Figure 1-A: Axial STIR image demonstrates a T2 hyperintense lesion in the right hepatic lobe.

Figure 1-B: Contrast enhanced axial VIBE image during arterial phase demonstrates predominantly peripheral enhancement of the lesion.

Figure 1-C: Contrast enhanced axial VIBE image during the portal venous phase demonstrates persistent enhancement of the lesion with contrast filling in the center of the lesion

Figure 1-D: Contrast enhanced axial VIBE image during the equlibirum phase demonstrates persistent enhancement of the lesion.

Figure 2-A: Contrast enhanced axial VIBE image during the arterial phase demonstrates a large lobulated enhancing mass in the left hepatic lobe with a central low intensity scar.

Figure 2-B: Contrast enhanced axial VIBE image during the portal venous phase demonstrates that the mass is almost isointense to the surrounding liver parenchyma.

Figure 2-C: Axial HASTE image demonstrates a very minimal T2 hyperintensity of the mass. The right hepatic lobe lesion from Figure 1 is also visualized.

Figures 1A-D: Hemangioma.
Figures 2A-C: Focal nodular hyperplasia (FNH).

The differential diagnosis for a solitary mass found in the liver on imaging studies includes: hepatocellular adenoma, hemangioma, metastatic tumor, inflammatory pseudotumor, bile-duct adenoma, and hepatocellular carcinoma.

FOCAL NODULAR HYPERPLASIA

Focal Nodular Hyperplasia (FNH) represents the second most common benign liver lesion, accounting for approximately 8% of primary hepatic tumors. FNH is most often a solitary lesion, although multiple foci of FNH occur in up to 23% of cases. Multiple FNH lesions can be found as part of the Multiple FNH Syndrome, which includes other lesions such as liver hemangioma, meningioma, astrocytoma, telangiectasia of the brain, and vein atresia. FNH is thought to represent a localized hepatocyte hyperplastic response of the liver to an underlying congenital vascular malformation. Pathologically, FNH is usually a well-circumscribed, non-encapsulated lesion that contains a central scar of vascular connective tissue, bile ductules, and inflammatory cells surrounded by abnormally arranged hepatocytes and Kupffer cells. The growth of FNH remains proportional to its blood supply; therefore, FNH does not commonly demonstrate internal hemorrhage or necrosis. Calcifications are rare.

Because FNH is a hyperplastic process and is composed of normal components of liver arranged in an abnormal fashion, the signal intensity of FNH is often similar to or indistinguishable form adjacent liver on T1- and T2- weighted magnetic resonance (MR) images. The central scar, which is often has a stellate configuration, appears hypointense on T1-weighted images and hyperintense on T2-weighted images. High signal intensity of the central scar on T2-weighted images is characteristic of FNH lesions but is observed only in 10-49% of patients. On contrast enhanced MR images, FNH lesions demonstrate dramatic enhancement during the arterial phase followed by isointensity during the portal venous phase. The central scar during arterial phase imaging does not enhance. On delayed phase imaging, especially in medium-to-large sized lesions, the central scar demonstrates high signal intensity due to the accumulation of contrast. There is a tendency for larger FNH lesions to have central scars that show only partial enhancement on delayed images, which may reflect more mature, less vascularized scar tissue.

In most instances, the typical MR features of FNH allow for a confident diagnosis, making biopsy and additional imaging studies unnecessary. However, atypical FNH features on MR imaging including large lesions, multiple lesions, internal necrosis, hemorrhagic foci, fatty infiltration, lesion heterogeneity, prominent hyperintensity on T1- and T2-weighted images, non-visualization of the central scar, non-enhancement of the central scar, hypointensity of the scar on T2-weighted images, and pseudocapsular enhancement on delayed imaging. The hypointensity on T2-weighted images, presumably caused by the loss or absences of vascular channels within the scar, is important to recognize because it can mimic the collageneous scar seen in fibrolamellar carcinoma, hepatocellular carcinoma, or intrahepatic cholangiocarcinoma.

HEMANGIOMA

Hemangioma is the most common benign hepatic neoplasm, with a prevalence ranging from 1% to 20% in the general population. Hemangiomas are more frequent in women. They can coexist with focal nodular hyperplasia (FNH) lesions, particularly in the setting of the multiple FNH syndrome. Like FNH, hemangiomas are most often asymptomatic and are usually detected incidentally. However, large hemangiomas, often referred to as giant hemangiomas, can result in symptoms such as abdominal discomfort, nausea, and vomiting secondary to extrinsic compression of adjacent bowel, rupture, hemorrhage, or thrombosis.

Pathologically, hemangiomas are characterized as well-circumscribed, blood-filled mesenchymal tumors. The great majority of these benign vascular lesions are cavernous hemangiomas. Hemangiomas are usually solitary (80%), often occur in the posterior segment of the right hepatic lobe, and are most often peripherally located. A giant hemangioma is larger than 10 cm and often contains a central cleft-like area of fibrosis or necrosis. With the exception of hemangiomas in pregnant women, which may enlarge because of the estrogen effect, the stability of these lesions is an important hallmark.

Since hemangiomas are often detected incidentally in patients undergoing imaging evaluation for known or suspected malignancy, the importance of hemangiomas lies in the fact that they must be differentiated from more clinically significant lesions, such as primary and secondary hepatic malignancies. In cases of typical hemangioma, imaging modalities are highly reliable for diagnosis, especially MRI, which has a sensitivity and specificity of greater than 90%. Typically hemangiomas are homogeneously hypointense relative to the liver on T1-weighted and markedly hyperintense on T2-weighted images relative to the liver. Low-intensity areas on T2-weighted images, usually associated with fibrosis, may sometimes be seen in the central portion of large hemangiomas.

On dynamic, contrast-enhanced MR imaging, hemangiomas can demonstrate three enhancement patterns: (1) immediate homogeneous enhancement (Type 1), usually seen in small tumors (< 1.5 cm); (2) a peripheral nodular centripetal enhancement pattern progressing to homogeneity (Type 2), usually seen in medium-sized hemangiomas (1.5-5.0 cm); and (3) peripheral nodular enhancement with centripetal fill-in and persistent central hypointense region (Type 3), commonly seen in larger lesions (> 5 cm) usually secondary to a central scar. Hemangiomas also vary in the rate and completeness of tumor enhancement. Rapidity of enhancement has been determined on 90-second images as slow (approximately 25% of tumor enhancement at the maximum transverse diameter), medium (approximately 50% enhancement), and fast (approximately 75% enhancement). Tumors at all sizes can enhance very slowly to very quickly and can demonstrate minimal to complete enhancement, with the exception that large tumors (> 5 cm) almost invariably demonstrate lack of central enhancement. Most hemangiomas demonstrate slow enhancement and this feature permits distinction from most tumors. Fast-enhancing hemangiomas show enhancement patterns that resemble other tumors, with metastases being the most difficult to distinguish. The most distinctive imaging feature of hemangiomas is the demonstration of a discontinuous ring of nodules immediately after gadolinium administration. Nodular enhancement is most frequently eccentric in location and my originate from the superior or inferior aspect of the hemangioma, simulating central enhancement on transverse images.

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