Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. 80-90% of cases develop in the setting of cirrhosis. Hepatitis B, hepatitis C, and alcoholic cirrhosis are the major risk factors. The ACR LI-RADS classification standardizes HCC probability assessment of focal lesions in cirrhotic patients. The combination of arterial hypervascularity with washout in portal venous/delayed phases is the strongest diagnostic criterion for HCC. AFP (alpha-fetoprotein) serum marker is supportive but has limited sensitivity (40-60%).
Age Range
40-80
Peak Age
65
Gender
Male predominant
Prevalence
Very Common
HCC follows the chronic liver injury → regeneration → dysplasia → malignancy pathway. In cirrhotic liver, regenerative nodules transform to dysplastic nodules (low → high grade), then early HCC, and finally advanced HCC. During hepatocarcinogenesis, the vascular supply critically changes: normal hepatic artery + portal vein supply is replaced by abnormal arterial neovascularization alone ('unpaired arteries'). This neoangiogenesis explains prominent arterial phase enhancement, while loss of portal venous supply explains washout in portal venous/delayed phases. Capsule formation is due to fibrous tissue proliferation and enhances in the delayed phase.
The triad of arterial phase hyperenhancement (APHE) → nonperipheral washout in portal venous/delayed phase → enhancing capsule in delayed phase is the signature finding of HCC. In LI-RADS classification, the combination of these three major features in a ≥10mm lesion categorizes it as LI-RADS 5 (definite HCC). This triad is sufficient for non-invasive diagnosis in the cirrhotic setting and does not require biopsy.
Intense enhancement reflecting hypervascularity compared to surrounding liver parenchyma in arterial phase (APHE). The most critical LI-RADS major feature for HCC diagnosis.
Report Sentence
A _mm lesion in liver segment _ demonstrates arterial phase hyperenhancement (APHE).
The lesion becoming hypodense compared to surrounding parenchyma in portal venous phase (washout). A LI-RADS major feature that strengthens HCC diagnosis when combined with APHE. 'Nonperipheral washout' is specific to HCC (peripheral washout suggests ICC).
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The lesion demonstrates nonperipheral washout in portal venous phase, consistent with HCC.
Thin, smooth enhancing rim surrounding the lesion in delayed phase ('enhancing capsule'). A LI-RADS major feature. The capsule is not visible in arterial phase and becomes apparent due to late enhancement of fibrous tissue in delayed phase.
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A thin enhancing capsule surrounding the lesion is observed in the delayed phase, consistent with the LI-RADS major feature of 'enhancing capsule'.
Mild to moderate hyperintense signal on T2-weighted images. Marked hyperintensity (hemangioma-level) is not typical. Mosaic pattern of internal structure (heterogeneous signal — necrosis, hemorrhage, fat, fibrosis areas) is characteristic of advanced HCC.
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The lesion demonstrates mild to moderate hyperintense signal and mosaic pattern on T2-weighted sequences.
Marked hypointensity of the lesion in hepatobiliary phase (gadoxetic acid — Primovist/Eovist, 20 minutes). OATP1B3 transporter expression is lost in HCC cells, so gadoxetic acid is not taken up. A LI-RADS ancillary feature.
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The lesion is markedly hypointense on hepatobiliary phase (gadoxetic acid), consistent with loss of OATP transporter expression.
Hyperintensity on diffusion-weighted imaging (DWI) and hypointensity on ADC map. Reflects high cellular density of the tumor. A LI-RADS ancillary feature.
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The lesion demonstrates diffusion restriction on DWI sequences, suggesting high cellularity.
On ultrasound, HCC appears as a mass of variable echogenicity: small HCC (<3 cm) is usually hypoechoic; large HCC is heterogeneous (due to necrosis, hemorrhage, fat content). Fat-containing HCC may be hyperechoic. Differentiation from regenerative/dysplastic nodules in cirrhosis is difficult.
Report Sentence
A _mm heterogeneous solid mass is observed in the liver, and further evaluation for HCC is recommended in the cirrhotic background.
Criteria
≤2 cm, well-differentiated, vaguely nodular type. May be a transitional lesion between dysplastic nodule and HCC.
Distinct Features
May not show APHE (neovascularization not fully developed yet). Hypointensity on hepatobiliary phase is the earliest MR finding. Washout may be mild or absent — may remain in LI-RADS 3-4 category.
Criteria
>2 cm, moderately to poorly differentiated, prominent neovascularization, expansile growth.
Distinct Features
Classic APHE + washout + capsule triad is prominent. Mosaic pattern (necrosis, hemorrhage, fat). Portal vein invasion (tumor thrombus) is common — LI-RADS M or LR-TIV category. May be giant HCC (>10 cm).
Criteria
Diffuse infiltrative growth pattern without distinct margins. Usually associated with portal vein thrombosis.
Distinct Features
Mass cannot be clearly delineated — diffuse heterogeneous enhancement. Portal vein tumor thrombus shows arterial enhancement (distinguishes from bland thrombus). AFP is usually very elevated. Poor prognosis.
Criteria
Pattern of numerous small nodules distributed throughout the liver. Very difficult to distinguish from regenerative nodules in cirrhotic liver.
Distinct Features
Miliary or multinodular pattern. Numerous small enhancing nodules in arterial phase. AFP may be very elevated. Transplantation is contraindicated.
Distinguishing Feature
Intrahepatic cholangiocarcinoma shows peripheral enhancement + progressive centripetal filling (fibrous stroma), different from APHE + washout in HCC. Capsular retraction is common in ICC (vs capsule bulging in HCC). ICC may show bile duct dilatation. Very rarely develops in cirrhosis.
Distinguishing Feature
High-grade dysplastic nodule may show APHE but washout is typically absent. May be hypointense on hepatobiliary phase (OATP loss initiated). May be T1 hyperintense (copper accumulation). Size usually <2 cm. High risk of transformation to HCC — requires close follow-up.
Distinguishing Feature
Hemangioma shows marked T2 hyperintensity ('light bulb sign') — HCC is mild-moderately hyperintense. Hemangioma shows peripheral nodular enhancement + centripetal filling — different from diffuse APHE in HCC. No washout in hemangioma, filling continues in delayed phase.
Distinguishing Feature
FNH shows intense homogeneous arterial enhancement but no washout — remains isointense in portal venous/delayed phases. Isointense/hyperintense on hepatobiliary phase (functional hepatocytes express OATP) distinguishes from HCC. FNH typically occurs in young women, non-cirrhotic liver.
Distinguishing Feature
Hepatic adenoma shows arterial enhancement but is not associated with cirrhosis. Seen in young women with OCP use. Hypointense on hepatobiliary phase (unlike FNH). Intracellular fat and hemorrhage may mimic HCC but washout pattern is different.
Urgency
urgentManagement
surgicalBiopsy
Not NeededFollow-up
3-monthHCC diagnosis can be made non-invasively in cirrhotic patients meeting LI-RADS 5 criteria — biopsy is not required. Treatment options are determined by stage: early stage (BCLC 0-A) → surgical resection or liver transplantation (Milan criteria: single ≤5 cm or up to 3 ≤3 cm); intermediate stage (BCLC B) → transarterial chemoembolization (TACE); advanced stage (BCLC C) → systemic therapy (sorafenib, lenvatinib, atezolizumab+bevacizumab); terminal stage (BCLC D) → palliative care. AFP is used for monitoring progression and treatment response. Multidisciplinary tumor board decision is recommended.
Early detection enables curative treatment (resection, transplantation, ablation) per Barcelona (BCLC) staging. Surveillance with US/AFP every 6 months is recommended for cirrhotic patients. LI-RADS 5 categorization allows diagnosis without biopsy.