Magnetic Resonance C o n t r a s t A g e n t s f o r Li v e r Imaging Mustafa R. Bashir, MD KEYWORDS  Gadolinium  Contrast  GBCA  GBCM

KEY POINTS  Intravenous contrast agents are important in the performance of high-quality liver MR imaging.  Contrast agents differ in their physical properties, biodistribution, and safety profiles and these differences can be exploited to optimize MR imaging examinations.  Practitioners administering contrast agents for MR imaging should be familiar with potential safety issues and establish rational guidelines for administration based on available safety and efficacy data.

Magnetic resonance (MR) imaging is an important tool for diagnosing and staging disease and for monitoring response to therapy. In the liver, MR imaging is frequently used for the characterization of masses, detection of primary and metastatic lesions, assessment of vascular structures and lesion vascularity, and evaluation of the biliary tree. MR imaging has an important role in the work-up of common clinical conditions, including abdominal pain, jaundice, and abnormal liver function tests. Compared with other imaging modalities, MR imaging has advantages for liver imaging in terms of the variety of available image contrast mechanisms. Conventional T1-weighted and T2-weighted imaging have been supplemented over time by additional contrast methods including chemical shift imaging, T2*/susceptibility-weighted imaging, and diffusion-weighted imaging, providing a wealth of synergistic data for characterizing disease. In addition, dynamic contrast-enhanced (DCE) sequences are considered vital for the characterization of most liver lesions, providing

insights into vascular features and improving detection of subtle abnormalities. Most (although not all) of the contrast agents used clinically in liver MR imaging are composed of the rare earth metal gadolinium bound within an organic chelate. Other types of contrast agents, based on manganese and iron, have been available, but gadolinium-based agents remain the most commonly used.1 The various contrast agents share many physical features but have important differences in relaxivity, protein binding, and biodistribution. These properties provide critical information for diagnosis in clinical liver imaging. This article reviews the characteristics of contrast agents used in liver MR imaging and their utility in clinical imaging. It also reviews the toxicities associated with these contrast agents and considerations for their use in at-risk populations.

CONTRAST AGENT PROPERTIES Table 1 lists a variety of intravenous gadoliniumbased contrast agents (GBCAs) used in clinical imaging. Most of these agents are not approved by the US Food and Drug Administration (FDA) specifically

Disclosure: M.R. Bashir is a consultant to Bayer Healthcare, the makers of gadoxetate disodium, gadobutrol, and gadopentetate dimeglumine. Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710, USA E-mail address: [email protected] Magn Reson Imaging Clin N Am - (2014) -– 1064-9689/14/$ – see front matter Published by Elsevier Inc.




Table 1 Intravenous gadolinium-based contrast agents used in clinical imaging


Trade Name

Gadofosveset trisodium


Gadoterate meglumine Gadoxetate disodium Gadobutrol Gadopentetate dimeglumine Gadobenate dimeglumine Gadodiamide Gadoversetamide

Dotarem Eovist Gadavist Magnevist MultiHance Omniscan OptiMARK



Manufacturer Lantheus Medical Imaging Guerbet Bayer Healthcare Bayer Healthcare Bayer Healthcare Bracco Diagnostics GE Healthcare Mallinckrodt Pharmaceuticals Bracco Diagnostics

for liver imaging. Most of these agents have received FDA approval for central nervous system applications (gadoterate meglumine, gadobutrol, gadopentetate dimeglumine, gadobenate dimeglumine, gadodiamide, gadoversetamide, and gadoteridol). Some are approved for general body indications (gadopentetate dimeglumine and gadodiamide), whereas others are approved for specific liver indications (gadoxetate disodium and gadoversetamide) or aortoiliac and peripheral vascular disease (gadofosveset trisodium). Ferumoxytol, an iron-based agent, is not currently approved for any imaging indications, although its use has been reported in patients who cannot receive a GBCA or for other unique applications, such as brain tumor, atherosclerotic plaque, and lymph node imaging.2–6 Although other iron-based agents (ferucarbotran, ferumoxide) and manganese-based agents (mangafodipir trisodium) have shown utility in liver and lymph node imaging, these compounds are no longer available in the United States.

Relaxivity The GBCAs are paramagnetic substances that induce changes in the local magnetic field, which in turn shortens the T1, T2, and T2* relaxation times of nearby nuclei. Their T1-shortening property is the most clinically useful, and the enhancement effect seen on T1-weighted images is used to detect the presence of GBCA and thus to evaluate tissue perfusion characteristics. The effect on T2 relaxation by GBCAs is very small and is typically ignored. For gradient echo pulse sequences with very short echo times, the effect on T2* can also generally be ignored. Pulse sequences can be modified to take advantage of the T2*-shortening

r1 at 1.5 T (37 C) in Blood (L mmolL1 sL1)

Chemical Structure



4.2 7.3 5.3 4.3 6.7 4.6 5.2

Cyclic Linear Cyclic Linear Linear Linear Linear



effect to precisely measure T2*, and by extension the concentration of GBCA, but this application is most frequently used in dynamic susceptibility contrast (DSC) perfusion measures in the brain, and is rarely used in clinical liver imaging. Compared with GBCAs, iron-based agents are ferromagnetic substances and have a much stronger T2*-shortening effects, and signal loss can be used to differentiate tissues that take up these agents to greater or lesser degrees. In addition, ferumoxytol causes adequate T1 shortening to provide strong enhancement on T1-weighted images for vascular imaging.2,7,8 The amount of subjective and quantitative enhancement seen on T1-weighted images after contrast administration depends on tissue concentration of the contrast agent, agent relaxivity, and magnetic field strength. The relaxivity constant r1 describes the inherent enhancement power of an agent, independent of the amount of the contrast material present. Most GBCAs have r1 values between 4.2 L mmol 1 s 1 and 5.3 L mmol 1 s 1 in blood at 1.5 T.9 However, because of transient binding interactions with serum albumin, 3 commonly used agents have higher r1 relaxivities: gadobenate dimeglumine (6.7 L mmol 1 s 1), gadoxetate disodium (7.3 L mmol 1 s 1), and gadofosveset trisodium (19 L mmol 1 s 1).9 Because the enhancement effect also depends on the concentration of the agent, this advantage is reduced or negated for gadoxetate disodium and gadofosveset trisodium at FDA-approved doses, because their approved dosing (0.025 mmol/kg for gadoxetate disodium; 0.03 mmol/kg for gadofosveset trisodium) is much lower than that of the other GBCAs (0.1 mmol/kg).10,11 In addition to being modified by protein-binding effects, r1 relaxivity also depends on magnetic

Liver MRI Contrast Agents field strength, and decreases at higher field strength.9 Although this results in lower r1 values at 3 T compared with 1.5 T for all of the GBCAs, tissue T1 times are also substantially longer at high field strength, resulting in a net increase in enhancement at 3 T for GBCAs.12 Thus there is generally thought to be an advantage to performing contrast-enhanced MR imaging and MR angiography at 3 T, although other effects including increased susceptibility, energy deposition caused by radiofrequency pulses, and the dielectric effect must be considered.

Biodistribution Extracellular contrast agents Known as extracellular or nonspecific contrast agents, most of the GBCAs in clinical use share a similar biodistribution with regard to the liver and other organs. Soon after bolus intravenous injection, the extracellular agents first reach the liver via the hepatic arteries. The result is mild enhancement of the hepatic parenchyma with preferentially greater enhancement of those solid liver lesions with arterial-dominant vascular supply, including focal nodular hyperplasia (FNH) and most hepatocellular carcinomas (HCCs) and hepatocellular adenomas (HCAs). This phenomenon is known as arterial hyperenhancement and typically occurs at about 20 to 30 seconds following intravenous contrast media administration. The hepatic arterial phase is particularly important for lesion detection and characterization, as well as delineation of normal and variant hepatic arterial anatomy. Soon after the hepatic arterial phase, additional contrast medium arrives in the liver via the portal vein from the splenic and bowel vasculature, causing further hepatic enhancement and creating the portal venous phase appearance. In this phase, many arterially enhancing lesions become less enhanced than the liver because of strong enhancement of the liver and weak additional enhancement of these lesions from the portal venous supply, resulting in the washout appearance. The portal venous phase typically occurs at about 60 to 70 seconds following intravenous contrast media administration. Following the portal venous phase, the administered extracellular GBCA recirculates and equilibrates between arterial and venous distributions, as well as the extravascular, extracellular interstitium, resulting in the interstitial or equilibrium phase appearance. In this phase, washout of hypervascular liver lesions may be better depicted than in the portal venous phase. The equilibrium phase may first be seen approximately 90 seconds following intravenous contrast injection in many

patients. The preferred timing for the equilibrium phase can be variable from institution to institution. The choice of timing depends on balancing the greater sensitivity for washout against reduced liver enhancement/signal-to-noise ratio with later timing. Most institutions have reported 3 to 8 minutes as their preferred postcontrast timing for the equilibrium phase. Taken together, the portal venous and equilibrium phases are used for both liver lesion characterization and assessment of the portal and hepatic veins. Liver lesions that maintain enhancement similar to the blood pool are often (but not always) benign hemangiomas or vascular shunts, whereas hypervascular lesions with washout often represent more ominous entities, such as HCCs and metastases. Representative liver MR imaging performed with an extracellular contrast agent is shown in Fig. 1. Hepatobiliary agents Two commercially available GBCAs, gadobenate dimeglumine and gadoxetate disodium, have the additional properties of hepatocyte uptake and biliary excretion, and thus have been termed hepatobiliary, hepatocyte-specific, or liver-specific agents. Both initially distribute in a manner similar to the extracellular contrast agents and show both the arterial phase enhancement and portal venous phase washout features of liver lesions. After reaching the hepatic sinusoids/interstitium, these agents are taken up directly into functioning hepatocytes by adenosine triphosphate (ATP)–driven cellular receptors, and are further excreted into the biliary canaliculi. It has been shown that gadoxetate disodium is taken up into hepatocytes by the organic anion-transporting polypeptide family of transport proteins and excreted into the biliary system by multidrug resistance–associated protein-2.13–15 Hyperintensity or hypointensity of liver lesions in the hepatobiliary phase of enhancement reflects the expression of these receptors or, in the case of FNH, trapping of the agent within disordered biliary canaliculi. Approximately 5% of the gadobenate dimeglumine injected is taken up by the normal liver, whereas 50% of injected gadoxetate disodium is taken up by the normal liver.16 After a variable period of time, the so-called hepatocyte or hepatobiliary phase is reached, in which T1-weighted imaging the liver and bile ducts are enhanced because of GBCA accumulation, whereas the blood vessels are dark because of GBCA clearance by the liver and kidneys. In this phase, many solid lesions (hemangiomas and most HCCs and HCAs) are visualized as hypointense to the liver parenchyma because of poor GBCA




Fig. 1. Representative images from a liver MR imaging examination performed with the administration of an extracellular contrast agent (gadobutrol). (A) Late hepatic arterial phase image shows enhancement of the hepatic artery and early enhancement of the portal vein, with minimal parenchymal enhancement and no antegrade hepatic vein enhancement. (B) Portal venous phase image shows enhancement of the portal and hepatic veins, as well as strong enhancement of the hepatic parenchyma. (C) Equilibrium phase image shows similar enhancement of all visible vessels. Enhancement of the liver in this phase is caused by a combination of intravascular enhancement and leakage of the contrast agent into the extravascular, extracellular interstitial space.

accumulation, whereas other lesions (FNH and a minority of HCCs) are isointense or hyperintense to the hepatic parenchyma.17 Because of the higher liver extraction fraction of gadoxetate disodium, hepatocyte phase imaging can be performed at around 20 minutes after injection (or sooner) in most patients, compared with 1 to 2 hours after injection for gadobenate dimeglumine.18 The strength and timing of peak hepatic enhancement depend on the individual patient’s expression of uptake receptors, presence and severity of chronic liver disease, and other factors.15 As a result, the precise time at which an adequate hepatocyte phase is achieved is highly patient dependent. Because hepatocyte extraction of hepatobiliary contrast agents begins with the first pass of the agents through the liver, this phenomenon can be superimposed on the washout phenomenon. For gadobenate dimeglumine, hepatocyte uptake is a slow process, and thus washout can reliably be assessed independently of hepatocyte uptake for several minutes following injection. However, hepatocyte uptake with gadoxetate disodium occurs much more rapidly. As a result, a true

equilibrium or interstitial phase may not be observed with gadoxetate disodium, but rather a transitional phase is seen in which the appearance of the liver and liver lesions is determined by a combination of vascular equilibrium, interstitial leakage, and hepatocyte uptake.1 In addition, imaging of the biliary tree has been described in the hepatobiliary phase using these contrast agents. This method may have value for showing sites of bile duct injury and bile leakage.19 The T1-weighted MR cholangiogram may also be complimentary to T2-weighted MR cholangiopancreatography sequences for evaluating the biliary system, particularly if the T2-weighted sequences are compromised by excessive/irregular respiration or other artifacts. Representative liver MR imaging performed with a hepatobiliary contrast agent is shown in Fig. 2. Blood pool agents One FDA-approved GBCA, gadofosveset trisodium, is considered a blood pool agent, because it is retained within the vascular compartment for an extended period of time. Because of strong binding to serum albumin, gadofosveset trisodium

Liver MRI Contrast Agents

Fig. 2. Representative images from a liver MR imaging examination performed with the administration of a hepatobiliary contrast agent (gadoxetate disodium). (A) Late hepatic arterial phase image shows enhancement of the hepatic artery and early enhancement of the portal vein, with minimal parenchymal enhancement and no antegrade hepatic vein enhancement. (B) Portal venous phase image shows enhancement of the portal and hepatic veins, as well as strong enhancement of the hepatic parenchyma. Note that hepatic parenchymal enhancement almost equals portal vein enhancement, because of early hepatocyte uptake of the contrast agent. (C) Late dynamic phase image shows strong enhancement of the liver with relative washout of all visible vessels. Enhancement of the liver in this phase is caused by a combination of residual intravascular enhancement, leakage of the contrast agent into the extravascular, extracellular interstitial space, and active hepatocyte uptake of the contrast agent. No true equilibrium or interstitial phase is seen because of hepatocyte uptake of the agent. (D) Hepatobiliary phase image shows strong enhancement of the liver, washout of the blood vessels, and excretion of the contrast agent into the bile ducts.

is cleared slowly by the renal glomeruli and shows little leakage into the interstitial compartment.20 As a result, this agent has a long serum half-life and provides little parenchymal enhancement of some organs (such as the kidneys), and can be used for imaging vascular abnormalities when a long temporal imaging window is desired. Ferumoxytol also behaves as a blood pool agent, with a distribution similar to gadofosveset trisodium immediately after injection. However, in contrast with gadofosveset trisodium, this distribution occurs because of ferumoxytol’s large molecular size (around 750 kDa), which prevents both leakage into the interstitial compartment and renal clearance.20 Ferumoxytol is ultimately taken up by macrophages, deposited in the Kupffer cells of the reticuloendothelial system, and retained in the liver, spleen, and bone marrow for months after administration.21 Both agents have shown utility in evaluating the abdominal vasculature.6,7,20,22 However, neither is routinely used to evaluate focal liver lesions, because the enhancement of lesions with other

available contrast agents is better described. In addition, because of lack of interstitial leakage, neither agent provides a conventional interstitial/ equilibrium phase. Hemangiomas and metastases have different appearances when imaged with gadofosveset trisodium in a late vascular equilibrium phase, because the agent is retained in hemangiomas.23 The same principle may apply to ferumoxytol, and that agent could have utility in characterizing small T2-hyperintense liver lesions in patients who cannot receive GBCAs, although this application has not yet been shown directly. Thus the role of these agents in liver imaging remains primarily in the evaluation of the hepatic vasculature, when parenchymal enhancement is not desired. Representative liver MR imaging performed with a blood pool contrast agent is shown in Fig. 3.

ADVERSE EVENTS AND TOXICITY Like other medications, intravenous contrast agents can cause a variety of adverse reactions.




Fig. 3. Representative images from a liver MR imaging examination performed with the administration of a blood pool contrast agent (gadofosveset trisodium). (A) Late hepatic arterial phase image shows enhancement of the hepatic artery and early enhancement of the portal vein, with minimal parenchymal enhancement and no antegrade hepatic vein enhancement. (B) Portal venous phase image shows enhancement of the portal and hepatic veins, as well as strong enhancement of the hepatic parenchyma. Liver enhancement is caused by small vessel enhancement, because the agent remains intravascular. (C) Equilibrium phase image shows similar enhancement of all visible vessels. Liver enhancement is caused by small vessel enhancement, because the agent remains intravascular and does not leak into the extravascular, extracellular interstitial space.

For the agents used in MR imaging, reactions are rare and typically mild. Unintentional extravascular injection of MR imaging contrast media, termed extravasation, is a rare event, occurring in approximately 1 in 2000 doses.24 When it does occur, significant injuries are rare, likely because of both the small injected volume and relative lack of toxicity to the skin and subcutaneous tissues.24

Gadolinium-based Agents For intravenous injection at standard clinical doses (0.025–0.1 mmol/kg), the reported adverse event rate for GBCAs is low (0.07%–2.4%).24 Most reactions are mild and self-limited, including nausea, hives, and taste disturbance.25 The incidence of these minor adverse reactions is similar among the commercially available GBCAs.26 Compared with iodine-based contrast agents used in computed tomography (CT), GBCAs are not associated with nephrotoxicity, although this is a common misconception among referring clinicians. Anaphylactoid reactions to GBCAs are very rare (0.001%–0.01% of administrations) but can be life threatening.24 The most important risk factor for acute adverse reaction to GBCA administration is a prior history of reaction to GBCA. In addition, a

history of allergy to other medications, foods, or iodinated contrast media also increases the risk of allergic reaction to GBCAs. The ACR Manual on Contrast Media advises precautions in patients with a history of contrast reactions receiving GBCAs.24 In particular, using a different brand of GBCA or administering a corticosteroid and/or antihistamine premedication should be considered.24 Acute adverse reactions to GBCAs are managed similarly to reactions to iodinated contrast media, including observation for mild reactions, and epinephrine and cardiopulmonary support if needed for more severe reactions. Caregivers should consider removing patients from the MR imaging suite when a reaction is identified, so that necessary non–MR imaging safe support equipment can be used. Nephrogenic systemic fibrosis (NSF) is a rare condition thought to be caused by GBCA exposure.24 It is characterized by multisystem fibrosis, particularly of the skin and subcutaneous tissues, and has been reported to occur within days or months after GBCA administration.27–31 The development of NSF has been associated with a variety of risk factors, including chronic renal insufficiency (estimated glomerular filtration rate [eGFR]

Liver MRI Contrast Agents 30 mL/min/ 1.7 m2), thus precautions for prevention of NSF have mainly focused on evaluation of renal function.24 Although no clear consensus guidelines exist regarding GBCA administration and renal function, all practitioners who administer or supervise the administration of GBCA should have a clear guideline in place. In particular, guidelines related to GBCA administration should address steps to minimize the risk of NSF development. Because the dissociation of gadolinium from its chelate (to form free gadolinium) is thought to be the main precipitator of NSF, stable chelate molecules are thought to be associated with lower risk. Macrocyclic agents (gadoteridol, gadoterate meglumine, and gadobutrol) have the lowest theoretic risks of NSF of the commercially available GBCAs. Some institutions have mandated the use of macrocyclic agents in at-risk populations, or in all patients, because of the lower risk of NSF.32 In addition, some clinicians have advocated lower dosing of GBCA in at-risk populations.32 Although no specific data exist showing reduced NSF risk with GBCA administration at less than FDA-recommended doses, greater risk has been shown with high (0.2 mmol/kg or higher) compared with conventional (0.1 mmol/kg) doses, and thus some have adopted a less-issafer philosophy.32 An example of an institutional guideline regarding GBCA administration in at-risk populations, which was in effect at Duke University Medical Center in 2013, is provided in Appendix 1. Note that gadodiamide and gadoversetamide, the two agents most strongly associated with NSF to date, are not considered in the policy because they were not included in the institutional formulary at the time the guideline was established. In addition, although renal dysfunction is the most commonly considered risk factor in GBCA administration, other at-risk populations, including pregnant and breast-feeding patients, must also be considered. Gadolinium-based agents have been shown to cross the placenta to the fetus in nonhuman primate experiments.33 Although no cases of adverse fetal or maternal events related to GBCA administration in pregnancy have been reported, such administrations are rare, and thus the precise risk remains unknown. If possible, imaging should be performed by other modalities or by noncontrast MR imaging while the mother

remains pregnant. In contrast, more data exist regarding GBCA administration in breast-feeding women. It has been shown that a small amount of administered GBCM is excreted in breast milk (less than 0.04% over 24 hours), and less than 1% of that amount is absorbed by the infant gastrointestinal tract.34–36 Thus the anticipated risk to the infant is minute. Example precautions for GBCA administration in pregnant and breastfeeding women are also provided in Appendix 1.

Iron-based Agents At present, ferumoxytol is the only commercially available iron-based agent in the United States, although it is FDA approved as an ironreplacement agent, not as a contrast agent. Nonetheless, the strict association between NSF and gadolinium administration has led the imaging community to explore alternative contrast agents, and ferumoxytol has been found to be efficacious in the evaluation of arterial and venous disease, without the risk of NSF associated with GBCAs.2,6–8,20,37 In phase II and III clinical trials, ferumoxytol had a low reported rate of adverse events (5.2% for ferumoxytol vs 4.5% for placebo), with the most common events including nausea, dizziness, and diarrhea.38 However, a few serious reactions have also been reported, including hypotension and anaphylaxis-type reactions.39,40 Thus, although such reactions are rare, ferumoxytol administration must be undertaken with caution, as with any medication or contrast agent. Ferumoxytol is classified as pregnancy category C by the FDA.41 Animal trials have shown that, at supratherapeutic doses, ferumoxytol administration in pregnancy was associated with decreased fetal weights and soft tissue malformations. No large human trials are available assessing the effect of maternal ferumoxytol administration on the fetus or on breast-feeding children. By comparison, GBCAs are also classified as pregnancy class C. Before administration of ferumoxytol in these populations, practitioners should consider available alternatives, including unenhanced imaging and CT, because pregnancy class B iodinated contrast agents are available for contrast-enhanced CT.42

INJECTION PROTOCOL AND ARTERIAL PHASE ACQUISITION With the exception of MR angiography, the goal of contrast-enhanced liver MR imaging is generally to obtain dynamic, multiphase data to aid in characterizing disease processes, which is generally performed using three-dimensional T1-weighted



Bashir gradient recalled echo–type pulse sequences. Precontrast imaging should be performed both to characterize intrinsic lesion properties and for comparison with postcontrast imaging, to differentiate intrinsically hyperintense structures from those that enhance with contrast material. Most examinations include a hepatic arterial phase acquisition, a portal venous phase acquisition, and one or more later phase acquisitions. Because the primary purpose of the hepatic arterial phase image set is to capture transient enhancement of liver lesions supplied predominantly by the hepatic arterial system, precise timing is important. This phase can be visually identified by strong enhancement of the hepatic arteries and early enhancement of the portal vein, which implies enhancement of arterially supplied lesions with little to no enhancement of the background liver parenchyma. Reliable late hepatic arterial phase timing can be achieved using test bolus or bolus tracking techniques.43–46 Although fixed timing methods do not reliably provide optimal late hepatic arterial phase timing, multiphase acquisitions with fixed timing have been shown to be more robust.47 In order to optimize the strength of enhancement in the arterial phase, contrast media injection should ideally be performed at a high flow rate, at least 2 mL/s. However, there are 2 notable exceptions. First, because gadobutrol is formulated at twice the concentration of other agents, it can be injected at 1 mL/s or diluted before injection. Second, ringing/truncation artifacts that can reduce image quality have been described in the arterial phase when gadoxetate disodium is injected at 2 mL/s.48 These artifacts are related to sudden changes in signal intensity during k-space filling, caused by the combination of high flow rate and high relaxivity of the agent. Some investigators have advocated reducing the flow rate to 1 mL/s, which can reduce artifacts, and also lengthening the contrast bolus to reduce the challenge of hepatic arterial phase timing.48,49 Other artifacts, including transient arterial phase motion, have also been described with gadoxetate disodium, and the multiphase hepatic arterial phase technique has been shown to reduce the impact of those transient artifacts (Fig. 4).47,49,50 Either gadobutrol or gadoxetate disodium can be injected undiluted at 2 mL/s, but short bolus length causes challenges in precise timing, and short temporal window acquisitions with precise or redundant timing may be required to achieve the ideal late hepatic arterial phase.47 In addition, using a saline chaser immediately after contrast material injection is recommended. The purpose of this chaser is both to clear any

Fig. 4. Arterial phase image from a 50-year-old man with cirrhosis, who developed severe motion in the arterial phase associated with injection of gadoxetate disodium for MR imaging.

residual contrast material in the inject tubing and to help preserve the bolus compactness, which optimizes peak contrast material concentration at the time of arterial phase imaging. Using a saline chaser has been shown to increase the amount of peak enhancement achieved using several GBCAs.51

SUMMARY In clinical practice, contrast-enhanced imaging is vital for high-quality liver MR imaging. It provides important insights including liver lesion characteristics and vascular anatomy and patency. Knowledge of the pharmacologic and imaging features of these agents is important for providers performing and interpreting liver MR imaging.

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APPENDIX 1 Example guidelines from Duke University Medical Center (2013) for administration of GBCAs in the setting of renal dysfunction. Note that the category designations described here do not correspond with the National Kidney Foundation system for staging chronic kidney disease. Category 0 (eGFR  60 mL/min/1.73 m2, measured within 3 months): normal renal function. GBCAs may be administered up to standard dosages. Category I (eGFR between 40 and 59 mL/min/ 1.73 m2, measured within 1 month): normal to mildly impaired renal function. Risk of developing NSF from GBCA administration in this patient population is extremely low. GBCAs may be administered up to standard dosages. Category II (eGFR between 30 and 39 mL/min/ 1.73 m2): borderline renal function. eGFR measurements can fluctuate from day to day. As a result, these patients must have eGFR rechecked within 24 hours of potential GBCA administration; this is done via point of care testing when the patient arrives for MR imaging for their scan if no other

Liver MRI Contrast Agents qualifying eGFR measurement is available. Patients with an eGFR greater than or equal to 30 mL/min/ 1.73 m2 within 24 hours of GBCA administration are managed as category I renal function. Those with eGFR less than 30 mL/min/1.73 m2 are managed as category III. If it is not possible to check the eGFR within 24 hours of MR imaging, then these patients are considered category III for the purposes of potential GBCA administration. Category III (eGFR

Magnetic resonance contrast agents for liver imaging.

Intravenous contrast agents are important in the performance of liver magnetic resonance (MR) imaging. These agents differ in their physical propertie...
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