Imaging of Benign Hepatic Masses

Using helical CT and rapid IV injection of contrast material, benign hepatic masses are discovered in at least 20% of subjects. To minimize expensive and invasive evaluation, an orderly approach to the interpretation of these lesions is necessary. Many benign lesions have a near pathognomonic appearance on a properly performed and interpreted CT scan. Others can have the diagnosis confirmed by a specific and well-chosen follow-up study, such as contrast-enhanced MR. In this article we present the most common types of benign hepatic masses and our approach to their diagnosis.

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KEYWORD

Computed tomography - imaging - liver - neoplasms

With the increasing use of cross-sectional imaging for evaluation of various abdominal signs and symptoms, benign hepatic masses are frequently discovered. This is especially true as imaging equipment and techniques become more sophisticated, allowing detection of small and hypervascular hepatic lesions that were virtually unknown to radiologists a decade ago. Many of these benign lesions are of no clinical concern but may be mistaken for malignant tumors, often resulting in overly aggressive evaluation and treatment.

The goal of this article is to present the most commonly encountered benign hepatic masses in adult patients along with an orderly plan for diagnosis and management. In most cases we are assuming that the hepatic mass has been detected first on abdominal computed tomography (CT), because this reflects the prevalent practice in North America in which abdominal magnetic resonance imaging (MRI) is used in a problem-solving mode, and ultrasonographically detected masses almost always have further evaluation by CT. We are also assuming that the CT evaluation of the hepatic mass includes multiphasic helical CT with rapid bolus injection of IV contrast material (see Federle and Blachar, pages 135-146). CT scans performed on nonhelical CT scanners or with drip or slow infusion of contrast material are markedly inferior for detection and characterization of hepatic masses.

The liver is a large, fairly homogeneous organ that is commonly involved secondarily by systemic or extrahepatic vascular, metabolic, infectious, and malignant processes. Our focus is on primary benign hepatic tumors and tumor-like conditions in adults. As listed in Table [1], these may be classified by cell of origin as hepatocellular, cholangiocellular, or mesenchymal. Other classification schemes can be useful, such as hypervascular hepatic masses or cystic masses, as demonstrated on bolus-enhanced multiphasic CT or MRI studies. We can also target specific cellular and functional aspects of liver masses by using certain radionuclide or MRI contrast agents that are designed for selective uptake as hepatobiliary or reticuloendothelial agents. These classification schemes allow us to narrow the differential diagnosis of focal hepatic lesions substantially. Using no more than one or two imaging tests, it is our experience that a confident diagnosis of benign liver masses is possible in most cases without the need for surgery, biopsy, or even follow-up imaging.

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HEPATIC CYSTS

Cystlike hepatic lesions may result from trauma (seroma or biloma), infection (pyogenic or parasitic abscess), or neoplasm (primary or metastatic). In most of these instances clinical evaluation is straightforward, and imaging will reveal some complexity of the cystic mass, such as thick septa, mural nodularity, or fluid-debris levels.

Simple, or developmental, cysts are believed to derive from biliary endothelium. They contain thin serous fluid, not bile, and are lined by a single layer of epithelium. They are reported to occur in 5 to 14% of the population and are more prevalent in women. Simple cysts are usually solitary to few in number, but innumerable cysts may occur in autosomal dominant or recessive polycystic disease, with or without involvement of the kidneys. Even with polycystic disease, liver function is rarely compromised; however, symptoms may occur due to large or multiple cysts or infection of the cyst. Most cysts are discovered incidentally and require no treatment unless they become infected.[1] [2]

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Imaging

On CT cysts appear as water-density (-10 to +10 Hounsfield units, or HU) sharply defined lesions with no visible wall and no more than two septa. No enhancement of the cyst contents or wall is found (Fig. [1]). The hepatic cysts in polycystic liver disease may vary in number (few to thousands), size (1-10 cm), and the cyst contents often are altered due to hemorrhage (Fig. [2]). Cysts are usually found in otherwise normal liver. Calcification of some cyst walls is frequent in polycystic disease.[1] [2]

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Further Evaluation

In most cases CT is definitive. In a patient with sepsis, needle aspiration might be warranted to exclude an abscess. A patient with a known malignancy, especially a primary cystic malignancy (e.g., ovarian cystadenocarcinoma) or sarcoma, may require further evaluation. Sonography is usually definitive in demonstrating simple cyst characteristics such as anechoic contents, thin wall, and through transmission of sound. Conversely, neoplastic or infected cysts invariably demonstrate debris, mural nodularity, thick septa, or other signs of complexity. MRI shows the same characteristics as CT, namely fluid contents and lack of enhancement. Unenhanced MRI may not be definitive, as cysts, hemangiomas, and certain neoplasms (necrotic and hypervascular) may all appear hypointense on T1-weighted images and markedly hyperintense on T2-weighted images.

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HEMANGIOMA

Hemangioma is the most common benign hepatic neoplasm, occurring in 5 to 20% of the population, the higher figure being derived from a thorough autopsy search for hemangiomas in an otherwise unselected population.[3] Women are affected more than men (5:1), and the lesions are commonly found in a subcapsular location in the right lobe of the liver. Hemangiomas occur sporadically without well-defined predisposing factors. Most lesions grow slowly and are uncommonly diagnosed in children. Even large and exophytic hemangiomas are usually asymptomatic, and spontaneous hemorrhage or other complications are extremely rare.

Hemangiomas consist of large endothelial-lined vascular spaces separated by fibrous septa. They can range in size from a few millimeters to more than 20 cm. While usually solitary, multiple hemangiomas are commonly encountered, and rare cases of hemangiomatosis have been reported.

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Imaging

In the era before helical CT, hemangiomas were diagnosed with confidence in only about 50% of cases.[4] Using proper CT technique and interpretive criteria, confident diagnosis should now be achieved in at least 90% of cases. Hemangiomas are nearly isodense to large blood vessels on unenhanced CT. After rapid intravenous (IV) bolus injection of contrast medium, hemangiomas show nodular or cloudlike peripheral enhancement that is isodense with large vessels, and they show progressive centripetal fill-in with enhancement over time (Fig. [3]).[5] [6] [7] [8] Hemangiomas more than 5 cm in diameter usually have a central area of necrosis or scar that may rarely calcify. If the other diagnostic criteria are met, this should not mitigate against the diagnosis of hemangioma. Small hemangiomas may demonstrate rapid uniform enhancement, similar to other hypervascular tumors (Fig. [4]). However, hemangiomas remain isodense to blood vessels on portal venous and delayed phases of enhancement, whereas other benign and malignant masses usually become hypodense to blood vessels and liver.[9]

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Further Evaluation

Small lesions considered too small to characterize on CT are often good candidates for sonography. Hemangiomas are usually very echogenic on sonography due to the fibrous septa between the vascular spaces (Fig. [4]). The fluid content may allow through transmission of sound. In most patients these sonographic signs can be considered definitive.

When sonography or CT is not definitive, MR can be helpful. Bolus IV administration of gadolinium (gadopentetate dimeglumine) demonstrates the same nodular peripheral enhancement and centripetal fill-in on T1-weighted images, and the lesions are intensely bright on heavily T2-weighted images (Fig. [3]).[7] Although Tc-labeled red blood cell radionuclide scintigraphy can also be definitive for hemangioma, most centers rely on MRI as the problem-solving technique of choice.

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FOCAL NODULAR HYPERPLASIA

Focal nodular hyperplasia (FNH) was rarely diagnosed by radiologists prior to the advent of helical CT and modern MRI techniques, but it may occur in some 2 to 5% of the population.[3] It is rarely symptomatic, although lesions may grow to more than 10 cm in diameter. Lesions are solitary in about 70% of patients and are few in number in the rest. Multiple lesions of FNH have been described in patients with certain brain neoplasms and vascular malformations of various organs[10] In our experience with 78 patients with FNH, 88% were women, with an average age at diagnosis of 37 years.[11] The use of exogenous steroids is certainly not necessary to develop FNH, although oral contraceptive use may stimulate the growth of FNH. We have uncommonly observed regression of FNH following cessation of oral contraceptive use.

FNH consists of a nonencapsulated firm nodule of normal hepatocytes with a distinct central scar and thin radiating fibrous septa containing Kupffer cells and primitive bile ductules.[12] Intratumoral calcification, fat, hemorrhage, and necrosis are all extremely rare.

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Imaging

Helical CT demonstrates characteristic and definitive findings in most patients with FNH.[11] [13] [14] The lesions are hypervascular and hyperdense to liver on arterial- phase CT images (30-45-sec delay) and enhance homogeneously (Fig. [5]). They are nearly isodense with liver on unenhanced, portal venous, and delayed-phase enhanced CT scans. They are usually subcapsular in location with ill-defined margins. For lesions more than 3 cm in diameter, CT demonstrates a central scar in 65% of cases, whereas only 35% of smaller lesions show a scar.[11] Multiplanar reformations can demonstrate the anomalous feeding artery and hepatic venous drainage, features that may help exclude malignant tumors, such as hepatocellular carcinoma (HCC), which predominantly have portal venous drainage.

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Further Evaluation

When CT demonstrates characteristic findings of FNH, particularly in a young asymptomatic patient, no further evaluation is usually required. MRI is probably more sensitive than CT in demonstrating the characteristic central scar, but otherwise shows the same morphologic and hemodynamic features as CT.[13] Radionuclide imaging has been helpful in confirming FNH. Because only benign lesions such as FNH have Kupffer cells as well as bile ductules, uptake of Tc-sulfur colloid (seen in some 50-60% of FNH) or Tc-hepatic iminodiacetic acid derivatives (seen in about 80-90% of FNH) has been considered definitive (Fig. [6]).[16]

More recently, we have had experience with 100 FNH lesions evaluated with a new hepatobiliary MRI contrast agent, gadobenate dimeglumine (Gd-BOPTA).[17] This agent can be given as a rapid IV bolus, and the characteristic bright homogeneous enhancement of FNH is observed. In addition, the agent is taken up by hepatocytes and is excreted in the bile. The disordered bile ductules that are characteristics of FNH result in prolonged enhancement of FNH lesions on 3-hr delayed MRI, a sign that appears to be specific for this diagnosis (Fig. [7]). Moreover, in our experience the Gd-BOPTA-enhanced MRI studies resulted in improved recognition of the central scar, which was visible in 53% of the enhanced scans (portal venous and delayed phases) versus 36% of the unenhanced MRI. As with CT, scars are more often recognized with FNH >3 cm in diameter (78% on Gd-BOPTA scans) rather than smaller lesions (31% on Gd-BOPTA scans).[17]

A tumor that is sometimes mistaken for FNH by radiologists is fibrolamellar HCC. As with FNH, fibrolamellar HCC usually occurs in young adults without cirrhosis, and it is a hypervascular tumor with a central scar. Key differential points, however, are that fibrolamellar HCC is, in our experience[18] with more than 40 cases, usually a large (>12 cm), well-defined (77% of cases), heterogeneous (100%) mass (Fig. [8]). The fibrous scar is large and central or eccentric with broad fibrous bands and calcification (68%). Moreover, lymph nodes or other metastases are evident in 65% of cases.

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HEPATOCELLULAR ADENOMA

Adenoma is a rare hepatic neoplasm that occurs almost exclusively in liver that has abnormal metabolism due to exogenous steroids or, less commonly, congenital abnormalities of carbohydrate metabolism (glycogen storage disease or diabetes). Over 90% of cases occur in women of reproductive age, and lesions may regress with withdrawal of oral contraceptives or other steroids. Adenoma is of clinical interest because of its tendency toward spontaneous rupture and hemorrhage. Rare cases of malignant degeneration are also recorded, particularly in patients with multiple or large adenomas. Patients with dozens of adenomas (adenomatosis) seem to constitute a distinct entity; these tumors are histologically identical to isolated adenomas but do not appear to be steroid-dependent. However, in our series of 15 patients with adenomatosis, 14 were in women.[19]

Most adenomas come to clinical attention as incidental findings on imaging studies or due to spontaneous hemorrhage. In our experience[20] with 25 cases, 13 lesions were solitary, with a mean diameter of 6 cm, whereas 12 patients had 2 or 3 adenomas.

Most adenomas are composed of cords of hepatocytes that occasionally form bile. However, adenomas lack bile ductules, portal tracts and hepatic veins, which results in necrosis and hemorrhage, as well as some characteristic imaging features. Excessive glycogen and lipids are characteristic histologic findings.

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Imaging

CT reliably demonstrates most adenomas as sharply defined masses with smooth borders. Unlike FNH, adenomas usually are heterogeneous due to the presence of hemorrhage, necrosis, and/or fat (lipid). CT is less definitive in detection of these specific features than MRI, but CT shows hemorrhage in 25%, fat in 7%, calcification in 5%, and a tumor capsule in 25%.[19] The prevalence of hemorrhage will obviously be increased in series where CT has been used to evaluate symptomatic patients. The nonhemorrhagic parts of adenoma are nearly isodense to liver on unenhanced CT, as well as on portal venous and delayed scans. On arterial-phase CT, portions of the adenoma are hyperdense due to hypervascularity (Fig. [9]). Patients with adenomatosis may have dozens of adenomas detected on CT or MRI, but even more adenomas are usually present on gross pathological exam that are missed on imaging.

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Further Evaluation

If CT depicts a large hemorrhagic mass in a young woman who is using oral contraceptives, further evaluation prior to surgery is usually not warranted. In a hemodynamically stable patient with a heterogeneous liver mass MRI is the best single imaging procedure. Various MRI sequences can be utilized to depict hemorrhage and focal fat, features that are quite characteristic of adenoma (Fig. [10]).[21] [22]

Even though adenomas contain well-differentiated hepatocytes and may form bile, they lack the bile ductules to excrete bile. Hepatobiliary radionuclide scans show some traces of uptake in some adenomas but, unlike FNH, no delayed excretion. Similarly, in our anectotal experience with hepatobiliary MRI contrast agents (Gd-BOPTA and mangafodipir), adenomas demonstrate poor uptake and no delayed enhancement.

There is some overlap in the imaging characteristics of adenoma and well-differentiated HCC. Moreover, needle biopsy specimens may not allow confident distinction. For these reasons, as well as the documented occurrence of spontaneous hemorrhage and malignant degeneration, most adenomas should be surgically excised. We have had limited experience with the management of multiple adenomas and adenomatosis, but surgical excision and even orthotopic liver transplantation have been successful in some patients.

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REGENERATIVE NODULES

Terminology and criteria to describe various nodular hepatocellular lesions have been confusing and are still evolving. Recently, the organizers of the World Congresses of Gastroenterology appointed an international working party to define and categorize these lesions. Their classification scheme (Table [2]) is based on two main sets of criteria: (1) whether the hepatic cells are regenerative or dysplastic and (2) the characteristics of the adjacent hepatic stroma.[23]

All regenerative nodules are the result of a localized proliferation of hepatocytes and their supporting stroma, in response to a focal or global hepatic injury, usually ischemic or toxic. Histologically, some of the lesions may be indistinguishable, but accurate diagnosis is often possible using clinical clues and imaging. Note that FNH and adenoma are also hepatocellular nodules that result from prior hepatic injury, but we have considered these separately.

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Nodular Regenerative Hyperplasia

Nodular regenerative hyperplasia is a response to disturbed hepatic circulation, usually obstruction of portal and/or hepatic veins, or the sinusoids. Well-recognized associated clinical conditions include Budd-Chiari syndrome, leukemia, polycythemia vera, and other hypercoagulable conditions. The lesions can be subdivided based on the presence or absence of fibrosis and the number of portal tracts within each nodule. When few fibrous septa are present and when the nodules are small (monoacinar), the individual nodules are about 1 mm in diameter, occasionally with clusters up to 10 mm. This manifestation of disease is not likely to be detectable on imaging studies as discrete focal masses.[24]

Multiacinar or large regenerating nodules can result from the same disorders of hepatic vasculature, such as Budd-Chiari or myeloproliferative disorders. When these nodules are surrounded by fibrous septa, they are indistinguishable from regenerating nodules within the cirrhotic liver.

Nodular regenerative hyperplasia occurs in patients with systemic disease, and most patients have abnormal hepatic function and portal hypertension, although, by definition, they do not have cirrhosis. Correct diagnosis of the nature of the diffuse and focal hepatic lesions is important but must be based on integration of clinical, histopathological, and imaging data. Attempts to interpret any of these tests in isolation will likely result in mistaken diagnosis of some other focal benign mass (e.g., adenoma or FNH) or hepatic malignancy.

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Imaging

CT does not directly display the monoacinar form of nodular regenerative hyperplasia, and the liver morphology may appear normal. More often, however, it demonstrates distortion of hepatic architecture reflecting the underlying hepatic injury. In Budd-Chiari syndrome, for instance, CT depicts ascites, enlargement of the caudate and deep right lobe, peripheral hepatic hypoperfusion. and narrowing or obstruction of the IVC or hepatic veins (Fig. [11]).[25] Multiacinar or large regenerating nodules may distort the liver surface or may be present in more central parts of the liver. When hepatic nodules are detected in Budd-Chiari syndrome, they are usually multiple (>10), small (1-4 cm), and homogeneous (Fig. [11]). Some nodules have a hypodense ring demonstrated on CT (or MRI). Hepatic arterial-phase CT (or MRI) demonstrates uniform enhancement. No central scar or capsule is evident.[26] [27]

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Further Evaluation

MRI shows many of the same features of the hepatic nodules as well as the underlying hepatic pathology, if any. MRI is more accurate than CT in demonstrating patency or occlusion of the hepatic veins and inferior vena cava (IVC), and may show more nodular lesions. The large regenerative nodules are usually hyperintense on T1-weighted images and hypointense on T2- weighted images and show hypervascular enhancement, helping to distinguish them from cirrhotic regenerative nodules and HCC (Fig. [12]). Our limited experience with Gd-BOPTA has demonstrated increased uptake and delayed clearance of the agent from these large regenerative nodules, similar to that in FNH, and reflecting their benign nature.

In patients with Budd-Chiari syndrome and other systemic disorders, hepatic malignancies can develop and may be difficult to diagnose. Vilgrain et al[26] studied 23 patients with Budd-Chiari syndrome and liver nodules. The HCC lesions tended to be fewer (1-3), larger (mean 7.3 cm), and more heterogeneous on MRI than the benign regenerative nodules. Close follow-up, screening for alpha-fetoprotein, and percutaneous image-guided biopsy are important for accurate diagnosis.

Regenerative nodules in cirrhosis may be indistinguishable on imaging and histology from nodular regenerative hyperplasia. Cirrhotic nodules are discussed more completely in other articles in this issue of Seminars.

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BILE DUCT HAMARTOMA

This lesion, also known as bile duct adenoma and von Meyenburg complex, is not a true neoplasm but consists of a benign disorganized proliferation of bile ductules and fibrocollagenous stroma. These lesions are small, usually 1 to 10 mm, but may coalesce into larger lesions. Radiologists have only recently become aware of these lesions as higher resolution imaging studies have come into use. These lesions are of no clinical importance, other than simulating metastases or microabscesses on imaging.

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Imaging

CT features are nonspecific, revealing multiple subcentimeter hypodense foci on a nonenhanced or contrast-enhanced scan (Fig. [13]). The lesions are too small to characterize by morphology or hemodynamics.

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Further Evaluation

As an isolated finding in an otherwise healthy, nononcologic patient, these lesions usually require no further evaluation. Sonography can confirm that they are not cysts, but MRI features are not likely to be diagnostic. If further work-up is necessary, biopsy can be attempted, although the small size of the hamartomas presents a challenge. Follow-up imaging usually shows no change.

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LIPOMATOUS MASSES

Focal steatosis (fatty infiltration) is very common and can simulate various masses and other hepatic lesions. Although hypodense to surrounding liver, focal steatosis is usually closer to water density on CT rather than to fat.

Hepatic neoplasms composed of fat are quite rare and include lipoma, angiomyolipoma, and myelolipoma, as well as metastatic liposarcoma and malignant teratoma. Hepatocellular adenomas and HCC may contain small foci of fat or generalized increase in cellular lipid, but these should rarely be mistaken for lipomatous neoplasms.

Lipoma and angiomyolipoma are usually encountered as incidental findings in patients with tuberous sclerosis. With rare exceptions they are of no clinical significance.

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Imaging

CT clearly shows the fat-density components of these tumors.[27] Lipomas are of uniform fat attenuation (-80-100 HU), whereas other tumors may contain smooth muscle, blood vessels, or other components as their names imply (Fig. [14]).

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Further Evaluation

The usual route to specific diagnosis in this setting is to inquire about any clinical evidence of tuberous sclerosis or a known liposarcoma or malignant teratoma. Other imaging studies, particularly MRI, are effective at revealing the fat component of these masses (high signal on T1- and T2- weighted images), although simple clinical follow-up is usually sufficient. Angiography can reveal large intratumoral vessels simulating aneurysms within angiomyolipomas.

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LYMPHANGIOMA

This is a rare hepatic mass that is usually part of a systemic disorder resulting in multiple masses of enlarged lymphatics that compress and distort the liver, spleen, skeleton, and other organs.

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BILIARY CYSTADENOMA

This tumor presents typically as a symptomatic large hepatic mass characterized by large cystic spaces surrounded and separated by thickened, nodular, enhancing walls. Although imaging features might overlap with a pyogenic or parasitic abscess, this is usually not a clinical dilemma. CT and all other imaging studies clearly demonstrate cystadenoma as an ``aggressive'' and complex neoplasm (Fig. [15]).[28] These are known to undergo malignant transformation, and there is no imaging technique capable of distinguishing between benign and malignant cystadenomas. For these reasons, these neoplasms should be resected and need no further work-up or discussion.

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SUMMARY

Evaluation of patients with focal hepatic masses is usually straightforward. Although primary or secondary malignant lesions often require biopsy, most benign hepatic masses can be diagnosed and managed confidently based on results of cross-sectional imaging coupled with clinical information. Radiologists must alter their CT protocols to make optimal use of the technical advances in helical CT technology, and referring physicians must contribute pertinent clinical information.

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ABBREVIATIONS

CT computed tomography

FNH focal nodular hyperplasia

Gd-BOPTA gadobenate dimeglumine

HCC hepatocellular carcinoma

HIDA hepatic iminodincetic acid

IV intravenous

MRI magnetic resonance imaging

*Figure 1* Simple hepatic cyst. Incidental finding in a 50-year-old woman. Sharply defined water density, nonenhancing, and nonseptated mass (C).

*Figure 2* Polycystic liver disease in a 63-year-old man. Innumerable cysts of varying size are present in the liver and kidneys. Some of the cysts have calcified walls (arrow) and higher than water density fluid contents due to hemorrhage.

*Figure 3* Large cavernous hemangiomas. A. Nonenhanced CT section demonstrates large masses (arrows). Except for areas of necrosis (N), the masses are isodense to the aorta (A). S = stomach. B. Portal venous-phase image shows cloudlike or nodular peripheral enhancement (arrows) of the hemangiomas that is isodense to the aorta (A). C. Ten-minute delayed section shows that the hemangiomas have opacified or ``filled in'' with contrast from the periphery and are isodense with the aorta except for the central areas of necrosis. D. T2-weighted MRI section. The hemangiomas (arrows) are very bright, or hyperintense, relative to the liver (L). E. T1-weighted gradient echo image during the portal venous phase of enhancement following IV bolus injection of Gd-DTPA. The hemangiomas (H) demonstrate the same nodular peripheral pattern of enhancement (arrows) as was demonstrated on CT. F. Later T1-weighted MRI shows progressive centripetal enhancement of the hemangiomas (H).

*Figure 4* Small hemangioma. A. Hepatic arterial-phase image demonstrates bright uniform enhancement of a lesion (arrow) almost isodense with the aorta (A). B. Portal venous-phase image shows that the hemangioma (H) remains isodense to the aorta and hepatic veins (HV). C. Ultrasonography in sagittal plane demonstrates the hemangioma (H) as a hyperechoic focus near the diaphragm (D).

*Figure 5* Focal nodular hyperplasia (FNH). A. A mass like lesion (arrow) is present in the liver that is only slightly hypodense to the liver on this nonenhanced CT image. B. Hepatic arterial-phase image demonstrates bright homogeneous enhancement of the FNH, except for the central scar (arrow). C. Ten-minute delayed CT. The FNH is isodense to liver and is invisible. The central scar (arrow) is slightly hyperdense due to retention of contrast in its fibrous stroma.

*Figure 6* Focal nodular hyperplasia (FNH). A. Late arterial-early portal venous-phase image shows uniform enhancement of the FNH except for the central scar (arrow). B. Tc-99m sulfur colloid scan, axial single photon emission computed tomography image in same plane as CT section. Unlike other hepatic masses (which lack Kupffer cells), the FNH (arrow) takes up and retains the radiotracer.

*Figure 7* Focal nodular hyperplasia (FNH). T1-weighted MRI section obtained 3 hr after the IV administration of Gd-BOPTA, a hepatobiliary MRI contrast agent. The marked and prolonged enhancement of the FNH indicates functioning hepatocytes and intact but disordered bile ductules, and seems to be specific for FNH.

*Figure 8* Fibrolamellar hepatocellular carcinoma in a 15-year-old girl. A. Nonenhanced CT demonstrates a mass (arrows) with a large central scar containing clumps of calcification (open arrow). B. Hepatic arterial-phase image shows bright heterogeneous enhancement of the mass. Note also the enlarged cardiophrenic node (CN), due to lymphatic metastasis, that also enhanced brightly. C. Portal venous-phase image. As with other hypervascular tumors, lesion conspicuity is decreased, as liver and tumor enhancement are now almost equal.

*Figure 9* Hepatic adenomas with spontaneous hemorrhage. A. Nonenhanced CT demonstrates hyperdense blood clot (C) and lower density lysed blood (B) in a subcapsular hematoma. The adenomas are difficult to identify. B. At least two large adenomas are evident as heterogeneous hypervascular masses (arrows) on this hepatic arterial phase image. C. Portal venous-phase image. The left lobe adenoma (A) is now homogeneously enhanced, whereas the right lobe lesion remains heterogeneous, presumably due to necrosis or fat content.

*Figure 10* Hepatic adenoma. A. T2-weighted MRI section demonstrates heterogeneous mild hyperintensity in the adenoma (arrow). B. Portal venous-phase image. T1-weighted image after IV bolus injection of Gd-DTPA shows bright heterogeneous enhancement of the adenoma (arrow).

*Figure 11* Budd-Chiari syndrome with large regenerating nodules (nodular regenerative hyperplasia). A. Nonenhanced CT section shows only enlargement of the caudate lobe (CL) and ascites (A). B. Hepatic arterial-phase image shows multiple hypervascular 1-cm nodules (arrows) and heterogeneous enhancement of the liver parenchyma.

*Figure 12* Budd-Chiari syndrome with large regenerating nodules. A. T1-weighted nonenhanced MRI section demonstrates a 2.5-cm slightly hyperintense nodule (arrow). Note tiny IVC. B. T1-weighted section during the bolus injection of Gd-DTPA shows several nodules with bright enhancement (arrows). C. T2-weighted MRI shows additional hypointense nodules (arrows). The appearance of these nodules on T1- and T2-weighted images is opposite to what is expected for malignant lesions such as HCC.

*Figure 13* Bile duct hamartomas (biopsy proven). Nonenhanced CT section shows innumerable subcentimeter hypodense foci in this asymptomatic patient.

*Figure 14* Angiomyolipoma. A. Portal venous-phase CT section shows a heterogeneous mass (arrow) with a bright hypervascular eccentric enhancement in its lateral half. B. T1-weighted MRI section, nonenhanced, shows the heterogeneous mass. The medial half of the mass is hyperintense, indicating fat or hemorrhage. Surgical resection demonstrated fat in this part of the tumor and enlarged abnormal blood vessels within the lateral component.

*Figure 15* Biliary cystadenoma. CT demonstrates a complex cystic mass with multiple locules separated by septa.

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