MR Characterization of Focal Liver Lesions




Magnetic resonance (MR) can characterize specific tissue subtypes, thus facilitating focal liver lesion diagnosis. Focal liver lesions that are isointense to hyperintense to liver on T1-weighted images are usually hepatocellular in origin. Chemical shift imaging can narrow the differential diagnosis by detecting the presence of lipid or iron. T2 and heavily T2-weigthed fast spin echo imaging can differentiate solid from nonsolid focal liver lesions. The authors illustrate these MR imaging pearls and the uncommon exceptions (pitfalls). The authors hope that you will find this less traditional contribution to the Magnetic Resonance Clinics of North America helpful in clinical practice.


Key points








  • Focal liver lesions that are isointense to hyperintense to liver on in-phase T1-weighted images are usually hepatocellular in origin.



  • Focal liver lesions that lose signal intensity on an opposed-phase image compared with the matched in-phase image contain lipid and are usually hepatocellular in origin.



  • Focal liver lesions that lose signal intensity on an in-phase image compared with an opposed-phase image are most often iron-containing siderotic nodules.



  • Focal liver lesions that are isointense to spleen on T2-weighted images are solid and often malignant, whereas focal liver lesions that are hyperintense to spleen on heavily T2-weighted images are usually nonsolid benign cysts or hemangiomas.






Pearl 1: the T1 pearl: a focal lesion that is isointense to hyperintense to liver on T1-weighted images is hepatocellular in origin


The first 3 imaging pearls discussed in this review are the 3 instances when focal liver lesion characterization is possible with T1-weighted gradient echo images.


The 3 most common focal liver lesions encountered in clinical practice are cysts, hemangiomas, and metastatic disease. Nonsolid benign hepatic lesions (cysts and hemangiomas) and almost all metastatic lesions are hypointense relative to liver on T1-weighted images ( Fig. 1 ). Normal liver has relative high signal intensity on T1-weighted images that has been attributed to high concentrations of protein, rough endoplasmic reticulum, and paramagnetic substances, such as manganese and copper. One study calculated the T1 relaxation times of liver at 1.5 T as 547 ms and that of solid lesions, hemangiomas, and cysts to be 1004, 1337, and 3143 ms, respectively. Thus, most liver lesions are initially detected on T1-weighted images as being hypointense to liver. The authors use other pulse sequences besides T1-weighted images in order to differentiate among cysts, hemangiomas, and solid liver lesions.




Fig. 1


Magnetic resonance demonstration of hepatic hemangioma and metastatic breast cancer in a 51-year-old woman. Metastases, cysts, and hemangiomas are almost all hypointense relative to liver on T1-weighted images. ( A ) Axial in-phase T1-weighted image shows low signal intensity hemangioma ( white arrow ) and infiltrative multifocal metastases ( smaller black arrows ). The metastases are isointense and the hemangioma is hypointense to spleen (S). However, the authors prefer to use T2-weighted images, diffusion-weighted images, and/or enhanced imaging to differentiate solid masses, such as metastatic disease, from nonsolid hepatic cysts and hemangiomas. ( B ) Corresponding opposed-phase image shows similar relative signal intensities of the hemangioma and metastatic disease. Geographic regions of lower signal intensity within the left lobe of liver ( black arrows ) represent steatosis. ( C, D ) T2-weighted fast-spin-echo images obtained with effective echo times of 90 ( C ) and 180 ms ( D ). The hemangioma is hyperintense to spleen, whereas the metastases are isointense. As the echo time increases, the contrast between the hemangioma and the adjacent metastases improve. This improvement is not because the hemangioma lights up or enhances; rather, the improved image contrast is because the hemangioma loses less signal as the echo time increases compared with liver, spleen, and metastases. ( E ) Opposed-phase T1-weighted imaging performed 2 years prior shows that the hemangioma ( arrow ) is hyperintense to the surrounding liver (L). When trying to establish the hepatocellular origin of a focal liver lesion by showing isointensity or hyperintensity to liver, one should use an in-phase image as steatotic liver can be of low signal intensity on opposed-phase imaging and can confound relative signal assessment. ( F ) Corresponding in-phase T1-weighted image shows that the hemangioma ( black arrow ) is hypointense to the steatotic liver.


If a focal liver lesion is isointense to hyperintense to liver on a T1-weighted image, then it is most commonly hepatocellular in origin. The 5 most common focal hepatocellular lesions encountered in clinical practice are regenerative nodules (RN), hepatocellular carcinoma (HCC), focal nodular hyperplasia (FNH), hepatocellular adenoma (HCA), and focal steatosis. In this section, the authors discuss FNH and the inflammatory subtype of HCA (IHCA). The reader is referred to the articles by Barr and Hussain and Sirlin in this issue of the Magnetic Resonance Imaging Clinics of North America concerning the evaluation of the cirrhotic liver and how to differentiate RN from HCC. Lipid and fat-containing liver lesions are discussed in “Pearl 2.”


FNH


FNH is the second most common benign hepatic tumor in adults after hemangioma. FNH composes approximately 8% of all primary liver tumors and has an estimated prevalence between 0.3% and 3.0%. FNH is not considered a neoplasm but instead is hypothesized to develop as a hyperplastic response of hepatic parenchyma around a central developmental vascular malformation. Individuals with FNH are more likely to have coexistent hepatic hemangiomas (20%) than would be expected by chance ; both hemangioma and FNH involve focal abnormalities in the hepatic blood supply.


FNH is typically detected in women aged 20 to 50 years and is uncommon in men (female-to-male ratio = 10:1). Unlike hepatic adenomas, there is no proven association of oral contraceptive use or pregnancy with the development or growth of FNH. Although up to 15% of FNH lesions can grow when followed longitudinally, this should not cause clinical concern. The authors are skeptical of reports of malignant transformation to fibrolamellar hepatoma or HCC, as most investigators think that malignant transformation of FNH does not occur.


The magnetic resonance (MR) features of FNH can be considered in 2 parts ( Fig. 2 ). The first component is the vascular nidus that forms the central scar of FNH, and the second is the surrounding hyperplastic response of adjacent liver. The vascular scar is hypointense to liver on both in-phase and opposed-phase imaging and is hyperintense to liver on T2-weighted imaging. The higher T2-weighted signal intensity is hypothesized to be secondary to slow flow within vessels. The scar does not enhance during the dynamic administration of gadolinium but does show delayed enhancement during the interstitial phase of enhancement when a conventional extracellular gadolinium contrast agent is used.




Fig. 2


MR findings of FNH and lipid-containing hepatocyte nuclear factor-1α inactivated hepatic adenoma in a 25-year-old woman. ( A, B ) Axial in-phase ( A ) and opposed-phase ( B ) T1-weighted images show 2 lesions: a larger FNH in segment 8 and a smaller adenoma in segment 2. The FNH has outer components ( thick arrow in A ) that are isointense to surrounding liver suggesting that it is hepatocellular in origin. There is a lower signal intensity central scar ( thin arrow in A ). The adenoma is isointense to liver and not perceptible on in-phase imaging; however, it loses signal and becomes recognizable on opposed-phase imaging ( arrow in B ). In-phase isointensity and loss of signal on opposed-phase image indicate that the lesion is lipid containing and hepatocellular in origin. ( C, D ) T2-weighted fast-spin-echo images (effective echo time = 95 ms) shows that both the FNH and adenoma ( thick arrows ) are hyperintense to liver and relatively isointense to spleen. The central scar of the FNH ( thin arrow ) is hyperintense to spleen. On the fat-suppressed image ( D ), there is similar contrast with the exception of lower signal intensity of the adenoma ( thick arrow in D ) because of the suppressed lipid. ( E ) Hepatobiliary-phase enhanced fat-suppressed T1-weighted image obtained after the intravenous administration of gadoxetate disodium shows hyperenhancement of the nonscar components of the FNH ( thick arrow ) and hypoenhancement of the adenoma ( thin arrow ). The adenoma showed hyperenhancement compared with adjacent liver on dynamic enhanced imaging (not shown).


The surrounding lesion of FNH itself is usually isointense to liver on both in-phase and opposed-phase imaging. Cases of lipid-containing FNH are uncommon and reportable ; many are associated with diffuse hepatic steatosis. On T2-weighted imaging, FNH is isointense to minimally hyperintense relative to liver. On arterial-phase dynamic gadolinium-enhanced imaging, FNH shows marked homogeneous enhancement, often with rapid washout during the portal and interstitial phases of enhancement.


If a gadolinium contrast agent with hepatobiliary excretion is used (eg, gadoxetate disodium), FNH will typically have components that are isointense to hyperintense relative to the surrounding liver on delayed hepatobiliary-phase imaging, which can be useful for distinguishing FNH from HCA for some lesions (see Fig. 2 E). In one study of 30 FNH lesions, only 2 showed homogenous low signal intensity on delayed hepatobiliary-phase images. If one uses gadoxetate disodium–enhanced MR to characterize FNH, the central scar may not show enhancement during the interstitial phase of contrast enhancement. The absent enhancement of the central scar is hypothesized to be from the more rapid removal of gadoxetate disodium from the circulation compared with other gadolinium contrast agents. The reader is referred to the article by Bashir for a detailed discussion concerning the use of the various MR contrast agents used for liver imaging.


Diffusion-weighted imaging and apparent diffusion coefficient (ADC) values alone should not be used to differentiate benign from malignant focal liver lesions as there can be substantial overlap. For example, many benign FNH and hepatic adenomas can show restricted diffusion similar to metastatic disease. For a review concerning the performance and interpretation of diffusion-weighted imaging of the liver, the reader is referred to the article by Taouli in this issue of the Magnetic Resonance Clinics of North America .


IHCA


Although pathologists had previously classified HCA into a single pathologic entity, recent molecular and immunohistochemical markers have determined that there are 4 distinct subtypes of HCAs. These subtypes include IHCAs and hepatocyte nuclear factor 1α inactivated (HNF-1α), β-catenin–activated, and unclassified HCAs. MR can often detect and characterize the subtype of HCA based on specific imaging features. Independent of the subtype, larger (>4 cm) adenomas are at risk of developing intralesional hemorrhage and are usually treated with surgical resection or with nonsurgical radiofrequency ablation or bland embolization. Smaller adenomas can be managed conservatively and followed by imaging. Women who take oral contraceptives should discontinue their use as some HCAs may subsequently decrease in size. Obesity and metabolic syndrome are associated with HCA ; patients are encouraged to modify their diet, develop an exercise program, and lose weight as part of a treatment plan.


Hepatic adenomatosis is a distinct entity that was originally described and defined in 1985 as the presence of greater than 10 HCAs ( Fig. 3 ). The HCA associated with adenomatosis is not limited to any one particular subtype, although patients with multiple adenomas are more likely to have steatosis. As with single lesions, management is based on lesion size and patients’ symptoms.




Fig. 3


MR imaging findings of pathology-proven hepatic steatosis and hepatic adenomatosis secondary to IHCA in a 43-year-old woman. The patient stopped taking oral contraceptives at the time of diagnosis and has been followed conservatively for the next 7 years. ( A ) Axial in-phase T1-weighted gradient echo image shows subtle foci of increased signal intensity relative to liver ( black arrows ). ( B ) Corresponding opposed-phase image shows loss of signal intensity within the liver confirming the presence of hepatic steatosis. There are multiple lesions that are hyperintense to the steatotic liver ( arrows ). Given that these lesions were isointense to liver on in-phase imaging, this pattern suggests they are hepatocellular in origin. ( C ) Subtraction image created by subtracting the opposed-phase image from the in-phase image (in-phase minus opposed-phase) depicts those voxels that contain both lipid and water protons. The highest signal intensity on the subtraction images occurs at fat-water interfaces (eg, junction of left kidney and perirenal fat [ thin arrows ]). This image confirms the presence of hepatic steatosis and the absence of lipid within the focal liver lesions ( thick arrows ). ( D, E ) Precontrast and arterial phase–enhanced fat-suppressed T1-weighted images show hyperenhancement of the adenomas ( arrows ) relative to the surrounding liver. The presence of arterial phase enhancement assists in differentiating IHCAs from masslike regions of focal sparing of steatosis.


The IHCA is the most common subtype of HCA and accounts for 40% to 60% of lesions in reported series. IHCA is associated with obesity and metabolic syndrome. In one study of 32 women with IHCA, the median body mass index was 32.5. In this same group of 32 women, steatosis was present in 59% on liver biopsies obtained distant from the tumor. In another series comparing 63 IHCA versus 46 HNF-1α adenomas, there was significantly less intralesional steatosis in the IHCA subgroup (43% vs 82%). Ten of the 63 patients with IHCA had findings of either intralesional or peritumoral hemorrhage, which was not significantly different than those found in the HNF-1α subtype.


On T1-weighted images, IHCAs are usually isointense to slightly hyperintense to surrounding liver. On opposed-phase imaging, the surrounding liver is more likely to lose signal intensity because of steatosis than the inflammatory adenoma itself (see Fig. 3 ; Fig. 4 ). On T2-weighted images, most IHCAs are minimally hyperintense relative to liver. In one series, 13 or 30 IHCAs revealed a specific atoll sign, consisting of a hyperintense rim that enhances on delayed gadolinium-enhanced imaging (see Fig. 4 C). It is hypothesized that the atoll sign is secondary to dilated sinusoids within the periphery of the adenoma. Like FNH, HCAs will enhance after gadolinium contrast. However, unlike FNH, IHCAs do not have a central scar and almost all IHCAs do not have components that are isointense to hyperintense to liver on delayed hepatobiliary-phase gadolinium-enhanced imaging. Thus, in a noncirrhotic woman with hepatic steatosis who has a solid enhancing mass that is isointense to liver on precontrast T1-weighted images and hypointense on hepatobiliary-phase enhanced images, one should consider an IHCA as the most likely cause.




Fig. 4


MR illustration of the atoll sign in a 26-year-old woman with a body mass index of 39 with a surgically proven IHCA. Obesity and metabolic syndrome are associated with hepatic adenomas. ( A, B ) Axial in ( A ) and opposed-phase ( B ) T1-weighted images show a subcapsular hyperintense hepatic mass ( arrow ) indicating it is hepatocellular in origin. Mild steatosis, which was confirmed at surgery, is most pronounced and best revealed as lower signal intensity within segment 4 on the opposed-phase image ( small arrows ). ( C ) Axial fast-spin-echo T2-weighted image (effective echo time = 93 ms) shows that the adenoma is hyperintense to liver and isointense to spleen. Not every focal lesion that is isointense to spleen is malignant, especially in individuals who do not have cirrhosis or history of a primary malignancy. A high-signal-intensity rim around the adenoma ( small arrows ) has been termed the atoll sign and is hypothesized to be secondary to dilated sinusoids. ( D ) Arterial-phase enhanced fat-suppressed T1-weighted image shows hyperenhancement of the adenoma and hypoenhancement of the peritumoral sinusoids.




Pearl 1: the T1 pearl: a focal lesion that is isointense to hyperintense to liver on T1-weighted images is hepatocellular in origin


The first 3 imaging pearls discussed in this review are the 3 instances when focal liver lesion characterization is possible with T1-weighted gradient echo images.


The 3 most common focal liver lesions encountered in clinical practice are cysts, hemangiomas, and metastatic disease. Nonsolid benign hepatic lesions (cysts and hemangiomas) and almost all metastatic lesions are hypointense relative to liver on T1-weighted images ( Fig. 1 ). Normal liver has relative high signal intensity on T1-weighted images that has been attributed to high concentrations of protein, rough endoplasmic reticulum, and paramagnetic substances, such as manganese and copper. One study calculated the T1 relaxation times of liver at 1.5 T as 547 ms and that of solid lesions, hemangiomas, and cysts to be 1004, 1337, and 3143 ms, respectively. Thus, most liver lesions are initially detected on T1-weighted images as being hypointense to liver. The authors use other pulse sequences besides T1-weighted images in order to differentiate among cysts, hemangiomas, and solid liver lesions.




Fig. 1


Magnetic resonance demonstration of hepatic hemangioma and metastatic breast cancer in a 51-year-old woman. Metastases, cysts, and hemangiomas are almost all hypointense relative to liver on T1-weighted images. ( A ) Axial in-phase T1-weighted image shows low signal intensity hemangioma ( white arrow ) and infiltrative multifocal metastases ( smaller black arrows ). The metastases are isointense and the hemangioma is hypointense to spleen (S). However, the authors prefer to use T2-weighted images, diffusion-weighted images, and/or enhanced imaging to differentiate solid masses, such as metastatic disease, from nonsolid hepatic cysts and hemangiomas. ( B ) Corresponding opposed-phase image shows similar relative signal intensities of the hemangioma and metastatic disease. Geographic regions of lower signal intensity within the left lobe of liver ( black arrows ) represent steatosis. ( C, D ) T2-weighted fast-spin-echo images obtained with effective echo times of 90 ( C ) and 180 ms ( D ). The hemangioma is hyperintense to spleen, whereas the metastases are isointense. As the echo time increases, the contrast between the hemangioma and the adjacent metastases improve. This improvement is not because the hemangioma lights up or enhances; rather, the improved image contrast is because the hemangioma loses less signal as the echo time increases compared with liver, spleen, and metastases. ( E ) Opposed-phase T1-weighted imaging performed 2 years prior shows that the hemangioma ( arrow ) is hyperintense to the surrounding liver (L). When trying to establish the hepatocellular origin of a focal liver lesion by showing isointensity or hyperintensity to liver, one should use an in-phase image as steatotic liver can be of low signal intensity on opposed-phase imaging and can confound relative signal assessment. ( F ) Corresponding in-phase T1-weighted image shows that the hemangioma ( black arrow ) is hypointense to the steatotic liver.


If a focal liver lesion is isointense to hyperintense to liver on a T1-weighted image, then it is most commonly hepatocellular in origin. The 5 most common focal hepatocellular lesions encountered in clinical practice are regenerative nodules (RN), hepatocellular carcinoma (HCC), focal nodular hyperplasia (FNH), hepatocellular adenoma (HCA), and focal steatosis. In this section, the authors discuss FNH and the inflammatory subtype of HCA (IHCA). The reader is referred to the articles by Barr and Hussain and Sirlin in this issue of the Magnetic Resonance Imaging Clinics of North America concerning the evaluation of the cirrhotic liver and how to differentiate RN from HCC. Lipid and fat-containing liver lesions are discussed in “Pearl 2.”


FNH


FNH is the second most common benign hepatic tumor in adults after hemangioma. FNH composes approximately 8% of all primary liver tumors and has an estimated prevalence between 0.3% and 3.0%. FNH is not considered a neoplasm but instead is hypothesized to develop as a hyperplastic response of hepatic parenchyma around a central developmental vascular malformation. Individuals with FNH are more likely to have coexistent hepatic hemangiomas (20%) than would be expected by chance ; both hemangioma and FNH involve focal abnormalities in the hepatic blood supply.


FNH is typically detected in women aged 20 to 50 years and is uncommon in men (female-to-male ratio = 10:1). Unlike hepatic adenomas, there is no proven association of oral contraceptive use or pregnancy with the development or growth of FNH. Although up to 15% of FNH lesions can grow when followed longitudinally, this should not cause clinical concern. The authors are skeptical of reports of malignant transformation to fibrolamellar hepatoma or HCC, as most investigators think that malignant transformation of FNH does not occur.


The magnetic resonance (MR) features of FNH can be considered in 2 parts ( Fig. 2 ). The first component is the vascular nidus that forms the central scar of FNH, and the second is the surrounding hyperplastic response of adjacent liver. The vascular scar is hypointense to liver on both in-phase and opposed-phase imaging and is hyperintense to liver on T2-weighted imaging. The higher T2-weighted signal intensity is hypothesized to be secondary to slow flow within vessels. The scar does not enhance during the dynamic administration of gadolinium but does show delayed enhancement during the interstitial phase of enhancement when a conventional extracellular gadolinium contrast agent is used.




Fig. 2


MR findings of FNH and lipid-containing hepatocyte nuclear factor-1α inactivated hepatic adenoma in a 25-year-old woman. ( A, B ) Axial in-phase ( A ) and opposed-phase ( B ) T1-weighted images show 2 lesions: a larger FNH in segment 8 and a smaller adenoma in segment 2. The FNH has outer components ( thick arrow in A ) that are isointense to surrounding liver suggesting that it is hepatocellular in origin. There is a lower signal intensity central scar ( thin arrow in A ). The adenoma is isointense to liver and not perceptible on in-phase imaging; however, it loses signal and becomes recognizable on opposed-phase imaging ( arrow in B ). In-phase isointensity and loss of signal on opposed-phase image indicate that the lesion is lipid containing and hepatocellular in origin. ( C, D ) T2-weighted fast-spin-echo images (effective echo time = 95 ms) shows that both the FNH and adenoma ( thick arrows ) are hyperintense to liver and relatively isointense to spleen. The central scar of the FNH ( thin arrow ) is hyperintense to spleen. On the fat-suppressed image ( D ), there is similar contrast with the exception of lower signal intensity of the adenoma ( thick arrow in D ) because of the suppressed lipid. ( E ) Hepatobiliary-phase enhanced fat-suppressed T1-weighted image obtained after the intravenous administration of gadoxetate disodium shows hyperenhancement of the nonscar components of the FNH ( thick arrow ) and hypoenhancement of the adenoma ( thin arrow ). The adenoma showed hyperenhancement compared with adjacent liver on dynamic enhanced imaging (not shown).


The surrounding lesion of FNH itself is usually isointense to liver on both in-phase and opposed-phase imaging. Cases of lipid-containing FNH are uncommon and reportable ; many are associated with diffuse hepatic steatosis. On T2-weighted imaging, FNH is isointense to minimally hyperintense relative to liver. On arterial-phase dynamic gadolinium-enhanced imaging, FNH shows marked homogeneous enhancement, often with rapid washout during the portal and interstitial phases of enhancement.


If a gadolinium contrast agent with hepatobiliary excretion is used (eg, gadoxetate disodium), FNH will typically have components that are isointense to hyperintense relative to the surrounding liver on delayed hepatobiliary-phase imaging, which can be useful for distinguishing FNH from HCA for some lesions (see Fig. 2 E). In one study of 30 FNH lesions, only 2 showed homogenous low signal intensity on delayed hepatobiliary-phase images. If one uses gadoxetate disodium–enhanced MR to characterize FNH, the central scar may not show enhancement during the interstitial phase of contrast enhancement. The absent enhancement of the central scar is hypothesized to be from the more rapid removal of gadoxetate disodium from the circulation compared with other gadolinium contrast agents. The reader is referred to the article by Bashir for a detailed discussion concerning the use of the various MR contrast agents used for liver imaging.


Diffusion-weighted imaging and apparent diffusion coefficient (ADC) values alone should not be used to differentiate benign from malignant focal liver lesions as there can be substantial overlap. For example, many benign FNH and hepatic adenomas can show restricted diffusion similar to metastatic disease. For a review concerning the performance and interpretation of diffusion-weighted imaging of the liver, the reader is referred to the article by Taouli in this issue of the Magnetic Resonance Clinics of North America .


IHCA


Although pathologists had previously classified HCA into a single pathologic entity, recent molecular and immunohistochemical markers have determined that there are 4 distinct subtypes of HCAs. These subtypes include IHCAs and hepatocyte nuclear factor 1α inactivated (HNF-1α), β-catenin–activated, and unclassified HCAs. MR can often detect and characterize the subtype of HCA based on specific imaging features. Independent of the subtype, larger (>4 cm) adenomas are at risk of developing intralesional hemorrhage and are usually treated with surgical resection or with nonsurgical radiofrequency ablation or bland embolization. Smaller adenomas can be managed conservatively and followed by imaging. Women who take oral contraceptives should discontinue their use as some HCAs may subsequently decrease in size. Obesity and metabolic syndrome are associated with HCA ; patients are encouraged to modify their diet, develop an exercise program, and lose weight as part of a treatment plan.


Hepatic adenomatosis is a distinct entity that was originally described and defined in 1985 as the presence of greater than 10 HCAs ( Fig. 3 ). The HCA associated with adenomatosis is not limited to any one particular subtype, although patients with multiple adenomas are more likely to have steatosis. As with single lesions, management is based on lesion size and patients’ symptoms.




Fig. 3


MR imaging findings of pathology-proven hepatic steatosis and hepatic adenomatosis secondary to IHCA in a 43-year-old woman. The patient stopped taking oral contraceptives at the time of diagnosis and has been followed conservatively for the next 7 years. ( A ) Axial in-phase T1-weighted gradient echo image shows subtle foci of increased signal intensity relative to liver ( black arrows ). ( B ) Corresponding opposed-phase image shows loss of signal intensity within the liver confirming the presence of hepatic steatosis. There are multiple lesions that are hyperintense to the steatotic liver ( arrows ). Given that these lesions were isointense to liver on in-phase imaging, this pattern suggests they are hepatocellular in origin. ( C ) Subtraction image created by subtracting the opposed-phase image from the in-phase image (in-phase minus opposed-phase) depicts those voxels that contain both lipid and water protons. The highest signal intensity on the subtraction images occurs at fat-water interfaces (eg, junction of left kidney and perirenal fat [ thin arrows ]). This image confirms the presence of hepatic steatosis and the absence of lipid within the focal liver lesions ( thick arrows ). ( D, E ) Precontrast and arterial phase–enhanced fat-suppressed T1-weighted images show hyperenhancement of the adenomas ( arrows ) relative to the surrounding liver. The presence of arterial phase enhancement assists in differentiating IHCAs from masslike regions of focal sparing of steatosis.


The IHCA is the most common subtype of HCA and accounts for 40% to 60% of lesions in reported series. IHCA is associated with obesity and metabolic syndrome. In one study of 32 women with IHCA, the median body mass index was 32.5. In this same group of 32 women, steatosis was present in 59% on liver biopsies obtained distant from the tumor. In another series comparing 63 IHCA versus 46 HNF-1α adenomas, there was significantly less intralesional steatosis in the IHCA subgroup (43% vs 82%). Ten of the 63 patients with IHCA had findings of either intralesional or peritumoral hemorrhage, which was not significantly different than those found in the HNF-1α subtype.


On T1-weighted images, IHCAs are usually isointense to slightly hyperintense to surrounding liver. On opposed-phase imaging, the surrounding liver is more likely to lose signal intensity because of steatosis than the inflammatory adenoma itself (see Fig. 3 ; Fig. 4 ). On T2-weighted images, most IHCAs are minimally hyperintense relative to liver. In one series, 13 or 30 IHCAs revealed a specific atoll sign, consisting of a hyperintense rim that enhances on delayed gadolinium-enhanced imaging (see Fig. 4 C). It is hypothesized that the atoll sign is secondary to dilated sinusoids within the periphery of the adenoma. Like FNH, HCAs will enhance after gadolinium contrast. However, unlike FNH, IHCAs do not have a central scar and almost all IHCAs do not have components that are isointense to hyperintense to liver on delayed hepatobiliary-phase gadolinium-enhanced imaging. Thus, in a noncirrhotic woman with hepatic steatosis who has a solid enhancing mass that is isointense to liver on precontrast T1-weighted images and hypointense on hepatobiliary-phase enhanced images, one should consider an IHCA as the most likely cause.




Fig. 4


MR illustration of the atoll sign in a 26-year-old woman with a body mass index of 39 with a surgically proven IHCA. Obesity and metabolic syndrome are associated with hepatic adenomas. ( A, B ) Axial in ( A ) and opposed-phase ( B ) T1-weighted images show a subcapsular hyperintense hepatic mass ( arrow ) indicating it is hepatocellular in origin. Mild steatosis, which was confirmed at surgery, is most pronounced and best revealed as lower signal intensity within segment 4 on the opposed-phase image ( small arrows ). ( C ) Axial fast-spin-echo T2-weighted image (effective echo time = 93 ms) shows that the adenoma is hyperintense to liver and isointense to spleen. Not every focal lesion that is isointense to spleen is malignant, especially in individuals who do not have cirrhosis or history of a primary malignancy. A high-signal-intensity rim around the adenoma ( small arrows ) has been termed the atoll sign and is hypothesized to be secondary to dilated sinusoids. ( D ) Arterial-phase enhanced fat-suppressed T1-weighted image shows hyperenhancement of the adenoma and hypoenhancement of the peritumoral sinusoids.




The exceptions


Nonhepatocellular Focal Liver Lesions in a Liver Containing Background Moderate or Marked Steatosis


On opposed-phase T1-weighted images, liver that is involved with moderate or severe steatosis will have very low signal intensity. Thus, if one were to evaluate the relative signal intensity of a focal liver lesion with surrounding steatotic liver on an opposed-phase T1-weighted image alone, then one may come to a false conclusion that the lesion is hepatocellular. For example, a benign hemangioma (see Fig. 1 E) or even a metastasis can appear hyperintense to steatotic liver on opposed-phase imaging. Therefore, one should use the in-phase image as the T1-weighted reference when using pearl 1.


Hemorrhagic Metastases to the Liver


Rare hepatic metastases can show T1 hyperintensity secondary to the T1 shortening properties of methemoglobin within subacute intralesional hemorrhage. This hyperintensity has been described in cases of metastatic renal, neuroendocrine, and lung cancers as well as choriocarcinoma. Focal liver lesion hyperintensity can also be secondary to the paramagnetic metals attached to melanin contained within metastatic melanoma ( Fig. 5 ). In these instances, patients’ primary tumor and the presence of metastatic disease are often known or apparent at the time of imaging.




Fig. 5


MR depiction of T1 hyperintense melanoma metastases to the liver in a 64-year-old woman. Some hemorrhagic metastases can be hyperintense to liver and should not necessarily be assumed to be hepatocellular in origin. ( A ) Axial in-phase T1-weighted gradient echo image shows multiple hypointense liver metastases. Two of the lesions have central high signal intensity ( arrows ). ( B ) Opposed-phase T1-weighted image shows persistent high internal signal intensity within 2 of the metastases ( arrows ). There is no loss of internal signal intensity to suggest intracellular lipid. Had the high signal intensity been secondary to macroscopic fat, one would have expected an etching artifact at the interface of the high signal intensity with the adjacent water-containing tissue (see Fig. 11 B). ( C ) Fat-suppressed T2-weighted image (effective echo time [TE] = 90 ms) shows that most of the metastases ( arrows ) are isointense to spleen (S). The hemorrhagic components of the metastases present within the liver and spleen ( small arrows ) are isointense to hypointense to liver secondary to intracellular methemoglobin and/or melanin.

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Sep 18, 2017 | Posted by in MAGNETIC RESONANCE IMAGING | Comments Off on MR Characterization of Focal Liver Lesions
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