DOI:10.2214/AJR.06.1076
AJR 2007; 189:67-72
© American Roentgen Ray Society
Imaging Features of Sclerosed Hemangioma
Deirdre J. Doyle1,
Korosh Khalili1,
Maha Guindi2 and
Mostafa Atri3
1 Department of Medical Imaging, University Health Network and Mount Sinai
Hospital, 610 University Ave., Toronto, Ontario, M5G 2M9, Canada.
2 Department of Pathology, University Health Network and Mount Sinai Hospital,
Toronto, Ontario, Canada.
3 Department of Medical Imaging, Sunnybrook and Women's Hospital, Toronto,
Ontario, Canada.
Received August 13, 2006;
accepted after revision October 31, 2006.
Address correspondence to D. J. Doyle
(Deirdre.Doyle{at}uhn.on.ca).
Abstract
OBJECTIVE. The purpose of this study was to review the imaging
features of sclerosed hemangioma.
CONCLUSION. In our series, suggestive features of sclerosed
hemangiomas include geographic outline, capsular retraction, decrease in size
over time, and loss of previously seen regions of enhancement. Additional
features include presence of transient hepatic attenuation difference (THAD),
rim enhancement, and nodular regions of intense enhancement as seen in typical
hemangiomas. Although not pathognomonic, some features of sclerosed hemangioma
can suggest it as a diagnostic possibility and lead to biopsy rather than more
extensive intervention.
Keywords: abdominal imaging • CT • liver • MRI • radiologic–pathologic correlation
Introduction
Cavernous hemangioma is the most common noncystic hepatic lesion, the
reported incidence being as high as 20%
[1]. Most hemangiomas remain
stable on follow-up imaging
[2]; growth and spontaneous
regression are reported to be very rare
[3]. Hemangiomas that undergo
degeneration and fibrous replacement are called sclerosed, thrombosed, or
hyalinized hemangiomas [4].
Although there have been isolated case reports of sclerosed hemangioma
[4–7],
no case series have been reported, to our knowledge. It has been suggested
that prospective diagnosis of sclerosed hemangioma is impossible
[5]. Our aim was to review the
imaging features of a series of proven sclerosed hemangiomas to determine
whether there are features that would allow prospective diagnosis.
Materials and Methods
This retrospective study was approved by our institutional research ethics
board, and informed consent was waived. A retrospective search through
pathology reports from August 2001 to January 2005 for the diagnosis of
sclerosed hemangioma in hepatectomy or liver biopsy specimens yielded seven
hemangiomas in five patients who underwent imaging before intervention.
Percutaneous biopsy was performed in four lesions, intraoperative biopsy was
performed in one lesion, and a right hepatectomy yielded two sclerosed
hemangiomas. Four of five patients had known primary malignant tumors (two of
the colon, one of the rectum, and one gastrointestinal stromal tumor). One
patient had a history of hepatitis B and C, but the liver did not appear
cirrhotic. Twenty-five additional patients were found through retrospective
review of the radiology information system from December 2000 through December
2004 with the search terms "sclerosed/sclerosing,"
"thrombosed/thrombosing," "hyalinized/hyalinizing,"
and "hemangioma." Inclusion criteria used for the imaging
diagnosis of sclerosed hemangioma were available previous triphasic CT scans
showing peripheral nodular enhancement with further filling of the lesion on
delayed images (Fig. 1A) and
follow-up CT scans showing change in morphologic characteristics over time
(Fig. 1B). Only three of these
25 patients were eligible for inclusion because they had undergone previous CT
that showed typical hemangioma with subsequent change in imaging
characteristics over 9–20 months. In total, 10 sclerosed hemangiomas
were identified in eight patients (four men, four women) with an age range of
46–77 years (mean, 58 years).
Imaging findings on CT (10 lesions), MRI (six lesions), and sonography
(five lesions) were analyzed. Lesion size, number, morphologic features,
calcification, relative attenuation, T1- and T2-weighted signal intensity, and
enhancement characteristics were analyzed. Follow-up images of six lesions
were available after the initial appearance of sclerosis, and these images
were assessed for changes in lesion size and enhancement pattern. CT was
performed with a 4-MDCT (n = 4), 8-MDCT (n = 3), 16-MDCT
(n = 1), or 64-MDCT (n = 2) scanner (LightSpeed QX/I or
Ultra, GE Healthcare; Sensation 16, Siemens Medical Solutions; Aquilion 64,
Toshiba). Protocols included portal venous phase only (70 seconds, 5-mm slice
thickness, 2.5-mm reconstruction interval) for three lesions and a triphasic
liver protocol for seven lesions (unenhanced, 25 and 65 seconds, 5-mm slice
thickness, 2.5-mm reconstruction interval). All patients were given IV
contrast material: iodixanol (Visipaque 270, GE Healthcare) in six cases and
iohexol (Omnipaque, GE Healthcare) in two cases. The dosage was a volume of
100–160 mL at a rate of 5 mL/s with exposure factors of 120 kV and
140–415 mA.
The following MR images were acquired with a 1.5-T system (Genesis Sigma
and Sigma Excite, GE Healthcare): axial spoiled gradient-recalled in- and
out-of-phase T1-weighted images (TE, 4.2 and 2.1), coronal single-shot fast
spin-echo T2-weighted, axial T2-weighted breath-hold fast-recovery fast
spin-echo (TE, 90), and axial single-shot fast spin-echo T2-weighted images
(TE, 180). Dynamic contrast-enhanced, fat-saturated, fast spoiled
gradient-recalled (minimum TE) images were obtained after administration of
gadodiamide (Omniscan, GE Healthcare) (four lesions) and gadobenate
dimeglumine (MultiHance, Bracco Diagnostics) (two lesions). Gadobenate
dimeglumine was used for improved detection of liver lesions in the delayed
parenchymal phase in the one patient with known metastatic disease. At
present, however, this agent is not routinely used at our institution for
detection of metastatic disease. Delayed contrast-enhanced spoiled
gradient-recalled T1-weighted images with fat saturation were also obtained 5
minutes after gadodiamide injection and 5 minutes and 3 hours after gadobenate
dimeglumine injection.
Results
Morphologic Appearance
Lesion size ranged from 1.4 to 7.7 cm (mean, 3.7 cm). All 10 lesions had a
geographic pattern (Fig. 2A).
Seven of 10 lesions exhibited volume loss, which manifested as capsular
retraction or concavity over the lesion. This finding appeared on follow-up
images of an additional lesion (Table
1). Calcification was found in only one lesion. In five patients,
additional hemangiomas found in the liver had a typical enhancement pattern
(Fig. 2A).
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Fig. 2A —56-year-old woman with colon cancer. Axial contrast-enhanced
CT scan at presentation shows two classic hemangiomas in left lobe
(arrows). Pathologically proven sclerosed hemangioma
(arrowheads) in segments VI and VII has geographic pattern, exhibits
hypoattenuation with capsular retraction, and exhibits no enhancement.
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Enhancement Characteristics
Dynamic enhancement characteristics were present in eight of 10 sclerosed
hemangiomas, three with CT, one with MRI, and four with both techniques.
Dynamic studies of the other two lesions showed no visual evidence of internal
enhancement (Figs. 2A and
2C). In one patient,
enhancement was found only in the venous phase of CT. Unenhanced CT images of
six lesions showed hypoattenuation compared with adjacent liver tissue.
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Fig. 2C —56-year-old woman with colon cancer. Axial MR image obtained
after administration of gadobenate dimeglumine shows rim enhancement of
metastatic lesion and absence of enhancement of sclerosing hemangioma
(arrowhead).
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Arterial phase—Nodular foci of enhancement, not necessarily
in the periphery of the lesions, were found in the arterial phase of CT of six
of eight lesions. In addition, wedge-shaped regions of transient hepatic
attenuation difference around the lesion were found in five of eight lesions
(Figs. 3 and
4A). Transient rim enhancement
was found in two of eight lesions (Figs.
1B,
3, and
4C).
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Fig. 3 —61-year-old woman with gastrointestinal stromal tumor and
biopsy-proven sclerosed hemangioma. Axial arterial phase CT scan shows
geographic lesion in left lobe of liver with rim and nodular enhancement and
peripheral transient hepatic attenuation difference (arrowhead).
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Fig. 4A —53-year-old man with hepatitis B and C and biopsy-proven
sclerosed hemangioma. Axial contrast-enhanced CT scan shows large
hypoattenuating lesion of liver segments VII and VIII with central and
peripheral nodular areas of enhancement and large peripheral transient hepatic
attenuation difference (arrowheads).
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Portal venous phase—In five of six lesions, the nodular foci
of enhancement were the same size in the venous phase but had grown in one of
six lesions (Figs. 3 and
4A). In one patient, slight
peripheral nodular enhancement was found in the venous phase only. In another
patient, rim enhancement also was found in the venous phase.
Delayed phase—Delayed-phase images were available for six of
the 10 lesions. Three of these lesions were visualized on CT, two on MRI, and
one on both CT and MRI. Images of five of the six lesions showed new,
irregular regions of delayed enhancement within the lesions that manifested as
areas of mild hyperattenuation or hyperintensity compared with adjacent liver
(Fig. 4D). In one patient who
received gadobenate dimeglumine, typical hemangiomas were homogeneously
hypointense with the liver on the delayed images. The two sclerosed
hemangiomas were homogeneously isointense or nearly isointense with the liver
and therefore were almost imperceptible
(Fig. 2D). This patient also
had a hepatic metastatic lesion from a colorectal primary lesion that
exhibited heterogeneous uptake of the contrast agent in the delayed phase
(Fig. 2D).
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Fig. 2D —56-year-old woman with colon cancer. Delayed MR image after
administration of gadobenate dimeglumine shows heterogenous signal intensity
of metastatic lesions, hypointense classic hemangioma, and isointense
sclerosing hemangioma (arrowhead).
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MRI Signal Intensity
Six lesions in four patients were evaluated with MRI. All lesions appeared
hypointense on T1-weighted images. High signal intensity such as that of
typical hemangioma on T2-weighted images with intermediate and long echo times
was present to variable degree in all lesions
(Fig. 4B). In two sclerosed
hemangiomas in the same patient, the entire lesion was of homogeneous high
signal intensity (greater than that of spleen but darker than that of CSF)
(Fig. 2B). In the other
lesions, variable degrees of peripherally based areas of high T2-weighted
signal intensity were mixed with areas of isointensity to hypointensity
compared with the liver. The areas of high signal intensity corresponded to
regions of early and nodular enhancement, whereas the isointense to
hypointense areas exhibited enhancement only on 5-minute delayed images (Figs.
4B and
4D).
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Fig. 4B —53-year-old man with hepatitis B and C and biopsy-proven
sclerosed hemangioma. Axial T2-weighted MR image shows central and peripheral
regions of increased signal intensity corresponding to foci of enhancement in
A and larger regions appearing isointense or hypointense.
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Fig. 2B —56-year-old woman with colon cancer. Follow-up T2-weighted
axial MR image 64 months after presentation shows interval development of
metastatic lesion of colon carcinoma in liver segments V and VI. Two classic
hemangiomas of high signal intensity persist. Previously seen sclerosing
hemangioma (arrowhead) in segments VI and VII has higher signal
intensity than spleen.
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Sonographic Features
Four lesions were heterogeneously hyperechoic. A 5.3-cm lesion in one
patient was not prospectively detected on sonography.
Follow-Up Imaging
Follow-up imaging of six lesions over 7–64 months (average, 32
months) showed that the size of four of the lesions decreased. In four
lesions, internal enhancement had been found in the venous phase of the
original scan. The follow-up images showed that in three of the four lesions,
the regions of enhancement decreased in size and number or entirely
disappeared.
Discussion
Many incidental benign liver lesions are found during routine examinations
and during staging of known malignant disease. In addition, the high incidence
of hemangioma increases the probability of encountering atypical
manifestations, including sclerosis. It has been suggested
[5] that prospective
differentiation of a sclerosed hemangioma from a malignant tumor is not
possible.
In our series of 10 lesions, we found features suggestive of sclerosed
hemangioma. All 10 lesions had a geographic pattern, and volume loss
manifested by capsular retraction eventually was seen in eight lesions. The
presence of transient hepatic attenuation difference in the arterial phase
(five of eight lesions), nodular regions of enhancement (six of eight
lesions), and additional typical hemangiomas (five of eight patients) further
increase suspicion. Rim enhancement, seen in three of 10 lesions, has been
described in case reports
[5–7].
Although it is not unique, this sign can be helpful when present. The
heterogeneity of signal intensity of sclerosed hemangiomas on T2-weighted
images in our series detract from the normally high specificity of high T2
signal in the recognition of hemangiomas. However, areas of typical high
T2-weighted signal intensity on the long TE (180 milliseconds) sequences,
which correspond to areas of enhancement, may be of minor help. Areas of
unusually low T2-weighted signal intensity, which may represent regions of
sclerosis (fibrosis) may also provide assistance. Ultimately, apart from
previous documentation of typical hemangioma, we have not found features
definitive for the diagnosis of sclerosis. However, the combination of
findings may be enough to suggest biopsy for diagnosis instead of definitive
therapy for some lesions.
The findings on 3-hour delayed gadobenate dimeglumine images of a patient
with rectal carcinoma and hepatic metastasis adjacent to the larger
hemangioma, which led to resection, were intriguing. The sclerosed hemangiomas
were long-standing and on delayed imaging became isointense to the adjacent
liver. The contrast agent was taken up by the hepatocytes in the adjacent
liver tissue and was retained in the lesions, presumably because of their
highly fibrous nature. The other typical hemangiomas appeared well defined and
hypointense, but the metastatic lesions had a highly heterogeneous appearance.
The finding of homogeneous delayed retention of contrast agent raises the
possibility of differentiating long-standing sclerosed hemangiomas with this
technique. This possibility warrants further study.
Haratake et al. [5] and
Takayasu et al. [6] described
histologically proven sclerosed hemangiomas that exhibited persistent
irregular ring and slight peripheral enhancement on CT. Yamashita et al.
[7] described a lesion with
marginal pooling of contrast material on CT and MRI. Those authors suggested
that sclerosing hemangioma be included in the differential diagnosis of
colorectal metastasis. Aibe et al.
[8] proposed that sclerosing
hemangioma be included in the differential diagnosis of hepatic lesions with
delayed enhancement. Another report
[9] describes nonenhancing,
well-demarcated nodular areas proven at pathologic examination to be sclerotic
nodules responsible for the atypical CT findings. Cheng et al.
[4] described hyalinized
hemangiomas showing lower signal intensity than CSF on T2-weighted images,
lack of early enhancement, and slight peripheral enhancement in the late
phase.
Ros et al. [10] found that
nodular areas of reduced signal intensity on T2-weighted images corresponded
to the histologic finding of fibrosis. Fibrosis when present occurs within the
body of a hemangioma, beginning in the center and extending more peripherally
to a variable degree [11].
Sometimes a sclerotic nodule can grow large enough to replace the entire
hemangioma, mimicking other solid tumors
[5]. Collagen-rich and
relatively acellular mature fibrous tissue is generally of lower signal
intensity than muscle on T2-weighted images because of decreased free-water
content and low mobile proton density
[6]. Tung et al.
[12] proposed that the
appearance of hemangiomas on T2-weighted images should reflect the opposing
influences on T2-weighted relaxation of slowly flowing blood in vascular
spaces and connective tissue. A complicating factor is the contribution to
signal heterogeneity of hemorrhage, thrombosis, hyalinization, calcification,
and cystic cavities [6,
10].
The process of sclerosis generally begins in the center of a hepatic
hemangioma and can extend to involve the entire lesion. The term
"sclerosed" is reserved for hemangiomas that are predominantly
fibrosed with near complete obliteration of the vascular spaces
[13]. The term
"sclerosing" is used to describe partially affected lesions. The
histologic appearance of sclerosed hemangiomas is different from the areas of
thrombosis seen in giant hemangioma. The extent to which sclerosing and
sclerosed hemangiomas are related is unresolved. Results of one study
[13] suggest that sclerosed
hemangiomas develop from capillary hemangiomas but that sclerosing hemangiomas
arise from cavernous hemangiomas. In our series, all of the lesions diagnosed
on the basis of pathologic findings fit the definition of sclerosed
hemangioma, not hemangioma with an area of sclerosis. Moreover, all of the
lesions had imaging appearances that did not fit the imaging criteria for
hemangioma, with or without scarring.
In our series, features suggestive of sclerosed hemangiomas included
geographic pattern, capsular retraction, decrease in size over time, and loss
of previously seen regions of enhancement. Additional features included the
presence of transient hepatic attenuation difference, rim enhancement, and
nodular regions of intense enhancement as seen in typical hemangioma. A
combination of these findings should raise the possibility of the presence of
sclerosed hemangioma, which can be diagnosed with biopsy before more complex
intervention is undertaken.
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Abstract
Introduction
