MRI Evaluation of Masses in the Noncirrhotic Liver

Kiran Gangahdar, MD; Deepa Santhosh, MD; Kedar N. Chintapalli, MD


Appl Radiol. 2014;43(12):20-28. 

In This Article

Benign Masses


Hemangioma is the most common benign hepatic tumor. The prevalence of hemangioma in the general population ranges from 1%–2%;[6] the female-to-male ratio varies from 2:1 to 5:1. Because hepatic hemangiomas are frequent, are most often asymptomatic, and have a very low rate of complications, this lesion does not require surgical resection.

Hemangiomas are composed of endothelial-cell–lined vascular channels with a supporting fibrous stroma. Hemangiomas demonstrate smooth, round, or lobular margins (Figures 1A,1B).[7] On T2-weighted images (Figure 1C), hemangiomas are hyperintense, approaching the signal intensity of cerebrospinal fluid.[7] Three types of contrast enhancement patterns are present in dynamic examinations: early homogenous enhancement and persistence of enhancement in the late phase (type 1); peripheral nodular enhancement (Figure 1D), centripetal dynamic uniform enhancement (type 2); peripheral nodular enhancement, centripetal dynamic enhancement, and non-enhancing central scar tissue in the late phase (type 3).[8] Centripetal enhancement (Figure 1E) is the most common enhancement pattern.[7] Immediate homogenous enhancement is seen in some hemangiomas smaller than 1.5 cm, rapid filling-in of these smaller hemangiomas is thought to be related to the smaller vascular spaces and larger interstitium present in these lesions.[9] On delayed gadolinium-enhanced images, regions of persistent central hypointensity in comparison with liver may be present in hemangiomas larger than 5.0 cm.[7] Heterogeneity of large or giant hemangiomas is related to the presence of hemorrhage, thrombosis, extensive hyalinization, liquefaction, and fibrosis.[10] On T2-weighted images, the central cleft-like portion of large hemangiomas is hyperintense in comparison with the remainder of the mass and corresponds to the region of hypointensity on the gadolinium-enhanced images reflecting cystic degeneration or liquefaction.[11]

Figure 1.

(A) Axial in-phase and (B) Axial out-of-phase showing hypointense lesion in segment IVb without foci of signal drop. (C) Axial T2 fat saturation reveals T2 hyperintense lesion. (D) Axial post contrast T1 THRIVE sequences demonstrate peripheral discontinuous nodular enhancement. Coronal post contrast delayed sequences showing progressive filling-in pattern, consistent with hemangioma.

Focal Nodular Hyperplasia

Focal nodular hyperplasia (FNH) of the liver is among the most common hepatic neoplasms. With current advances in radiologic imaging, it has become an even more frequent diagnosis. FNH typically presents as a single lesion in 70% of patients and with two to four lesions in the remaining 30%.[12] FNH is more common in premenopausal women, although up to 10% may occur in men.[13] These lesions are often detected incidentally during imaging for non-specific abdominal symptoms. Once the diagnosis has been established, active treatment is almost never required.

The pathogenesis of FNH is unclear; however, Wanless et al[14] have suggested that FNH develops as hyperplastic nodules caused by blood flow in an anomalous hepatic artery branch. Kondo[15] has also proposed that FNH lesions are a result of regional abnormalities in either portal or hepatic arterial blood flow. Certainly FNH lesions are characterized macroscopically by the presence of abnormal, dilated capsular blood vessels.[16] They are known to occur simultaneously with other vascular hepatic lesions such as hemangiomas and adenomas[17] and their incidence may be increased following blunt abdominal trauma[18] and chemotherapy,[19] both of which are associated with intrahepatic vascular damage. In addition, an Italian case control study found that cigarette smoking was an indicator of elevated risk of FNH.[20] Currently, FNH is divided into two types: classic and nonclassic. The nonclassic type contains three subtypes: (a) telangiectatic FNH, (b) FNH with cytologic atypia, and (c) mixed hyperplastic and adenomatous FNH.[16]

The lesion varies from mildly hypointense to isointense on T1-weighted (Figures 2A, 2B) MRI and from mildly hyperintense to isointense on T2-weighted images. Unlike fibrolamellar HCC, the central scar in FNH is not a true scar, but represents a confluence of blood vessels, bile ducts, and sometimes a focal area of fibrosis. This "central scar" (Figure 2C and 2D) is characteristically hyperintense on T2-weighted images. The mild hyperintensity of the lesion on T2-weighted images may be related to the presence of vascular channels or edema throughout the lesion. FNH is perfused by the hepatic arterial system and shows marked, nearly uniform arterial phase enhancement (Figure 2E). The degree of lesion enhancement lessens on subsequent contrast-enhanced images, with lesion signal intensity approaching that of the surrounding liver parenchyma. The central scar has low signal intensity on early phase contrast-enhanced images, but gradually enhances to become hyperintense relative to the rest of the lesion on delayed phase images (Figure 2F).[21]

Figure 2.

(A) Axial in-phase and (B) axial out-of-phase images display a well-defined encapsulated hypointense lesion within segment VI without foci of signal drop showing T1 hypointense central scar. Also note the diffuse hepatic steatosis with loss of signal on out-of-phase sequences. (C) and (D) Axial T2 fat-saturation and axial T2-weighted image discloses T2 iso/hypointense lesion with central hyperintense scar, consistent with focal nodular hyperplasia. (E) Axial post-contrast T1 THRIVE sequence show intense homogenous enhancement of the lesion with nonenhancing central scar. (F) Axial postcontrast, 10-minute-delayed T1 THRIVE sequence demonstrates delayed persistent enhancement of the lesion with diffuse enhancing background, consistent with FNH representing normal excretory function of hepatocytes.

Hepatic Adenoma

Although the precise pathogenic mechanism leading to hepatic adenomas is still unknown, the use of estrogen-containing[3] or androgen-containing[4] steroid medications clearly increases their prevalence, number, and size within the affected population and often within individual patients. Moreover, this causal relationship is related to dose and duration, with the greatest risk encountered in patients taking large doses of estrogen or androgen for prolonged periods of time.[4] In women who have never used oral contraceptives, the annual incidence of hepatic adenoma is about 1 per million. This increases to 30 – 40 per million in long-term users of oral contraceptives.[22]

Small HCA is generally asymptomatic. Right upper abdominal quadrant fullness or discomfort is present in 40% of cases due to mass effect. Typical clinical manifestation is spontaneous rupture or hemorrhage leading to acute abdominal pain with possible progression to hypotension and even death. HCA rarely undergoes malignant transformation to hepatocellular carcinoma (HCC).

Image-guided biopsy or surgical resection with histopathologic and immunohistochemical analysis is necessary for complete characterization of HCAs but MR imaging plays an important role in diagnosis and subtype characterization as well as identification of complications and surveillance.[23,24]

On MRI, adenomas have variable signal intensity but can show hyperintense foci on unenhanced T1-weighted images (Figures 3A, 3B) secondary to hemorrhage or intracellular lipid. The visualization of fat within the lesion on fat-suppressed or opposed-phase T1-weighted images (Figure 3B) helps distinguish an adenoma from FNH. On T2-weighted images, hepatic adenomas can have variable signal intensity, but they are often mildly hyperintense relative to the liver. On dynamic contrast-enhanced images, adenomas show heterogeneous hypervascularity during the arterial phase (Figure 3C). These masses often show no washout of contrast material, becoming isointense to the liver parenchyma on portal venous and subsequent dynamic series, and they may have a delayed-enhancing pseudocapsule.[24]

Figure 3.

(A) Axial in-phase and (B) Axial out-of-phase exhibits a well-defined encapsulated iso/hypointense lesion within segment VI with foci of signal drop on OP sequence. (C) Axial postcontrast THRIVE sequence confirms heterogenous intense enhancement.

Geographic Fatty Liver

Geographic fatty liver disease is a frequently encountered variant of hepatic steatosis. Different geographic patterns can be attributed to specific causes. For example, fat accumulation sometimes occurs only in the right lobe. One hypothesis to explain this distribution is that blood from the superior mesenteric vein containing lipogenic alimentary factors that are preferentially distributed to the right lobe.[25] Geographic patterns may be secondary to an insult to the liver parenchyma. For example, fatty liver deposition can be distributed in territories previously affected by cholangitis.

Focal fat deposition is slightly less common and can mimic other hepatic benign or malignant lesions on ultrasound and CT (Figure 4D). MRI is very useful for making the diagnosis of focal hepatic steatosis, which appears isointense or hyperintense to liver on in-phase images (Figure 4A) and loses signal on out of-phase images (Figure 4B). Fat accumulation does not show diffusion restriction on any T2 correlate (Figure 4C), which may also be useful to differentiate steatosis from other liver abnormalities. Moreover, focal fat accumulation tends to show wedge–shaped margins, no mass effect on adjacent blood vessels or the biliary tree, sharp boundaries, and lobar or segmental distribution.[26]

Figure 4.

(A) Axial in-phase and (B) axial out-of-phase images showing a geographic area of signal drop on OP images in the right lobe without correlating T2-weighted lesion (C). (D) CT reveals diffuse hypodensity representing geographic steatosis (arrows).

Mesenchymal Hamartoma

Mesenchymal hamartoma is a rare, benign, developmental tumor of the liver, with occasional risk of malignancy. The pathogenesis of mesenchymal hamartomas is still debated. A handful of series have shown an association with mesenchymal stem villous hyperplasia of the placenta.[27] Histologically, it appears as a disordered arrangement of the mesenchyme, bile ducts, and hepatic parenchyma. Cords of normal appearing hepatocytes are separated by zones of loose, poorly cellular mesenchyme. The porous nature of the mesenchyme permits accumulation of fluid.[28] The typical presentation is one of asymptomatic, rapid abdominal distention with a palpable mass on physical examination. The rapid expansion of the tumor is believed to be due to degeneration of the mesenchyme and fluid accumulation. Other uncommon associated symptoms are vomiting, fever, constipation, diarrhea and weight loss.[29]

On CT (Figure 5A), mesenchymal hamartomas usually appear as well-defined masses with a central area of homogeneous low attenuation with internal septations. On sonography cystic mesenchymal hamartomas are described as large cysts with internal septae or trabeculae. Less commonly of the lesion manifests as smaller cysts with thickened septations.[30] An article by Bin-Bin Ye et al demonstrated that MR images showed enlarged liver with smooth border, multiple foci with slightly low signal intensity on T1-weighted images and slightly high signal intensity on T2-weighted images (Figure 5B). After intravenous administration of a gadolinium-based contrast agent (Figure 5C), the lesions demonstrated annular, heterogenous or no enhancement in the arterial phase, moderate enhancement in the portal phase and hyper enhancement in delayed phase.[31]

Figure 5.

(A) CECT showing heterogeneous hypodense mass lesions involving both lobes. (B) Axial T2-weighted image indicates T2 hyperintense masses involving both lobes. (C) Axial postcontrast THRIVE sequence demonstrates heterogenous peripheral enhancement.