Imaging of hepatocellular carcinoma: diagnosis, staging and treatment monitoring

Tiffany Hennedige, Sudhakar Kundapur Venkatesh, Tiffany Hennedige, Sudhakar Kundapur Venkatesh

Abstract

Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Imaging is important for establishing a diagnosis of HCC. Several imaging modalities including ultrasonography (US), computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET) and angiography are used in evaluating patients with chronic liver disease and suspected HCC. CT, MRI and contrast-enhanced US have replaced biopsy for diagnosis of HCC. Dynamic multiphase contrast-enhanced CT or MRI is the current standard for imaging diagnosis of HCC. Functional imaging techniques such as perfusion CT and diffusion-weighted MRI provide additional information about tumor angiogenesis that may be useful for treatment. Techniques evaluating tissue mechanical properties such as magnetic resonance elastography, and acoustic radiation force impulse imaging are being explored for characterizing liver lesions. The role of PET in the evaluation of HCC is evolving with promise seen especially with the use of a hepatocyte-specific PET tracer. Imaging is also critical for assessment of treatment response and detection of recurrence following locoregional treatment. Knowledge of the post-treatment appearance of HCC is essential for correct interpretation. This review article provides an overview of the role of imaging in the diagnosis, staging and post-treatment follow-up of HCC.

Figures

Figure 1
Figure 1
HCC in a 58-year-old man with chronic hepatitis B. Unenhanced (a), arterial phase (b), portal venous phase (c) and delayed phase (d) CT images showing a rounded HCC (white arrow) that enhances in arterial phase and washes out in portal venous and delayed phases. A thin enhancing pseudocapsule (black arrow head) is best demonstrated in the delayed phase.
Figure 2
Figure 2
MRI of HCC in a 54-year-old woman with chronic hepatitis C. HCC (white arrow) appears mildly hyperintense to liver on the T2-weighted image (a), hypo- to isointense on the T1-weighted image, shows restricted diffusion on DWI (c), arterial phase enhancement (d) and washout in both portal venous (e) and delayed (f) phases. Note the enhancing capsule (black arrow) in both portal venous and delayed phases.
Figure 3
Figure 3
Large HCC (black arrow) in the right lobe of the liver showing heterogeneous enhancement in the arterial phase (a) and washout and mosaic appearance in the portal venous phase (b).
Figure 4
Figure 4
Fatty HCC. Unenhanced CT (a), in-phase (b) and opposed phase (c) MR images in the same patient showing heterogeneous HCC with fat component (arrow).
Figure 5
Figure 5
Large HCC (*) with portal vein invasion. Tumor thrombus within the portal vein (black arrow) showing enhancement in the arterial phase (a) and washout in the portal venous phase (b) similar to the main tumor.
Figure 6
Figure 6
Large HCC with portal vein tumor thrombus. The portal vein is expanded and completely filled with tumor thrombus (black arrow). The tumor thrombus demonstrates neovascularity of cast of vessels in the arterial phase (a) and washout in the portal venous phase (b). The primary tumor (curved arrow) does not show arterial phase enhancement but appears hypodense in the both phases.
Figure 7
Figure 7
Multifocal HCCs well demonstrated using super paramagnetic iron oxide particle imaging. A T2-weighted image following SPIO administration shows a large mass in the left lobe and multiple smaller lesions in the right lobe.
Figure 8
Figure 8
A 37-year-old man with chronic hepatitis B and raised AFP and histology proven HCC. Unenhanced (a) T1-weighted image showing a hypointense nodule (white arrow) in the left lobe and minimal enhancement in the arterial phase (b) and appears hypointense on the portal venous and delayed phases (not shown). Features are not typical for HCC. However, the nodule shows restricted diffusion on DWI with b = 500 and no uptake in the hepatocyte phase (d) after intravenous Gd-EOB-DTPA injection.
Figure 9
Figure 9
MR elastography of HCC in a background of cryptogenic liver cirrhosis. T2-weighted (a), unenhanced T1-weighted (b) and arterial phase (c) T1-weighted images showing typical HCC. Stiffness map from MR elastography (d) showing a high stiffness value of 10.6 kPa in the tumor. The stiffness of the liver parenchyma is 6.3 kPa, higher than the normal liver stiffness cut-off value of 2.93 kPa.
Figure 10
Figure 10
CEUS of HCC. Prompt intense enhancement of the segment 4 nodule (arrow) in the arterial phase (a) which is hypoechoic to surrounding liver on the grayscale image (b).
Figure 11
Figure 11
Unenhanced CT (a) and fused PET/CT image (b) of an FDG-avid moderately differentiated HCC (arrow).
Figure 12
Figure 12
CT arteriography of HCC (arrow) in a 66-year-old patient with cryptogenic cirrhosis. Intense enhancement in the arterial phase (a) and washout in the central portion of the tumor in the delayed phase (b).
Figure 13
Figure 13
CT appearances before and after RFA of HCC. Top row: arterial (a) and portal venous phase (b) CT images showing an HCC (black arrow) before RFA. Bottom row: CT after 6 weeks of ablation; the HCC is replaced by a zone of hypodensity that is larger than the tumor and shows no enhancement (white arrow) in both the arterial (c) and portal venous phase (d).
Figure 14
Figure 14
MR appearances of HCC before and after RF ablation. Before ablation (a–d), HCC is iso- to mildly hyperintense on the T2-weighted image (a), hypointense on the T1-weighted image (b), enhances in the arterial phase (c) and washes out in the portal venous phase (d). Post-ablation MRI (e–h) after 4 weeks showing a larger heterogeneous hypointensity on the T2-weighted image (e) and mixed hyperintensity on the T1-weighted image (f) representing the ablation zone (white arrows). There is no enhancement in the arterial phase (g) but a thin rim of post-ablation inflammatory enhancement (black arrow) seen in the portal venous phase (h).
Figure 15
Figure 15
Examples of post-RFA recurrence. Top row (a–c), a case of HCC (black arrow) in the background of non-alcoholic steatohepatitis and cirrhosis. Arterial phase CT before (a), 3 months after (b) and 1 year (c) after RFA. There is no recurrence at 3 months and the large ablation zone covers the tumor region. Nodular recurrence (white arrowheads) seen at 1 year at the margins of the ablation zone. Bottom row (d–f) is another example of nodular recurrence at the margin of the RFA zone illustrated on MRI. The recurrence is seen as hyperintense nodule on the T2-weighted image (d) and hypointense nodule on the T1-weighted image (e) in contrast to the ablated zone (curved arrow) and enhances in the arterial phase (f). (Image courtesy of Dr Grant Schmitt, MD, Mayo Clinic, Rochester, MN, USA.)
Figure 16
Figure 16
Examples of complete and partial response to TACE. Top row (a,b) showing a small HCC in the left lobe before (a) and 4 weeks after (b) TACE. There is mild reduction in the size of the tumor and no enhancement (black arrow). Bottom row (c,d) showing an HCC in the right lobe of the liver before (c) and 4 weeks after (d) TACE with residual tumor (black arrow head) seen in the post-TACE scan.
Figure 17
Figure 17
Examples of post-TARE response. Top row (a,b) showing arterial phase CT before (a) and 8 weeks after (b) TARE of a segment 6 HCC. There is complete necrosis of the tumor. (c,d) Arterial phase CT images in a patient with multifocal HCCs and partial response to TARE at 6 weeks. There is partial necrosis of the tumor (black arrowheads) and progression of tumor in segment 4 (white arrow).

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