| Hepatocellular | Focal nodular hyperplasia Hepatocellular adenoma Nodular regenerative hyperplasia Dysplastic nodules |
| Cholangiocellular | Hepatic cysts and Polycystic liver disease Cystadenoma Bile duct adenoma (biliary hamartoma/Von Meyenburg complexes) Intraductal papillary neoplasm of the bile duct |
| Mesenchymal | Liver haemangioma Lipoma Angiolipoma |
| Inflammatory | Hepatic abscess (Pyogenic liver abscess, Amoebic liver abscess) Hydatid cysts |
| Others | Mesenchymal hamartoma Focal fatty infiltration Hepatic pseudotumours |
| Imagine advice from Emma |
- Most lesions are T2 intermediate or bright
- CSF/fluid is also bright
- Haemangiomas and cysts are very bright on T2
- Anything bad diffusion restricts
- Primavist - FNH and adenoma enhance
- HCC arterially enhance then washout
- Haemangioma have slow fill in cause they are slow flow venous malformations
- Post contrast sequences are always T1 - because most things are dark you can see what enhances. Things that are bright on T1 are fat, blood, mineralisation, contrast an melanin
Summary of Primovist Findings
| Lesion | Arterial Phase | Hepatobiliary Phase | Key Feature |
|---|---|---|---|
| FNH | Hyperintense | Iso-/Hyperintense | Central scar |
| Adenoma | Hyperintense | Hypointense | No scar, possible fat signal loss |
| HCC | Hyperintense + Washout | Hypointense | Capsule, vascular invasion |