontrast abdominal images were obtained, the
patient was injected with 20 mL of gadolinium. The liver
was reported to be normal in morphology, volume, and signal characteristics. No inflammation, fatty infiltration, or
cirrhosis was visualized. The liver lesion was seen as a
solitary mass that initially had the same appearance as the
surrounding parenchyma on precontrast images (Figure 6).
The mass was best demonstrated on the arterial phase postcontrast. On these images, the mass transiently enhanced
brighter than the liver but, shortly after, faded back to its
original isointensity (Figure 7). The delayed-phase images

Figure 8. Magnetic resonance image showing the presence


of the central scar (black arrow) within the tumor, providing a
definitive diagnosis of focal nodular hyperplasia.

demonstrated enhancement of a central scar within the


lesion (Figure 8). This finding was consistent with the
diagnosis of focal nodular hyperplasia (FNH). The mass
measured 3.2 3.8 3.5 cm on MRI, with a volume of
28 mL. It was noted to be located subjacent to the confluence of the hepatic veins and was in contact with the intrahepatic inferior vena cava, without effacement. The middle
hepatic vein was located over the anterior border of the
FNH, and it was effaced, with no indication of outflow
obstruction or limitations. The spleen, pancreas, kidneys,
adrenal glands, gallbladder, biliary system, retroperitoneum, and mesentery were all normal. The patient was
given the definitive diagnosis of focal nodular hyperplasia.
No follow-up care has been suggested or required.

Discussion
FNH is one of the most common benign hepatic masses.
Its incidence is second only to the frequently encountered
cavernous hemangioma of the liver.1,2 FNH was originally
mentioned in the literature by Edmundson in 1958 and
officially recognized as a distinct hepatic lesion by the
World Health Organization in 1975.3,4 Prior to this
acknowledgment, FNH may have been misdiagnosed as a
hepatic adenoma, also termed focal nodular cirrhosis or
benign hepatoma.5 Nonetheless, with more than a halfcentury of research, there still appears to be much conjecture and ongoing exploration into the etiology of the mass
frequently portrayed as the stealth lesion of the liver.

Composition of FNH
Differing studies have mentioned FNH as either a lesion
that is neoplastic in nature, consisting of polyclonal cells,

20
or nonneoplastic, consisting of monoclonal cells. Lesions
that are polyclonal consist of different types of cells,
whereas monoclonal lesions are composed of similar
cells. The determination as to whether FNH is a true neoplasm is significant, however, specifically because a differentiation usually needs to be made between FNH and
other hepatic masses, as prognosis and follow-up can vary
considerably. A recent study by Gong et al4 in 2009 established that FNH is indeed more likely a mass consisting
of proliferated polyclonal cells and that it is nonneoplastic in nature, thus confirming that FNH is a hyperplastic
rather than a neoplastic process.6
Histologically, FNH consists of hyperplastic units of
hepatocytes fixed together in an abnormal arrangement
with dense fibrous tissue.2,7 The mass also contains proliferating bile ducts, Kupffer cells, connective tissue, and a
central stellate (an arrangement resembling that of a radiating pattern, like that of a star) scar.7,8 The stellate scar
contains a large artery that courses within it, causing
hyperperfusion and arterializations of sinusoids.5 Radiating
out from the scar are often dense fibrous septa, often in a
spoke-wheel pattern toward the periphery.6,9,10 Surrounding
the FNH is a pseudo-capsule, although with imaging, the
pseudo-capsule often appears as a genuine capsule surrounding the FNH because of the compression of adjacent liver parenchyma.10
The average size of an FNH at the time of discovery is
approximately 6 cm.11 Three criteria typically have to be
recognized to differentiate FNH from other hepatic masses
microscopically: (1) the existence of a central stellate scar
within the mass, (2) the presence of multiple bile ducts in
fibrous intervals, and (3) a mass that lacks small cell
changes.12 The appreciation of this latter characteristic is
crucial, for small cell change is a fundamental step in
hepatocarcinogenesis. Moreover, it is significant to note
that the central scar can be absent in anywhere between
20% and 50% of FNH cases.4,11

Etiology of FNH
The etiology of FNH has been an area of concentrated
research. FNH has a low occurrence rate in males but is
often discovered incidentally in females of childbearing
age, which correlates with the case study discussed in
this article.12,13 These findings support a theory that
proposes that the mass is the outcome of an estrogenstimulating vascular alteration combined with hepatocyte
hyperplasia.4 The role that estrogen, and specifically the
use of oral contraceptives (OCs), plays in the development of FNH has not been clearly established. It should
be noted that FNH has been found in children, males, and
females who are not taking OCs.14 One small study
revealed no change in the character of tumors on followup imaging in patients who continued to take OCs.12 It

Journal of Diagnostic Medical Sonography 29(1)


has been suggested that patients on OCs may have a risk
of tumor enlargement, however, therefore signifying that
FNH may be responsive to estrogen, but that estrogen is
not a causative factor in its development.15,16 Younger
women tend to have larger lesions than do postmenopausal women and men, and although not predictive, one
study demonstrated that a pregnant patient with FNH did
have an increase in the size of her tumor.11,17 Some
research has revealed that a decrease in size or regression
of FNH is seen after abandonment of oral contraceptives.17 Furthermore, most investigators agree that OCs
are not responsible for FNH, but they discourage the
further use of OCs in patients with FNH secondary to the
risk of complications such as enlargement of the tumor,
hemorrhage, rupture, or necrosis.5
Irregular blood flow patterns, vascular abnormalities,
and preexisting arterial malformations have been proposed
as the origin of FNH.5 Altered blood flow patterns in association with an elevated angiopoietin 1/angiopoietin 2
mRNA ratio can result in FNH.7 The angiopoietins are protein growth factors that encourage angiogenesis from preexisting blood vessels. One study has suggested that FNH
is a result of the development of hyperplastic nodules in an
area of the liver secondary to blood flow in an irregular
hepatic artery branch.6 Another source states that the origin
of FNH results from a vascular anomaly that occurs before
birth, which leads to a hyperplastic response within the
hepatocytes.6 This theory is supported by the consistently
confirmed link between FNH and hereditary hemorrhagic
telangiectasia (HHT), an inherited disease linked with
numerous vascular anomalies.17,18
Finally, an additional hypothesis that strengthens the
vascular association is that FNH may be the result of the
development of an abnormal, spider-like, arterial malformation that produces an excessive amount of cells in a
localized area, thus resulting in a change in the sinusoidal
pressure and the development of a focal area of hyperplasia.11 The theory that FNH is the result of a vascular malformation of the liver is supported by the fact that FNH is
often accompanied by other vascular lesions of the liver,
such as cavernous hemangioma.13 The coexistence of
FNH and hepatic hemangioma is 23%.17 Although not as
common, FNH also has been discovered in patients with
hepatic adenomas and hepatocellular carcinoma.
In the past, it was once assumed that abnormalities
of the portal vein were not associated with FNH, but
recent studies have shown that mild abnormalities of
the portal vein were present in a significant number of
cases. One such case of FNH was reported in a patient
with portal hypertension, which was thought to be associated with the anomalous portal tract syndrome, in
which abnormal portal veins and arteries cause hyperplastic nodules to develop such as those seen in the
presence of FNH.19

McCann and Penny


There appears to be no risk for FNH to undergo malignant degeneration, although FNH was discovered adjacent to an area of hepatocellular carcinoma (HCC) in one
case study mentioned in the literature.20 However, FNH in
association with HCC is rare, with an incidence of only
2%.11,21 One study examined 77 patients with FNH who
underwent surgical resection, and of those patients, only
2 had evidence of HCC, with one of the patients ultimately
having a recurrence of HCC shortly after the removal of
the tumor.22 Although this rate is extremely low, there has
been speculation by some that FNH has the potential to
lead to HCC, although this has not been definitively
demonstrated.4

Risk Factors and


Clinical Presentation of FNH
FNH is more often seen in females in reproductive years,
although it can be discovered in both sexes and at any
age. Patients who smoke, have undergone chemotherapy,
or have experienced blunt abdominal trauma are also at
risk for developing FNH.6 Patients with a history of cirrhosis and those who have been exposed to azathioprine,
a drug that may be used to treat rheumatoid arthritis, have
an increased risk for developing FNH as well.7
Patients with FNH typically lack any clinical signs or
symptoms. Acute abdominal pain can be a presenting
symptom, although this has occurred in very few documented cases.11,16 The abdominal pain caused by FNH is
thought to be the result of a large FNH that impinges
upon adjacent hepatic structures, leading to a feeling of
bloatedness for some individuals.12 Patients with FNH
may begin to experience symptoms and pain if the lesion
suddenly begins to increase in size and certainly if the
mass undergoes hemorrhage or rupture.12 Five cases of
intraperitoneal hemorrhage from FNH have been recorded
since 1975, with four of the five cases being reported
between 2000 and 2006.5

Imaging Findings of FNH


FNH is most often incidentally discovered during an
imaging study such as sonography, accounting for an
estimated 3% to 8% of all primary hepatic tumors.12,13
Sonography is often the initial imaging modality for the
identification of FNH, especially in asymptomatic
patients. The sonographic appearance of FNH is variable,
with a mixture of lesions that may be isoechoic,
hypoechoic, or hyperechoic.8 The isoechoic lesions can
be overlooked without careful sonographic investigation.
This attribute leads to the tumors descriptive nickname as
the stealth lesion of the liver because of the possibility
that the mass can be practically invisible on sonography.1

21
For these instances, the use of B-color to highlight the
borders of the mass can be beneficial, and a vigilant
analysis of contour changes within the liver will help
identify these masses.
Within the tumor, sonography may demonstrate the
presence of the aforementioned central scar. This scar
may appear hyperechoic or hypoechoic and contain
prominent vasculature. Color Doppler may demonstrate
evidence of vascularity surrounding the mass.23 Although
not yet approved by the US Food and Drug Administration
(FDA) for this application, contrast-enhanced ultrasound
(CEUS) is a dependable modality for the evaluation of
focal liver lesions, with a 96% success rate at differentiating FNH from the hepatic adenoma.11,24 An FNH under
CEUS interrogation will yield hypervascularity on the
arterial phase and demonstrate the presence of stellate
lesional vessels and a tortoise feeding artery.1 Germany
and France have both participated in well-known multicenter studies involving focal liver lesions and CEUS.
The German study consisted of 1349 patients with focal
liver lesions, and although the CEUS study was compared primarily with biopsy, some cases were compared
with computed tomography (CT) or MRI. The study presented an accuracy rate of 90.3%, a sensitivity rate of
95.8%, and a specificity rate of 83.1%.24 In this particular study, CEUS correctly diagnosed 87.1% of FNHs.24
The French study consisted of 1034 focal liver lesions,
and CEUS provided an accuracy rate of 86.1% compared
with standard ultrasound, which had an accuracy of only
62.4%.
CT and MRI are especially useful in differentiating
FNH from other hepatic tumors and are typically used
subsequent to the incidental identification of FNH during a sonographic study. On an unenhanced CT, FNH
will appear as a hypoattenuating or isoattenuating mass,
with about one-third of the cases presenting with a
prominent hypoattenuating central scar.9,16 Contrastenhanced CT findings typically show a mass that is
homogeneous, with some enhancement of the scar noted
during the arterial phase and possibly on delayed images
as well.9
MRI has become the gold standard in diagnosing liver
lesions, as it is considered to have a higher sensitivity and
specificity compared with CT.5,12 On T1-weighted MRI
images, FNH will appear either isointense or slightly
hypointense compared with the normal hepatic parenchyma, whereas T2-weighted images may show a relatively hyperintense mass.9 The central scar, when present,
is readily identified with MRI. Specific contrast media
used in MRI can also be used to identify the presence of
Kupffer cells.10 This is beneficial in the differential diagnosis between FNH and hepatic adenoma because adenomas do not typically contain Kupffer cells.13

22

Journal of Diagnostic Medical Sonography 29(1)

Prognosis and Treatment

Declaration of Conflicting Interests

Since there is a low risk for malignancy, current medical


treatment remains conservative for the patient with an
asymptomatic FNH with no need for medical intervention. The termination of oral contraception may be indicated secondary to a possible increase in the growth of
the lesion, although as mentioned earlier, the link has not
been clearly established. Close monitoring of a known
FNH during pregnancy could be easily managed with
routine sonographic examinations, possibly at the time of
scheduled antenatal sonograms.
Surgical intervention may be necessary in a small number of individuals. The surgery can be performed by open
surgery or laparoscopic resection.11 However, this is typically only considered for patients who are symptomatic
and have a previous history of bleeding episodes, hepatomegaly, elevated hepatic enzyme levels, or jaundice from
compression on the biliary system.7,22 A sudden increase
in the size of the lesion may warrant surgical intervention,
however, even in the asymptomatic patient.6,17 In one
study of 120 patients with hepatic lesions, 27 of whom
had FNH, only one had an increase in the size of FNH
located on her caudate lobe, which occurred during pregnancy. She had surgical intervention and did not survive
the surgery.17 Liver masses that measure over 5 cm have
shown some increased risk for rupture, hemorrhage, or
abnormal growth and may need to be managed and monitored more closely.5 When masses cannot be definitively
diagnosed with imaging, biopsy may be necessary.

The authors declared no potential conflicts of interest with


respect to the research, authorship, and/or publication of this
article.

Conclusion
FNH is a benign hepatic mass that may appear as a welldefined lesion of varying sonographic echogenicity. The
role of the sonographer in the diagnosis of FNH is apparent. Sonographers are obligated to identify the lesion,
measure it, and describe the sonographic appearance and
location relative to other hepatic anatomy. Sonographers
should also use critical thinking while obtaining clinical
history information and employ every technical tool to
examine a hepatic mass when discovered, including the
use of image optimization and color Doppler. The identification of a central scar may be difficult with sonography. Although MRI may play a larger role in obtaining a
more definitive diagnosis of FNH, it is the obligation of
the sonographer to understand any diagnostic differentiations and attempt to show these sonographic variations when a hepatic mass is identified. By obtaining an
accurate, thorough clinical history from our patients, we
can collect valuable information that can be used both
during and after the sonographic examination of a
hepatic mass, thus ultimately contributing to a definitive
diagnosis of FNH.

Funding
The authors received no financial support for the research,
authorship, and/or publication of this article.

References
1. Rumack CM, Wilson SR, Charboneau JW, Levin D:
Diagnostic Ultrasound. 4th ed. Philadelphia, PA, Elsevier
Mosby, 2011, pp 118119.
2. Brant WE: The Core Curriculum, Ultrasound. Philadelphia,
PA, Lippincott Williams & Wilkins, 2001.
3. Sugito K, Kusafuka T, Kawashima H, et al: Usefulness of
power Doppler ultrasonography and supraparamagnetic iron
oxide enhanced magnetic resonance imaging for diagnosis
of focal nodular hyperplasia of the liver after treatment of
neuroblastoma. Pediatr Hematol Oncol 2010;27:250256.
4. Gong L, Li Y, Su G, et al: Use of X-chromosome inactivation pattern and laser microdissection to determine the
origin of focal nodular hyperplasia of the liver. Pathology
2009;41(4):348355.
5. Li T, Qin L, Ji Y, et al: Atypical hepatic focal nodular
hyperplasia presenting as acute abdomen and misdiagnosed as hepatocelluar carcinoma. Hepatol Res 2007;37:
11001105.
6. Hsee L, McCall J, Koea J: Focal nodular hyperplasia: what
are the indications for resection? HPB 2005;7:298302.
7. McPhee ST, Papadakis MA: Current Medical Diagnosis
and Treatment. 49th ed. New York, McGraw-Hill, 2010.
8. Kawamura DM, Lunsford BM: Diagnostic Medical Sonography: Abdomen and Superficial Structures. 3rd ed. Baltimore, MD, Lippincott Williams & Wilkins, 2012.
9. Lee JKT, Sagel SS, Stanley RJ, Heiken JP: Computed Body
Tomography With MRI Correlation. Vol. 2, 4th ed. Philadelphia, PA, Lippincott Williams & Wilkins, 2006.
10. Rasmussen F: Focal nodular hyperplasia. Acta Radiologica
2006;47(4):338.
11. Wasif N, Sasu S, Conway W, Bilchik A: Focal nodular
hyperplasia: report of an unusual case and review of the literature. Am Surg 2008;74:11001103.
12. Bonney G, Gomez D, Al-Mukhtar A, et al: Indication for
treatment and long-term outcome of focal nodular hyperplasia. HPB 2007;9:368372.
13. Demarco M, Shen P, Bradley R, et al: Intraperitoneal hemorrhage in a patient with hepatic focal nodular hyperplasia.
Am Surg 2006;72:555559.
14. Sudour H, Mainard L, Baumann C, Clement L, Salmon A,
Bordigoni P: Focal nodular hyperplasia of the liver following hematopoietic SCT. Bone Marrow Transplant 2009;
43:127132.

McCann and Penny


15. Di Carlo I, Urrico GS, Ursino V, Russello D, Puleo S, Latteri
F: Simultaneous occurrence of adenoma, focal nodular hyperplasia, and hemangioma of the liver: are they derived from a
common origin? J Gastroenterol Hepatol 2003;18:227230.
16. Bahirwani R, Reddy KR: Review article: the evaluation of solitary liver masses. Aliment Pharmocol Ther 2008;28:953965.
17. Reddy K, Kligerman S, Levi J, et al: Benign and solid
tumors of the liver: relationship to sex, age, size of tumors,
and outcome. Am Surg 2001;67:173178.
18. Weik C, Greiner L: The liver in hereditary hemorrhagic
teleangiectasia (Weber-Rendu-Osler disease). Scand J Gastroenterol 1999;34:12411246.
19. Inada M, Kita K, Kondo F, et al: Large regenerative nodule perfused by the portal vein. J Gastroenterol Hepatol
2005;20:17941798.

23
20. Coopersmith CM, Lowell JA, Hassan A, Howard TK:
Hepatocellular carcinoma in a patient with focal nodular
hyperplasia. HPB 2002;4(3):135138.
21. Sotiropoulos GC, Bockhorn M, Molmenti EP, Fouzas I,
Broelsch CE, Lang H: Hepatocellular carcinoma as a coincidental finding in a patient undergoing surgery for focal
nodular hyperplasia. Liver Int 2008;28(4):578579.
22. Langrehe JM, Pfitzmann R, Radke H, et al: Hepatocellular
carcinoma in association with hepatic focal nodular hyperplasia. Acta Radiol 2006;4:340344.
23. Hagen-Ansert SL: Textbook of Diagnostic Sonography. 7th
ed. St. Louis, MO, Elsevier Mosby, 2012.
24. Sirli R, Sporea I, Martie A, et al: Contrast enhances ultrasound in focal liver lesionsa cost efficiency study. Med
Ultrasonography 2012;12(4):280285.

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Article: Focal Nodular Hyperplasia: Case Study,


Imaging, and Treatment
Authors: Chelsey N. McCann, RT(R), RDMS, and
Steven M. Penny, BS, RT(R), RDMS
Category: Abdomen
Credit: 1.0 SDMS CME Credit

2. FNH is coexistent with hepatic hemangioma in


approximately what percentage of patients?
a. 10%15%
b. 15%20%
c. 20%25%
d. 25%30%

Objectives: After studying the article entitled Focal


Nodular Hyperplasia: Case Study, Imaging, and
Treatment, you will be able to:

3. FNH is coexistent with hepatocellular carcinoma


in approximately what percentage of patients?
a. 2%
b. 3%
c. 4%
d. 5%

1. Explain the risk factors for development of


focal nodular hyperplasia
2. Describe the sonographic imaging findings
associated with focal nodular hyperplasia
3. Determine the role of ultrasound contrast in the
evaluation of liver lesions
1. Focal nodular hyperplasia (FNH) is the _______
most common benign hepatic mass.
a. First
b. Second
c. Third
d. Fourth

4. The typical size of an FNH at the time of discovery


is approximately
a. 3 mm
b. 6 mm
c. 8 mm
d. 10 mm
5. Recent studies suggest that FNH is a mass
consisting of
a. Monoclonal cells and is neoplastic in origin
b. Monoclonal cells and is nonneoplastic in origin

25

JDMS CME ArticleSDMS CME Credit


c. Polyclonal cells and is neoplastic in origin
d. Polyclonal cells and is nonneoplastic in origin
6. FNH typically presents clinically with
a. No symptoms
b. Abdominal pain
c. Right flank pain
d. Intraperitoneal bleeding
7. A sonographic feature of FNH is a central scar
with prominent vasculature, which may appear on
imaging to be
a. Hypoechoic or hyperechoic
b. Always hypoechoic
c. Always hyperechoic
d. Isoechoic
8. With contrast-enhanced ultrasound, FNH shows
hypervascularity during the
a. Injection phase
b. Arterial phase
c. Venous phase
d. Washout phase

9. Contrast-enhanced ultrasound detects FNH with


an accuracy of approximately
a. 60%65%
b. 70%75%
c. 85%90%
d. >95%
10. C
 urrent recommended management of asymptomatic FNH is
a. Surgical resection
b. Cryoablation
c. Embolization of the central vessel
d. Routine sonographic surveillance