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MRI of Focal Liver Lesions
▪ Introduction
Magnetic resonance imaging (MRI) is the most comprehensive and definitive noninvasive modality for evaluating the liver. A combination of enhancement characteristics and exquisite tissue contrast allows for the characterization of liver lesions. Unique artifacts—such as susceptibility and chemical shift—allow for sensitive detection of hepatic iron and lipid deposition, respectively. Common indications for liver MRI include liver lesion characterization, hepatic steatosis quantification and surveillance, liver surveillance in patients with risk factors for hepatocellular carcinoma (HCC), metastatic workup in patients diagnosed with cancer, and further investigation for patients with abnormal liver enzymes of unknown etiology ( Table 2.1 ).
TABLE 2.1
Common Indications for Liver Magnetic Resonance Imaging
| Indication | Imaging Objective | Details |
|---|---|---|
| Liver lesion characterization | Definitive lesion diagnosis (usually detected by US or CT) | Consider Eovist for suspected FNH |
| Known or suspected metastatic disease | Exclude or detect metastases from extrahepatic primary malignancies | Consider Eovist |
| Elevated LFTs | Exclude or detect biliary obstruction and potential obstructing mass or stones, parenchymal disease as a result of inflammation or underlying lesions | Eovist less useful with hepatocyte dysfunction |
| Chronic liver disease/cirrhosis | Exclude or detect hepatocellular carcinoma, evaluate vascular structures for patency, assess for portal hypertension, assess degree of cirrhosis | Eovist less useful with hepatocyte dysfunction |
| Portal venous patency | Identify normal enhancement and absence of filling defect, recanalization, or collateralization | Consider ⇑dose gadolinium, SSFP |
| Hepatic steatosis | Quantify degree of steatosis, assess for development of cirrhosis | Consider fat quantification technique |
| Iron deposition | Liver iron quantification; involvement of pancreas, spleen, bone marrow, myocardium | Consider iron quantification technique; T2 and T2 correlate with iron content |
| Response to treatment | Identification of residual/recurrent viable tumor after percutaneous, intra-arterial, or systemic therapy | Consider extracellular GCA |
| Hepatocellular carcinoma | Assess size, multifocality, and vascular invasion | Correlate with alpha-fetoprotein levels |
| Cholangiocarcinoma | Assess size, extent of biliary involvement, lobar atrophy, lymphadenopathy, vascular invasion | Include MRCP sequences |
▪ Normal Features
Morphology, signal, and texture are the currency used to describe the MRI appearance of the liver. The normal liver is usually described from a negative reference point—“lack of nodularity” or “atrophy/hypertrophy pattern” (or “trophic pattern”). Normal liver texture is smooth, reflected by an absence of both surface nodularity and reticulated fibrosis that develops with cirrhosis. The liver occupies most of the right upper quadrant and its morphology generally conforms to the available space in the right upper quadrant, bounded by the right hemidiaphragm and abdominal wall. Mentally deconstruct the liver into segments—right lobe, medial segment, lateral segment, and caudate lobe—to establish the basis for normal and morphologic derangements associated with cirrhosis (the former two atrophy and the latter two hypertrophy) ( Fig. 2.1 ).
Further deconstruct the liver spatially into segments, according to the Couinaud system, in order to facilitate communication with referring physicians and specifically locate lesions and pathology. Each Couinaud segment functions independently with unique vascular inflow, outflow, and biliary drainage; the central portal vein, hepatic artery, and bile duct define the segment. Consequently, each segment is independently resectable without affecting neighboring liver tissue. The horizontal plane of the portal vein bifurcation transects the vertical planes of the hepatic veins to delineate the Couinaud segments.
Relatively low water content accounts for hepatic parenchymal signal characteristics—relative T1 hyper- and T2 hypointensity. Hepatic T1 signal nearly matches pancreatic T1 hyperintensity, and most tumors contain more water and appear relatively T1 hypo- and T2 hyperintense to the normal liver. Isointensity between in- and out-of-phase images reflects an absence of fat and iron deposition under normal circumstances.
The liver experiences a unique biphasic enhancement pattern as a consequence of its dual blood supply. The portal vein delivers 75% of blood flow to the liver, with the hepatic artery accounting for the rest. Four discrete phases describe the transit of intravenous contrast through the liver: the hepatic artery–only phase (HAOP), the hepatic artery–dominant phase (HADP; also known as the capillary phase ), the portal venous phase (PVP; also known as the early hepatic venous phase ), and the hepatic venous phase (HVP; otherwise known as the interstitial phase ) ( Fig. 2.2 ).
Liver imaging relies heavily on the HADP. HADP image acquisition begins approximately 15 seconds after contrast administration. Modest tissue enhancement, or relative T1 hyperintensity compared with unenhanced images, and contrast within the hepatic arteries and portal veins characterize the HADP in which the parenchyma has been perfused by the hepatic arterial circulation ( Fig. 2.3 ). Arterial contrast preceding parenchymal and portal venous enhancement corresponds to the HAOP, preceding the HADP. Successful acquisition of an HADP phase permits lesion enhancement stratification into four categories relative to liver parenchyma: hypervascular (more arterial perfusion), isovascular, hypovascular, and avascular ( Fig. 2.4 ). Correlating relative HADP signal with relative intensity on subsequent timepoints often yields specific diagnostic information. Before making this assessment, confirm adequate timing of the intended HADP; early or late timing often obscures hypervascular lesions.
PVP acquisition time begins approximately 45 to 60 seconds after contrast administration and corresponds to peak parenchymal enhancement. All vessels, including hepatic veins, are enhanced. Liver features during the HVP resemble the PVP, and underlying lesion enhancement changes, such as washout, may be more conspicuous with time. HVP timing constraints are less rigorous and may be obtained between 90 seconds and 5 minutes after contrast administration.
▪ Focal Lesions
Exquisite tissue contrast and enhancement conspicuity distinguish MRI as the definitive noninvasive diagnostic authority for liver lesions. Like ultrasound, MRI unequivocally discriminates solid from cystic lesions and, like CT, incorporates enhancement characteristics into the diagnostic analysis. T2 values differentiate cystic (almost always benign) from solid (benign or malignant) lesions with virtually no overlap. Review the heavily T2-weighted images to identify cystic lesions; visibility on these images connotes fluid content and excludes solid masses. Cysts, biliary hamartomas, and hemangiomas—all benign lesions—dominate this category, referred to as cystic lesions for the purpose of this discussion. Inflammatory lesions, such as echinococcal cysts and abscesses, enter the differential only in the appropriate clinical setting. In the neoplastic category, only the exceedingly rare biliary cystadenoma (and cystadenocarcinoma) merit consideration in the cystic liver lesion differential only when characteristic features coexist. Whereas cystic or necrotic metastases feature cystic components, peripheral solid tissue excludes true cystic etiology. Enhancement indicates solid tissue, excluding cystic etiologies, and serves as the basis for solid versus cystic lesion classification and diagnosis (supplemented by T2 characteristics). Within the solid category, lesions are stratified into 1 of 2 groups according to the degree of enhancement (hyper- versus hypovascularity) ( Table 2.2 ).
TABLE 2.2
Liver Lesion Classification Scheme
| Cystic | Hypervascular | Hypovascular |
|---|---|---|
| Simple hepatic cyst | Hepatic adenoma | Hypovascular metastases |
| Biliary hamartoma | ||
| Focal nodular hyperplasia | Lymphoma | |
| Hemangioma | ||
| Biliary cystadenoma (-adenocarcinoma) |
Transient hepatic arterial difference | Ablated lesions |
| Echinococcal cyst | Cirrhotic nodules (prehypervascular) | Cholangiocarcinoma |
| Pyogenic abscess | ||
| Amebic abscess | Hepatocellular carcinoma | Angiomyolipoma |
| Fungal abscess | Fibrolamellar carcinoma | Lipoma |
| Hematoma | ||
| Biloma | Hypervascular metastases | Steatotic nodule |
Cystic Lesions
Establish cystic status using heavily T2-weighted images and pre- and postcontrast images. As T2-weighting increases, signal decays from everything but unbound water protons and free fluid. Consequently on heavily T2-weighted images, all hyperintense lesions are effectively cystic. Cystic designation effectively connotes benign etiology. Simple cysts and biliary hamartomas define the highest end of the T2 signal intensity spectrum as purely fluid-filled structures ( Fig. 2.5 ). Hemangiomas are slightly less intense and frame the lower limit of signal intensity for fluid-intensive liver lesions. Echinococcal cysts are generally similar in intensity to simple cysts, but might be complicated with wall thickening, septation (pericyst), (daughter cyst), and/or internal debris (matrix, hydatid sand). Fungal and pyogenic abscesses are usually not technically cystic and are more accurately described as “liquefying,” but for the purposes of our discussion, they are included in the cystic category. The only neoplastic lesion—biliary cystadenoma/cystadenocarcinoma—is predominantly cystic with variable septation and scant solid tissue (unless rarely flagrantly malignant).
Developmental Lesions
Simple Hepatic Cyst
Simple hepatic (bile duct) cysts are benign incidental lesions not communicating with the biliary tree, although lined with biliary endothelium. They arise from a defect in bile duct formation. Hepatic cyst prevalence has been reported in the 2.5% range, although anecdotal experience suggests a higher prevalence. These lesions are almost always incidental, unless associated with an inherited polycystic syndrome.
The water content of cysts dictates the imaging appearance—uniform T2 hyper- and T1 hypointensity equivalent to the cerebrospinal fluid ( Fig. 2.6 ). No solid tissue complicates the appearance, and the wall is imperceptible. Size ranges from a few millimeters to (usually) less than 10 cm. Occasional thin (essentially unmeasurable) septa are present. Simple cysts maintain maximum signal intensity even on heavily T2-weighted images, whereas other relatively high fluid content substances (such as hemangiomas) lose signal compared with moderately T2-weighted images. Lack of enhancement confirms the absence of solid tissue—the water-filled cyst remains a T1 signal void. Complications explain aberrancy in the monotonous appearance of simple cysts and include infection, rupture, and hemorrhage. Infected cysts may contain septa and debris, which changes the internal signal profile. Hemorrhagic cysts usually exhibit T1 hyperintense internal contents with possible fluid-fluid levels. Although minimal reactive rim enhancement may accompany these complications, lack of enhancement is otherwise maintained.
Of course, the probability of complications increases with an increased number of cysts. With more than 10 cysts, the possibility of polycystic liver disease (PCLD) should be considered (see Fig. 2.6 ). PCLD is in the family of fibropolycystic liver diseases that include bile duct hamartoma, Caroli’s disease, congenital hepatic fibrosis, and choledochal cysts. Imaging features do not distinguish these cysts from simple hepatic cysts, and histology is identical. Although commonly associated with polycystic kidney disease, PCLD also occurs in isolation.
Bile Duct Hamartoma
The bile duct hamartoma (von Meyenburg complex) is another liver lesion that is usually cystic. It is a focal cluster of disorganized bile ducts and ductules surrounded by fibrous stroma. Bile duct hamartomas are incidental developmental lesions of uncertain pathogenesis—possibly ischemia, inflammation, or genetic anomalies. Although present in 3% of autopsy specimens, more than half evade detection on imaging studies. Lesions range in size from 2 to 15 mm, and they tend to be peripherally distributed. The MRI appearance is defined by a spectrum extending from simple fluid with no enhancement on one end to solid, enhancing tissue (fibrous stroma) on the other. The simple fluid appearance dominates, simulating a hepatic cyst, although a thin, peripheral rim of enhancement occasionally coexists ( Fig. 2.7 ). When solid, these lesions exhibit intermediate signal intensity on T2-weighed images and generally gradually solidly enhance. Progressive enhancement of the fibrous tissue simulates metastases and follow-up imaging to confirm stability or biopsy ensues.
Caroli’s Disease
Caroli’s disease (or “congenital communicating cavernous ectasia of the biliary tract,” if you prefer—less mellifluous but descriptive) simulates other polycystic liver diseases—PCLD, multiple simple (biliary) hepatic cysts, and biliary hamartomas. Many of these cystic diseases (except the simple hepatic cyst) derive from primordial ductal plate disorders. Caroli’s disease represents one of the family of fibrocystic ductal plate diseases to which the following diseases also belong: autosomal recessive polycystic kidney disease, congenital hepatic fibrosis, autosomal dominant polycystic kidney disease, biliary hamartomas, and mesenchymal hamartomas ( Table 2.3 ). The ductal plate represents the anlage of the intrahepatic biliary system. Ductal plate remodeling into the mature intrahepatic biliary dilatation follows a complex series of precisely timed events. In the case of Caroli’s disease, arrest in ductal plate remodeling involves the larger bile ducts (interlobular and more central); Caroli’s syndrome affects the smaller, peripheral, intrahepatic ducts, which undergo remodeling later in embryonic life and manifest with coexistent hepatic fibrosis. A pattern of segmental inflammation and stricturing alternating with saccular and fusiform dilatation of the involved ducts results.
TABLE 2.3
Fibrocystic Ductal Plate Diseases
| Disease | Hepatic Disease | Renal Disease | Associated Features |
|---|---|---|---|
| Congenital hepatic fibrosis (CHF) | Progressive fibrosis of portal tracts with portal hypertension, association with Caroli’s disease | Polycystic kidney disease | None |
| Autosomal recessive polycystic kidney disease (ARPKD) | CHF | Cystic dilatation of collecting tubule | None |
| Autosomal dominant polycystic kidney disease (ADPKD) | Cysts derived from bile ducts (noncommunicating), DPM, CHF, rarely Caroli’s disease | Cysts arising from all segments of tubule | None |
| Autosomal dominant polycystic liver disease | Cysts arising from biliary microhamartomas and periductal glands | None | Mitral leaflet abnormalities, intracranial aneurysms |
| Caroli’s disease | Cystic dilatation of segmental intrahepatic bile ducts, CHF | Medullary sponge kidney, ARPKD, ADPKD | None |
| Choledochal cyst | Intra- or intra- and extrahepatic biliary ductal involvement | None | None |
| Biliary hamartoma | Dilated ducts embedded in fibrous stroma | None | None |
MRI reveals innumerable round and/or tubular fluid collections within the liver measuring up to 5 cm in Caroli’s disease. Although the presence of multiple cystic intrahepatic foci simulates PCLD or biliary hamartomas, communication with the biliary tree discriminates Caroli’s disease from these entities. An additional discriminating feature—the central dot sign —seen on enhanced images, reflects the portal vein branch within the dilated biliary radicle. Intraductal/intracystic filling defects (usually bilirubin stones) may also differentiate Caroli’s disease from the other cystic liver disorders and are best visualized on fluid-sensitive sequences—either heavily T2-weighted or MRCP images.
Other diseases to consider in the differential diagnosis include primary sclerosing cholangitis (PSC) and recurrent pyogenic cholangitis (RPC). Ductal dilatation is less severe and more cylindrical (as opposed to saccular) in PSC and RPC, compared with Caroli’s disease. Involvement of the extrahepatic duct often characterizes PSC and RPC and excludes Caroli’s disease. Complications in Caroli’s disease occur as a consequence of bile stagnation and include stones, cholangitis, hepatic abscesses, postinflammatory strictures, and secondary biliary cirrhosis. Cholangiocarcinoma develops in 7% of patients.
Cavernous Hemangioma
Hemangiomas (cavernous hemangiomas) are classified as cystic for the purpose of this discussion because of the high fluid content and MR signal characteristics similar to fluid—even though the internal contents are blood, instead of water (or serous fluid). Blood flowing slowly enough to avoid flow artifacts, and/or flow voids, accounts for the signal characteristics; a single layer of endothelial lining suspended by fibrous stroma constitutes the only solid component. Hemangiomas are almost invariably incidental lesions representing a collection of dilated vascular channels replacing hepatic parenchyma. Hemangiomas are found in 7% of patients with a slight female predominance (1.5 : 1). Multiple hemangiomas are present in up to 50% of patients.
Hemangiomas range in size from a few millimeters to well over 10 cm, and their complexity is generally proportional to size. The prototypic hemangioma exhibits homogeneous near-isointensity to simple fluid (cyst) on heavily T2-weighted images with well-defined, lobulated borders and a unique enhancement pattern. Early peripheral, nodular, and discontinuous enhancement centripetally progressively fills in on successive delayed images until uniform hyperattenuation (relative to hepatic parenchyma) is achieved ( Fig. 2.8 ).
The aforementioned imaging features define the standard appearance of hemangiomas (type 2; Fig. 2.9 ). Relatively smaller and larger hemangiomas have a predilection for variant enhancement patterns. Small hemangiomas (<2 cm) more often demonstrate uniform early and persistent hyperenhancement (type 1; Fig. 2.10 ). Early hyperenhancement also characterizes other benign and malignant lesions, such as FNH, adenoma, HCC, and hypervascular metastases. Marked T2 hyperintensity and persistent hyperenhancement single out the so-called flash-filling hemangioma from the other hypervascular lesions (none of which exhibit marked T2 hyperintensity and all of which either washout or fade on delayed images). Perilesional perfusional alterations most commonly accompany the smaller flash-filling hemangiomas (see Fig. 2.10 ). Segmental or nodular hyperattenuation (usually peripheral to the lesion) on HADP images fades to isointensity on delayed images and reflects either increased arterial inflow or arterioportal shunting resulting in contrast overflow into perilesional sinusoids.
Giant hemangiomas often display complex imaging features. The definition of giant hemangioma applies to hemangiomas exceeding 4 to 5 cm. The enhancement pattern of the giant hemangioma often reiterates the typical pattern with peripheral, nodular, discontinuous centripetal propagation, except for the presence of a central nonenhancing “scar.” The central variably shaped “scar” (linear, round, oval, cleft-like, or irregular) conforms to cystic degeneration, liquefaction, or myxoid change and usually appears relatively T1 hypo- and T2 hyperintense to the surrounding lesion ( Fig. 2.11 ). Although other liver lesions possess central scars, such as FNH, fibrolamellar HCC, and cholangiocarcinoma, these scars usually enhance late, and overall lesion enhancement features are distinctly different (FNH and fibrolamellar HCC hyperenhance and then washout, whereas rim enhancement with patchy, irregular progression typifies cholangiocarcinoma).
Less common features complicate the MR appearance of hemangiomas, such as pedunculation, calcification, capsular retraction, and hyalinization or thrombosis ( Fig. 2.12 ). Whereas torsion and/or ischemia may complicate the appearance of an exophytic or pedunculated hemangioma, the appearance is otherwise typical—albeit exceedingly rare. Reported prevalence of calcification varies from 1% to 20%, and anecdotally, the actual prevalence seems to be closer to the lower end of the range, or even lower. Calcification in a hemangioma corresponds to phleboliths and/or dystrophic changes in areas of fibrosis and thrombosis. Practically speaking, calcification rarely, if ever, confounds the MR appearance of hemangiomas, and if present, most likely manifests as a signal void. When peripheral, fibrosis associated with a hemangioma potentially results in capsular retraction. The other focal hepatic lesion known to induce capsular retraction is cholangiocarcinoma, which should not present diagnostic difficulty. Hyalinization indicates hemangioma involution and histologically corresponds to thrombosis of vascular channels. Hyalinization decreases T2 signal to slightly hyperintense to liver, and enhancement is variably absent with as little as minimal peripheral delayed enhancement.
A few parting thoughts about hemangiomas are worth mentioning. Although usually static, hemangiomas have been shown to grow on occasion (sometimes with exogenous estrogens), and conversely, they are usually eradicated in the setting of cirrhosis. Malignant transformation has never been described, and spontaneous rupture is exceedingly rare (∼30 cases have been reported). There is no known association with other tumors or other diseases, except Kasabach-Merritt syndrome (KMS). KMS involves a vascular tumor—such as a hemangioma or hemangioendothelioma—sequestering platelets causing thrombocytopenia. Consumption of clotting factors ensues, leading to disseminated intravascular coagulation (DIC). Unless associated with KMS or DIC, for which surgical resection may be warranted, no treatment or follow-up is necessary.
Hemangiomatosis refers to diffuse replacement of hepatic parenchyma by multiple, often innumerable, ill-defined hemangiomas. Diffuse enlargement of the liver with multiple lesions with signal and enhancement characteristics typical of hemangiomas—albeit frequently with ill-defined margins—often profoundly disfigures the liver, rendering it virtually unrecognizable ( Fig. 2.13 ). Although commonly resulting in high-output cardiac failure and mortality in infants, hemangiomatosis usually symptomatically spares adults—only potentially generating diagnostic uncertainty on imaging studies.
Unlike the previously discussed lesions, the remaining cystic liver lesions—biliary cystadenoma/cystadenocarcinoma and infectious lesions—exhibit more complexity and variability. Multilocularity and wall thickening are common features, and these lesions rarely simulate the other simple cystic lesions already discussed. Clinical factors assume a greater role in diagnosis, which is important because all of these lesions require further treatment.
Neoplastic Lesions
Biliary Cystadenoma (-Adenocarcinoma)
Biliary cystadenomas and cystadenocarcinomas require surgical resection for treatment and potential cure. These lesions arise from bile duct epithelium—derived from mucin-secreting epithelial cells. Approximately 85% of these tumors arise from intrahepatic bile ducts (as opposed to extrahepatic bile ducts and gallbladder). Most commonly affecting middle-aged females, two histologic subtypes—with or without ovarian stroma (accounting for the female preponderance)—confer different prognostic outcomes. Lesions with ovarian stroma exhibit a more indolent course compared with lesions with absent ovarian stroma. Differentiating benign (cystadenoma) from malignant (cystadenocarcinoma) is less relevant than discriminating neoplastic from nonneoplastic etiologies, because of the treatment implications—biopsy and ultimately resection. In any event, no imaging features reliably discriminate benign from malignant.
To put things in perspective, these lesions reportedly constitute less than 5% of cystic liver lesions and empirically far less than that. Size ranges from a few centimeters to up to 40 cm, and when detected on imaging studies, these lesions are usually fairly large ( Fig. 2.14 ). Although occasionally unilocular, multilocularity, septation, and nodularity distinguish these lesions from other cystic liver lesions. Variable signal intensity of internal contents depends on mucin content and occasional hemorrhage. Whereas mild wall thickening is common and nonspecific, associated T2 hypointensity from hemorrhage excludes many other potential confounders. Septal and mural calcification best visualized on CT usually evades detection on MRI ( Fig. 2.15 ). Despite the derivation from biliary epithelium, communication with the biliary tree is rarely evident radiographically and more likely noted on endoscopic retrograde cholangiopancreatography (ERCP); upstream biliary dilatation occasionally develops as a result of extrinsic compression or an intraductal component.
Nonneoplastic cystic lesions dominate the differential diagnostic possibilities. Echinococcal cyst, pyogenic abscess, and complicated (hemorrhagic) bile duct cyst most closely approximate the MR appearance of biliary cystadenoma. Rare cystic HCC and cystic metastases are worth considering in the differential, but usually manifest a greater solid component, irregular margins, and suggestive clinical features.
Infectious Lesions
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