FIGURE 1
Geographical distribution of main risk factors for hepatocellular carcinoma (HCC) worldwide.
FIGURE 2
Graphic demonstrating hepatocarcinogenesis from regenerative nodules to progressed hepatocellular carcinoma (HCC), emphasizing the proportion of portal triad, neoangiogenesis, and organic anionic transporting polypeptides, and, consequently, the pattern of enhancement on late arterial, portal, and hepatobiliary phases.
TABLE 1
Main indications of MRI for hepatocellular carcinoma (HCC)
| Main indications of MRI for HCC evaluation |
|---|
| Nodules larger than 1.0 cm identified on ultrasound |
| For patients on the orthotopic liver transplantation waiting list |
| When the imaging features of the nodule on CT are not elucidative |
| History of allergy to iodinated contrast agent used on CT scans |
| After locoregional therapy |
TABLE 2
MRI sequences and hepatocellular carcinoma (HCC) features that can be assessed in each sequence
| MRI sequences | HCC imaging features |
|---|---|
| T2WI | Usually hyperintense |
| T1WI opposed and in-phase | Intralesional microscopic fat (lower signal on opposed-phase) or iron (lower signal on in-phase) |
| T1WI with fat saturation pre-contrast | Demonstrates the presence of macroscopic fat and blood products After locoregional therapies, hyperintensity indicates coagulative necrosis |
| Dynamic late arterial phase | Hyperenhancement |
| Dynamic portal venous phase | Washout and capsule appearance |
| Dynamic delayed phase | Washout and capsule appearance |
| Diffusion weighted imaging | Restricted diffusion (helps to identify small lesions) |
| Subtraction imaging | Characterizes contrast enhancement in spontaneously hyperintense nodules on T1WI pre-contrast (especially important for lesions with blood products and after locoregional treatment) |
| Multi-planar acquisition | Helps to differentiate HCC from mass-like lesions or extra-hepatic lesions |
| Hepatobiliary phase | Generally hypointense |
[i] T1W1 = T1 weighted image; T2WI = T2 weighted image
FIGURE 3
53-year-old man with cirrhosis due to hepatitis B and hepatocellular carcinoma. Hepatic nodule in segment VII with high signal intensity on T2 weighted image (T2WI) (A); with fat content (B, C) demonstrated by reduction of signal intensity on T1 weighted image (T1WI) opposite phase (C) when compared with T1WI in-phase (B); restriction on diffusion (D, E) characterized by high signal on diffusion weighted imaging (DWI) (D) and low signal on the apparent diffusion coefficients (ADC) map (E). On dynamic phases (F-I), the nodule showed arterial hypervascular enhancement in the late arterial phase (F); mosaic architecture (F-I); washout appearance in the portal venous (H) and delayed (I) phases; and capsule (dashed arrows) (H-I) and satellites nodules (arrows) with the same pattern of enhancement (F-I).
FIGURE 4
63-year-old man with chronic hepatitis C and HCC with tumor invasion within the portal vein. Main and right portal veins demonstrate dilation (arrows), high signal intensity on T2 weighted image (T2WI) (A), restriction on diffusion weighted imaging (DWI) (B,C).
FIGURE 5
49-year-old woman with cirrhosis due to chronic hepatitis C had a new hepatic nodule detected on screening ultrasound which was confirmed as HCC on MRI with hepatobiliary contrast agent. Hepatic nodule in segment VII (arrows) with high signal intensity on T2 weighted image (T2WI) (A), hyperenhancement in the late arterial phase (B), washout appearance (C), and hypointense appearance in the hepatobiliary phase.
FIGURE 6
62-year-old man with cirrhosis due to alcohol with a history of percutaneous radiofrequency ablation of a nodule in segment IV. On pre-contrast T1 weighted image (T1WI) with fat suppression (A) there is high signal intensity within the treated area (arrows) that was maintained in the arterial phase (B); however, on subtraction no enhancement is detected (C), which is compatible with no viable tumor. New HCC appeared during the follow-up in the segment VI (dashed arrow) with a true arterial hyperenhancement.
FIGURE 7
59-year-old woman with cirrhosis due to chronic hepatitis B and small HCC. Small nodule (arrows) in segment V with arterial phase hyperenhancement (A), without washout appearance (B), and with diffusion restriction (C, D). The patient underwent percutaneous biopsy with the diagnosis of well-differentiated HCC.
TABLE 3
Main imaging features of hepatocellular carcinoma (HCC)
| Imaging features | Description |
|---|---|
| Arterial hyperenhancement | Increased enhancement in the arterial phase. Reflects tumor neoangiogenesis. |
| Washout appearance | Hypoenhancement of the lesion compared with background liver tissue. Secondary to HCC extracellular reduced volume, rapid venous drainage and reduced intranodular portal venous supply. |
| Capsule appearance | Observed in approximately 80% of HCCs, detected on delayed phase, secondary to the lack of portal supply to malignant nodules. Corresponds to a pseudocapsule consisting of compressed adjacent liver parenchyma with occasional nonspecific inflammatory cells on histology. |
| Portal vein tumoral thrombosis | HCC invades and grows within the lumen. The vein appears dilated and with the same pattern of enhancement observed in the nodule. |
| T2 hyperintensity | The elevated signal intensity on T2WI can be useful to differentiate HCC from dysplastic nodules. |
| Restricted diffusion | Mildly elevated signal relative to the surrounding liver parenchyma on diffusion weighted imaging (DWI) and low signal intensity on apparent diffusion coefficients (ADC) map. |
| Corona enhancement | Enhancement of the peritumoral parenchyma after enhancement of the tumor itself, because of the passage of contrast through the draining sinusoids and portal venules into the surrounding sinusoids. |
| Intralesional fat | Loss of signal on the opposed-phase T1WI compared with the in-phase images. |
| Lesion iron sparing | Siderotic nodule is likely to be a dysplastic nodule. Development of an iron-free around the nodule suggests HCC foci. |
| Mosaic architecture | Nodular areas interspersed by areas of fibrosis, hemorrhage, arteriovenous shunting and necrosis. Characteristic of progressed HCCs. |
| Nodule-in-nodule architecture | Mildly elevated signal intensity on T2WI within nodule with low signal intensity, representing the focus of HCC within the low density dysplastic nodule, that may also enhance in the arterial phase. |
| Transitional phase hypointensity | Hypointensity compared with background liver following administration of a hepatobiliary contrast agent (2–5 minutes after contrast media administration). |
| Hepatobiliary phase hypointensity | Hypointensity compared with background liver following administration of a hepatobiliary contrast agent (20 minutes after). |
[i] T1W1 = T1 weighted image; T2WI = T2 weighted image
FIGURE 8
69-year-old man with cirrhosis due to alcohol with diffuse infiltrative HCC (A). Diffuse hepatic mass with areas of hypervascular arterial phase (B) and washout appearance (C), with tumoral thrombus within the right portal vein (arrows).
FIGURE 9
65-year-old woman without liver disease with surgically-proven intrahepatic cholangiocarcinoma confirmed. Nodule in the left hepatic lobe with peripheral restricted diffusion (arrows) (A, B), rim of arterial hyperenhancement (dashed arrow), and peripheral washout appearance (arrowhead).
TABLE 4
Main classifications used to assess tumor response after locoregional treatment
| Criteria | System | Response | Definition |
|---|---|---|---|
| Size | WHO | CR | Disappearance of all TL |
| PR | ≥ 50% decrease in CP of TL | ||
| SD | < 50% decrease to ≤25% increase in CP of TL | ||
| PD | > 25% increase from maximum response of TL | ||
| RECIST | CR | Disappearance of all TL | |
| PR | ≥ 30% decrease in MD of TL | ||
| SD | < 30% decrease to ≤20% increase in MD of TL | ||
| PD | > 20% increase from maximum response of TL | ||
| Necrosis | mRECIST | CR | Disappearance of any intratumoral enhancement in all TL |
| PR | ≥ 30% decrease in SMD of enhancing tissue in TL | ||
| SD | < 30% decrease to ≤20% in SMD of enhancing tissue in TL | ||
| PD | > 20% increase in amount of enhancing tissue in TL | ||
| EASLmeas | CR | Disappearance of any intratumoral enhancement in all TL | |
| and | PR | ≥ 50% decrease in amount of enhancing tissue in TL | |
| EASLest | SD | < 50% decrease in amount of enhancing tissue in TL | |
| PD | > 25% increase in amount of enhancing tissue in TL and/or new enhancement in previously treated lesions | ||
| LI-RADS | Nonviable | No suspicious lesion enhancement | |
| Equivocal | Atypical enhancement not meeting criteria to viable tumor | ||
| Viable | Nodular, mass-like, or thick irregular tissue in or along the treated lesion with any of the following: arterial phase hyperenhancement or washout appearance or enhanced similar to pretreatment 100% of tumor necrosis or reduction | ||
| RECICL | TE4 a | Necrotized area larger than the tumor (enough ablative margin) | |
| b | Necrotized area similar in size to the tumor (insufficient ablative margin) | ||
| TE3 | 50–100% of tumor necrosis or reduction | ||
| TE2 | Other effect than TE3 and TE1 | ||
| TE1 | Tumor enlargement of > 25% regardless of necrosis |
[i] CR = complete response, CP = cross-product, EASL = European Association for the Study of Liver, LI-RADS = Liver Imaging Reporting and Data System, MD = maximum diameter, PD = progressive disease, PR = partial response, RECIST = Response Evaluation Criteria for Solid Tumors, mRECIST = modified RECIST, RECICL = Response Evaluation Criteria in Cancer of the Liver, SD = stable disease, SMD = sum of maximum diameters, TE = treatment effect, TL = target lesion(s), WHO = World Health Organization