Focal hepatic lesions in Gd-EOB-DTPA enhanced MRI: the atlas

Abstract

Objective: This article reviews the different technical aspects and pitfalls of gadolinium (Gd)-ethoxibenzyl (EOB)-diethylenetriamine pentaacetic acid (DTPA) and the advantages of the hepatocellular phase (HCP) and defines its specific imaging features of liver lesions.

Background: Gd-EOB-DTPA is a contrast agent with combined properties of a conventional non-specific extracellular and a hepatocyte-specific contrast agent. Benign cirrhosis-associated nodules are characterised by isointensity in dynamic imaging and the HCP. Hepatocellular carcinomas (HCCs) usually show hyperenhancement in the arterial phase, with washout in the portal vein pressure (PVP) and hypointensity in the HCP. Among other characteristic findings, we have the mosaic pattern, a capsule, the "nodule-in-nodule" appearance and the satellite nodules. The fibrolamellar HCC is a large enhancing heterogeneous lesion, on a non-cirrhotic liver, with a hypointense scar in every sequence. THIDs (transient hepatic intensity differences) are perfusional alterations, characterised by hyperintensity in the arterial phase, with no alterations in the rest of the sequences including the HCP. Adenoma and focal nodular hyperplasia (FNH) are lesions, occurring more frequently in young women, with brisk arterial enhancement, differentiated by the scar and the uptake of Gd-EOB-DTPA in the HCP. Focal eosinophilic infiltration is a difficult diagnosis, with characteristics such as a non-spherical shape and irregular borders suggesting it. Besides these lesions, in which Gd-EOB-DTPA has a clear advantage, there are a few where the specificities of this agent can be troublesome: haemangiomas, focal fat/sparing, foreign body reaction, cholangiocarcinoma and metastases.

Conclusion: Gd-EOB-DTPA is comparable to extracellular agents, and uptake by functioning hepatocytes in the delayed phase provides additional information that further improves detection and characterisation of many hepatic lesions.

Main messages: Gd-EOB-DTPA offers advantages for the imaging of many liver lesions including HCC, fibrolamellar HCC, FNH and adenoma. • The properties of Gd-EOB-DTPA can pose problems when dealing with haemangiomas, cholangiocarcinoma and metastases among others. • The uptake of Gd-EOB-DTPA by functioning hepatocytes in the delayed phase provides additional information that further improves detection and characterisation of many hepatic lesions.

Fig. 1

Molecular structure of Gd-EOB-DTPA

Fig. 2

A benign cirrhosis-associated nodule in a 38-year-old woman with chronic liver disease. a Pre-contrast MRI, b, c arterial phase, d PV phase, e delayed phase, f hepatocellular phase. The image shows a liver with a lobulated contour and a nodular parenchyma (cirrhosis). The solid arrows point to a small rounded focal lesion, markedly hypointense in all sequences (more conspicuous with the increase of the TE), showing no enhancement with the contrast agent. The curved arrow points to multiple Gamna-gandy bodies (hemosiderin deposition)

Fig. 3

A benign cirrhosis-associated nodule in a 39-year-old man with chronic liver disease. Gd-EOB-DTPA enhanced MRI. a arterial phase, b PV phase, c delayed phase, d 5 min, e 10 min, f hepatocellular phase. The image shows a liver with a nodular contour and a heterogeneous parenchyma. The arrows point to a small rounded focal lesion accumulating Gd-EOB-DTPA- benign nodule

Fig. 4

An FNH-like lesion in a 41-year-old man with chronic liver disease. a Pre-contrast MRI, b arterial phase, c PV phase, d 5 min, e 10 min, f hepatocellular phase. The image shows a liver with a lobulated contour. The arrows point to a small rounded focal lesion, isointense in the Pre-contrast sequence, showing brisk arterial enhancement. In the HCP it accumulates Gd-EOB-DTPA, exposing the typical FNH internal architecture

Fig. 5

Fatty HCC in a 45-year-old man with chronic liver disease. a Pre-contrast MRI, b, c arterial phase, d 3 min, f 4 min, f 8 min, g IP, h OP, i SSFSE, j b0, k b500, l T1-weighted PDFF. The arrows point to a rounded focal lesion, with arterial enhancement, PV washout and hypointensity in the HCP. It also shows heterogeneous loss of signal in OP (fat), expressed likewise in the fat fraction map as bright areas in the lesion

Fig. 6

Hypervascular HCCs in a 50-year-old man with chronic liver disease. a Pre-contrast MRI, b arterial phase, c portal vein pressure (PVP), d 3 min, f 4 min, f HCP. Marked heterogeneous liver with nodular contour, with reticulation in the HCP- cirrhotic The arrows point to two rounded focal lesions, with arterial enhancement (one less prominent), PV washout and hypointensity in the HCP

Fig. 7

A 52-year-old man with chronic liver disease. a Arterial phase, b HCP. Imaging findings of a cirrhotic liver, with a lesion (large arrows) with areas of enhancement (thin arrow) and non-enhancing areas—mosaic pattern. In the HCP we found a similar appearance with areas taking up Gd-EOB-DTPA and others not

Fig. 8

HCC in a 42-year-old woman with chronic liver disease. a Pre-contrast MRI, b arterial phase, c PV phase, d 5 min, e 10 min, f HCP. Hypervascular HCC, with washout in the PV phase and uptake of Gd-EOB-DTPA (arrows)

Fig. 9

Fibrolamellar-HCC in a 34-year-old man without liver disease. a Pre-contrast MRI, b arterial phase, c PV phase, d HCP. Big nodular lesion in the left lobe isointense in pre-contrast imaging, with arterial enhancement, washout in the PV phase and no uptake of Gd-EOB-DTPA in the HCP (thick arrow). The central scar (thin arrow) remains hypointense in all sequences

Fig. 10

THIDs in a 38-year-old man with chronic liver disease. a Pre-contrast MRI, b arterial phase, c 2 min, d 3 min, e IP, f OP, g T2, h DWI B500. Heterogeneous liver with nodular contour. Fluffy hyperintense areas in the arterial phase (arrows), not seen in the other sequences

Fig. 11

Multiple THIDs and a big HCC in a 47-year-old man with chronic liver disease. a Pre-contrast MRI, b arterial phase, c PV phase, d delayed phase. Big nodular lesion in the left lobe hypointense in pre-contrast imaging, with arterial enhancement, internal arteries, washout in the PV phase and heterogeneous uptake of Gd-EOB-DTPA in the HCP (*). There also seen multiple nodulariform hyperintense areas in the arterial phase (arrows), not seen in the other sequences—THIDs

Fig. 12

FNH in a 37-year-old woman with no liver disease. a Pre-contrast MRI, b, c arterial phase, d 3 min, e 5 min, f 8 min, g 10 min, h HCP. Big nodular lesion (thick arrows), with lobulated contours isointense in pre-contrast imaging, with arterial enhancement, washout in the PV phase and uptake of Gd-EOB-DTPA in the HCP—note the fine reticular architecture typical of a FNH. The central scar (thin arrow) remains hypointense in all sequences

Fig. 13

Liver adenoma in a 35-year-old woman on oral contraceptives, with no liver disease. a Pre-contrast MRI, b, c arterial phase, d 3 min, e 5 min, f HCP. Lobulated lesion in the right lobe isointense in pre-contrast imaging, with arterial enhancement, internal arteries and no uptake of Gd-EOB-DTPA in the HCP (arrow)

Fig. 14

Focal hypereosinophilic necrosis nodule in a 55-year-old man with no liver disease. a Arterial phase, b PV phase, c HCP, d T2-weighted. Small non-spherical lesion with ill-defined margins in the right lobe with poor enhancement in the arterial and PV phase, mixed hypointensity on the HCP and slightly hyperintense in T2-weighted (black arrows). This lesion was biopsy proven to be a lesion of focal eosinophilic infiltration

Fig. 15

Confluent fibrosis in a 56-year-old man with cirrhosis. a Pre-contrast, b, c arterial phase, d PV phase, e 3 min, f 5 min, g 8 min, h HCP. Wedge-shaped ill-defined areas associated with capsular retraction, with decreased enhancement in the dynamic phases and with no uptake of Gd-EOB-DTPA in the HCP (arrows)

Fig. 16

Haemangioma in a 39-year-old woman with no liver disease. a, b Arterial phase, c PV phase, d 3 min, e 5 min, f HCP. Right lobe hypointense lesion with arterial nodular peripherical enhancement (thin arrow) with centripetal progression. Note that the hepatocellular uptake starts immediately (curved arrow). The intralesional enhancement follows the blood pool. In the HCP the lesion is hypointense because of rapid uptake of Gd-EOB-DTPA by the surrounding normal liver during equilibrium phase (thick arrow)

Fig. 17

Focal fat sparing area and a FNH, in a 36-year-old woman with no liver disease. a OP, b IP, c PDFF, d T2-weighted, e T1 fat-sat, f arterial phase, g PV phase, h HCP. Triangular-shaped periportal area (arrows) hyperintense to the rest of the liver in OP and Fat Sat imaging mimicking uptake of Gd-EOB-DTPA, corresponding to a fat spared area. This is confirmed in the fat-fraction map. Of note, is a lesion (*) compatible with a FNH

Fig. 18

Cholangiocarcinoma with a satellite lesion, in a 62-year-old man. a Pre-contrast, b, c arterial, d 3 min, e 5 min, f HCP. Large mass-forming lesion, irregular contour, with mild heterogeneous enhancement in the dynamic phases, with no uptake of Gd-EOB-DTPA in the HCP (thick arrow) There is another lesion (thin arrow) in the left lobe with similar contrast uptake proprieties and a necrotic centre, compatible with a metastasis

Fig. 19

Multiple hypervascular metastases, in a 39-year-old woman with breast cancer. a Pre-contrast, b arterial phase, c PVP, d 3 min, e 5 min, f HCP. Multiple nodular lesions are seen, hyperenhancing in the arterial phase, with washout in the PVP, some with a hypointense necrotic centre (solid arrow). In the HCP, some of these lesions paradoxically uptake Gd-EOB-DTPA in the necrotic centre (thin arrow)

Fig. 20

Multiple hypovascular metastases, in a 60-year-old man with an NE tumour. a Pre-contrast, b, c arterial, d 3 min, e 5 min, f 8 min, g 10 min, h HCP. Multiple hypointense nodular lesions, with no significant enhancement in the dynamic phases, one of large dimensions in the right lobe (arrows), with progressive central pooling of Gd-EOB-DTPA, more evident in the HCP

Fig. 21

Foreign body reaction, in a 41-year-old man that suffered a car accident after a New Year’s dinner. a, b Arterial phase, c PVP, d 5 min, e 8 min, f HCP. In the posterior aspect of the left lobe we see a fluffy heterogeneous hyperenhancing area, that progressively washes out and gives origin to a Gd-EOB-DTPA defect (thin arrows). Histologically proven, after surgery, to be an inflammatory reaction to a small carrot fragment

Fig. 22

Multiple hepatic cysts, in a 47-year-old woman, with no liver disease. a Pre-contrast, b arterial, c PVP, d 3 min, e 5 min, f 8 min, g 10 min, h HCP. Multiple rounded hypointense lesions (arrows), with no enhancement during all the phases. These lesions were also markedly hyperintense in T2-weighted imaging (not shown)

Fig. 23

Angiomyolipoma in a 40-year-old man with a history of renal lesions. a Arterial phase, b T2 fat sat, c OP, d IP. Large mass-forming lesion, irregular contour, with mild heterogeneous enhancement in the arterial phase (arrow). It loses internal signal in OP, indicating the presence of intracellular fat (black arrow). These were histologically proven to be an angiomyolipoma

Fig. 24

Pseudolipoma (Glisson’s capsule lipoma). a IP b OP c arterial d HCP. Small, no enhancing peripheral lesion (arrow), losing internal signal in OP, indicating the presence of intracellular fat. Histologically proven, after surgery, to be a pseudolipoma

Fig. 25

Inflammatory pseudotumour, in a 52-year-old man with PSC. a, b Arterial phase, c PVP, d 3 min, e 5 min, f HCP. Ill-defined hypointense area, in the right lobe (arrows), seen in the dynamic phases, not visualised in the HCP, proven to represent an inflammatory pseudolesion

Fig. 26

TP granulomas, in a 42-year-old man with active pulmonary TP. a Arterial phase, b PVP, c delayed phase, d HCP. There are two nodular lesions (arrows), with faint peripheral enhancement, that appear as defects in the HCP, as they have no hepatocytes to uptake Gd-EOB-DTPA

Fig. 27

Liver abscess, in a 54-year-old man with history of choledocal litiasis. a Pre-contrast, b, c arterial, d 3 min, e 5 min, f HCP. On the posterior aspect of the liver, there is a thick-walled hypointense lesion (solid arrow), with no internal enhancement during the dynamic phases. Note the excretion of Gd-EOB-DTPA on the HCP, proving the connection of this abscess with the biliary tree

Fig. 28

Liver Lymphoma, in a 39-year-old woman. a Pre-contrast, b arterial phase, c PVP, d HCP. Large infiltrative lesion in the right lobe (arrows), hypointense in the pre-contrast phase, with faint heterogeneous arterial enhancement, with washout in the PVP, not taking up Gd-EOB-DTPA in the HCP. Note involvement of the tumour along the periportal route (black arrow) and right adrenal gland (white arrows)