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AJR Integrative Imaging LIFELONG LEARNING FOR RADIOLOGY |
1 Division of Abdominal Imaging and Interventional Radiology, Department of
Radiology, Massachusetts General Hospital and Harvard Medical School, White
270, 55 Fruit St., Boston, MA 02114.
2 Department of Radiology, Tri-Service General Hospital and National Defense
Medical Center, Taipei, Taiwan.
3 Department of Radiology, Azienda Ospedaliera di Benevento G. Rummo, Beltiglio,
BN, Italy.
Received May 16, 2007; accepted after revision June 11, 2007.
Address correspondence to C. H. Liu
(cute610627{at}gmail.com).
Keywords: CT • hepatic actinomycosis • MRI
OBJECTIVE
A 45-year-old woman presented with a lobulated, hypoechoic mass in the left lobe of the liver on abdominal sonography. Abdominal CT showed a hyperdense to isodense hepatic mass with a peripheral low-density rim in portal venous phase images. Abdominal MRI showed a hypointense mass on T1- and T2-weighted images. The peripheral rim of the mass was T1 hypointense and T2 hyperintense. On dynamic series, the mass showed marked enhancement in the arterial phase and subsequent progressive washout in the delayed phase. The peripheral rim exhibited delayed enhancement. The final pathologic diagnosis was hepatic actinomycosis.
CONCLUSION
Hepatic actinomycosis is a rare granulomatous disorder. Imaging findings of hepatic actinomycosis are various and may mimic those of neoplasms. Abdominal MRI offers the benefit of tissue contrast that is superior to that of CT in the differentiation of inflammatory pseudotumor from other solitary hepatic neoplasms. Fine-needle biopsy or surgery is necessary for definite diagnosis and management.
Case History
A 45-year-old woman was admitted because of a 1-week history of
intermittent high fever, general malaise, and poor appetite. She had a history
of chronic hepatitis B and had never undergone surgery or abdominal trauma.
Physical examination revealed a fever of 39°C, hepatomegaly, and a
palpable mass with local tenderness over the right upper quadrant of the
abdomen.
Abnormal laboratory values included WBC, 13.7 x 103/mL;
hemoglobin, 7.8 g/dL; platelet count, 530 x 103/mL; and
lactate dehydrogenase, 887 U/L. Liver transaminase and alkaline phosphatase
values were normal; and tumor markers, including 
-fetoprotein and
carcinoembryonic antigen, were negative. After admission, broad-spectrum
antibiotics (cefazolin and gentamicin) were used to treat the underlying
inflammatory process.
Abdominal sonography revealed a 6.1 x 4.3 cm lobulated, inhomogeneous hypoechoic lesion in the left lobe of liver (Fig. 1A). The liver parenchyma showed a normal contour but increased echogenicity. No splenomegaly was identified. Abdominal CT was subsequently performed.
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Contrast-enhanced abdominal CT shows a homogeneous, mildly hyper- to isodense mass with a peripheral low-density rim on portal venous phase images. The differential diagnosis includes hepatocellular adenoma, hepatocellular carcinoma, hypervascular metastases, peripheral cho langio car cinoma, and inflammatory pseudo tumor. The history of chronic hepatitis B and the CT findings of a hyper- to isodense solitary hepatic mass place hepatocellular carcinoma at the top of the differential diagnosis list. However, the possibility of other differential diagnoses exists.
MRI
An MRI examination (1.5-T scanner, Vista, Picker) of the liver is performed
2 days after the CT study. It reveals a well-defined mass with a mildly
irregular contour in the left lobe of the liver, with hypointensity on both
T1- and T2-weighted images (Figs.
1H and
1I). A peripheral rim of
hypointensity on T1-weighted images and hyperintensity on T2-weighted images,
suggesting edematous change, circumscribes the mass (Figs.
1C and
1D). Multiphasic dynamic MR
images are obtained at 30 seconds (arterial phase), 70 seconds (portal venous
phase), and 3, 6, and 10 minutes (delayed phase). On the dynamic images, the
mass shows marked enhancement in the arterial phase images
(Fig. 1E) and subsequent
progressive washout, resulting in a punctate appearance on the delayed phase
images (Figs. 1F,
1G,
1H, and
1I). The peripheral rim
exhibits delayed enhancement (Figs.
1H and
1I).
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Expert Discussion (Dr. Liu)
MRI was performed to characterize the hepatic mass. According to the
enhancing pattern of the mass—marked enhancement on arterial phase
images and subsequent progression washout on delayed phase images—the
differential diagnosis includes hepatocellular adenoma, hepatocellular
carcinoma, hypervascular metastasis, peripheral cholangiocarcinoma, and
inflammatory pseudotumor. We will consider each of these in turn.
Hepatocellular adenoma has an incidence of 1/1,000,000 and is predominant in women of child-bearing age. The use of oral contraceptives in women or steroids in men seems to lead to an increased incidence of hepatocellular adenoma. These adenomas are usually solitary in 70–80% of cases, may have a fibrous capsule, and have a tendency to hemorrhage. They frequently show heterogeneous hypointensity on T1-weighted images and heterogeneous hyperintensity on T2-weighted images. Occasionally they have a peripheral hypointense rim on both T1- and T2-weighted images corresponding to a fibrous capsule. On dynamic images, they show enhancement during the arterial phase and isointensity or slight hyperintensity on portal venous and delayed phase images.
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1-antitrypsin deficiency, excessive androgen and oral
contraceptive use, hemochromatosis, and exposure to aflatoxin or vinyl
chloride. On MRI, hepatocellular carcinomas are often hypointense on
T1-weighted images and hyperintense on T2-weighted images. On dynamic images,
most hepatocellular carcinomas are homogeneously hyperintense to the liver on
arterial phase images and hypointense on the portal venous and delayed phase
images. Hepatocellular carcinoma is called "encapsulated" when it
is completely surrounded by a fibrous capsule. The capsule usually enhances
prominently on portal venous phase images. Thereafter, enhancement persists,
with signs of washout into the delayed phase. This is due to the slow flow in
the blood vessels that are present in the abundant fibrous granulation
tissue. Metastases are the most common malignant focal liver lesions in the noncirrhotic liver. Hypervascular metastases frequently arise from renal cell carcinomas, breast cancer, islet cell carcinomas, melanomas, sarcomas, pheochromocytomas, carcinoid, and thyroid carcinomas, and are best seen on arterial phase images. During the portal venous phase, these lesions often are isodense with the normal liver and difficult to detect. On MRI, the signal intensity of hypervascular metastases varies considerably, depending on the degree of vascularity, necrosis, and hemorrhage. They often show hypo- to isointensity relative to the surrounding parenchyma on T1-weighted images and hyperintensity on T2-weighted images. On dynamic imaging, they reveal strong transient enhancement in the arterial phase, followed by isointensity in the portal venous and delayed phases.
Cholangiocarcinomas are malignant tumors of the biliary system and constitute 15–25% of all liver and biliary tract cancers. They are divided according to their location into hilar adenocarcinoma (Klatskin tumor), intrahepatic cholangiocarcinoma (peripheral type), and carcinoma of the extrahepatic bile ducts (distal type). Peripheral cholangiocarcinoma arises from small biliary intrahepatic radicals and usually presents as a large hepatic mass. They are typically hypovascular masses and show isointensity or hypointensity relative to the normal liver on T1-weighted images that may range from marked to mild hyperintensity on T2-weighted images. On dynamic imaging, minimal or moderate incomplete enhancement is seen at the tumor periphery in the arterial phase, whereas progressive central enhancement is seen in the delayed phase. This pattern of enhancement reflects the hypovascular, desmoplastic composition of most cholangiocarcinomas.
Inflammatory pseudotumor is a rare benign mass in the liver. The lesion may appear in almost every tissue and anatomic location and mimics malignancy on imaging findings. The etiology of inflammatory pseudotumor remains unclear. It may be due to a post-inflammatory regenerative process or a primary neoplastic process. Hepatic inflammatory pseudotumors are usually solitary, but they have been reported to be multiple and synchronous in 20% of cases. On MRI, these pseudotumors are moderately hypointense on T1-weighted images and usually mildly hyperintense on T2-weighted images. On dynamic imaging, they show late enhancement in the delayed phase due to hypovascularity.
In this patient, the mass showed hypointensity on T2-weighted images, indicating fibrous composition, calcification, or hemosiderin deposition. However, no calcifications in the mass were seen on sonography, and no different stages of blood were identified on MRI. The finding of a hepatic mass with fibrous tissue narrows the differential diagnosis to peripheral cholangiocarcinoma and inflammatory pseudotumor. Additionally, the peripheral rim of the mass showed hypointensity on T1-weighted images, hyperintensity on T2-weighted images, and delayed enhancement on delayed phase images, indicating edematous change. Unlike hepatic neoplasm, inflammatory pseudotumor usually has a marked peripheral edematous area. Delineation of progressive contrast washout, resulting in a punctate appearance on delayed phase MR images, strongly suggests the diagnosis of an inflammatory pseudotumor with fibrous tissue and multiple small necrotic areas.
The mass in the spleen was suggestive of hamartoma by radiographic findings and showed no interval change after 2 years of follow-up.
Clinical Management
Sonographically guided fine-needle biopsy of the mass was performed, and
mixed acute and chronic inflammatory tissues were found. The specific organism
was not identified, and the symptoms of intermittent high-grade fever and
local tenderness over the right upper quadrant persisted; therefore, a left
hepatic lobectomy was performed. At surgery a yellowish inflammatory mass with
puslike content was removed. The microscopic findings included inflammatory
cell infiltration and fibroblastic tissue in the mass accompanied by
filamentous organisms showing sulfur granules, which is consistent with the
diagnosis of hepatic actinomycosis (Fig.
1J).
The patient was prescribed penicillin, 6 million U per day for 8 days, and discharged receiving oral tetracycline. Follow-up continued, and 24 months after discharge the patient is doing well clinically.
Commentary
Hepatic actinomycosis is an uncommon suppurative infection that was first
described in 1878 [1]. It is
characterized by chronic, localized inflammatory process associated with
fever, leucocytosis, hypergammaglobulinemia, and an elevated alkaline
phosphatase level. It is thought to be related to previous abdominal
inflammation, trauma, or surgery, causing secondary hepatic spread.
Actinomycosis is caused by actinomycetes, usually Actinomyces
israelii [2], a
gram-positive, non-spore-forming anaerobic bacterium, found as a normal
commensal in the oral cavity, tonsillar crypts, and colon
[3]. A common site of infection
is the cervicofacial region, at a rate of 70–90% of cases; it is also
seen in the thoracic and abdominal regions
[1]. Hepatic actinomycosis is
found in 5% of all cases of actinomycotic infections and 15% of those with
abdominal actinomycotic infections. It is usually secondary to an
actinomycotic infection elsewhere, especially in the gastrointestinal tract,
most commonly in the ileocecal area
[1–6].
Although the direct spread of actinomycosis is usual, hematogenous
dissemination via the portal system or a hepatic artery from an intraabdominal
focus occurs in only a few cases
[4]. In the case presented,
there is no abdominal trauma or surgical history; therefore, a primary hepatic
actinomycosis should be considered
[5].
The clinical presentation of hepatic actinomycosis is variable and nonspecific. Signs and symptoms include tender hepatomegaly, jaundice, progressive palpable mass, and fever [2, 3]. Peripheral blood leucocytosis, hypergammaglobulinemia, an elevated alkaline phosphatase level, and mild to moderate impairment of other liver biochemical tests are characteristic, but not invariably present [3]. Our patient had leucocytosis, but other blood test results were within normal limits and therefore misleading.
The diagnosis of hepatic actinomycosis is established by histopathologic findings. The characteristic appearance is that of an inflammatory pseudotumor, with effacement of liver parenchyma by foamy histocytes and an inflammatory infiltrate composed of eosinophiles and plasma cells in a fibrous stroma [6]. On H- and E-stained tissue sections, classic sulfur granules are the hallmark for the diagnosis. Most patients with this disorder respond favorably to treatment with penicillin [1, 3].
Diagnostic imaging may reveal one of the three patterns of hepatic actinomycosis: a solitary intrahepatic mass mimicking a neoplasm, multiple liver abscesses, and a disseminated pattern [3]. The CT features of hepatic actinomycosis have been reported in several English-language articles [1–4, 7, 8]. On CT images, it usually appears as an ill-defined low-density mass on unenhanced scans. After contrast administration, it usually shows a poorly enhancing center with a thickened and enhanced wall [1-4, 7, 8]. Boucenna and Arrivé [9] also reported a solitary hepatic actinomycosis with transient contrast enhancement during the arterial phase and hypodensity during the portal venous phase, mimicking malignancy. In our patient, a mildly hyperdense to isodense mass, with a low-density rim, was shown on the contrast-enhanced CT images. Because the patient had a hepatitis B viral infection, the initial diagnosis of hepatocellular carcinoma has not been completely ruled out.
The MRI features of hepatic actinomycosis have been discussed rarely [10–12]. Nazarian et al. [10] first described the MRI features of multiple actinomycotic liver abscesses and revealed the mass was hypointense to the liver on T1-weighted images and hyperintense on T2-weighted images, with some parenchymal edema surrounding it. After the IV administration of gadopentetate dimeglumine, the lesions showed no central enhancement on either early or delayed T1-weighted gradient-echo images. Only mild early enhancement of a thick peripheral rim was identified. In our patient, dynamic MR images revealed intense central enhancement of the lesion in the arterial phase and progressive washout in the delayed phase. Persistent enhancement of the peripheral rim in the delayed phase was also seen. These imaging findings corresponded with the microscopic findings of increased neovascularization in the inflammatory mass surrounded by a marked edematous area.
In summary, solitary hepatic actinomycosis frequently mimics malignancy. Imaging studies, especially MRI, can be helpful in differentiating solitary inflammatory pseudotumor from malignancy. Fine-needle biopsy or surgery is essential for appropriate diagnosis and treatment.
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  C.-H. Liu, D. C. Rivard, A. C. Silva, K. J. Burkholz, and S. D. Beaty Imaging of Focal Hepatic Lesions: Self-Assessment Module Am. J. Roentgenol., June 1, 2008; 190(6_Supplement): S65 - S68. [Abstract] [Full Text] [PDF]
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