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Original Research |
1 All authors: Department of Radiology, Abdominal Imaging, New York University School of Medicine, Tisch Hospital, 560 First Ave., Ste. HW 202, New York, NY 10016.
Received February 22, 2007;
accepted after revision June 10, 2007.
Address correspondence to M. Macari
(michael.macari{at}nyumc.org).
Abstract
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MATERIALS AND METHODS. From a radiology information system, we identified 174 consecutive patients who underwent contrast-enhanced abdominal MRI. Subjects with diffuse liver disease were excluded. The presence of geographic low signal adjacent to the falciform ligament in the anterior medial aspect of the medial segment of the liver during dynamic gadolinium-enhanced imaging was assessed during the arterial, portal venous, and equilibrium phases of enhancement. If this finding was present on any contrast-enhanced sequence, in- and opposed-phase images were qualitatively evaluated to determine if signal loss occurred on opposed-phase imaging.
RESULTS. Fifty-three patients were excluded because of diffuse liver disease. Twenty-one (17.4%) of the remaining 121 patients showed focal low signal during gadolinium-enhanced MRI. This finding was present in all 21 patients during the portal venous phase and in seven and five during the arterial and equilibrium phases of enhancement, respectively. Of the 21 patients, three showed signal loss on opposed-phase imaging and 18 (85.7%) did not.
CONCLUSION. Although low attenuation or signal adjacent to the falciform ligament may represent focal fat, it usually does not and is likely related to anomalous venous drainage into the liver.
Keywords: focal fat in- and opposed-phase imaging liver MRI
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In cases of diffuse fatty liver, common locations for fatty sparing occur around the gallbladder, in the posterior medial segment, and around tumors such as hemangiomas. The cause is likely related to a lack of direct portal venous inflow into these areas of the liver [4–6]. It has been suggested that for fatty liver to occur, superior mesenteric venous inflow to the liver parenchyma is required. If superior mesenteric venous inflow is lacking or reduced, fatty sparing may occur. The typical areas of fatty sparing seen in the posterior medial segment and around the gallbladder are explained by aberrant right gastric and direct cholecystic venous drainage directly into these regions of the liver, respectively [6]. Similarly, around tumors, the portal venous supply may be reduced because of direct venous compression or because of increased arterial flow resulting in focal fatty sparing [4].
The cause of focal fatty deposition in the liver is not so easy to explain and has many imaging manifestations. It has been described as being round and occasionally multifocal and in these cases may mimic tumors [7, 8]. Rarely, focal fatty infiltration may be perivascular and mimic hepatic inflammation [3]. Although focal abnormalities in the posterior aspect of the medial segment of the liver are usually due to focal sparing as previously described, a case of focal fatty deposition has been described in this location [9].
A common location for focal fatty infiltration in the liver has been described as occurring in the medial segment of the left lobe, usually anteriorly, and adjacent to the falciform ligament [1, 9, 10]. This is usually seen as a geographic area of decreased attenuation relative to the background liver parenchyma at contrast-enhanced CT [10, 11]. The exact cause for the development of focal fatty infiltration in this region of the liver is poorly understood but thought to be due to aberration in blood flow with direct blood flow into the liver from anterior abdominal wall veins (the inferior vein of Sappey) somehow causing disturbances in the metabolic activity of the liver with resultant fatty change [12, 13].
We have observed areas of decreased signal intensity in this area at contrast-enhanced MRI that did not show signal loss on opposed-phase T1-weighted gradient-echo sequences. Therefore, using imaging data obtained at in- and opposed-phase gradient-echo T1-weighted sequences as a surrogate for fatty deposition, we performed this retrospective study to determine how often geographic decreased signal at contrast-enhanced MRI in the anterior medial segment of the left lobe of the liver actually represented focal fatty deposition.
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MRI Technique
All 174 patients underwent abdominal MRI at 1.5 T using either a Vento or
Symphony magnet (Siemens Medical Solutions) and a torso phased-array coil. A
22-gauge IV catheter was inserted into an arm vein. All patients underwent a
breath-hold spoiled gradient-echo T1-weighted sequence using a dual-echo for
in-phase (TR/TE, 180/4.7) and opposed-phase (TR/first- and second-echo TEs,
180/1.9, 2.3) imaging with 80° flip angle and 6- to 8-mm-thick sections
with a 1.6-mm gap.
All patients underwent breath-hold T2-weighted imaging with a HASTE sequence with parameters TR/TEeff, 900/88; 150° flip angle; 5-mm-thick sections; and no gap. In addition, heavily T2-weighted sequences were obtained using either a STIR sequence with parameters TR/TE, 4,350/85; inversion time, 180 milliseconds; 144° flip angle; 8-mm-thick sections;1.6-mm gap (n = 16) or a fat-suppressed fast spin-echo technique with parameters 3,570/101, 180° flip angle, 8-mm-thick sections, 1.6-mm gap (n = 9).
Contrast-enhanced imaging was performed using a volumetrically acquired 3D fat-suppressed gradient-recalled echo (GRE) sequence with parameters 3.3/1.3; 12° flip angle; and slice thickness, 2.4 mm. This sequence was run before and during a dual arterial phase acquisition, and at approximately 60 (venous phase) and 180 (equilibrium phase) seconds after the IV administration of 20 mL of gadopentetate dimeglumine (Magnevist, Berlex Laboratories).
The arterial phase acquisition was determined after a test bolus of 1 mL of gadolinium was injected followed by a 20-mL saline flush using serially acquired T1-weighted images. The parameters were 500/1.66 with 10-mm-thick sections. The time-to-peak was calculated on the basis of visual observation and was used as the time to initiate the first arterial phase acquisition. The second arterial phase was obtained 5 seconds after the completion of the first arterial phase. All data were sent to a PACS workstation.
Data Interpretation
All MR data were retrospectively evaluated by two reviewers in consensus on
a PACS workstation in the following manner. Patients with diffuse hepatic
disease (cirrhosis, diffuse fatty infiltration or diffuse iron deposition,
prior liver transplantation, or multiple metastases or hepatocellular
carcinoma [HCC]) were excluded from the analysis. Exclusion was based on
consensus review of MRI data. Exclusion was based solely on the MRI
appearance. Laboratory data were not used as criteria for exclusion.
Fifty-three (30.5%) of the 174 patients were excluded due to the presence of
cirrhosis (n = 37), diffuse fatty infiltration (n = 5),
multiple liver metastases or HCC (n = 7), liver transplant
(n = 3), and hemochromatosis (n = 1).
In patients without diffuse liver disease, the multiphase volumetrically acquired 3D fat-suppressed GRE T1-weighted sequences acquired during the arterial, portal venous, and equilibrium phases of contrast enhancement were reviewed for the presence of geographic low signal intensity adjacent to the falciform ligament in the anterior medial aspect of the medial segment of the left lobe of the liver. The contrast-enhanced data were evaluated to determine if the low signal was present on either of the two arterial, venous, or equilibrium phases of enhancement. When present, the size of the area was measured in millimeters. The greatest transverse diameter of the decreased enhancement was measured by a single reviewer using electronic calipers on the PACS. Measurements were made on axial images during the contrast-enhanced sequence that showed the focal area as being most visually conspicuous.
If this finding was present on any of these contrast-enhanced sequences, the in- and opposed-phase images and the axial T2-weighted sequences were reviewed and qualitatively assessed to evaluate for signal loss on opposed-phase imaging when compared with the in-phase images, which served as surrogate markers for focal fatty deposition. The T2-weighted images were qualitatively evaluated for focal areas of high or low signal in the area. If an abnormality was seen on the opposed-phase or the T2-weighted sequence it was measured in millimeters as previously described. The exact z-axis position was used from data on the images to correlate the gradient-echo T1-weighted and T2-weighted sequences to the contrast-enhanced images.
Statistical Analysis
The prevalence of decreased signal on the contrast-enhanced sequences and
of signal loss on opposed-phase imaging when decreased signal was observed
were expressed as percentages. The Blyth-Still-Casella procedure was used to
derive exact CIs for these percentages. All statistical computations were
performed using StatXact, version 6.2.0 (Cytel Software).
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When correlating the decreased signal on the contrast-enhanced sequences with the T2-weighted sequences, no focal abnormality in T2 signal was seen in any of the patients. When correlating the decreased signal on the contrast-enhanced sequences, three patients showed signal loss on opposed-phase imaging when compared with the in-phase sequences at the same z-axis level. Eighteen (85.7%) of 21 did not show signal loss on opposed-phase imaging (Figs. 1A, 1B, 1C, 1D, 1E, 2A, 2B, 2C, 2D, 2E, 3A, 3B, 3C, and 3D). All 21 patients showed no focal signal abnormality on the in-phase images.
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The process may be confused for a primary hepatic neoplasm or more commonly as a metastasis in a patient with a known extrahepatic neoplasm. There are a number of imaging findings that suggest its benign nature including the typical location, presence of geometric borders, and visualization of the hepatic vasculature traversing the region without distortion or interruption. On unenhanced CT, nonspecific low attenuation may be seen in this region. At MRI, the diagnosis of focal fatty deposition can be made by exploiting in- and opposed-phase gradient-echo T1-weighted sequences [14, 15].
In- and opposed-phase imaging takes advantage of the fact that MR voxels that contain similar amounts of fat and water will lose signal on opposed-phase imaging when compared with in-phase images. This is because during gradient-echo sequences, the protons in fat and water resonate in phase and out of phase depending on the TE and field strength of the magnet. At 1.5 T, protons are in phase at approximately 4.4 milliseconds and out of phase at 2.2 milliseconds [15]. Current data acquisition techniques allow both of these echoes to be obtained in the same sequence during a single short breath-hold. The in- and opposed-phase images can then be interleaved. By viewing the in- and opposed-phase sequences interleaved, subtle changes of fatty infiltration (which appear dark on opposed-phase images relative to in-phase images) or T2* susceptibility effects such as iron deposition (which appear dark on in-phase images when compared with opposed-phase images) may be detected.
It is unclear why geographic fatty infiltration should affect the anterior medial aspect of the medial segment of the liver. It has been hypothesized that fatty infiltration and focal areas of fatty sparing in the liver are likely related to local disturbances in hepatic blood flow that cause alterations in metabolism [1, 4–10]. Several studies using combined CT hepatic arteriography and CT arterioportography have shown aberrant vascular supply and drainage corresponding to these geometric regions of decreased enhancement [12, 13]. Another angiographic study found that a draining abdominal wall vein, the vein of Sappey, drained directly into the anterior medial aspect of the medial segment of the liver [10]. In this patient, fatty deposition was present in the region based on low attenuation on unenhanced CT. Moreover, in patients who have superior vena cava obstruction, increased venous collateral flow into the medial segment of the left lobe of the liver may be present on early phase imaging in exactly the same location as typically seen with focal fatty deposition [16]. The early hyperenhancement seen in this area of the liver in superior vena cava obstruction usually becomes isoenhanced to adjacent hepatic parenchyma on delayed phase imaging. This observation has been shown to be due to aberrant non–portal venous drainage into the left lobe of the liver [16].
We have observed that the geographic low signal in the medial segment seen on contrast-enhanced imaging does not always correlate with loss of signal on opposed-phase imaging. In the current study, we attempted to determine how often this finding was present on contrast-enhanced MRI and how often it reflected underlying focal fatty infiltration. We found that in the majority of cases in which this finding was present on contrast-enhanced imaging, it was not seen as signal loss on opposed-phase imaging. In fact, in 18 (85.7%) of the 21 patients in whom the finding was present during the portal venous phase of hepatic enhancement, signal loss on opposed-phase imaging was not shown.
Our findings are similar to a previous study evaluating geometric low-signal perfusion abnormalities in the liver at contrast-enhanced MRI [11]. In that study, low-signal perfusion abnormalities were seen in 15 (13%) of 103 patients [11]. Twelve were in segment IV, and all were seen during the venous phase of enhancement with variable visualization during the arterial and equilibrium phases. Moreover, in only one of the 15 cases was signal loss shown on opposed-phase imaging. Our study, in contrast to the prior study, used a breath-hold dual-echo in- and opposed-phase acquisition. On the PACS, these images can be interleaved, which allows improved z-axis location evaluation of the in- and opposed-phase imaging data. This theoretically should allow better evaluation of subtle changes in signal intensity differences between in- and opposed-phase data.
As has been previously shown, and as we have shown, focal decreased signal seen on contrast-enhanced MRI in the anterior medial aspect of segment IV is common. These areas are likely related to different venous inflows and drainages and not focal fatty deposition [11–13]. Indeed, during the arterial and equilibrium phases of hepatic enhancement, the focal area of decreased signal was not present in 14 and 16, respectively, of the 21 patients with decreased signal on the venous phase. This observation, coupled with the fact that in the majority of cases no signal loss was seen on opposed-phase imaging, suggests that the process is usually due to variations in hepatic blood flow without focal fatty deposition.
There are several limitations to this study. First, histologic proof was not present. However, MRI using in- and opposed-phase dual-echo acquisition has become the imaging standard for diagnosing fatty deposition and is used not only in the liver but in the adrenal gland to diagnose lipid-rich adenomas and in the kidney to diagnose angiomyolipomas [1, 3, 14, 15]. Moreover, the T1-weighted in-phase images and the T2-weighted imaging sequences showed no focal abnormality in the region. On none of the contrast-enhanced acquisitions was a capsule or pseudocapsule present to suggest neoplasm. Second, confirmation that the cause of the low signal at venous phase imaging was due to accessory venous drainage was not established. However, to confirm this angiographically would be invasive, and accessory venous drainage into this region of the liver has been previously established [12, 13]. In addition, the lack of signal loss on opposed-phase imaging and the change in appearance during different phases of contrast enhancement strongly support a perfusion abnormality as the cause.
In conclusion, our study showed that focal decreased signal in the anterior medial aspect of the medial segment of the liver is not rare and is seen in up to 16.5% of cases during the venous phase of hepatic enhancement at gadolinium-enhanced MRI. We noted fatty deposition in only 14% of cases. In most cases, signal loss on opposed-phase imaging was not present at the same z-axis position as the decreased signal on the venous phase of enhancement. Our results suggest that there is 99% confidence that low signal at gadolinium-enhanced MRI in this location will be associated with signal loss on opposed-phase imaging in less than 40% of cases.
Thus, although low attenuation or signal adjacent to the falciform ligament may represent focal fatty infiltration, it usually does not. When geographic low signal is seen on contrast-enhanced imaging in the anterior medial segment but does not show focal fat on opposed-phase imaging, a perfusion abnormality should be considered rather than a neoplasm.
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