Small tumors (< 3 cm without vascular invasion) are curable with resection, ablation, transplantation
Achievable goal of surveillance program using US, CT, &/or MR (properly performed and interpreted)
Use LI-RADS classification system for focal lesions in cirrhotic liver
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Key imaging features
Heterogeneous hypervascularity on arterial phase (CT or MR) with washout on venous and delayed
Presence of a capsule or fat content
Evidence of portal or hepatic vein invasion
Hypointense lesion on hepatobiliary phase of gadoxetate-enhanced MR
Bright lesion on diffusion-weighted MR
TOP DIFFERENTIAL DIAGNOSES
•
Regenerative and dysplastic nodules
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Cholangiocarcinoma (peripheral)
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Nodular regenerative hyperplasia
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Hypervascular metastases
CLINICAL ISSUES
•
Which imaging modality should be used?
Sonography
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Effective in expert hands in screening thin patients with relatively nonfibrotic livers
Triphasic CT or MR (arterial, venous, and delayed phases) is mandatory in more advanced disease
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Any focal lesion; fibrotic, nodular liver; strong clinical concern for HCC
–
MR with gadoxetate enhancement has greater sensitivity and specificity for analyzing nodules
TERMINOLOGY
Abbreviations
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Hepatocellular carcinoma (HCC)
Definitions
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Most common primary malignant liver tumor, usually arising in a cirrhotic liver
IMAGING
General Features
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Best diagnostic clue
Heterogeneous hypervascular mass with “washout” of contrast enhancement and portal vein invasion
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Size
Small tumors < 2 cm
Large tumors > 5 cm
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Diffuse: Subcentimeter to few cm lesions throughout liver
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Morphology
Usually spherical
•
Key concepts
Most frequent primary visceral malignancy in world
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Accounts for 80-90% of all primary liver malignancies
2nd most common malignant liver tumor in children after hepatoblastoma
Important to detect and stage accurately
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Small tumors are curable with resection, ablation, or transplantation
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Multiple, large, or those with venous invasion can be palliated with chemoembolization
Signs of
portal vein invasion by HCC
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Expansion of portal vein lumen
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Enhancement of tumor within vein
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Contiguity of tumor and portal vein
CT Findings
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NECT
In noncirrhotic liver (usually a symptomatic patient, as with pain or rupture)
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Solitary HCC: Large hypodense mass; ± necrosis, fat, calcification
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Encapsulated HCC: Well-defined, rounded, hypodense mass
Dominant hypodense mass with decreased attenuation “satellite” nodules
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Multifocal HCC: Multiple hypodense lesions rarely with central necrotic portion
In cirrhotic liver (usually detected as part of a surveillance program)
–
HCC may be hypodense to liver
–
Regenerative nodules may be hyperdense to liver
•
CECT
Hepatic arterial phase (HAP) scan
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Heterogeneous hypervascular enhancement (for moderately and poorly differentiated HCC)
Well-differentiated tumor may be hypodense to liver on all phases of enhancement
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Wedge-shaped areas of ↑ density on HAP: Perfusion abnormality due to portal vein occlusion by tumor thrombus and ↑ arterial flow
Portal venous phase (PVP) scan
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HCC often nearly isodense to surrounding liver
Delayed scan: HCC hypodense to surrounding liver
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Washout of contrast enhancement is key finding
Helps to distinguish HCC from regenerative nodules and arterioportal shunts (both common in cirrhosis)
Small hypervascular HCC
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Early and late arterial phases: Hyperattenuating, more on 2nd or later arterial phase
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Later (portal venous and delayed): HCC washes out to become hypodense to liver
MR Findings
•
Variable intensity depending on degree of fatty change, fibrosis, necrosis
•
T1WI
HCC may be hypo-, iso-, or hyperintense to liver
Tumors with fat or hemorrhage are hyperintense
•
T2WI
Usually hyperintense to liver
–
Regenerative nodules are hypointense on T2WI
HCC arising within dysplastic nodule
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“Nodule within nodule” pattern
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HCC appears as small focus of increased signal intensity within decreased signal intensity nodule
•
T1 C+ (gadolinium)
Heterogeneously hyperintense, with washout on portal venous and delayed phase
Rapid central washout with residual capsular enhancement = HCC,
not arterioportal shunt
•
Hepatobiliary contrast agent (gadoxetate)
Trade names: Eovist or Primovist
On 20 minute delayed phase
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Normal liver (and some portions of cirrhotic liver) enhance brightly
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Most HCCs are seen as hypointense focal masses
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Rare for well-differentiated HCC to show delayed persistent enhancement with gadoxetate
Increases sensitivity of MR in diagnosing small HCC
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Diffusion-weighted MR
Restricted diffusion within HCC often detected as bright signal in focal lesion
Adds sensitivity and specificity to MR detection of HCC
Ultrasonographic Findings
•
Grayscale ultrasound
Lower sensitivity and specificity than CT or MR in diagnosing HCC
–
Especially within nodular, fibrotic, cirrhotic liver
Mixed echogenicity due to tumor necrosis and hypervascularity
Hypoechoic: Due to solid tumor
Hyperechoic: Due to fatty metamorphosis
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Small hyperechoic HCC can simulate hemangioma
Capsule: In encapsulated HCC
•
Color Doppler
Shows hypervascularity and tumor shunting
Small HCC: Indistinguishable from regenerative and dysplastic nodules
Angiographic Findings
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Conventional
Hypervascular tumor
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Marked neovascularity and AV shunting
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Large hepatic artery and vascular invasion
Threads and streaks sign
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Sign of tumor thrombus in portal vein
Nuclear Medicine Findings
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Hepatobiliary scan
Uptake in 50% of lesions
•
Technetium sulfur colloid
HCC in cirrhotic liver: Seen as defect
HCC in noncirrhotic liver: Heterogeneous uptake
•
Gallium scan
HCC is gallium avid in 90% of cases
Imaging Recommendations
•
Best imaging tool
In cirrhotic patient, multiphasic CT or MR
Triphasic CT or MR (arterial, venous, and delayed phases)
–
MR with gadoxetate enhancement has greater sensitivity and specificity
DIFFERENTIAL DIAGNOSIS
Regenerative and Dysplastic Nodules
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Diagnostic Imaging_ Gastrointes - Michael P Federle