Lesion Definable characteristics US CT MRI Focal nodular hyperplasia arterial enhancement but slow washout Usually progressively enhancing ...
| Lesion | Definable characteristics | US | CT | MRI |
|---|---|---|---|---|
| Focal nodular hyperplasia | arterial enhancement but slow washout Usually progressively enhancing central scar Scar high T2 Usually takes up SPIO—implying it is benign and contains Kupffer cells No cirrhosis No pseudocapsule | Well-defined lesion Large central vessel that may be detectable on Doppler | Unenhanced Isodense Well-circumscribed, slightly hypoattenuating mass Contrast – Arterial Intense transient arterial enhancement Contrast – Portal phase Isodense Contrast – Delayed Central scar may demonstrate enhancement | T2 fat saturated Isointense High signal of the central scar due to vascular channels and oedema Central scar bright on T2, but fibrolamellar carcinoma is dark T1 fat saturated Isointense Low signal scar Aortic-gadolinium-arterial Enhancement of the lesion 1 hour post-gadolinium Isointense apart from scar, which enhances Hepatobiliary contrast agents (MultiHance or Gd-BOPTA) not taken up by adenoma Increased diagnostic significance with gadobenate FNH will retain gadobenate and appear isointense building to hyperintense in the liver on hepatobiliary (HPB) phase images (1-3 hours post-gadolinium) |
| Hepatic adenoma | Peripheral arterial enhancement, variable washout Has pseudocapsule No cirrhosis Minimal SPIO uptake Non-enhancing scar Usually large with areas of haemorrhage May contain fat— high T1 | Large hyperechoic lesion Central areas of low density caused by haemorrhage or necrosis | Hypodense Contrast – Arterial phase Transient arterial enhancement Isodense portal phase | Most lesions are low T1 including FNH Adenoma are high T1 Due to the presence of glycogen and fat Isointense on in-phase T1 Isointense on T2 Loses signal on out-of-phase images Immediate and intense enhancement with gadolinium Equilibrate in the portal phase |
| Fibrolamellar carcinoma | Calcification Central scar that does not enhance and is low T2 | Solid Hyperechoic scar | Lobulated margin Hypodense, particularly the central scar Contrast – Arterial phase Enhances moderately and peripherally Contrast – Venous phase Isointense in the venous phase Scar often contains calcification | T1—low signal T2—high signal This differentiates it from focal nodular hyperplasia as FNH does not contain calcification Central scar is typically low signal on T1 and T2—this differentiates it from FNH, for which the scar is high T2 + scar enhances with FNH |
| HCC | Arterial enhancement with washout in venous phase and pseudocapsule HCCs wash out more avidly than the other lesions Usually does not take up SPIO Associated with cirrhosis Often shows invasion of portal veins | May be hyper- or hypo-echoic May occlude the portal vein May show arterial vascularity Heterogeneous reflectivity due to areas of necrosis Smaller lesions are typically of homogeneous low reflectivity | Unenhanced Encapsulated Hypodense mass Contrast – Arterial Rapid enhancement during arterial phase Hyperenhancing in the acute phase Contrast – Portal phase Early washout of contrast on delayed images Washout in the venous phase | Dynamic T1 MRI Marked enhancement on the arterial phase—the arterial phase is at 20 seconds Less marked on the venous phase—the venous phase is at 60 seconds The peripheral enhancement in the venous phase is due to the pseudocapsule T2* post-SPIO Dark, iron-laden liver with the bright lesion, as this does not take up SPIO T2 hyperintensity |
| Metastases | Peripheral washout sign is diagnostic of mets | Homogeneous Hyper- or hypoechoic May be cystic | May show complete peripheral enhancement rather than nodular Only haemangiomas show nodular Washout on delayed phase | T1—low T2—high T2 fat sat—high T1 arterial phase Early peripheral enhancement T1 equilibrium phase Prolonged central enhancement with low signal peripherally Peripheral washout sign |
| Dysplastic nodules | Cirrhosis No raised AFP Often take up SPIO Bright enhancement Usually no pseudocapsule Simple regenerative nodules do not usually enhance | The nodules are generally hypoechoic | — | T1 high signal intensity |
| Regenerative nodules | High T1 <1 cm Cirrhosis Isodense on unenhanced CT | — | Isodense on unenhanced <1 cm | High T1 |
| Haemangioma | Early peripheral enhancement with gradual filling in on delayed imaging High signal on heavily T2 sequences Does not take up SPIO However, atypical haemangiomas do occur, which can be difficult to diagnose | Hyperechoic lesions | Hypodense Early periperal nodular enhancement Centripetal fill in on delayed phase | T1—hypointense T2 fat sat—hyperintense Lobulated, well-defined margin T1 post-gad arterial phase Early peripheral nodular discontinuous enhancement T1 post-gad portal venous and delayed phases Progressive enhancement Enhancement is equal to the vessels |
| Cholangiocarcinoma | Does not take up SPIO | Nodules/focal bile duct wall thickening Hyperechoic bile duct walls | Tumour mass is often isodense Peripheral enhancement Demonstrates delayed enhancement—best seen on late venous enhancement (10 minutes) Intrahepatic duct dilatation May contain calcification | Peripheral enhancement in cholangiocarcinoma, but less than in the vessels Capsular retraction T1—hypointense T2—hyperintense |
Note: CT: computed tomography; HCC: hepatocellular carcinoma; MRI: magnetic resonance imaging; SPIO: superparamagnetic
iron oxide; US: ultrasound.
iron oxide; US: ultrasound.
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