Comparing Single And Multiple Ring Enhancing Lesions Table

Fig. 18. Larger SPIO particles such as ferumoxides are administered by drip infusion and T2-weighted images are acquired more than 20 min after injection

Zaim Zeck Homeopathy

Fig. 19. Smaller USPIO particles such as SH U 555 A can be administered as a bolus, whereupon they distribute initially in the intravascu-lar-extravascular space permitting dynamic T1-weighted imaging. Thereafter, like ferumoxides, SH U 555 A particles are taken up by Kupffer cells allowing T2-weighted delayed imaging

Fig. 19. Smaller USPIO particles such as SH U 555 A can be administered as a bolus, whereupon they distribute initially in the intravascu-lar-extravascular space permitting dynamic T1-weighted imaging. Thereafter, like ferumoxides, SH U 555 A particles are taken up by Kupffer cells allowing T2-weighted delayed imaging unenhanced imaging for the depiction of hepatic tumors [21]. More recent studies, however, have shown that SPIO-enhanced MRI has significantly greater detection capability for liver malignancies compared to spiral CT [125, 134, 145, 146]. Although comparisons of SPIO-enhanced MRI with other gadolinium-enhanced MR techniques have been somewhat limited until recently [7,38,48,49, 50, 85, 133, 139], the general conclusion is that gadolinium-enhanced imaging is the more valuable approach for the detection of hepatocellular lesions such as HCC and FNH [38,85,133].

Limitations of SPIO-enhanced MRI include an increased incidence of false positive lesions due to the possibility of vessels mimicking lesions against a background of black liver, and a longer imaging protocol that requires pre- and post-contrast imaging over a period of 30 min or more. Further more, the use of SPIO in patients with cirrhosis is also challenging due to the diminished uptake and heterogeneous signal arising from fibrosis [24, 151]. However, in this regard a recent study has suggested a lower dose of SPIO agent might be useful in patients with cirrhotic liver [1].

The availability of SH U 555 A may go some way towards overcoming the problems inherent to the larger SPIO agents in that this agent can be administered as a fast bolus in order to observe the early perfusion characteristics of the liver using T1- or T2*-weighted sequences [95, 96, 126] (Fig. 20). This, combined with the enhancement patterns observed on delayed T1-weighted and T2-weighted images (Figs. 21, 22) may prove clinically useful for both the detection and characterization of lesions. Unfortunately, the enhancement observed on SH U 555 A-enhanced dynamic im-

. " * /

b

" -y t

h

|L A d

Fig. 20a-d. Dynamic Tl-weighted MR imaging of focal nodular hyperplasia with SH U 555 A. A large homogeneously hyperintense lesion can be seen on the arterial phase Tl-weighted GRE images acquired 30 sec after the administration of SH U 555 A (a). A central hy-pointense scar is also apparent on this image. On the portal-venous (b) and equilibrium (c) phase images acquired after 75 sec and 4 min, respectively, the lesion is seen as slightly hyperintense compared to the surrounding parenchyma. On the delayed phase image acquired after 10 min (d), the lesion appears isointense compared to the surrounding parenchyma while the central scar is seen as slightly hy-pointense. The isointense appearance on the delayed Tl-weighted GRE image indicates that the lesion contains functioning Kupffer cells that are able to take up SH U 555 A. This suggests the lesion is benign in nature

Fig. 20a-d. Dynamic Tl-weighted MR imaging of focal nodular hyperplasia with SH U 555 A. A large homogeneously hyperintense lesion can be seen on the arterial phase Tl-weighted GRE images acquired 30 sec after the administration of SH U 555 A (a). A central hy-pointense scar is also apparent on this image. On the portal-venous (b) and equilibrium (c) phase images acquired after 75 sec and 4 min, respectively, the lesion is seen as slightly hyperintense compared to the surrounding parenchyma. On the delayed phase image acquired after 10 min (d), the lesion appears isointense compared to the surrounding parenchyma while the central scar is seen as slightly hy-pointense. The isointense appearance on the delayed Tl-weighted GRE image indicates that the lesion contains functioning Kupffer cells that are able to take up SH U 555 A. This suggests the lesion is benign in nature

Weighted And Weighed

Fig. 21a-d. T2-weighted and T1-weighted MR imaging of nodular regenerative hyperplasia with SH U 555 A. The unenhanced GE T1-weighted image (a) reveals several faintly hyperintense nodules (arrows) in the right liver lobe. On the corresponding unenhanced TSE T2-weighted image (b) these nodules are again seen as slightly hyperintense. On the T1-weighted and T2-weighted images acquired 10 min after the administration of SH U 555 A (c and d, respectively) the nodules appear slightly hypointense against the surrounding parenchyma. This indicates that the lesions are able to take up contrast agent and are therefore likely to be benign in nature

Fig. 21a-d. T2-weighted and T1-weighted MR imaging of nodular regenerative hyperplasia with SH U 555 A. The unenhanced GE T1-weighted image (a) reveals several faintly hyperintense nodules (arrows) in the right liver lobe. On the corresponding unenhanced TSE T2-weighted image (b) these nodules are again seen as slightly hyperintense. On the T1-weighted and T2-weighted images acquired 10 min after the administration of SH U 555 A (c and d, respectively) the nodules appear slightly hypointense against the surrounding parenchyma. This indicates that the lesions are able to take up contrast agent and are therefore likely to be benign in nature

Steve Mcqueen Mri Contrast Dye

Fig. 22a-d. T2- and T1-weighted MR imaging of peripheral cholangiocellular carcinoma with SH U 555 A. The unenhanced GE T1-weighted image (a) reveals a hypointense mass (arrow) in the right liver lobe. Slight capsular retraction is also apparent. The lesion is less well seen on the corresponding unenhanced TSE T2-weighted image (b). The lesion does not indicate a capacity to take up the contrast agent on the delayed T1-weighted image acquired 10 min after the administration of SH U 555 A (c) and remains slightly hypointense compared to the surrounding parenchyma. On the corresponding post-contrast T2-weighted image (d) the lesion is clearly delineated with a peripheral hyperintense rim. This enhancement pattern indicates that the lesion is likely to be malignant in nature

Fig. 22a-d. T2- and T1-weighted MR imaging of peripheral cholangiocellular carcinoma with SH U 555 A. The unenhanced GE T1-weighted image (a) reveals a hypointense mass (arrow) in the right liver lobe. Slight capsular retraction is also apparent. The lesion is less well seen on the corresponding unenhanced TSE T2-weighted image (b). The lesion does not indicate a capacity to take up the contrast agent on the delayed T1-weighted image acquired 10 min after the administration of SH U 555 A (c) and remains slightly hypointense compared to the surrounding parenchyma. On the corresponding post-contrast T2-weighted image (d) the lesion is clearly delineated with a peripheral hyperintense rim. This enhancement pattern indicates that the lesion is likely to be malignant in nature ages is relatively weak due to the small dose (1 ml) that is injected from the prefilled syringes. Thus, it remains to be seen whether this agent will have widespread clinical impact on MRI of the liver.

In addition to possessing both T1 and T2 effects, the newer ultrasmall formulations currently under development have a longer intravascular residence than the larger SPIO agents. As with the larger SPIO particles, the Kupffer cells of the RES take up and eventually clear these USPIO particles over a period of about 24 hrs. The prolonged imaging window, however, allows for more favorable image resolution and signal-to-noise ratio because the acquisition parameters are less constrained by time. For liver imaging, the blood pool effect and combined T1 and T2 effects have shown promise for the detection and characterization of lesions [42, 110]. A specific advantage is that vessels and lesions show opposite enhancement. On T1-weighted images vessels are bright while lesions are dark, whereas on T2-weighted images the reverse is true. An additional advantage is that MR angiography may also be performed with these agents. An early study to evaluate the abdominal vasculature on delayed (45 min) images acquired following the infusion of AMI-227 revealed significant enhancement of all vessels [75]. Similarly, time of flight (TOF) MR angiography prior to and following AMI-227 administration demonstrated that the depicted renal artery lengths increased significantly following contrast administration [131]. Unfortunately, the use of blood pool agents is hindered at the present time by the presence of increased background signals and the superimposition of venous structures.

Injection Schemes for Liver MRI with Different Contrast Agents

Non-Specific Gadolinium Chelates

Gadopentetate dimeglumine (Magnevist®, Gd-DT-PA; Berlex Laboratories/Schering AG) Gadoteridol (ProHance®, Gd-HP-DO3A; Bracco Diagnostics),

Gadodiamide (Omniscan®, Gd-DTPA-BMA; GE Healthcare)

Gadoversetamide (Optimark®, Gd-DTPA-BMEA; Mallinckrodt)

Gadoterate meglumine (Dotarem®, Gd-DOTA; Guerbet)

Gadobutrol (Gadovist®, Gd-BT-DO3A; Schering AG)

These contrast agents are injected as a bolus, typically at a dose of 0.1 mmol/kg bodyweight and at a flow-rate of 2-3 ml/sec. The injection of the contrast agent should be followed by a saline flush of 20 ml at the same injection rate.

Contrast enhanced T1-weighted or T1-weighted fat-suppressed imaging of the entire liver is typically performed in a single breath-hold at:

20-25 sec post-injection (Arterial phase imaging)

60-80 sec post-injection (Portal-venous phase imaging)

3-5 min post-injection (Equilibrium phase imaging)

Hepatocyte-Targeted Contrast Agents

Mangafodipir trisodium (Teslascan®, Mn-DPDP; GE Healthcare)

This agent has to be administered as a drip infusion over a period of approximately 10 min at a dose of 5 |mol/kg bodyweight (0.5 mL/kg; maximum dose, 50 mL). Alternatively, some investigators have used a hand injection over a 1 or 2 min period, followed by a flush of 10 mL of normal saline. However, when this fast injection scheme is employed, there is potentially an increased incidence of adverse events.

Imaging with T1-weighted and T1-weighted fat-suppressed sequences is usually performed at 15-20 min post-injection.

Agents with Combined Extracellular and Hepa-tocyte-Specific Distribution

Gadobenate dimeglumine (MultiHance®, Gd-BOP-TA; Bracco Imaging SpA)

Gadolinium ethoxybenzyldiethylenetriaminepen-taacetic acid (Primovist®, Gd-EOB-DTPA; Schering AG, Germany)

Imaging with contrast agents that have a combined extracellular and hepatocyte-specific distribution can be performed during the dynamic phase of contrast enhancement in a manner identical to that used with the non-specific Gd-chelates that have a purely extracellular distribution. For this purpose, these agents are injected as a bolus, typically at a dose of 0.05-0.1 mmol/kg BW (0.1-0.2 mL/kg bodyweight) for Gd-BOPTA and 0.025 mmol/kg BW (0.1 mL/kg bodyweight) for Gd-EOB-DTPA, at a flow-rate of 2-3 ml/sec. The injection of the contrast agent should be followed by a saline flush (0.9% sodium chloride solution) of 20 ml at the same injection rate.

Contrast enhanced T1-weighted or T1-weighted fat-suppressed imaging of the entire liver is typically performed in a single breath-hold at:

20-25 sec post-injection (Arterial phase imaging)

60-80 sec post-injection (Portal-venous phase imaging)

3-5 min post-injection (Equilibrium phase imaging)

In addition to imaging in the dynamic phase of contrast enhancement, the hepatocyte-specific distribution of these agents permits imaging to be performed in a more delayed hepatobiliary phase. Hepatobiliary imaging after injection of Gd-BOP-TA is typically performed at 45 min to 3 hrs postinjection. Conversely, with Gd-EOB-DTPA imaging in the hepatobiliary phase is usually performed between 20 min and 2 hrs post-injection.

Typically 2D or 3D T1-weighted and T1-weighted fat-suppressed GRE images are acquired in the hepatobiliary phase.

RES-Specific Agents SPIO Agents:

Ferumoxides (Feridex®, Berlex Laboratories and Endorem®, Laboratoire Guerbet)

A SPIO dose of 15 |mol/kg of bodyweight from the stock solution (0.075 mL/kg bodyweight) is diluted in 100 mL of a 5% glucose solution, before being administered as a drip infusion over a period of at least 30 min.

The incidence and severity of adverse events such as back pain, thoracic pain or decreased blood pressure correlates with the speed of infusion. Therefore, if patients experience side effects, the drip infusion should be stopped until the symptoms disappear and then recommenced at a lower infusion speed under medical supervision. However, if reactions such as nausea, urticaria or other allergic skin reactions occur, the administration should be stopped immediately and not recommenced.

The optimal time-point for imaging in the accumulation phase after SPIO administration is between 30 min and 6 hrs after injection of the complete dose of contrast medium.

Imaging protocols typically include T2-weight-ed TSE sequences, T2*-weighted sequences and in certain cases T1-weighted GRE sequences.

USPIO Agents:

Unlike Ferumoxides, this iron oxide-based agent can be administered as a bolus.

The dose for patients with a bodyweight of less than 60 kg is 0.9 mL (total iron dose 0.45 mmol); patients with a bodyweight of more than 60 kg receive a dose of 1.4 mL (total iron dose 0.7 mmol). The contrast agent is administered as a bolus using an included 5 |m-filter followed by a saline flush (0.9% sodium chloride solution) of approximately 20 mL.

Following bolus injection, dynamic contrast-enhanced T1-weighted or T2*-weighted GRE imaging of the entire liver is typically performed in a single breath-hold at:

20-25 sec post-injection (Arterial phase imaging)

60-80 sec post-injection (Portal-venous phase imaging)

3-5 min post-injection (Equilibrium phase imaging)

The time-point for imaging in the accumulation phase after USPIO injection is between 10 min and 8 hrs post-administration of the contrast medium.

At this time point T2-weighted or T2*-weighted SE or TSE images should be acquired. If information about the intrahepatic vessels is needed, the imaging study can be augmented by a TOF MR an-giography sequence within the first 20 min after injection. During this time span a fraction of the administered dose of USPIO is still circulating in the blood thereby increasing the vessel signal on TOF images.

Radiologic Classification of Focal Liver Lesions on Unenhanced and Contrast-Enhanced MRI

Liver lesions can be classified on the basis of both unenhanced and contrast-enhanced images (Table 3). On unenhanced imaging, classification can be based upon the signal intensity and delineation of lesions on conventional T2-weighted and Tl-weighted images as well as on opposed phase Tl-weighted images or Tl-weighted images acquired with fat suppression. Tables 4 and 5 show the characteristic appearances of many of the more common lesion types on unenhanced T2-weighted and T1-weighted images, respectively. Thus, on unen-hanced imaging, lesions with a high fluid content, lesions containing fat and lesions with internal hemorrhage can be detected and readily diagnosed. Unfortunately, unenhanced imaging alone cannot always differentiate reliably between benign and malignant lesions and, in many cases, addi tional information from contrast-enhanced imaging is necessary for accurate differential diagnosis.

The availability of contrast agents with markedly different properties means that lesions can be classified on the basis of different enhancement patterns on contrast-enhanced imaging (Table 3). Thus, lesions can be classified according to their behavior on dynamic imaging following the administration of extracellular contrast agents (in a similar manner to that which occurs on dual phase spiral CT imaging), and to their behavior on delayed imaging following the administration of contrast agents targeted either to the hepatocytes or the Kupffer cells.

In the dynamic phase of contrast enhancement after the administration of gadolinium-based contrast agents, lesions can be classified according to whether they demonstrate hypervascular or hypo-vascular enhancement patterns or delayed persistent enhancement on T1-weighted acquisitions during the arterial, portal-venous and equilibrium phases, respectively (Table 6). Within these three major groups of lesions, lesions can be classified further according to the presence or absence of certain characteristic features. For example, a central scar within a hypervascular lesion in a non-cirrhotic liver that shows low signal intensity on T1-weighted images and high signal intensity on T2-weighted images may be indicative of FNH (Table 7). Similarly, a hypovascular lesion with a hypervascular rim that shows contrast agent washout at 10-15 min post-injection and a dough-nut or halo sign on T2-weighted images may be indicative of a metastasis of adenocarcinoma (Table 8). Finally, a lesion that shows nodular enhancement in the arterial phase followed by centripetal filling-in in the subsequent phases and high signal intensity on T2-weighted images may be indicative of a hemangioma (Table 9).

Whereas the enhancement seen on dynamic T1-weighted imaging gives information on the morphologic characteristics of lesions, that seen on delayed phase images after the injection of agents targeted either to the hepatocytes (e.g. Gd-BOPTA (Table 10), Gd-EOB-DTPA (Table 11), Mn-DPDP (Table 12)) or Kupffer cells (SPIO agents (Table 13), USPIO agents (Table 14, 15 and 16)) gives information on the cellular content and cellular functionality of lesions. In the case of Gd-BOPTA, the information gained in the delayed phase is additional to that seen in the dynamic phase and may serve to distinguish lesions of he-patocellular origin such as FNH that may be able to take up the agent, from lesions of hepatocellular origin such as HCC that have lost this ability and lesions of non-hepatocellular origin that are also unable to take up the agent (Table 10). Similarly, lesions can be classified into different groups on the basis of their ability to take up Gd-EOB-DTPA

(Table 11), Mn-DPDP (Table 12) and iron oxide particles (Tables 13, 14, 15 and 16). However, the lack of a dynamic imaging capability combined with the sometimes overlapping levels of enhancement of different primary benign and malignant liver lesions often makes accurate differential diagnosis difficult with these agents.

The tables that follow demonstrate schematically an approach to the classification of liver lesions based on imaging features on unenhanced MR imaging and enhanced imaging after administration of both extracellular and liver-specific contrast agents.

Summary

Various categories of MR contrast agents are available for clinical use, all of which permit the demonstration of more liver lesions than can be depicted on unenhanced imaging alone. The biggest impediment to the more widespread use of contrast agents for liver imaging in the USA in particular is that reimbursement schemes have not yet been established. Thus, these products have so far received only a cautious welcome in the market place. In addition, the added cost of the extended imaging time needed for the tissue-specific (RES and hepatocyte) agents makes their use less attractive at the current time. On the other hand, it is possible the added value and cost-effectiveness of some of the newer agents will become apparent through clinical use.

Until recently, the absence of an approved contrast agent with combined extracellular and hepa-tobiliary distribution in the USA led various authors to propose sequential same-session imaging with both a tissue-specific agent and an extracellular gadolinium agent to improve liver lesion detection and characterization [63,109]. The downside of this approach, however, is the need for two injections of two different contrast agents and the associated additional costs involved. The development of contrast agents such as gadobenate dimeglumine, which has the characteristics of both extracellular and hepatobiliary agents, allows functional information to be gained on hepatobil-iary phase imaging in addition to that gained on standard dynamic phase imaging. In this regard, the use of agents with combined extracellular/he-patobiliary properties would appear to offer advantages not only in comparison to other MR contrast agents, but also in comparison to other imaging modalities such as MDCT.

Table 3. Classification of focal liver lesions

Table 4

Table 5

unenhanced

T1w dynamic imaging

extracellular contrast agents

T1w hepatobiliary imaging

T2w iron oxide enhanced imaging

Dual

(extracellular and hepatobiliary) contrast agents Gd-BOPTA Table 10 Gd-EOB-DTPA Table 11

Hepatobiliary contrast agent Mn-DPDP

Table 12

Tables 13 - 16

liver specific contrast agents

Table 4. DDX of focal liver lesions on T2w imaging hyperintense

Cysts

Hemangioma

Metastases of neuroendocrine tumors

Cystic metastases

Bilioma

AV malformation (low flow)

Hemangiosarcoma

Hemangiosarcoma slightly hyperintense

Metastases of adenocarcinoma

(e.g., colorectal), "halo-sign", "doughnut-sign"

Undifferentiated HCC

Focal Fatty Liver isointense

Adenoma

Well-differentiated HCC

Metastases of neuroendocrine tumors after chemotherapy

hypointense

Regenerative nodules

(low signal caused by hemosiderin deposits)

Calcification

AV malformation with high flow

(flow void)

Fibrosis

Non-acute hemorrhage

Table 5. DDX of focal liver lesions on T1w images hyperintense fluid with fat hemorrhage protein content fluid with fat hemorrhage protein content

fs

and/or

fs

fs

opposed

imaging

imaging

phase

imaging

SI I

(due to magnetic field inhomogeneities

SI I

(due to magnetic field inhomogeneities susceptibility artefacts)

hemosiderotic nodules in cirrhotic liver fs imaging

regenerative nodule (T2w SI I)

susceptibility artefacts)

Cirrhotic Hyperplastic Nodules Mri

hemosiderotic nodules in cirrhotic liver

regenerative nodule (T2w SI I)

Dynamic Liver Mri

hypointense most benign and malignant focal liver lesions

Mets

Table 6. DDX of focal liver lesions on T1w dynamic imaging (extracellular Gd-chelates (e.g., Gd-DTPA), dual Gd-chelates (e.g., Gd-BOPTA))

hypervascular liver lesions in arterial phase hypovascular liver lesions in arterial / portal venous phase liver lesions with delayed persistent enhancement in equilibrium phase

Oral Lesions Hypervascular

Table 7. DDX of hypervascular liver lesions on dynamic imaging no cirrhosis

Central scar true scar with low SI in T1w and T2w images;

no delayed enhancement of central scar

Fibrolamellar carcinoma (FLC)

Central scar with low SI in T1w and high SI in T2w images;

delayed enhancement of central scar no scar hemorrhage regressive changes

Typically young female patients, related to use of oral contraceptives

Focal nodular hyperplasia (FNH)

Focal nodular hyperplasia (FNH)

cirrhotic liver

Irregular internal lesion morphology

Homogeneous or inhomogeneous hyper-vascularization; high SI in T2w images

Hepatocellular carcinoma (HCC) (pseudocapsule, diffuse, solitary or micronodular)

Dysplastic nodule

+/- known primary neoplasm

Homogeneous low SI in T2w images I

low SI in T2w images due to hemosiderin deposition, homogeneous SI, homogeneous vascularization

Metastases of neuroendocrine tumors (e.g., insulinoma, gastrinoma, carcinoid)

Homogeneous, typically very high SI in T2w images, strong vascularization

Metastases of different primary neoplasms [e.g., hypernephroma, pheochromo-cytoma, melanoma, breast cancer (also hypo-vascular)]

Metastases of leiomyo-sarcoma

Incidental regional hyper-vascularization

Inhomogeneous Homogeneous high SI in T2w SI in T2w images, necrotic images, slightly areas but homo geneous hyper-vascularization, isointense in images 5 min after CMA

Focal attenuation difference (FAD)

Table 8. DDX of hypovascular liver lesions on dynamic imaging cystic appearance

Sharply demarcated, no irregular regional vascularization low SI rim, internal septation, daughter cysts

■ Cysts (solitary, multiple) • Carolis disease polycystic kidney disease hypervascular rim in arterial phase

Wash-out sign 10-15 min after CMA, T2w: doughnut sign / halo sign

Cystic appearance, irregular cyst wall with focal cystic

Hypovascular in arterial and portal venous phase, isointense on images 5 min after CMA

Irregular areas of low SI in T1w images, increased SI or isointense in T2w images

Cystic appearance, irregular cyst wall with focal cystic

Hypervascular rim with persistent enhancement, no central CM uptake

High SI in T2w images (almost cystic appearance), occasionally gas formation

History of abdominal trauma or surgery

Cystic appearance, tends to increase in size, dislocation of vessels, high SI in T2w images

Irregular borders, inhomo-geneous SI in T1w and T2w images, hyperintense rim due to extracellular methemoglobin, with time increase of central SI

Table 9. DDX of liver lesions with delayed persistent enhancement

Nodular peripheral enhancement in arterial phase, centripetal filling

High SI in T2w images (light bulb appearance), in large lesions central areas may remain unenhanced after CM application due to thrombosis/fibrosis sharply demarcated

Hemangioma infiltrating along portal tracts, segmental biliary obstruction

Hypovascular with hypervascular peripheral enhancement in arterial phase

Intrahepatic cholangiocellular carcinoma (CCC)

+/- known primary neoplasm

Hypo- or slightly hypervascular in arterial phase, low SI in T1w and high SI in T2w images, sometimes peripheral wash-out

Metastases of leiomyosarcoma and gastrointestinal stromal tumors (GIST)

Irregular, partially nodular enhancement in arterial phase, irregular filling

Centrifugal or irregular filling, irregular borders

- Hemangiosarcoma

- Hemangioendothelioma

- Hemangiopericytoma

Homogeneous, sometimes early enhancement, irregular shape

High SI in T2w images, iso- or hyperintense in delayed-phase images

Peliosis hepatis

Table 10. DDX of focal liver lesions in the hepatobiliary phase after Gd-BOPTA

contrast agent uptake ■

.SIt no contrast agent uptake inhomogeneous more than normal live tissue more than normal live tissue

inhomogeneous

- Adenoma

(without hemorrhage/ regression)

(well-differentiated)

- Adenoma

(with hemorrhage/ regression)

- Cysts

- Metastases

(often peripheral wash-out and unspecific CM-retention in regressive changes)

- HCC (undifferentiated)

- hemangioma

(-> diagnosis made by T2w SI and dynamic imaging)

m

Cysts

Mets

Table 11. DDX of focal liver lesions in the hepatobiliary phase after Gd-EOB-DTPA

no contrast agent uptake inhomogeneous more than normal liver tissue more than normal liver tissue

inhomogeneous

- Cysts

- Metastases

(often peripheral wash-out and unspecific CM-retention in regressive changes)

- HCC (undifferentiated)

- hemangioma

(-> diagnosis made by T2w SI and dynamic imaging)

Table 12. DDX of focal liver lesions in the hepatobiliary phase after Mn-DPDP

contrast agent uptake no contrast agent uptake

Iron Liver Tabel

Table 13. DDX of focal liver lesions on SPIO enhanced T2w images in the RES-specific phase iron oxide uptake (SI i )

comparable to slightly less than liver tissue liver tissue less than liver tissue comparable to slightly less than liver tissue liver tissue less than liver tissue

no iron oxide uptake (CNR f )

Table 14. DDX of focal liver lesions on USPIO enhanced T1w and T2*w dynamic CE imaging hypervascularized discretely hypervascularized delayed persistent enhancement delayed persistent enhancement

FNH NRH HCC

(early wash-out effect)

Metastases

FNH Adenoma HCC

(early wash-out effect)

Hemangioma

(rim enhancement)

Cysts Metastases

Table 15. DDX of focal liver lesions on USPIO enhanced T1w images in the RES-specific phase hyperintense slightly hyperintense isointense hypointense hypointense

FNH NRH Hemangioma

CCC Cysts HCC

(undifferentiated)

Metastases

Table 16. DDX of focal liver lesions on USPIO enhanced T2w/T2*w images in the RES-specific phase comparable to liver tissue

iron oxide uptake

slightly less than liver tissue

Adenoma

(well-differentiated)

Adenoma

HCC FLC

iso-

slightly hyper-

less than liver tissue

HCC FLC

hemangioma hyperintense no iron oxide uptake (CNR f)

Cysts

Metastases

HCC (undifferentiated)

hyperintense

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