Definition:

The hepatobiliary phase (HBP) is a post-contrast injection time range after administration of a hepatobiliary agent (HBA) in which images have the following characteristics:

• the hepatic parenchyma is hyperintense to the hepatic blood vessels, and
• there is excretion of contrast into the biliary system

Comments:

• Although there is a broad temporal window for hepatobiliary phase imaging, most available data suggest that in non-cirrhotic livers a delay of 15-20 minutes for gadoxetate disodium and a delay of 1 hour for gadobenate dimeglumine consistently provide high-quality hepatobiliary phase imaging.
• The cirrhotic liver may have diminished parenchymal enhancement during the hepatobiliary phase, and the time to peak enhancement may be delayed, possibly due to reduced number of functional hepatocytes or dysfunctional cellular transport mechanisms.
• In the setting of cirrhosis and severe hepatic dysfunction, increasing the delay for hepatobiliary phase imaging to 30 minutes or more for gadoxetate disodium and 2-3 hours for gadobenate dimeglumine may improve parenchymal enhancement somewhat; however, it is difficult to predict which patients will have diminished and/or delayed hepatic parenchymal enhancement.
• Enhancement of the hepatic parenchyma during the hepatobiliary phase should be considered suboptimal if the hepatic parenchyma is not unequivocally hyperintense relative to the hepatic blood vessels.
• If the hepatobiliary phase parenchymal enhancement is suboptimal, characterization of hepatobiliary phase intensity of liver observations may be difficult. If an observation is hypointense in the hepatobiliary phase despite suboptimal hepatobiliary phase parenchymal enhancement, the observation may be characterized as hypointense. If an observation is iso- or hyperintense, characterization of hepatobiliary phase intensity may be unreliable.

Potential pitfalls and challenges:

• Most HCCs appear hypointense to liver during the hepatobiliary phase, but HCC with overexpression of uptake transporter OATP1B3/OATP8 may demonstrate iso- or hyperintensity in the hepatobiliary phase.
• A small percentage of HCCs may demonstrate iso- or hyperintensity in the hepatobiliary phase. Such HCCs may be misinterpreted as non-malignant nodules (e.g., FNHs and dysplastic nodules). Ancillary imaging features reported to favor the diagnosis of HCC include HBP hypointense rim, nodule-in-nodule architecture, and focal defect in HBP uptake.
• Infiltrative HCC may be difficult to identify and delineate from background cirrhotic liver in the hepatobiliary phase after administration of HBA, due to ill-defined margins and frequent low lesion to parenchyma contrast.
• High-grade dysplatic nodules and sometimes low-grade dysplastic nodules may be hypointense in the hepatobiliary phase due to underexpression of uptake transporters; thus, not all cirrhotic nodules with HBP hypointensity are HCC.
• Siderotic nodules may be hypointense in the hepatobiliary phase. The mechanism has not yet been determined but may be related to T2* shortening effects of iron and/or underexpression of uptake transporters.
• Focal steatosis may be hypointense in the hepatobiliary phase. The mechanism has not yet been determined but may be related to suppression of fat containing voxels on fat-suppressed T1w images and/or underexpression of uptake transporters.