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Shear Stiffness (kPa)
68
14 Magnetic Resonance Elastography (MRE) to Assess Hepatic Fibrosis
115
postprocessing employs a multimodel direct inversion
(MMDI) algorithm [17]. A condence map, indicating where
the inversion algorithm is unreliable (noisy data), is displayed as a checkerboard overlay on the stiffness map to
highlight regions of low condence. Liver stiffness is calculated as an average of measurements from ROIs placed at
multiple liver slice levels while avoiding the checkered
regions [14].
14.2 MRE Performance
Technical failure rates with MRE are small, reportedly
occurring in 2–5% of scans [14, 18]. Liver MRE is repeatable and reproducible with high inter- and intra-observer
agreement [19–22]. Liver stiffness measurements with MRE
have also shown to be comparable across vendors [23, 24],
and the reported accuracy is superior to routine serum liver
function tests for detection of signicant and advanced brosis [25–27]. The major advantage of MRE over ultrasound-
< 2.5 = Normal
2.5 to 2.9 = N or Inflammation
2.9 to 3.5 = Stage 1-2
3.5 to 4.0 = Stage 2-3
4.0 to 5.0 = Stage 3-4
> 5.0 = Stage 4
Fig. 14.2 Range of MRE stiffness values (kPa) used to stage liver
brosis and color representation of liver stiffness range on elastograms
associated with brosis stage
Normal
Stg. 1 Stg. 2
Stg. 3
024
Infl.
Stg. 4
based techniques is the large eld of view enabling
assessment over a much larger liver volume. This is particularly important given the heterogeneous distribution of diffuse liver disease. Patient factors are also less likely to affect
MRE compared to ultrasound-based quantitative elastography. In a review of 153 studies, MRE was the only noninvasive technique with reasonable accuracy for diagnosis of
mild brosis [27]. Furthermore, it has been suggested that
MRE may be useful for predicting inammatory change in
patients with nonalcoholic steatohepatitis before development of brosis [28].
Fibrosis detection and staging: The normal liver is soft and
has a mean stiffness value of 2.05–2.44kPa with reported
ranges from 1.54 to 2.87 [23, 29–31]. Liver stiffness increases
with the development of brosis. MRE detects liver brosis
before the development of morphological changes seen on
cross-sectional imaging. MRE has a reported accuracy of
89–99%, sensitivity of 80–98%, and specicity of 90–100%
[13, 25, 26, 28–32]. The threshold for detecting liver brosis
ranges from 2.4 to 2.93kPa [13, 16, 25, 28–33]. The variation
in threshold for detection may be related to population variation with different liver disease etiologies. MRE stiffness
thresholds used for staging liver brosis are shown in Fig.14.2
[14]. The overlap between threshold values for brosis stage
indicates the importance of interpreting liver stiffness measurements within clinical context and test results.
Liver stiffness is calculated as an average using regionsof- interest placed at four to six axial levels through the liver.
A liver stiffness of less than 2.5kPa is generally considered
normal. Images from a patient with an average liver stiffness
of 1.6 kPa consistent with normal liver (no brosis) are
shown in Fig.14.3.
The severity of liver brosis can be readily identied with
application of a color scale to the stiffness values of the elastogram. For example, the images of two patients with a different
brosis stage due to chronic liver disease are shown in Fig.14.4.
Typically, diffuse liver disease is heterogeneous as shown
in Fig. 14.5. The variation in liver brosis can be readily
a b c
Fig. 14.3 MRI images from a patient with a normal liver. (a) Axial
T2-weighted image showing liver outlined by a white line. (b) MRE
phase/wave image through the liver. (c) Color elastogram with checker-
board overlay to highlight regions of low condence; the liver is purple/
blue based on the color scale. The average liver stiffness was 1.6kPa
indicating normal stiffness
116
ab
ce
A. Qayyum
Fig. 14.4 Color elastograms from two patients with chronic liver dis-
ease. (a) In the rst patient, the average stiffness of the liver (outlined
by broken line) was 3.5kPa (mainly green) corresponding to a brosis
stage of 2–3. (b) In the second patient, the average liver stiffness was
8kPa (mainly red) corresponding to brosis stage 4
a
bd f
Fig. 14.5 Patient with nonalcoholic steatohepatitis. (a) T1-weighted
image of the liver (outlined by a white line). (b) Fat fraction map; the
estimated liver fat fraction was seven (mild steatosis). (c) MRE magnitude image. (d) MRE wave image. (e) Color MR elastogram demonstrating heterogeneous liver color/stiffness. (f) MR elastogram with
checkerboard overlay to highlight regions of low condence. The liver
biopsy of this patient demonstrated stage 1 portal brosis. However, the
average liver stiffness derived from measurements obtained at multiple
levels in the liver was 3.9kPa corresponding to a higher overall brosis
stage of 2–3
identied on the color MRE elastogram and highlights how
a liver biopsy can result in incorrect estimation of brosis
stage depending on the region sampled.
As mentioned above, shear waves propagate faster in
stiffer tissue and are associated with a longer wavelength.
The longer wavelength is represented by the width of propa-
gating waves on the MRE wave as shown in Fig.14.6. The
longer wavelength is reected in the arbitrary color scale
assigned to the shear stiffness values.
Liver brosis that is detected on MRE may not be apparent on conventional MR images as shown in Fig.14.7. The
greater sensitivity of MRE for detection of liver brosis has
14 Magnetic Resonance Elastography (MRE) to Assess Hepatic Fibrosis
abc
117
Fig. 14.6 Patient with stage 4 brosis. (a) Gray scale and (b) Color
MRE wave images demonstrate wide shear waves (arrows) in the liver
due to long wavelength. (c) Color elastogram with large regions of red
a
arbitrarily selected to indicate higher stiffness within the liver (outlined
by white line). The liver stiffness was 6.8kPa consistent with stage 4
brosis
b
Fig. 14.7 Liver images from a patient with nonalcoholic fatty liver
disease, which affects one in three Americans. The conventional liver
MRI exam showed no evidence of brosis. (a) T1-weighted image of
resulted in an increased incorporation of MRE to routine
liver MRI for assessment of liver disease.
14.3 Pitfalls inStiness Measurement
Liver stiffness measurements require manual segmentation
of the liver on the MR images while avoiding regions of low
condence in the liver. It is also important to avoid nonhepatocyte tissues such as major blood vessels, and areas suscep-
the liver (outlined in white). (b) MRE color elastogram demonstrating
extensive red color within the liver consistent with increased liver stiffness and advanced brosis
tible to artifact such as the left liver (cardiac pulsation
artifact), diaphragm and liver edges (partial volume averaging effect causing an articial increased stiffness). Tumors
within the liver should not be included when assessing background liver stiffness since tumors and tumor thrombus are
associated with higher stiffness levels compared to nontumor
liver parenchyma. For example, Fig. 14.8 shows images
from a patient with extensive inltrating hepatocellular carcinoma (HCC) and portal vein tumor thrombus resulting in
marked increased stiffness of the liver. However, the
118
A. Qayyum
a
ce
bd f
Fig. 14.8 A 44-year-old man with inltrating HCC and tumor throm-
bus. (a) T2-weighted image. The liver (outlined by white broken line)
has extensive high T2-signal intensity due to inltrating HCC (asterisk). Expansile tumor thrombus (arrow) is seen in the right and left portal vein. (b) Contrast-enhanced image. (c) MRE magnitude image. (d)
MRE wave image with color. The wide bands of color indicate longer
wavelength and faster wave speed. (e) Color elastogram showing predominantly red color within the liver consistent with increased stiffness. (f) Color elastogram with checkerboard overlay to highlight
regions of low condence. Although the liver stiffness is measured at
>6kPa, this cannot be interpreted as brosis since the tumor and portal
vein tumor thrombus will contribute to the high liver stiffness
increased stiffness is likely due to tumor and tumor thrombus
in the portal vein rather than reecting liver brosis. When
measuring liver stiffness, it is helpful to use the magnitude
image for anatomical guidance in order to correctly match
locations to the elastogram (use table position/slice location
parameters). Matching anatomy facilitates identication of
focal lesions on the elastogram. Follow-up imaging should
use similar liver locations to the baseline scan [34].
14.4 Technical Limitations
There are several technical and biological factors that can
affect the success of an MRE exam including:
1. Transducer failure and incorrect settings (e.g., incorrect wave
frequency and amplitude) and incorrect placement of the passive driver (driver does not overlie the liver). Additional factors that result in MRE failure are poor contact between the
passive driver and patient, loose connection between the plastic tube and passive driver and failure to synchronize the
active driver with the MRE sequence (Fig.14.9).
2. Patient motion, as shown in Fig.14.10, can degrade the
MRE image, and intrinsic confounders, e.g. increased
liver iron (reduces MRI signal), and post-prandial
increased portal blood ow to the liver (increases liver
stiffness). In the past, failure rates were more common at
higher eld strengths (3T) but these have been addressed
by the improvement in pulse sequences. For example,
ascites and high BMI are not signicant causes of technical failure with up-to-date MRE techniques. Based on a
recent meta-analyses, the overall technical failure rate of
MRE is approximately 2%, and most commonly due to
iron overload in the liver.
Several tactics can enhance the diagnostic quality of MRE
exams. MRE data should be obtained at end expiration since
this enables a more repeatable diaphragm position than endinspiration and reduces respiratory motion artifact.
Performing MRE with sequences that have a shorter echo
time, such as spin-echo echo-planar imaging (EPI), reduces
signal loss from increased liver iron. Imaging patients in a
fasting state (4–6h) reduces the likelihood of post-prandial
portal blood ow related articial increase in liver stiffness
[35, 36]. The time-to-echo (TE) for MRE should be near or
at the TE of in-phase imaging to maximize signal intensity of
the liver parenchyma and avoid loss of signal from liver fat.
Updated postprocessing techniques should be used as they
continue to evolve. For example, the newer multimodel
direct inversion (MMDI) algorithm has better image quality
and slightly lower stiffness values compared to the previously used multiscale direct inversion algorithm (MSDI) at
3T magnet strengths [17]. An average liver stiffness should
be obtained using multiple regions-of-interest carefully
placed in the liver to reduce the effects of heterogeneous disease distribution.
ab
cd
14 Magnetic Resonance Elastography (MRE) to Assess Hepatic Fibrosis
ab c
119
Fig. 14.9 Driver failure due to improper connection of coupling tube.
(a) Phase image which appears “at” without wave visualization. (b)
Color map of waves on phase image showing signal loss (dark region).
(c) Elastogram with checkerboard overlay showing regions of low condence throughout the image. Stiffness measurements are not possible
Fig. 14.10 MRE failure due to severe respiratory motion artifact. (a)
Magnitude image demonstrating phase encoding artifact causing an
overlap/ghosting in the image. (b) Color map of waves on phase image
showing signal loss (dark region). (c) Color map of elastogram (stiff-
ness map) with motion artifact. (d) Elastogram with checkerboard overlay highlights regions of low condence throughout the image. Stiffness
measurements are not possible
120
A. Qayyum
Advances in MRE: Current commercially available
MRE packages employ a two-dimensional wave propagation model (2D MRE), which assumes that shear waves
propagate in the plane of acquisition while ignoring waves
traveling in an oblique direction. This assumption may
result in an overestimation of liver stiffness. More recently,
3D MRE has been introduced, employing imaging the wave
motion and processing the wave images in three dimensions to calculate tissue stiffness. The 3D MRE offers more
reliable and repeatable measures of liver stiffness with
larger liver coverage, as well more accurate assessment of
focal liver lesions. In addition, 3D MRE allows measurement of the subcomponents of the complex shear modulus,
i.e. the real and imaginary components, which represent the
elastic (storage modulus, G’) and viscous (loss modulus,
G”) properties of tissue, respectively. Such quantitative
biomarkers are promising for the non-invasive assessment
of histopathologic processes such as inammation UCSF
[14, 37, 38].
14.5 Summary
Liver MRE is a robust technique for liver stiffness quantication. Currently MRE is the most accurate non-invasive method
for detection and staging of liver brosis. Advances in MRE
technology may further our understanding of diffuse and focal
liver disease and improve patient management in the future.
Acknowledgments Richard L. Ehman, M.D. Mayo Clinic,
Rochester,MN.
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FDG-PET forManagement
onHepato- Pancreato- Biliary Disease
KojiMurakami
15
Abstract
PET (Positron Emission Tomography) has a unique feature that is visualized “metabolic activities” of cell, or tissue. Malignant tumors including hepato-pancreato-biliary
cancer (HPBC) usually shows hypermetabolism of glucose to be depicted clearly by using FDG-PET.PET has
the advantage of being able to survey the entire body
because it covers a wide area, but on the other hand,
because of its low spatial resolution, it is not suitable for
detecting small lesions. From such features on FDG-PET,
the major roles for HPBC are staging (detecting lymph
node, distant metastases), response assessment for
chemo(radiation) therapy, and early detection of recurrence (surveillance). But recent advancement of PET/CT
camera enables us to detect small lesions which were
missed by other imaging modalities. We should have a
good understanding of the characteristics of FDG-PET
and use it successfully in the management on HPBC
patients.
15.1 Introduction
FDG-PET is said to be one of the most rapidly popular diagnostic imaging modalities in this century not only in Japan
but in major advanced countries. However, since PET examination requires a large amount of capital investment, facilities at which PET is available are still limited. PET equipment
has been introduced mainly in major institutions or diagnostic imaging centers in big cities. Although numerous middlesized and small hospitals cannot economically afford to
introduce PET, physicians can refer their patients to facilities
where PET is available. Therefore, it is essential for general
K. Murakami (*)
Department of Radiology, Graduate School of Medicine, Juntendo
University, Tokyo, Japan
e-mail: k-murakami@juntendo.ac.jp
physicians to gain accurate knowledge about PET, including
the appropriate indications for PET in order to select patients
for referral to PET facilities.
General speaking, PET is not always a useful tool especially for detecting small lesions because of its low spatial
resolutions. Main purpose of performing PET in malignant
tumor are to detect lymph node and distant metastases for
staging, response assessment for chemo (and/or radiation)
therapy, and early detection of recurrence (surveillance). But
these indications of PET are a little bit different according to
the organs and disease. In this article, we review the indications for PET (or PET/computed tomography [CT]) using
FDG of the liver, biliary tract, and pancreas.
15.2 FDG-PET Examination forLiver
Cancer
15.2.1 PET forHepatocellular Carcinoma (HCC)
HCC is known to show low FDG accumulation. This can be
explained based on the mechanism of FDG uptake in tumors.
FDG is an analogue of glucose, and when injected into the
body, it is taken up by the cells and phosphorylated in the
same pathway as glucose. The metabolic process of FDG is
the same as that of glucose up to this point, but the reactions
of FDG do not proceed further (Fig.15.1). In other words, the
FDG remains in the cells as phosphorylated FDG. On the
other hand, because dephosphorylating enzyme activity is
higher in hepatocytes than in other tissues, it is likely that the
glucose accumulated in normal hepatocyte is dephosphorylated again and excreted out of the cells. As activity of dephosphorylating enzyme is retained in well-differentiated HCC,
the tumor shows relatively low FDG accumulation (Fig.15.2).
Another reason of low FDG uptake in well- differentiated
HCC is that the expression of the glucose transporter at the
surface of cell is fewer compared to other types of malignant
tumors. On the other hand, poorly- differentiated HCC has
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022
M. Makuuchi et al. (eds.), The IASGO Textbook of Multi-Disciplinary Management of Hepato-Pancreato-Biliary Diseases,
https://doi.org/10.1007/978-981-19-0063-1_15
123
124
*
Glu-Trans
K. Murakami
ATP ADP
Glycogen
Hexokinase
Glucose
18
FDG
Fig. 15.1 Schema of metabolic pathway in cells of glucose and 18-F-
FDG.FDG take same pathway as glucose till phosphorylation, though
it does not progress further. Most malignant cell is known to have over-
Glucose
18
FDG
Phosphatase
Hexokinase
Phosphatase
weak enzyme activity to show strong FDG uptake [1, 2]. As
the FDG uptake vary with the degree of differentiation of
HCC, we may be able to predict, to some extent the degree of
differentiation of HCC by the degree of FDG uptake, even
though FDG-PET is not useful for the detection. Furthermore,
because poorly differentiated HCC is frequently associated
with metastasis and recurrence, FDG/PET is useful for detecting such metastasis/recurrence to be able to survey whole
body (Fig.15.3) [3]. The degree of histological differentiation
is thought to be correlated with the prognosis, and the poorer
the degree of differentiation of the HCC, the poorer the prognosis is. Thus, FDG-PET offers the promising tool for predicting the prognosis of HCC [4, 5].
15.2.2 PET forCholangiocellular Carcinoma
(CCC)
CCC is histologically classied as adenocarcinoma, and usually shows increased FDG uptake (Fig.15.4) [6, 7]. However,
since both poorly differentiated HCC and metastatic hepatic
carcinoma usually shows marked FDG uptake, it is difcult
to differentiate these malignant liver tumors based on the
uptake of FDG alone. Other morphological diagnostic imaging such as dynamic CT or magnetic resonance imaging
(MRI) are indispensable for reference.
G-6-PO
4
CO
2
H2O
18
FDG-6-PO
TCA
cycle
4
**
expression of glucose transporter (asterisk) and low activity of phosphatase (double asterisk)
Moreover, diagnostic “high-resolution” imaging tools,
such as direct contrast radiography, endoscopic ultrasound
(EUS), intraductal ultrasound (IDUS), contrast-enhanced
CT and MRI, are sufcient for diagnosing the stage of primary lesions, so that clinical signicance of PET is of little
value for the diagnosis of the T factor in CCC.On the other
hand, PET may be used as a complementary diagnostic tool
for the diagnosis of lymph node metastases when diameter of
which are below 10 mm. FDG positive lymph nodes less
than 10mm in diameter suggests a high probability of metastatic lymph node that is difcult to estimate as metastasis
only by CT criteria.
PET is also expected to be useful for detecting the presence/absence of distant metastases and diagnosing recurrent
disease in CCC.In particular, PET is useful for the diagnosis
of distant metastasis, as demonstrated by a study which
showed that the treatment policy was determined by PET in
17% of the cases [8], or changing the treatment policy in
30% of the cases [9]. PET also has an excellent ability to
diagnose recurrent disease, which is difcult to detect after
hepatic resection or bile duct resection, in view of its excellent contrast resolution.
There are two major pitfalls to be known. One is FDG
uptake in inammatory tissue, such as cholangitis which causes
false positive. Another is weak FDG uptake in slow growing or
brosis abundant tumor which cause false negative.
15 FDG-PET forManagement onHepato-Pancreato-Biliary Disease
125
a
b
c
Fig. 15.2 A case of well-differentiated HCC. (a, b) Arterial and portal phase of dynamic CT.Typical enhancement pattern of HCC was shown;
(c) FDG-PET.There was no FDG uptake
15.2.3 PET Examination forMetastatic Liver
Cancer
glucose level, respiratory movements during data acquisition
as external factors, so and so. Thus, the FDG uptake may dif-
fer between the primary and metastatic lesions depending on
The visualization of liver metastases may depend on the histological characters of the primary lesion. In general, when
the primary lesion shows marked FDG uptake, the metastases also shows increased FDG uptake. However, the visualization of metastases on PET is also inuenced by other
factors, e.g., such as the tumor size, cell density, presence of
bleeding/necrosis as tumor-related factors, and the blood
the aforementioned factors.
As compared with other imaging modalities, PET is not
the most suitable for the detection of small lesions because
of its poor spatial resolution. Even if liver tumors show FDG
avidity, tumor uptake of FDG must be stronger than the
physiological liver uptake to be clearly recognized. Even
considering these factors, it is sure that both the contrast