Review
FOCUS ON: Gastrointestinal Imaging
June 22, 2018

Spectrum of Pitfalls, Pseudolesions, and Misdiagnoses in Noncirrhotic Liver

Abstract

OBJECTIVE. The purpose of this article is to illustrate the various pitfalls, mimics, and atypical features that can lead to inaccurate diagnosis of focal lesions in a noncirrhotic liver. The content includes relevant pathogenesis and background as well as specific clues that can be used to reach an accurate diagnosis.
CONCLUSION. When assessing focal hepatic lesions, it is important to avoid pitfalls and misdiagnoses that can alter the management plan. Helpful strategies for avoiding pitfalls include paying close attention to the clinical history of the patient, carefully evaluating all of the available imaging studies, and being aware of the various radiologic mimics.
Despite advances in cross-sectional abdominal imaging, detection and characterization of focal hepatic lesions continue to present a daily challenge in clinical practice. Reaching an accurate diagnosis often requires tailoring the imaging protocol to each patient's clinical question. It also requires review of and access to relevant clinical data, including previous images and reports [1]. The differential diagnosis of focal hepatic lesions is long and comprises both benign and malignant entities. Characteristic imaging features for the diagnosis of these liver lesions are well known for CT and MRI of the liver. MRI with hepatobiliary contrast agents and T1- and T2-weighted sequences can narrow this differential diagnosis and provide information to help guide appropriate management. Several benign entities—including focal nodular hyperplasia, hemangiomas, and cysts—have a classic imaging appearance to allow definitive characterization with MRI [2]. Likewise, many malignant entities—such as hepatocellular carcinoma (HCC), cholangiocarcinoma, and metastases—have well-defined typical imaging features [2]. The imaging appearance of HCC is so well defined that in the appropriate clinical setting of a patient at high risk (i.e., someone with cirrhosis), there is no need for histopathologic confirmation [3, 4].
In practice, the clinical context is not always clear at the time of interpretation of imaging studies, and many pitfalls, mimics, and atypical presentations challenge accurate interpretation. Differentiation of benign from malignant lesions is essential for appropriate patient care and best outcomes [5]. The purposes of this article are to review the challenges posed by mimics and pitfalls in the noncirrhotic liver and to describe clues that may lead the interpreter to an accurate radiologic diagnosis.

Benign Lesions Mimicking Malignant Processes

Sclerosed Hemangioma

Cavernous hemangiomas are one of the most common types of hepatic lesions, the reported incidence being as high as 20% [6]. They are benign vascular tumors characterized by initial excessive angiogenesis followed by regression and inhibition of newly formed blood vessels [7]. Hemangiomas have classic enhancement patterns in the form of peripheral nodular discontinuous enhancement with gradual centripetal fill-in on delayed phase with similar degree of enhancement to blood pool.
Sclerosed hemangiomas (also known as thrombosed or hyalinized hemangiomas) are much less common than other patterns of hepatic hemangiomas. Sclerosed hemangiomas have undergone degeneration and fibrosis [8, 9]. A much more diverse enhancement profile has been described for these lesions, including heterogeneous enhancement, no enhancement, peripheral discontinuous nodular enhancement, and continuous rim enhancement. At MRI, unlike typical hemangiomas, sclerosed hemangiomas may have decreased signal intensity on T2-weighted images. Relative hypoenhancement and delayed enhancement due to fibrosis and obliteration of blood vessels have been described [5, 9]. Owing to the presence of atypical features, sclerosed hemangiomas, especially those with peripheral rim enhancement and capsular retraction, can be misinterpreted as metastases or intrahepatic cholangiocarcinomas (Fig. 1).
Fig. 1A —69-year-old woman with ovarian cancer and sclerosed hemangioma in liver.
A, Axial gadolinium-enhanced T1-weighted MR images of liver show ovoid, nonenhancing mass (arrow) in both late arterial (left) and portal venous (right) phases.
Fig. 1B —69-year-old woman with ovarian cancer and sclerosed hemangioma in liver.
B, Axial T2-weighted MR image shows that lesion is moderately T2 hyperintense. Capsular retraction (arrow) is evident.
Fig. 1C —69-year-old woman with ovarian cancer and sclerosed hemangioma in liver.
C, Follow-up contrast-enhanced portal venous phase CT image of liver obtained 1 year after A and B shows stable size of lesion and heterogeneous delayed enhancement (arrow).
Clues to the correct diagnosis of sclerosed hemangioma include a well-defined margin, capsular retraction (seen in malignancy), a decrease in size over time, loss of previously enhancing regions, presence of associated transient hepatic attenuation difference (THAD) and transient hepatic intensity difference (THID), and rim enhancement in the arterial phase [10]. It is a clinical challenge to definitively diagnose these lesions with imaging when they are encountered for the first time. It is often necessary to recommend follow-up imaging or biopsy to confirm the diagnosis. Recognizing the possibility of this diagnosis may allow a patient to undergo conservative measures instead of hepatic resection.

Large Regenerative Nodules

Large regenerative nodules are hyperplastic lesions that are typically associated with Budd-Chiari syndrome and are due to venous outflow obstruction of the hepatic veins or vena cava. Decreased hepatic venous outflow results in venous stasis and injury to hepatocytes. In response to decreased perfusion, the liver forms nodules that consist of multiple layers of hepatocytes and appear as hypervascular masses at contrast-enhanced CT and MRI [11, 12].
On contrast-enhanced images (CT and MRI), large regenerative nodules are enhancing in the late arterial and portal venous phases. On T2-weighted images, they are commonly isointense to hypointense. Large regenerative nodules may be misinterpreted as adenomas, focal nodular hyperplasia, multifocal HCC, or metastases (Fig. 2A). Clues to the correct diagnosis include a history of Budd-Chiari syndrome, homogeneous intense enhancement in the hepatic arterial phase, and absence of washout in the portal venous phase, unlike HCC and metastases, which typically have a washout appearance [13]. Given that they contain hepatocytes, these nodules may also exhibit hepatobiliary contrast retention.
Fig. 2A —Large regenerative nodules.
A, 38-year-old woman with Budd-Chiari syndrome and regenerative nodules. Axial gadolinium-enhanced T1-weighted MR images of liver show enhancing nodule (arrow) in late arterial (left) and portal venous (center) phases. Round, enhancing mass (arrow) in segment VII of liver is evident, as are additional smaller hypervascular nodules. Nodule in segment VII and smaller liver nodules are isointense to slightly hyperintense to liver in portal venous phase. Axial T2-weighted MR image of liver (right) shows dominant nodule is isointense to liver and has hypointense rim (arrow), whereas other nodules are isointense to hypointense.
Fig. 2B —Large regenerative nodules.
B, 28-year-old woman who has undergone Fontan operation. Axial late arterial phase contrast-enhanced CT scan of liver (left) shows multiple enhancing nodules and dominant lesion (arrow) in left lobe. Axial delayed phase contrast-enhanced CT scan (right) shows nodule in left liver has low attenuation and rim of enhancement (arrow). Additional liver nodules are isointense to liver in portal venous phase.
Management of large regenerative nodules is usually directed at the underlying liver condition [11]. Because of the presence of these atypical nodules, Budd-Chiari syndrome as a cause of chronic liver disease is an exclusion criterion for noninvasive definitive diagnosis of HCC in the 2017 version of the Liver Imaging Reporting and Data System [4]. Similarly, the conditions of patients who have undergone a Fontan operation and have chronically elevated systemic venous pressure and low cardiac output progress to chronic liver inflammation. Arterially enhancing benign masses with washout may subsequently develop and mimic HCC (Fig. 2B). Being on the lookout for portal phase washout, mosaic architecture, elevated α-fetoprotein and threshold growth at follow-up imaging is the key to identifying HCC in patients who have undergone a Fontan operation [14, 15].

Inflammatory Pseudotumor

Inflammatory pseudotumor (IPT) is a rare entity that occurs most commonly in the lungs [16]. It is characterized by inflammatory cellular infiltration and areas of fibrosis, which is why it is also known as plasma cell granuloma [17]. The hepatic variant of IPT accounts for 8% of extrapulmonary IPTs and has an incidence of 0.7% [1820]. IPT in the liver may present as a malignant masquerade variably misinterpreted as atypical HCC, cholangiocarcinoma, or metastasis [21, 22] (Fig. 3). IPTs in the liver are classified pathologically as IgG4-related and non–IgG4-related [23]. Although the two types have different pathologic and clinical features, imaging alone is not enough to differentiate them [24]. IPT carries a good prognosis with conservative management.
Fig. 3A —48-year-old man with Epstein-Barr virus–positive pseudotumor.
A, PET/CT image shows multiple lesions in liver with increased radiotracer uptake (arrows).
Fig. 3B —48-year-old man with Epstein-Barr virus–positive pseudotumor.
B, Axial portal venous phase contrast-enhanced CT image shows peripheral enhancement of corresponding lesion with central hypoattenuation (arrows).
Fig. 3C —48-year-old man with Epstein-Barr virus–positive pseudotumor.
C, Axial delayed phase contrast-enhanced CT image shows retention of contrast material (arrows).
CT and MRI are useful for reaching the correct diagnosis of IPT. IPTs usually appear as heterogeneous peripherally enhancing lesions with central low attenuation and occasional delayed enhancement at contrast-enhanced CT. T2-weighted MR images may show heterogeneous signal intensity with high intensity in the periphery of the mass. However, because of the lack of pathognomonic imaging features, histologic confirmation of the diagnosis is often required to avoid unwarranted procedures [25]. Suspicion should be high for IPT in patients with solid liver lesions and one or more of the following: systemic illness with elevated serum inflammatory markers, normal α-fetoprotein and carbohydrate antigen 19 levels and a history of IPTs elsewhere. IPTs are usually successfully treated with antibiotics or nonsteroidal antiinflammatory drugs [26].

Hepatic Radiation Injury

Radiation treatment of the distal esophagus, lung bases, and pancreatic masses can result in inflammation and necrosis in the nearby liver parenchyma. The imaging characteristics of irradiated liver parenchyma reflect the increased water content and impaired perfusion. CT shows decreased attenuation and decreased enhancement in the arterial and venous phases and progressive enhancement in the delayed phase [27]. PET typically shows an area of increased FDG uptake [28] (Fig. 4). At MRI, use of a hepatobiliary agent may show decreased uptake 20 minutes after the injection owing to hepatic injury [29]. Clues to the diagnosis of radiation injury include typical location within the radiation field, a less distinct appearance at follow-up imaging, and a history of radiation within the previous 6 months.
Fig. 4A —58-year-old man with gastric lymphoma and radiation-induced changes in liver.
A, PET/CT image shows hypermetabolic masslike finding (arrow) in left hepatic lobe adjacent to stomach.
Fig. 4B —58-year-old man with gastric lymphoma and radiation-induced changes in liver.
B, Axial T2-weighted MR image of liver shows masslike area of high signal intensity (arrow).
Fig. 4C —58-year-old man with gastric lymphoma and radiation-induced changes in liver.
C, Coronal gadoxetate disodium–enhanced hepatobiliary phase MR image of liver shows hypointense area (arrow) with corresponding atrophic lateral segment.

Giant Biliary Hamartoma

Biliary hamartomas are usually multiple small (< 1.5 cm) benign cystic lesions containing dilated bile ducts and surrounded by fibrous stroma [30]. They are seen as areas of high signal intensity on T2-weighted MR images and as low-attenuation lesions at CT. Larger lesions mimicking cystic neoplasms (i.e., cystadenocarcinomas) are rare but have been reported [31]. Altered fluid content secondary to hemorrhage and proteinaceous material with resultant increased attenuation on CT scans and increased signal intensity on T1-weighted images have been described. Clues to the correct diagnosis include a fibrous capsule that produces a hypointense rim on T2-weighted images and smooth, delayed peripheral enhancement on contrast-enhanced images (Fig. 5).
Fig. 5A —71-year-old man with abdominal pain due to giant biliary hamartoma.
A, Axial T1-weighted unenhanced fat-suppressed MR image (left) and portal venous phase image after injection of gadolinium-based contrast agent (right) show large cystic lesion (arrow) in right hepatic lobe with fluid content and slight increase in signal intensity on unenhanced image (left), indicating hemorrhagic or proteinaceous content. Slight peripheral enhancement (arrow, right) is evident.
Fig. 5B —71-year-old man with abdominal pain due to giant biliary hamartoma.
B, Axial T2-weighted fat-suppressed MR image of liver (left) shows hyperintense lesion. Coronal T2-weighted MR image (right) shows hyperintense lesion with hypointense capsule (arrow).

Posttreatment Pitfalls

Omental Packing

Indications for the use of omental packing during surgical intervention include hepatic trauma, tumor resection, removal of a large cyst to prevent bleeding, biliary leakage, and abscess formation [32]. The imaging features can mimic those of adipose tissue. Thus, omental packing can be misinterpreted as a hepatic fat-containing lesion such as lipoma, angiomyolipoma, liposarcoma, or HCC [33]. CT shows that the area of packing has very low attenuation (−10 to −100 HU) compared with the liver parenchyma (Fig. 6). MRI shows a loss of signal intensity on fat-suppressed images compared with non–fat-suppressed pulse images and an India ink artifact between the finding and the adjacent liver on dual-phase gradient-echo images [33]. To help reach the correct diagnosis, branching intralesional vessels can be traced to omental vessels. In addition, close review of the clinical history, particularly any history of surgery, should be helpful for avoiding misinterpretation.
Fig. 6A —55-year-old man undergoing CT follow-up after partial hepatic resection with omental packing.
A, Axial portal venous phase contrast-enhanced CT image of liver (left) shows fat-attenuation masslike lesion in left lobe corresponding to omental packing (arrow). Coronal contrast-enhanced CT image (right) shows fatty masslike lesion traced to adjacent omental origin (arrow).
Fig. 6B —55-year-old man undergoing CT follow-up after partial hepatic resection with omental packing.
B, Axial T2-weighted MR image of liver (left) shows hyperintense masslike lesion and traversing vascular structures (arrow). Axial fat-suppressed late arterial phase gadolinium-enhanced T1-weighted MR image (right) shows hypointense masslike lesion (arrow).

Tissue Sealants

In addition to omental packing, hemostatic agents and tissue sealants can be used for hemostasis during surgery and percutaneous intervention [34]. In some instances, air can be trapped in the interstices of the packing material. This can result in imaging features that mimic abscesses. Blood, interstitial fluid, and granulation tissue can also infiltrate the packing material, producing imaging features similar to those of a soft-tissue mass. These observations often take on an irregular in shape over time and gradually decrease in size, ultimately disappearing [35]. At CT, they appear homogeneous and non-enhancing, but they may also mimic complicated fluid collections because they have high attenuation (Fig. 7). The presence of granulation tissue, however, can cause enhancement that can be misinterpreted as a recurrent mass in the case of oncologic resection. Close review of the patient history and the position of the lesion in relation to surgical clips often leads to the correct diagnosis.
Fig. 7A —78-year-old woman 6 days after en bloc gallbladder resection for gallbladder cancer with hepatic wedge resection and placement of tissue sealant.
A, Axial portal venous phase contrast-enhanced CT image of liver (A) and coronal reformat (B) show well-circumscribed masslike lesion with gas bubbles (arrow) mimicking abscess in hepatic wedge resection bed.
Fig. 7B —78-year-old woman 6 days after en bloc gallbladder resection for gallbladder cancer with hepatic wedge resection and placement of tissue sealant.
B, Axial portal venous phase contrast-enhanced CT image of liver (A) and coronal reformat (B) show well-circumscribed masslike lesion with gas bubbles (arrow) mimicking abscess in hepatic wedge resection bed.

Malignant Lesions Mimicking Benign Conditions

Metastases With Delayed Phase Enhancement

The liver is a common site for metastatic lesions originating in the colon, breast, lung, pancreas, and stomach, most of these metastases being hypovascular [36]. At CT, hypovascular metastases appear as hypoattenuating lesions with peripheral continuous rim enhancement in the arterial phase. At MRI, they appear hypointense on T1-weighted and slightly hyperintense on T2-weighted images with less contrast enhancement than the liver parenchyma [37]. Some metastases exhibit delayed phase enhancement, mimicking hepatic hemangioma (Fig. 8). This delayed enhancement is usually due to contrast retention in fibrosis and abundant interstitial tissue. The clues to a correct diagnosis include a history of primary malignancy, continuous rather than discontinuous rim enhancement, CT isoattenuation and MRI isointensity in the delayed phase, unenhanced T1 hypointensity, peripheral washout in the delayed phase, intermediate T2 signal intensity, indistinct margins, and the presence of hemorrhage or necrosis [38]. In contradistinction, hemangiomas typically parallel the blood pool in enhancement and are more markedly T2 hyperintense than the liver parenchyma.
Fig. 8A —73-year-old man with colon adenocarcinoma with liver metastases mimicking hemangioma.
A, Axial portal venous (A) and delayed (B) phase contrast-enhanced CT images of liver show hypoenhancing mass (arrow) in left hepatic lobe consistent with metastatic deposit. Mass retains contrast material (arrow) in delayed phase (B). These findings can be misinterpreted as hemangioma.
Fig. 8B —73-year-old man with colon adenocarcinoma with liver metastases mimicking hemangioma.
B, Axial portal venous (A) and delayed (B) phase contrast-enhanced CT images of liver show hypoenhancing mass (arrow) in left hepatic lobe consistent with metastatic deposit. Mass retains contrast material (arrow) in delayed phase (B). These findings can be misinterpreted as hemangioma.

Cystic Liver Metastases

Truly cystic liver metastases are rare; their incidence varies according to the type of the primary neoplasm. Tumors known to present with cystic-appearing metastases include cystadenoma, cystadenocarcinoma, colonic mucinous adenocarcinoma, neuroendocrine tumors, thyroid carcinoma, and gastrointestinal stromal tumors [36]. The cystic appearance is usually attributed either to necrosis due to growth beyond the vascular supply or to mucin overproduction, as in tumors of colorectal or ovarian origin or in gastrointestinal stromal tumors after imatinib therapy [39, 40]. Treatment of liver metastases with antiangiogenic therapy may result in visualization of cystic lesions that were previously present but seen only after treatment. This should not be regarded as progression of disease but rather interval necrosis of previously nonvisualized liver metastasis.
At CT, cystic metastases appear as hypoattenuating or hyperattenuating masses owing to the presence of mucin or hemorrhage, respectively, with occasional peripheral and septal enhancement (Fig. 9). At MRI, cystic metastases appear hypointense on T1-weighted and hyperintense on T2-weighted images with occasional peripheral enhancement [41]. Cystic metastases can be misinterpreted as simple or complex benign cystic lesions. The clues to a correct diagnosis include relevant clinical history, presence of mural nodules or enhancing components, irregular enhancing septations, irregular inner margin, and multifocality.
Fig. 9A —44-year-old woman with gastrointestinal stromal tumor and cystic metastases to liver.
A, Axial T2-weighted MR image (left) shows well-circumscribed large hyperintense lesion (arrow) with smaller adjacent hyperintense lesion (arrowhead) in right hepatic lobe. Axial late arterial phase T1-weighted MR image acquired after injection of gadolinium-based contrast agent (right) shows both lesions are hypointense compared with adjacent liver parenchyma.
Fig. 9B —44-year-old woman with gastrointestinal stromal tumor and cystic metastases to liver.
B, DW image (left) and apparent diffusion coefficient map (right) show nonrestricted diffusion (arrow). Arrowhead indicates smaller adjacent hyperintense lesion.

Fat-Related Pitfalls

Focal Hepatic Steatosis

Hepatic steatosis is one of the most common abnormalities encountered in cross-sectional imaging [42]. It is most commonly caused by alcoholic liver disease, toxicity related to chemotherapy, or nonalcoholic fatty liver disease. The prevalence in the general population is 15%, compared with the prevalence of 75% among patients with obesity, 50% among those with hyperlipidemia, and 45% among those with alcoholism [43]. Different patterns of steatosis can be seen, including diffuse hepatic steatosis, diffuse fatty change with areas of focal sparing, and focal fat in an otherwise normal liver.
At CT, focal fat appears as a low-attenuation geographic area with vessels passing through it, typically with an attenuation less than 40 HU, or 10 HU less than that of the spleen [44]. Focal steatosis is classically present near the falciform ligament, in periportal distribution, or around the gallbladder. At MRI, there may be a characteristic decrease in signal intensity on opposed-phase compared with in-phase gradient-echo images [45] (Fig. 10A). Heterogeneous or nonuniform fat accumulation may lead to an erroneous diagnosis by mimicking neoplastic or inflammatory conditions. Focal fat can remain hypointense on hepatobiliary phase MR images but is usually not as hypointense as metastases (Fig. 10B). The relative enhancement of focal fat mimics that of normal liver. The finding of steatosis at CT can be misinterpreted as metastatic disease because of its low attenuation relative to spared liver [38]. Clues to the correct diagnosis include recognizing the typical locations of focal steatosis, lack of a diffusion correlate, relative mildly decreased hepatobiliary contrast retention, lack of mass effect, and vessels traversing the areas of abnormal attenuation or signal intensity on CT and MR images.
Fig. 10A —Focal hepatic steatosis.
A, 42-year-old woman with breast cancer undergoing surveillance imaging with finding of focal fat deposition in liver. Axial portal venous phase contrast-enhanced CT image of liver (left) shows scattered ill-defined low-attenuation areas (arrows) throughout liver. Opposed-phase (center) and in-phase (right) MR images of liver show loss of signal intensity in these lesions (arrows) in out-of-phase-series. Findings are consistent with lipid-containing lesions.
Fig. 10B —Focal hepatic steatosis.
B, 46-year-old woman with focal fat deposition in liver. Opposed-phase (left) T1-weighted MR images of liver show decreased signal intensity (arrow) in area of focal fatty changes, which appear slightly hypointense on unenhanced T1-weighted image (center). This finding is consistent with lipid-containing lesions. Axial gadoxetate disodium–enhanced T1-weighted fat-suppressed MR image of liver (right) shows focal fatty area (arrow) remains slightly hypointense in hepatobiliary phase.

Nodular Fatty Sparing

Nodular fatty sparing can occur in a background of diffuse hepatic steatosis. Usually, it has a geographic shape and occurs at specific locations, such as near the porta hepatis or in segments IV and V near the gallbladder fossa (similar locations to focal steatosis). At CT, the focal sparing has increased attenuation compared with the adjacent fatty liver parenchyma. At MRI, a focal area of high signal intensity is visible against a background of low intensity on out-of-phase images [46, 47] (Fig. 11). These nodular spared areas can be misinterpreted as metastatic deposits or other focal lesions [48]. Fatty sparing can also occur around a focal lesion, such as a metastatic lesion. In this case, DWI and contrast-enhanced imaging may help to accurately delineate the metastatic deposit from the background spared liver [38].
Fig. 11A —60-year-old woman with nodular lesion due to focal fatty sparing in liver.
A, Axial in-phase T1-weighted MR image of liver shows homogeneous liver parenchyma and no focal lesions.
Fig. 11B —60-year-old woman with nodular lesion due to focal fatty sparing in liver.
B, Axial opposed-phase T1-weighted image shows diffuse loss of liver parenchymal signal intensity and well-defined nodule (arrow) of higher signal intensity than parenchyma, corresponding to area of focal fatty sparing.

Diffuse Hepatic Steatosis

Diffuse hepatic steatosis can obscure an underlying focal hepatic lesion or alter its typical imaging features. Severe steatosis can reduce the sensitivity of metastatic lesion detection with CT. In this situation, MRI may be more sensitive for detection of metastatic lesions because of the capability of improved soft-tissue contrast, DWI, and hepatobiliary phase imaging [36, 37]. At MRI, liver metastases may be hyperintense on out-of-phase images but appear hypointense on in-phase T1-weighted images. Also at MRI, when steatosis is severe, metastases that would typically be hypointense to normal liver may appear hyperintense to steatotic liver (Fig. 12).
Fig. 12A —68-year-old man with colon cancer and metastatic liver lesions in fatty liver.
A, Axial unenhanced T1-weighted MR image of liver (left) shows hyperintense metastatic lesion (arrow). Axial hepatobiliary phase contrast-enhanced T1-weighted image (right) shows liver metastasis as hyperintense relative to background liver. Typically, colon cancer metastases appear hypointense on unenhanced T1-weighted images and hypoenhancing on contrast-enhanced T1-weighted images.
Fig. 12B —68-year-old man with colon cancer and metastatic liver lesions in fatty liver.
B, Axial in-phase (left) and opposed-phase (right) T1-weighted MR images of liver show loss of signal intensity of liver in opposed phase due to severe diffuse hepatic steatosis (arrow).

Diffuse Confluent Metastases

Diffuse confluent metastases can seed the liver through the portal vein. The evaluation of hepatic masses may be challenging in this scenario because of the lack of normal background liver for reference. Coalescent metastases can mimic steatosis or diffuse liver disease. Differentiation requires recognition of the expected changes in attenuation or signal intensity described for steatosis at CT and MRI [44, 45]. Unlike simple steatosis, diffuse metastases do cause a mass effect and possible hepatomegaly along with distortion of the bile ducts and blood vessels. At MRI, the liver may have increased T2 signal intensity (greater than background muscle) but should not exhibit a typical decrease in signal intensity on out-of-phase images and often exhibits diffusion restriction or signal intensity on high b value images that nears that of the spleen [36, 37] (Fig. 13). Bulging of the liver capsule and nodular liver contour in the absence of cirrhosis are additional clues.
Fig. 13A —72-year-old woman with diffuse confluent metastases secondary to gastric carcinoma.
A, Axial portal venous phase contrast-enhanced CT image shows diffuse area of increased attenuation in periphery of liver (arrows).
Fig. 13B —72-year-old woman with diffuse confluent metastases secondary to gastric carcinoma.
B, Axial T2-weighted MR image shows geographic areas of hyperintensity (arrows) at periphery of liver.
Fig. 13C —72-year-old woman with diffuse confluent metastases secondary to gastric carcinoma.
C, Axial late arterial phase gadolinium-enhanced image shows enhancement (arrows) and bulging of liver capsule (arrowheads). Findings are in keeping with confluent hepatic metastases.

Pseudolesions Secondary to Anomalous Vascular Supply

Aberrant Hepatopetal Venous Flow

Hepatopetal venous flow normally occurs through the portal venous system. Aberrant hepatopetal flow, also known as third inflow, can be a result of aberrant right or left gastric, cystic, paraumbilical, and caudate veins [49, 50]. Aberrant venous flow may result in focal areas of fatty deposition, fatty sparing, and perfusion changes, which result in the appearance of an enhancing pseudolesion and mimic a focal hepatic lesion [51, 52]. These areas can be mistaken for enhancing metastases in patients with a known primary tumor (Fig. 14). Pseudolesions associated with aberrant right gastric vein are usually seen in segment IV, whereas those associated with aberrant left gastric vein more typically involve segments II and III of the liver. Pseudolesions caused by the cystic vein are usually seen adjacent to the gallbladder, whereas those associated with the caudate vein are seen within the caudate lobe [53, 54].
Fig. 14 —54-year-old man with aberrant hepatopetal venous flow and history of melanoma. Axial portal venous phase contrast-enhanced CT image of liver shows geographic area of enhancement (arrow) in posterior aspect of segment IV. Right gastric vein (arrowhead) courses through segment without obstruction or displacement.
MRI can be used to differentiate pseudolesions from true lesions [45]. Clues to the correct diagnosis of a hepatic pseudolesion include a location that is typically based on the associated vein, typical segmental or geographic pattern, and visualization of an anomalous vein coursing through the enhancing area with no associated mass effect from the lesion [38].

Superior Vena Caval Obstruction

Obstruction of the superior vena cava (SVC) often produces multiple chest and upper abdominal wall venous collaterals that can communicate with portal venous branches, resulting in portosystemic venous shunting. Drainage of systemic blood through portal collaterals increases intrahepatic blood flow and can result in a focal hot spot or hot quadrate sign [55, 56]. Causes of SVC obstruction include occlusion related to an in-dwelling catheter, constriction from mediastinal fibrosis, and mass effect from thoracic malignancies. On contrast-enhanced images, a focal hot spot appears as a wedge-shaped area of enhancement in segment IV of the liver that mimics an enhancing liver mass [57] (Fig. 15). Clues to the correct diagnosis include recognizing the presence of chest and abdominal wall collaterals that can be indicative of SVC obstruction along with the classic distribution of enhancement within the liver. Once the diagnosis is suspected, dedicated imaging of the chest to confirm SVC obstruction should be recommended.
Fig. 15A —27-year-old man with systemic lupus erythematosus and occlusion of superior vena cava.
A, Coronal contrast-enhanced CT image of chest and upper abdomen (left) shows focal occlusion of superior vena cava (long arrow) with blood being shunted into subclavian and axillary veins (short arrow). Coronal contrast-enhanced CT image of upper abdomen (right) shows large venous collateral (short arrow) draining into liver with resultant parenchymal area of hyperenhancement (long arrow) in segment IV.
Fig. 15B —27-year-old man with systemic lupus erythematosus and occlusion of superior vena cava.
B, Axial early arterial phase contrast-enhanced CT image of liver (left) shows oblong area (long arrow) with central vessel (arrowhead) and large anterior abdominal wall collateral vessels (short arrow). Axial portal venous phase contrast-enhanced CT image (right) shows corresponding area with increased enhancement (arrow).

Hepatic Pseudoaneurysm

Hepatic pseudoaneurysm is a rare complication that can occur after biopsy, trauma, percutaneous intervention, or liver transplant [5860]. It occurs when blood leaking from an artery into the adjacent tissue produces an open communication between the artery and the resultant cavity. As elsewhere in the body, hepatic pseudoaneurysm poses a risk of rupture and life-threatening hemorrhage [61]. On images, it may appear as an enhancing mass mimicking an intrahepatic or exophytic parenchymal tumor, especially in patients with chronic liver disease. Clues to the correct diagnosis include a clinical history of hepatic intervention, enhancement similar to that of arteries in all phases, visualization of a direct communication with an artery, a vascular yin-yang ultrasound pattern, and a signal-intensity void on T1- and T2-weighted MR images.

Transient Hepatic Attenuation and Intensity Differences

THAD and THID represent an area of abnormal parenchymal enhancement in the arterial phase of CT and MRI. It is a result of the dual nature of the liver's blood supply (portal vein, 75%; hepatic artery, 25%) [62]. The phenomenon is explained by the compensatory increase in arterial flow when there is a decrease in portal flow. THAD and THID are often idiopathic but can be a direct result of focal lesions due to a siphoning effect, which causes a lobar multisegmental shape, or an indirect result of portal hypoperfusion, which produces a sectorial shape with straight borders [63]. It can also result from portal vein thrombosis or flow diversion due to an arterioportal shunt [63]. At imaging, THAD and THID appear as a wedge-shaped area that is enhancing in the arterial phase but fades to become isoattenuating or isointense in the portal venous phase. The size of the abnormality relates directly to the location of the insult relative to the portal vein branch size. More central lesions produce larger regions of THAD and THID. THAD and THID can be mistaken for other enhancing hepatic focal lesions, particularly if they have a rounded configuration. Although THAD and THID are frequently idiopathic, a thorough search should be conducted for possible underlying causes [38]. THAD and THID can also look like regions of confluent fibrosis and atrophy, which instead of equilibrating with background liver persistently are more enhancing than the background.

Conclusion

When assessing focal hepatic lesions, it is important to avoid pitfalls and misdiagnoses that can alter the management plan. Helpful strategies for avoiding pitfalls include paying close attention to the clinical history of the patient, carefully evaluating all available imaging studies, and being aware of the various radiologic mimics.

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FOR YOUR INFORMATION

The reader's attention is directed to a related article, titled “Spectrum of Pitfalls, Pseudolesions, and Potential Misdiagnoses in Cirrhosis,” which begins on page 87.

Information & Authors

Information

Published In

American Journal of Roentgenology
Pages: 97 - 108
PubMed: 29932762

History

Submitted: March 12, 2018
Accepted: March 16, 2018

Keywords

  1. CT
  2. hepatic focal lesions
  3. hepatocellular carcinoma
  4. imaging mimics
  5. MRI pitfalls

Authors

Affiliations

Khaled M. Elsayes
Department of Radiology, The University of Texas MD Anderson Cancer Center, 1400 Pressler St, Houston, TX 77030.
Christine O. Menias
Department of Radiology, Mayo Clinic, Scottsdale, AZ.
Ali I. Morshid
Department of Radiology, The University of Texas MD Anderson Cancer Center, 1400 Pressler St, Houston, TX 77030.
Akram M. Shaaban
Department of Radiology and Imaging Sciences, University of Utah Health, Salt Lake City, UT.
Kathryn J. Fowler
Mallinckrodt Institute of Radiology, Washington University in Saint Louis, Saint Louis, MO.
An Tang
Department of Radiology, Centre Hospitalier de l'Université de Montréal, Montréal, QC, Canada.
Victoria Chernyak
Department of Radiology, Montefiore Medical Center, Bronx, NY.
Janio Szklaruk
Department of Radiology, The University of Texas MD Anderson Cancer Center, 1400 Pressler St, Houston, TX 77030.
Mustafa R. Bashir
Department of Radiology and Center for Advanced Magnetic Resonance Development, Duke University Medical Center, Durham, NC.

Notes

Address correspondence to K. M. Elsayes ([email protected]).

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