Fundamentals of

Body MRI
 Fundamentals of
Body MRI

Christopher G. Roth, MD
Vice Chairman
Methodist Division
Department of Radiology
Thomas Jefferson University
Philadelphia, Pennsylvania
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

FUNDAMENTALS OF BODY MRI ISBN: 978-1-4160-5183-1

Copyright © 2012 by Saunders, an imprint of Elsevier Inc.

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I dedicate this book to my family …
… to my grandparents whose spiritual will to pursue intellectual advancement
provided me role models and confidence to pursue my own education and intel-
lectual enrichment.
… to my mother whose support and academic and professional achievements
served as my inspiration.
… to my father whose support, intellectual curiosity, encouragement, and liter-
ary exploits helped guide me through my academic and literary endeavors.
… to my fiancée, Stephanie, whose unconditional love and support provided
me the sustenance I needed to complete this work.
… I dedicate this book to our future.
Contributor
Sandeep Deshmukh, MD
Clinical Assistant Professor
Methodist Division
Department of Radiology
Thomas Jefferson University
Philadelphia, Pennsylvania
MRI of the Pancreaticobiliary System

vii
Preface
I wrote this book rebelling against a number appearance, which is more in sync with the
of trends in medical literature—a tendency to reader’s perspective than the encyclopedic style
write exclusively in the passive tense, a predi- of organizing by disease entity. This format
lection for the encyclopedic method, a distaste more closely mirrors the reader’s experience at
for visual aids (e.g., diagrams, tables), and an the workstation, providing a useful reference for
aversion to the basic science behind the scenes a problematic case or imaging pattern and facili-
of our clinical practice. Some of these trends are tating differential diagnoses. Hopefully, absten-
easier to avoid than others. Tackling the science tion from the passive tense further enhances the
of body MRI and composing a basic introduction readability of this text.
to MRI physics was definitely the most difficult. In writing a “fundamentals” text, my goal was
Once you pull at the thread, there is no end to to provide a stepping stone to a comfort level
the unraveling; in MRI physics, each of the many with body MRI—both technically and clinically.
abstract concepts are predicated on multiple My intent was to provide in-depth useful infor-
others, inviting an endless series of intercon- mation and commentary on the bread-and-
nected explanations, and I feel like an inhabitant butter material accounting for most of what is
in the M. C. Escher lithograph, “Relativity” seen in clinical practice, deferring on the more
(depicting a network of impossibly intercon- advanced applications and exotic diseases.
nected staircases constructed in different dimen- Advanced body MRI applications, such as pros-
sions). I sacrificed comprehensiveness in this tate, breast, and cardiovascular MRI, were con-
regard for a concise, common sense approach sciously excluded. For these topics, I refer you
to MRI physics and introductory concepts in to many worthy texts and review articles.1–9
Chapter 1 with the liberal use of visual aids This book has been long overdue—as one of
and sparing use of abstract concepts and the most complex fields in radiology, body MRI
equations. needs a “fundamentals” text. It’s my hope that
In the clinical chapters (Chapters 2 to 5), this book fulfills this need and it was my honor
I resisted the encyclopedic style in favor of and privilege to write it.
a reader-oriented approach, where possible. Christopher G. Roth
Most of the text is arranged by the imaging

1. Siegelman ES. Body MRI. Philadelphia: Saunders, 2005. 6. Morris EA, Liberman L. Breast MRI. New York: Springer,
2. Semelka RC. Abdominal-Pelvic MRI, 2nd ed. Hoboken, 2005.
NJ: Wiley-Liss, 2006. 7. Hendrick RE. Breast MRI: Fundamentals and Technical
3. Lee VS. Cardiovascular MRI: Physical Principles to Practi- Aspects. Secaucus, NJ: Springer Science and Business
cal Protocols. Philadelphia: Lippincott Williams & Media, 2008.
Wilkins, 2006. 8. Bard RL. Dynamic Contrast-Enhanced MRI Atlas of Pros-
4. Bogaert J, Dymarkowski S, Taylor AM. Clinical Cardiac tate Cancer. Berlin: Springer, 2009.
MRI. Berlin: Springer, 2005. 9. Verma S, Rajesh A. A clinically relevant approach to
5. Kwong RY. Cardiovascular Magnetic Resonance Imaging. imaging prostate cancer: Review. AJR Am J Roentgenol
Totowa, NJ: Humana Press, 2008. 196:S1–S10, 2011.

ix
Acknowledgments
Without the guidance and support of my who generated the images that I display in my
mentors, this work would not have been possi- book, although there are too many to name
ble. I credit the visionary leadership of our individually.
chair—Vijay Rao—for the fertile clinical and Without the help of my friend and colleague
academic environment of our department in Sandeep Deshmukh, this book would be fodder
which I was able to compose this work. for future generations of radiologists. With his
I largely owe my interest, aptitude, and under- help in finishing the last written (MRI of the
standing of MRI to Don Mitchell. His book, MRI Pancreaticobiliary System) chapter, I was able to
Principles, attracted me to MRI and TJU for complete the work in a reasonable timeframe
fellowship training and provided the foundation and bring the project to fruition.
of my understanding of MRI physics. With his I owe the privilege of writing this book to my
own unique brand of mentorship, George friend Rob Ward, whose recommendation ulti-
Holland also endowed me with a deeper appre- mately landed me this opportunity. I also owe
ciation and understanding of body MRI. him gratitude for suggesting the unique reader-
I’d be remiss not to acknowledge the dili- oriented organization of the chapters and other
gence, efficiency, and industriousness of helpful suggestions along the way. Without his
Angelique Burke, who assisted me with printing friendship and insight, this would not have been
and reprinting and collating drafts during the possible.
revision process. I’d also be remiss in not Christopher G. Roth
acknowledging the countless technologists

xi
 CHAPTER ONE 

Introduction to Body MRI

“spin up”) or (2) anti-parallel to (or “spin down”)
MAGNETIC RESONANCE
to the magnetic field.
IMAGING: WHAT IS THE
The second phenomenon—spin, or angular
OBJECTIVE?
momentum—describes the propensity of a
Magnetic resonance imaging (MRI) exploits the nucleus with net charge to oscillate like a gyro­
inherent magnetism in the protons that consti­ scope (or “precess”) in the presence of a mag­
tute the human body in a creative way by mani­ netic field (Fig. 1-3). The rate of precession is
pulating them with radiofrequency (Rf) energy nucleus-specific and defined by a variable known
in the presence of a strong magnetic field. as the gyromagnetic ratio (γ).
This manipulation induces the protons to emit Resonance capitalizes on nuclear precession
energy, which is detected and reconstructed in MRI. Energy absorption by a precessing
into an image. The human body—not ostensibly nucleus exposed to oscillating energy of equal
magnetic—is effectively magnetized by a strong frequency defines resonance. By altering the
magnet. Once magnetized, Rf energy shifts oscillating frequency, only specific nuclei are
magnetized protons to a higher energy state. selected and energized, establishing the spectro­
Subsequently, the protons release this energy in scopic basis of MRI.
the process of returning to their original low- MRI is founded on these two nuclear
energy state. The released energy is detected in phenomena—spin and magnetic moment—
a specialized receiver (referred to as a coil in occurring only in nuclei with net charge and
MRI parlance). With this information, ultimately applicable only to few nuclei in the human body
images with spatial and molecular information (see Fig. 1-1). Among the biologically occurring
are reconstructed without harmful effects to the magnetically active nuclei, it is the hydrogen
patient (such as ionizing radiation). nucleus (1H) that serves as the substrate for MRI
because of its large magnetic moment (propor­
tional to the magnetic resonance [MR] “signal,”
MAGNETISM: HOW IS THE
or emitted energy converted to visual images)
HUMAN BODY MAGNETIZED?
and abundance in the human body (i.e., fat and
The process of magnetizing the human body water molecules).
actually invsolves only select magnetically active
nuclei (Fig. 1-1). The term magnetically active
nuclei refers to those nuclei with unpaired THE COMPONENTS
protons or neutrons. These magnetically active
The Magnet
nuclei harbor a net charge—the requisite pro­
perty for interaction with a magnetic field The heart of the MRI apparatus is the magnet,
(although neutrons have no actual net charge, or main magnetic field—referred to as B0.
the distribution of component charges is not Without a strong external magnetic field, the
uniform). body’s protons align themselves randomly,
This interaction involves two phenomena— yielding no net magnetization and, therefore, no
magnetic alignment and spin, or angular potential signal to convert to an image when
momentum. Magnetic alignment describes the subjected to Rf energy. The vector sum of the
tendency of the magnetically active nucleus (or randomly aligned proton magnetic poles is
“magnetic moment,” or “spin”)—a miniature zero—they cancel each other out. In the pres­
magnet itself—to align along the orientation of ence of a strong magnetic field—B0—protons
an external magnetic field (Fig. 1-2). The align­ align themselves parallel and anti-parallel to the
ment of these magnetic moments is quantized magnetic field (see Fig. 1-2).1 Because more
into one of two energy states: (1) parallel to (or protons align parallel versus anti-parallel to the
1
2  •  Fundamentals of Body MRI

Element Protons Neutrons Nuclear Gyromagnetic Natural Angular

Spin Ratio Abundance Momentum
(MHz/T) (%) (MHz)
1H 1 0 1/2 42.5774 99.985 63.8646
(Protium)
2H 1 1 1 6.53896 0.015 9.8036
(Deuterium)
3He 2 1 1/2 32.436 0.000138 48.6540

12C 6 6 0 0 98.90 0
13C 6 7 1/2 10.7084 1.10 16.0621
14N 7 7 1 3.07770 99.634 4.6164
15N 7 8 1/2 4.3173 0.366 6.4759
16O 8 8 0 0 99.762 0
17O 8 9 5/2 5.7743 0.038 8.6614
23Na 11 12 3/2 11.2686 100 16.9029
31P 15 16 1/2 17.2514 100 25.8771

FIGURE 1-1.  Biologically relevant nuclei.

No B0

B0

FIGURE 1-2.  Proton alignment with and without a magnetic field. Left, Randomly oriented protons in the absence of a magnetic field.
Right, Protons oriented parallel and anti-parallel to the magnetic field.

magnetic field, a net magnetic vector (NMV) is a larger NMV—the currency used to fashion MR
created from the protons in an external mag­ images.
netic field (Fig. 1-4). This magnetic vector, rep­ Whereas different types of commercially used
resenting net magnetism, is the basis for creating magnets exist, the superconducting type is most
MR images—the sine qua non of MRI. Creating clinically relevant to body MRI. Body MRI appli­
this magnetism explains the need for a strong cations require high magnetic field strength (at
magnetic field. The stronger the magnetic field, least 1.0 Tesla and optimally 1.5 Tesla) in order
the greater the discrepancy between parallel to image rapidly with adequate signal-to-noise
and anti-parallel spins, with fewer aligning anti- ratio (SNR). Resistive magnets top out at 0.5
parallel in the higher energy state. The result is Tesla and permanent magnets are also generally
 Introduction to Body MRI  •  3

manufactured at lower magnetic field strengths the Rf pulse exciting the magnetized protons.
(≤0.7 Tesla) not optimized for body MRI appli­ Four components constitute the Rf transmitter
cations. Conceptually, the superconducting system: the frequency synthesizer, the digital
magnet is a large solenoid composed of super­ envelope of Rfs, a high-power amplifier, and an
conducting wire (i.e., niobium-titanium or antenna in the form of a “coil.” The net effect is
niobium-tin), which is supercooled (with liquid generation of an Rf pulse to excite the magne­
helium or nitrogen) (Fig. 1-5).2 Superconducting tized protons by exploiting MR.
wire cooled appropriately permits the flow of In order to explain this process and the
electric current with virtually no resistance. By concept of MR, a basic understanding of nuclear
virtue of the thumb rule (officially Ampere’s physics and magnetism is necessary. As men­
Law), the result is a magnetic field oriented tioned earlier, protons in a magnetic field
along the axis of the solenoid (B0). become aligned, and the body becomes
magnetized. In addition to aligning parallel or
anti-parallel to B0, the protons rotate—or
Rf System
precess—around their magnetic axis, referred
Another key component of the MRI apparatus to as magnetic spin (see Fig. 1-3). The angular
is the Rf transmitter system that generates momentum (ω0) and, accordingly, the frequency
of precession (f0) vary according to the strength
of the magnetic field (B0) and the gyromagnetic
ω0 = γB0/2π ratio (γ), which is a function of the specific
or
F0 = γB0 properties of the nucleus—expressed by the
Larmor equation:

ω 0 = γ B 0 / 2π

which simplifies to

f0 = γ B 0

Magnetic spins precessing at the frequency of

the Rf pulse will absorb energy and move to the
higher energy state. Thereafter, excited pro­­tons
B0 “relax,” emitting the absorbed energy and
returning to their original low-energy state. The
FIGURE 1-3.  The concept of a nuclear spin. emitted Rf energy constitutes the signal that

Parallel
(low energy)

Net
magnetic
vector

Anti-parallel
(high energy)
B0

FIGURE 1-4.  The net magnetic vector (NMV) concept.

4  •  Fundamentals of Body MRI

ultimately generates an MR image. Conceptu­ distorts the magnetic environment in order to

ally, the NMV is aligned parallel to B0 preceding selectively excite a region—or slice—of tissue at
the Rf excitation pulse. The Rf excitation pulse a time to facilitate image generation and to send
shifts spins into the higher energy state and the spatial information into the excited volume of
NMV away from the longitudinal axis of B0 into protons. The gradient system includes three sep­
the transverse plane. So, initially, the NMV is arate gradients each designed for its designated
longitudinal—parallel to B0—and tilted by the Rf orthogonal plane: x, y, and z (Fig. 1-7). Each gra­
excitation pulse away from B0 into the trans­ dient is a coil through which current passes to
verse plane (Fig. 1-6). The transverse compo­ induce changes in B0. Each gradient induces a
nent of the spin vector ultimately constitutes the linear variation in the main magnetic field (B0)
MR signal.3 along its respective axis. In other words, a gradi­
ent alters the B0 along a scale such that the mag­
netic field strength at one end of the gradient is
The Gradient System
stronger than the other (see Fig. 1-7).
A gradient system (a spatially varying magnetic The z—or slice-select—gradient (Gz or Gs)
field superimposed on spatially uniform B0) establishes the environment in which a specific
slice of protons is excited. By varying the mag­
Current netic field strength along the axis of B0, the
slice-select gradient concordantly varies the pre­
cessional frequency of the protons along the B0
B0 axis. Consequently, an Rf pulse emitted with a
narrow range of frequencies excites only a thin
slice of protons (Fig. 1-8). The narrow range of
frequencies included in the Rf pulse—the trans­
mit bandwidth—thereby determines the thick­
ness of the excited slice protons. This slice of
B

excited protons ultimately constitutes the MR

The hand grip or
thumb rule
image.
X- and y-gradients incorporate additional
spatial information into the excited slice of
protons, allowing the emitted MR energy to
FIGURE 1-5.  Schematic of a superconducting magnet. be converted into an MR image. The gradients

More spins in
higher energy state
Low High
energy energy

Spins moving to
higher energy state

NMV Rf
excitation
pulse
NMV

FIGURE 1-6.  Net magnetic vector (NMV)

tilted by the radiofrequency (Rf) excita- B0
tion pulse.
 Introduction to Body MRI  •  5

X Gradient (Gx) Y Gradient (Gy) Z Gradient (Gz)

B0 B0 B0
B0
z
B0 z
z
y x
x y
x
y
B0

x
y

FIGURE 1-7.  Schematic of a magnetic field gradient.

Gp
B0
Excited
protons

B0

Slower Faster
spins spins
Transmit bandwidth
Gf
FIGURE 1-9.  The frequency-encoding gradient.

Rf pulse 90°
FIGURE 1-8.  Slice-select gradient and the radiofrequency (Rf)
pulse. Rf

Dephasing
lobe
are applied in axes orthogonal to the slice- Gf
Rephasing
select gradient. The x-gradient—or frequency- lobe
encoding gradient or readout gradient (Gx or
Gf)—applied perpendicular to B0—functions Phase
analogously to the slice-select gradient. By
orchestrating a gradient magnetic field, spins FIGURE 1-10.  Frequency-encoding gradient scheme.
vary in precessional frequency along a spectrum
from one end of the excited slice of protons to
the other (Fig. 1-9). Because spins precessing at ortho­gonal axis. Applied briefly, the phase-
different frequencies results in destructive inter­ encoding gradient induces a magnetic field gra­
ference, which reduces the emitted signal, the dient along the final orthogonal axis such that
frequency-encoding gradient is applied in two spins at one end transiently spin faster than
separate phases, or lobes—the dephasing and spins at the opposite end (Fig. 1-11). Thereafter,
rephasing lobes (Fig. 1-10). when turned off, the spins retain their differen­
The y-gradient—or phase-encoding gradient tial phase varying across the phase-encoding
(Gy or Gp)—encodes spatial information into direction. This phase variation constitutes the
the excited slice of protons along the final spatial information along the phase-encoding
6  •  Fundamentals of Body MRI

axis, which is incorporated into the emitted and MRI in Practice, C. Westbrook and C.
resonance signal. Kaut.5-9
This complex sequence of Rf energy and mag­
netic field gradients is precisely timed to accom­
The Receiver System
plish the feat of coaxing a coherent emission of
resonance energy from a specific slice or volume The next pertinent hardware component is the
of protons that can be received by a specialized system designed to receive or capture the
antenna, or coil (Fig. 1-12). Variations on this emitted resonance energy. To review, the com­
basic theme constitute the different pulse ponents discussed to this point include the main
sequences used in MRI—such as spin-echo (SE), magnetic field (B0), the Rf transmitter system,
fast spin-echo (FSE), single-shot fast spin-echo and the gradient magnetic field system. The
(SSFSE), gradient-echo (GE), steady-state free receiver system includes a receiver coil, a
precession (SSFP), and echo planar imaging receiver amplifier, and an analog-to-digital con­
(EPI).4 For a brief discussion of different pulse verter (ADC). A component of the Rf system
sequences, refer to the upcoming section in this previously mentioned—the transmit coil—often
chapter; for more detail on this subject, refer to doubles as the receiver coil. In other words,
texts dedicated to MRI physics—MRI Principles, some coils are send-receive coils—they perform
D. G. Mitchell; MRI Basic Principles and Appli- the dual function of emitting the Rf excitation
cations, M. A. Brown and R. C. Semelka; The pulse and receiving the emitted resonance
MRI Manual, R. B. Lufkin; MRI The Basics, R. signal. Body—abdominal and pelvic—MRI appli­
H. Hashemi, W. G. Bradley Jr., and C. J. Lisanti; cations demand the use of a dedicated torso coil.
Although these devices vary from manufacturer
to manufacturer and from device to device,
Gp torso coils are designed to closely encircle the
body to enhance reception of the emitted reso­
y nance energy. Most torso coils take advantage
of the phased-array configuration, combining
multiple coil elements into a single coil device,
which facilitates the reception of signal and the
performance of parallel imaging (discussed
later).
Because the amplitude of the received signal
is so miniscule (on the order of nanovolts or
Time microvolts), a signal amplifier is a requisite com­
FIGURE 1-11.  The phase-encoding gradient. ponent of the receiver system. The ADC

180°
Spin Refocusing
echo pulse

B0 Excitation
pulse
Rf Phase
encoding
gradient

Gs Excited slice Gf Gp
Volume of protons Slice-select of protons
within magnetic field gradient
Inverted
Gradient frequency
–Gf encoding
echo
gradient

FIGURE 1-12.  Basic pulse sequence schematic.

 Introduction to Body MRI  •  7

converts the received analog signal into digital increasing k-space plotting area augments spatial
data to be processed into image data. resolution.
Each point in k space contains information
from the entire excited cohort of protons. The
K Space and the Fourier Transform
number and distribution of k-space coordi­
The final phase of the process involves decoding nates set by the pulse sequence dictate the
this digitized data into the visual medium of an time required for signal acquisition or “k-space
MR image. This process happens on a computer filling.” K-space filling follows a trajectory
storing the digital data and empowered with the determined by the spatial encoding scheme,
mystical Fourier transform.10 The digital data which varies by pulse sequence. The trajectory
resides in an abstract formulation known as k begins at the origin of k space and is deflected
space. K space is a metaphysical construct peripherally by spatial gradients. For example,
serving as the repository for the raw (pre– consider a simple GE pulse sequence in which
Fourier transform–deciphered) data with fre­ the strongest negative phase-encoding gradient
quency and phase coordinates (Fig. 1-13). The is applied first (Fig. 1-14A). At time zero—the
difficulty in understanding k space arises from Rf excitation pulse—the journey through k
the lack of a visual frame of reference; K-space space begins at the origin—kx0, ky0. The
data bear no direct resemblance to image data. strong negative phase-encoding gradient trans­
Instead of spatial coordinates, k-space data plot ports k space sampling trajectory to point kx0,
along frequency and phase coordinates (in ky-max (maximally negative phase-encoding
cycles/meter). Dividing k space into peripheral gradient strength with no frequency-encoding
versus central regions facilitates understanding gradient). Thereafter, frequency-encoding gra­
its place in image formation. dient dephasing and rephasing yield data
The echoes acquired for each slice of raw data points (the readout) transversely across that
plot into a corresponding k space map for that line of k space horizontally, at the end of
particular slice. K-space coordinates correspond which a single line of k space has been filled.
to the frequency and phase-encoding gradient At the next Rf excitation pulse, the journey
strengths at which the signal is obtained. Central begins at the k-space origin again to be
points in k space represent the data acquired deflected to the next, slightly less negative,
with the weakest gradients. Conversely, the line in k space by a slightly weaker phase-
periphery of k space coincides with signal encoding gradient. Frequency-encoding fills
obtained with the strongest gradients. Stronger this line in the same fashion and the process is
gradients discriminate fine detail at the expense repeated for each line in k space until k space
of signal loss due to dephasing. Weaker gradi­ is filled. The scheme exemplifies cartesian
ents fail to discriminate fine detail, but preserve k-space filling, which rigidly follows a coordi­
signal. Central k-space plots image contrast nate system in k space. Noncartesian k space
information; peripheral k-space plots image trajectory schemes include radial, PROPELLER
detail information. Increasing k-space plotting (Periodically Rotated Overlapping Parallel
density expands the field of view (FOV); Lines with Enhanced Reconstruction), and
kf0, kp0

Kfmax, kpmax kfmax, kpmax

Signal
amplitude ↑ Phase ↓ Signal
↑ Frequency amplitude

Kp 0 Phase ↑ Signal
cycles/m X
0 Frequency amplitude
kf0, kp0
↑ Phase ↓ Signal
↑ Frequency amplitude
Kfmax, kpmax kf cycles/m kfmax, kpmin
FIGURE 1-13.  K-space.
8  •  Fundamentals of Body MRI

kf cycles/m
Following the initial excitation pulse,

Step 1: phase encoding gradient (Gp) deflects

the potential signal to point kx0, kymax

Step 2: frequency encoding (Gf) dephasing

gradient deflects k space trajectory to point
kxmax, kymax
Kp
cycles/m
Step 3: frequency encoding (Gf) rephasing
gradient applied with opposite polarity drives 4
trajectory to kxmax, kymax during which
time readout datapoints 1–7 are collected 1
Gp
Step 4: the next radiofrequency excitation
1 2 3 4 5 6 7
pulse deflects the trajectory back to the
origin of k space

Gf dephasing
2 Gf rephasing
A 3

Radial k Spiral k
B space filling space filling
FIGURE 1-14.  A, Basic (gradient echo) Cartesian k-space trajectory. B, Examples of noncartesian k-space trajectory schemes.

Shim system

Operator’s console Gradient coil

Host computer Transmitter system Magnet

FIGURE 1-15.  Magnetic resonance imaging (MRI) system

System disc Receiver system
schematic.

Operator’s Console
spiral k-space trajectories (see Fig. 1-14B).
These k-space filling techniques involve com­ On the user’s (technologist’s) side, the main
bining gradients during the readout to fill k component is the operator’s console. The oper­
space in novel, potentially more efficient ator’s console is the portal of entry into the main
ways. system computer, which subsequently executes
The purpose of the Fourier transform is to instructions from the operator’s console to the
translate the k-space data in the frequency and system hardware and channels incoming image
phase domain into image data with spatial data to the operator’s console and storage
coordinates. The Fourier transform “solves” module (Fig. 1-15). This is the computer that the
k space for pixel data. The numeric value technologist uses to select the imaging protocol
assigned to each Fourier transform–solved pixel and the sequence parameters and that receives
corresponds to the MR signal amplitude, or the image data decoded by the Fourier trans­
signal. form for review by the technologist.
 Introduction to Body MRI  •  9

180°

90° α°

Rf Rf
TE TE

Gz

Gx

Gy
Spin echo Gradient echo
FIGURE 1-16.  Spin-echo and gradient-echo pulse sequences. TE, time to excitation.

PULSE SEQUENCES
180°, the refocusing pulse inverts the phase
The process of filling k space depends on the difference between spins so that spins ahead in
pulse sequence chosen. Two major types of phase become equally behind in phase after the
pulse sequences dominate body MRI and MRI refocusing pulse. Therefore, in a time period
in general: (1) SE and (2) GE sequences. equal to the time period preceding the refocus­
The presence or absence of a “refocusing pulse” ing pulse, the spins will be aligned. Conse­
characterizes the SE and GE sequences, respec­ quently, the duration of echo generation in an
tively. These two pulse sequences represent dif­ SE pulse sequence (TE) is generally twice the
ferent approaches to the problem of generating time preceding the refocusing pulse, which
signal after the initial Rf excitation pulse. incurs the passage of a significant amount of
The frequency-encoding gradient dephases the time compared with a GE pulse sequence.
excited spins (i.e., destructive interference), However, the benefits outweigh this disadvan­
which must be rephased in order to yield tage under many circumstances. Spins dephase
signal—referred to as an echo of the original Rf not only as a consequence of the frequency-
excitation pulse, reverberating at time TE (time encoding gradient but also because of magnetic
to excitation) after the Rf excitation pulse. Of field inhomogeneities and inherent microenvi­
course, these pulse sequences usually need to ronmental factors (spin-spin interactions)—
be repeated multiple times in order to acquire known as T2* decay. The 180° refocusing pulse
enough data to fill k space for a single image. corrects for these dephasing artifacts at the cost
The interval between Rf excitation pulses is of image acquisition time. In the end, spectral
referred to as TR (time to repetition). considerations dictate the use of these two
In the SE pulse sequence experiment, the types of pulse sequences. The increased time
excited spins are inverted by a 180° refocusing required to obtain T2-weighted sequences
pulse prior to a rephasing lobe of the frequency- demands a longer acquisition time (which is
encoding gradient of equal polarity (Fig. 1-16). discussed in more detail later), conforming to
In the GE experiment, the refocusing pulse is the specifications of the SE sequence. Mean­
omitted and a frequency-encoding rephasing while, T1-weighted sequences benefit from
lobe of reversed polarity reestablishes phase shorter acquisition times, which also minimize
coherence. Advantages and disadvantages of T2* artifacts, favoring the use of GE sequences.
each technique must be acknowledged when Practically speaking, modifications of the pro­
devising MRI protocols.11 totypic SE and GE sequences already described
The implementation of a refocusing pulse are implemented in modern-day body MRI pro­
furnishes SE sequences with two distinctive tocols. These sequences have been adapted to
attributes: (1) increased imaging time and acquire multiple echoes with a single excitation
(2) resistance to artifacts. By flipping the spins pulse, rather than the single-echo scenario
10  •  Fundamentals of Body MRI

180° 180° 180° 180° 180° 180°

90°

Rf

Gz

Gx

Gy
TEeffective

Fast spin echo

FIGURE 1-17.  Multiecho spin-echo and gradient-echo pulse sequence diagrams. TE, time to excitation.

previously described, in order to save time. In transform “solves” the 3-D k-space data in the
the case of the SE sequence, multiple refocusing same way as the 2-D Fourier transform previ­
pulses follow the Rf excitation pulse, each ously described for each individual slice while
producing an echo (Fig. 1-17). The extreme using the z-axis phase-encoded data to partition
example of this multiecho technique is the the information along the slice axis.
SSFSE sequence in which all echoes necessary Using 3-D k-space filling techniques, each Rf
to fill k space for a given image are acquired pulse excites the entire volume of tissue (rather
after a single excitation pulse. Consequently, than a single slice), magnifying SNR compared
the SSFSE sequence robustly corrects suscepti­ with 2-D techniques. In 3-D pulse sequences,
bility artifact and minimizes acquisition time. each voxel of tissue benefits from every excita­
The FSE sequence includes at least two and less tion pulse in the entire sequence, whereas voxels
than all of the refocusing pulses and echoes in 2-D schemes receive only slice-selective exci­
necessary to fill k space; acquisition time and tation pulses (none from the other slices in the
susceptibility artifact resistance of an FSE prescribed ROI). Consequently, 3-D sequences
sequence are greater than a conventional SE yield higher SNRs, permitting the partition of the
sequence and less than an SSFSE sequence. data into smaller fragments, or voxels, generating
GE sequences have also been adapted as mul­ higher spatial resolution and image detail.
tiecho sequences to minimize acquisition time Other GE sequence types used in body MRI
(see Fig. 1-17). Another pulse sequence modifi­ include SSFP and EPI sequences. The SSFP
cation frequently adapted to GE sequences in sequence is a specialized sequence in which an
body MRI is three-dimensional (3-D) imaging. equilibrium quantity of transverse and longitudi­
The basic premise of a 3-D pulse sequence is the nal magnetization is maintained in a steady state.
excitation of a volume of tissue instead of a slice. Tissue contrast—to be discussed in greater
Rather than covering the region of interest detail—is T2-/T1-weighted. The EPI sequence is
(ROI) with individual contiguous slices, the ROI a GE sequence that acquires all the data neces­
is covered with a single volume. Instead of sary to fill k space with 1 Rf excitation pulse. In
acquiring multiple images independently, the body MRI, the EPI sequence is commandeered
3-D technique acquires the volume data set all for diffusion-weighted imaging (DWI). An addi­
at once. During 3-D image acquisition, the tional gradient applied in two phases—with sen­
rephasing lobe of the slice-select gradient serves sitizing and desensitizing lobes—favors signal
as a phase-encoding gradient in the slice axis, from static tissue, which phases and dephases
thereby encoding z-axis spatial information into from the diffusion gradient, yielding no net
the excited volume. While the two-dimensional phase shift. Moving—or diffusing—tissue unpre­
(2-D) approach preempts the problem of spa­ dictably experiences the diffusion gradient,
tially localizing along the z-axis by preselecting resulting in some degree of dephasing and pro­
targeted tissue, the 3-D approach adds another portionally negating signal. The DWI sequence
gradient, adding another dimension to k space is T2-weighted—an exception to the GE rule in
and the Fourier transform. The 3-D Fourier body MRI.
 Introduction to Body MRI  •  11

Mlong = max Mlong = 0

B0
Mlong = MlongTE

NMV NMV

NMV
Rf
TE

T1 relaxation
Excitation T2 decay
pulse
Mtrans = 0 Mtrans = max Mtrans = MtransTE

FIGURE 1-18.  Rf excitation and T1 recovery and T2 decay. NMV, net magnetic vector; TE, time to excitation.

TISSUE CONTRAST Mxy Mz

T2 decay
One of the remarkable qualities of MRI is the T1 recovery
ability to render spectroscopic images. The 0.63 M0
behavior of a proton in a magnetic field varies
depending on its unique microenvironment. For 0.37 M0
all intents and purposes, the protons relevant to
MR imaging are hydrogen (1H) protons. 1H
protons in fat and water behave differently; dif­
0 T2 T1
ferent fat protons in the same fat molecule
Time
behave differently; and free water protons in
liquid form versus bound water protons in solid FIGURE 1-19.  T1 and T2 relaxation curves and values for different
tissue (such as visceral organs) behave differ­ tissues.
ently. These differences are exploited in MRI
with the use of targeted pulse sequences with (or spin-lattice relaxation); the T1 relaxation
characteristic parameters. time is the time to recover 63% of the original
T1- and T2-weighting are the main pulse longitudinal magnetization after an Rf excita­
sequence strategies employed to yield spectro­ tion pulse. Decaying transverse magnetization
scopic information, or tissue contrast.12 is T2 relaxation (or spin-spin relaxation) and
T1-weighting enhances the differences in T1 the T2 value of a tissue corresponds to the time
values between tissues, whereas T2-weighting elapsed after 63% of the original transverse
enhances the differences in T2 values between magnetization has decayed. The (oversimpli­
tissues. In order to understand these concepts, fied) premise that spins are simple vectors of
consider the proton spin magnetic moment ini­ magnetization that are tipped into the trans­
tially parallel to B0 and subsequently tilted per­ verse plane and reorient parallel to the longitu­
pendicular to B0 into the transverse plane by dinal plane suggests that these processes occur
the Rf excitation pulse (Fig. 1-18). At this point, at equal rates. However, premise fails. Whereas
the longitudinal component of the vector is these values usually approximate that rule—
minimized and the transverse component is that is, spins with long T2 values also have long
maximized. Immediately thereafter, spins lose T1 values—they do not always directly follow
transverse and regain longitudinal magnetiza­ one another. T2 decay generally outpaces T1
tion according to their unique microenviron­ recovery and the T1 relaxation rate of a proton
ment. Regaining, or recovering, longitudinal defines the potential upper limit of the T2
magnetization is referred to as T1 relaxation decay time (Fig. 1-19).
12  •  Fundamentals of Body MRI

T1 (msec)

Tissue 0.5T 1.5T 3.0T

Free Water >4000 >4000 >4000

Muscle 560 870 898

Fat 192 200 382

Liver 395 570 809

FIGURE 1-20.  T1 values at different Spleen 760 1025 1328

magnetic field strengths.

The T1 value of a proton defines its ability to the refocusing pulse in an SE sequence elimi­
release energy and return to its original state. nates T2* effects. Therefore, the term T2 con-
The T1 is a function of the proton microenviron­ trast applies to SE imaging, whereas T2* contrast
ment, or lattice, and the magnetic field strength. is reserved for GE sequences.
T1 values decrease with greater structural orga­ The TR and TE of a pulse sequence are mani­
nization and increase with increasing magnetic pulated to favor signal from protons with either
field strength. This is another counterintuitive short T1 values or long T2 values. Colloquially
principle—stronger magnetic field strength speaking, when favoring short T1 values, the
would seem to draw spins back to equilibrium pulse sequence is “T1-weighted,” and when
faster. Suspend that notion and remember that favoring long T2 values, the pulse sequence is
T1 relaxation depends on the internal structure “T2-weighted.” Actually the T1-weighted pulse
of the proton. A stronger magnetic field over­ sequence is short–T1-value-weighted and the
whelms the facilitating effects of a proton’s T2-weighted pulse sequence is long–T2-value-
structure, and T1 values for all spins generally weighted; for obvious reasons, the more
increase and converge with increasing field succinct “T1-weighted” and “T2-weighted”
strength (Fig. 1-20). desig­nations suffice.
T2 values are not affected by magnetic field In order to understand how to isolate signal
strength. T2 values also decrease with structural from protons with short T1 values versus
organization facilitating the dissipation of protons with long T2 values, consider the fol­
energy. The T2 value measures the length of lowing experiment. In order to receive signal
time that transverse magnetization remains from all protons in a substance, the TE is set
coherent. In other words, after the Rf excitation to zero to negate spin-spin (T2) relaxation and
pulse, the NMV is deflected into the transverse the TR is maximized to ensure that all spins
plane, at which time all spins are in phase. Even­ have fully recovered longitudinal magnetiza­
tually, spins dephase because some precess tion. Under these circumstances, all spins yield
faster than others owing to local differences in signal regardless of their T1 and T2 values (Fig.
the magnetic microenvironment—hence, the 1-21). Therefore, signal generated from this
term spin-spin relaxation. Other factors affect pulse sequence represents a map of proton
transverse magnetization in addition to intrinsic density—hence, the designation proton density
T2 decay, referred to as T2* (T2 star) decay. (PD). Using the PD pulse sequence as a starting
Factors that induce T2* decay include heteroge­ point, decreasing the TR below the T1 relax­
neity of the local magnetic field and heterogene­ ation rates of spins with long T1 values dimin­
ity of tissue chemical shifts (or susceptibility ishes the signal contribution from these spins
artifact). While transverse magnetization under­ (Fig. 1-22A). After the Rf excitation pulse, these
goes T2* decay during GE sequences, the opera­ spins incompletely recover longitudinal magne­
tional mechanism of transverse magnetization tization before the next Rf excitation pulse.
decay in spin echo imaging is T2 decay, since Therefore, the longitudinal magnetization
 Introduction to Body MRI  •  13

180° 180°
90° PD 90°

Rf
TE TE
TR
T1
180° 180°
TR
↓
90° 90°

Rf

↑ TE
TE TE

TR 180° 180°
90° T2 90°

Rf
TE TE

TR
FIGURE 1-21.  Pulse sequence schemes: PDW, T1W, T2W. PD, proton density; TE, time to excitation; TR, time to repetition.

Contrast
with long TR
Short T1
Contrast
Signal intensity

with Long T1
short TR Contrast
Signal intensity

with
short TE

Long T2
Contrast
with Short T2
↓ TR ↑ TR long TE

A TR (msec) B TE (msec)
FIGURE 1-22.  A, T1 contrast mechanism. B, T2 contrast mechanism. TR, time to repetition. TE, time to excitation.

converted to transverse magnetization by suc­ Only spins with short T1 values recover enough
cessive Rf excitation pulses is continuously longitudinal magnetization to be excited into
diminished for spins with long T1 values, effec­ the transverse plane and avoid saturation.
tively eliminating the signal contribution of Incomplete, fractional longitudinal magnetiza­
these spins to the resulting image and isolating tion recovery is repeated mathematically. In
the signal from spins with short T1 values other words, if initial longitudinal magnetization
(T1-weighting). equals L and the TR occurs when only half of L
Parenthetically, another method of achieving has recovered, then
T1-weighting involves modifying the flip angle After the first Rf pulse, longitudinal
(FA). The FA refers to the degree of deflection
of NMV away from B0 by the Rf excitation pulse. magnetization = 1 2 L
SE pulse sequences conventionally fix FA at 90° After the second Rf pulse, longitudinal
and T1-weighting relies on the TR. However, GE
magnetization = 1 4 L
sequences generally employ lower FAs and
commonly rely on FA to modify T1-weighting. After the third Rf pulse, longitudinal
Increasing the FA increases the amount of—and
magnetization = 1 8 L
time for—longitudinal magnetization to be
recovered before the next Rf excitation pulse. and so on.
14  •  Fundamentals of Body MRI

180° 180°

90°

Rf
T1
TE

Flipped parallel to B0 by 90° Rf pulse

↓
No transverse magnetization
↓
No signal

Flipped between 90° and B0

↓
Residual transverse magnetization
↓
FIGURE 1-23.  Inversion recovery pulse
Signal
sequence. TE, time to excitation. B0

This sequence of events exemplifies saturation. eliminating signal from fat. The inversion pulse
Because longitudinal magnetization is an­ deflects all protons 180° preceding the 90° Rf
alogous to potential energy, the decremental excitation pulse, which is timed to occur when
impact on longitudinal magnetization translates fat protons are at the 90° position; this time
to vanishing signal potential. interval is referred to as the inversion time (TI)
Starting with the PD sequence template with (Fig. 1-23). Consequently, the fat protons are
minimal TE and maximal TR, increasing the TE tilted to the 0° position, yielding no signal. The
favors signal from spins with long T2 values. short T1 value of fat protons expedites their T1
Spins with short T2 values experience rapid loss recovery ahead of most other protons, which
of transverse magnetization with little to no are at some value between 180° and 90° at the
residual signal at the time the echo is sampled time of the Rf excitation pulse. Therefore, lon­
(TE) (see Fig. 1-22B). Maintaining a long TR gitudinal magnetization is an intermediate value,
ensures that spins with long T1 values (which which results in relatively lower SNRs for inver­
usually characterize spins with long T2 values) sion recovery sequences. This type of inversion
will not be saturated. This pulse sequence recovery pulse sequence is known as the STIR
scheme—T2-weighting—therefore ensures that (short tau inversion recovery) sequence.
signal yield primarily results from spins with Changing the TI targets protons with different
long T2 values. T1 relaxation rates. For example, a long TI is
A few pulse sequence modifications bear applied to eliminate signal from water protons,
consideration in order to explain the ability to which have a long T1 value, so that the 90° Rf
selectively image protons in body MRI: the excitation pulse reverts them to the 0° position.
spectrally selective pulse, the inversion pulse, This technique is usually applied to brain
and chemical shift. The spectrally selective imaging, and is known as the FLAIR (fluid atten-
pulse most commonly manifests in body MRI as uation inversion recovery) sequence.
the “fat-saturation pulse” or “fat-suppression Chemical shift refers to the difference
pulse.” This is an Rf pulse set to the resonant (or shift) in precessional frequency between
frequency of fat followed by a spoiler gradient, different proton species, such as water and fat,
which dephases the excited fat protons, which is a function of the proton microenviron­
eliminating their transverse magnetization. ment (remember the Larmor equation express­
Thereafter, the Rf excitation pulse is applied in ing the precessional frequency incorporates
the absence of signal contribution from fat the nucleus-specific gyromagnetic ratio). At
protons. some point, spins with different rates of preces­
The inversion pulse serves as an alternative sion rotate out-of-phase with one another (180°
to the spectrally selective pulse as a method of apart). If the TE occurs at this timepoint,
 Introduction to Body MRI  •  15

destructive interference ensues negating signal. To summarize, a number of physical phenom­

The most popular practical application of ena and parameter manipulations empower MRI
this phenomenon is fat-water chemical shift to exploit the unique behavior of different
imaging—colloquially referred to as in- and protons in the presence of a magnetic field.
out-of-phase imaging. This technique is neces­ Decreasing the TR isolates signal from protons
sarily applied to a GE pulse sequence (the 180° with short T1 values, whereas increasing the TE
refocusing pulse in an SE sequence eliminates isolates signal from protons with long T2 values.
chemical shift). Echoes are timed to coincide T1- and T2-weighted sequence design follows
with out-of-phase and in-phase timepoints of these parameter prescriptions. In the case of GE
the relevant spins (Fig. 1-24). In the case of sequences, T1-weighting involves increasing the
fat and water protons at 1.5 Tesla, water FA to favor signal from spins with long T1
protons precess an additional 360° in 4.4 values. Fat saturation techniques supplement
msec. Therefore, after an Rf excitation pulse, pulse sequences to eliminate signal from lipid
echoes acquired at 2.2 msec and 4.4 msec are protons, isolating signal from the remaining
out-of-phase and in-phase, respectively. Coexis­ protons. Spectrally selective and inversion
tent fat and water protons deprive signal from recovery techniques are commonly used
the imaging voxel in out-of-phase images and methods. Fat-water chemical shift imaging is
both contribute signal to the imaging voxel in used to identify the coexistence of these protons
in-phase images (Fig. 1-25). by synchronizing echoes with the out-of-phase
and in-phase precessional timepoints.

α°

Rf
THE PULSE SEQUENCE SCHEME
TEoop Body MRI pulse sequences fall into two main
TEip categories: T1- and T2-weighted sequences (Fig.
1-26). Each pulse sequence is designed with
b a tissue-specific objective in mind, which
ab
a° a necessitates a familiarity of the different tissues
ab encountered (see Fig. 1-26). The two major
categories of protons encountered in body
MRI—water and fat protons—require further
subdivision to generate a rational pulse sequence
Out-of-phase In-phase scheme. Water protons split into two major
FIGURE 1-24.  Chemical shift imaging. Rf, radiofrequency; TE, categories: bound water and free water protons.
time to excitation. Bound (intracellular) water protons exist in solid

A B
FIGURE 1-25.  Out-of-phase imaging shows microscopic fat. The marked signal loss in the liver on the out-of-phase image (A) compared
with the in-phase image (B) indicates the presence of microscopic fat. The etched appearance at the fat-water interfaces (arrows) on the
out-of-phase image is referred to as “India ink” artifact.
16  •  Fundamentals of Body MRI

Pulse Sequence Application Sequence Type Other

Out-of-phase Microscopic fat GRE India ink artifact

In-phase Susceptibility artifact GRE Acquired with

(iron, metal, etc.) OOP as single
dual-echo
acquisition
Pre-contrast Paramagnetic (3-D) GRE Optimally with
T1 substances (blood, fat suppression
melanin, etc.)

Dynamic post- Solid tissue and (3-D) GRE Same as above

contrast vascular structures
Delayed post- Extracellular space GRE Same as above
contrast (fibrous tissue,
inflammation)
Moderately T2- Bound Water FSE Optimally with
weighted (malignant lesions) fat suppression,
TE ≈ 80
T2 Heavily T2- Free Water SSFSE TE ≈ 180
weighted (fluid)

MRCP Free water only SSFSE TE > 500

FIGURE 1-26.  Body MRI pulse sequences. FSE, fast spin-echo; GRE, gradient-recalled echo; MRCP, magnetic resonance cholangiopan-
creatography; OOP, out of phase; SSFSE, single-shot fast spin-echo; TE, time to excitation.

tissues bound in close proximity to large Relevant paramagnetic substances include

molecules, such as protein. Free (extracellular) methemoglobin (present in hemorrhage),
water protons exist in solution (e.g., bile, melanin, protein, and gadolinium. Concentrated
urine, cerebrospinal fluid). Fat protons experi­ gadolinium—typically used as an intravenous
ence a similar distribution—macroscopic (or injection—is an example of a relevant super­
extracellular) fat versus microscopic (or intra­ paramagnetic substance. Iron, cobalt, and nickel
cellular) fat. Macroscopic fat occurs in subcuta­ are examples of ferromagnetic substances.
neous, retroperitoneal, and intraperitoneal MRI pulse sequences each generally target
distributions and in certain types of tumors, such one or more of these substances. Although pro­
as angiomyolipoma, dermoid cyst, and myeloli­ tocols vary between different institutions, body
poma. Microscopic fat infiltrates solid organs parts, and manufacturers, a general tissue-based
(such as the liver) and certain tumors (such as pulse sequence scheme transcends provincial
hepatic adenomas and renal cell carcinoma). differences, providing a universally applicable
A third category includes substances with system. T1-weighted sequences usually include
magnetic susceptibility. Magnetic susceptibility an in- and out-of-phase sequence, a pre- and
describes the tendency of a substance to become postcontrast dynamic sequence and a delayed
magnetized in a magnetic field. Magnetism is postcontrast sequence. T2-weighted sequences
denoted by the Greek symbol χ. Substances not include moderately T2-weighted, heavily T2-
magnetizable—diagmagnetic—have χ values weighted, and extremely heavily T2-weighted
less than or equal to zero—which characterizes (or MRCP [magnetic resonance cholangiopan­
most of the tissues of the human body. Paramag­ creatography] or MRU [magnetic resonance
netic substances are weakly magnetic and have urography]) sequences.
χ values greater than zero, but less than super­ T1-weighted sequences evoke signal from
paramagnetic substances with χ values 100 to substances with short T1 values, such as fat
1000 times stronger. At the far end of the spec­ and protons experiencing paramagnetic effects
trum, ferromagnetic materials have the highest (e.g., protons in protein-rich organs such as the
χ value. Paramagnetic substances enhance the pancreas and liver). Sequence-specific attri­
efficiency of T1 and T2 relaxation. These sub­ butes, such as fat saturation and chemical shift,
stances have unpaired electrons that facilitate confer greater specificity, isolating or highlight­
proton relaxation—usually in aqueous solution. ing individual proton species.
 Introduction to Body MRI  •  17

In- and out-of-phase images are usually After injecting gadolinium (usually adminis­
acquired simultaneously in a single pulse tered as an extracellular agent), vascular struc­
sequence with two different TEs. The data are tures followed by perfused tissues followed
subsequently separated into two image sets by interstitial spaces enhance, according to
covering the same anatomy. The out-of-phase the sequential delivery of gadolinium to the dif­
sequence is T1-weighted sequence with sensi­ ferent compartments of the extracellular space.
tivity to microscopic fat—“the microscopic fat The postcontrast phases of the dynamic
sequence.” Wherever fat and water protons sequence usually include an arterial phase, a
coexist, destructive interference and signal loss portal venous phase, and occasionally, a venous
ensue (see Fig. 1-25). These images distinguish phase. In addition to rendering its respective
themselves with the unique “India ink” artifact, vascular network, each phase of this sequence
alluding to the etched appearance at the inter­ confirms viable tissue by demonstrating an
face between water-rich substances and fat (see increase in signal compared with the precon­
Fig. 1-25)—another manifestation of destructive trast phase. Therefore, this multiphasic sequence
interference. is referred to as the vascular, or solid/viable
The in-phase sequence is T1-weighted with tissue sequence.
sensitivity to susceptibility artifact—“the The delayed postcontrast sequence usually
susceptibility sequence.” Whereas most T1- mirrors the parameters of the dynamic sequence.
weighted sequences in body imaging are GE The timing of the delayed sequence most closely
sequences and inherently possess sensitivity to approximates the delivery of contrast to the
susceptibility artifact, the in-phase sequence interstitium. The dynamic sequence precedes
benefits from a relatively long TE and a refer­ delivery of gadolinium to the interstitium and
ence standard in the form of its cohort—the exhibits no enhancement. Consequently, fibrous
out-of-phase sequence. Susceptibility artifact is tissue and interstitial edema (i.e., associated
induced by substances with drastically different with inflammation) enhance preferentially on
χ values from the substances around them and the delayed phase (Fig. 1-30)—hence, the desig­
most commonly arises from metallic substances, nation interstitial sequence.
such as surgical hardware and iron—manifesting Whereas T1-weighted sequences used in body
signal loss. Because of the doubled TE, the MRI are usually GE sequences, the T2-weighted
in-phase sequence exaggerates susceptibility sequences are mostly SE-based sequences,
artifact compared with the out-of-phase sequ­ removing consideration of chemical shift and
ence (Fig. 1-27). The appearance ranges from susceptibility phenomena. The need to attain
modest signal loss, such as in the case of depo­ higher TE values for T2-weighting increases
sitional iron disease, to a dramatic signal void, acquisition time, imposing prohibitive suscepti­
in the case of embolization coils and metallic bility artifact, decreasing SNR, and increasing
surgical devices. breathhold demands on GE images. SE sequences
The dynamic sequence involves multiphasic are better adapted to the needs of T2-weighting
repetition of the same sequence before and mul­ for most applications. T2-weighted SE pulse
tiple times after intravenous gadolinium admini­ sequences used in body MRI benefit from the
stration (Fig. 1-28). This sequence is designed to refocusing pulse, which eliminates potentially
detect enhancement, or the paramagnetic effect prohibitive susceptibility artifact and also helps
of gadolinium. The sequence parameters are to preserve SNR.
adjusted to detect the T1-shortening effects of T2-weighted sequences differ chiefly in their
administered gadolinium. In order to select for targeted water molecule—free water versus
substances only experiencing the paramagnetic bound water. The main difference between
effects of gadolinium, fat, the dominant sub­ these sequences is the TE. A relatively lower TE
stance with a short T1 value, is selectively is adapted to identify differences in bound water
removed with a spectrally selective pulse. There­ content between solid tissues. Increasingly
fore, on the precontrast set of images before higher TE values more selectively isolate signal
gadolinium is administered, paramagnetic sub­ from free water protons and eliminate signal
stances other than gadolinium—methemoglobin from solid tissues.
(blood), melanin, and protein—are conspicuous The moderately T2-weighted sequence
(Fig. 1-29) and this sequence is appropriately approximates the T2 values of solid organs, such
termed the paramagnetic sequence. as the liver. The typical TE value of a moderately
18  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 1-27.  In-phase imaging shows susceptibility artifact. The magnification or “blooming” of the central signal void (arrow) from
embolization coils on the in-phase image (B) compared with the out-of-phase image (A) is a function of the longer time to excitation
(TE). C, The artifact on the corresponding single-shot fast spin-echo (SSFSE) image is better controlled owing to the refocusing pulses
(despite the much longer TE). D, Susceptibility artifact also arises from endogenous structures, such as gas-containing bowel, as seen
in the out-of-phase image (arrow) in a different patient. E, Blooming (arrow) is evidence on the susceptibility (in-phase) image.

T2-weighted sequence used in abdominal The heavily T2-weighted sequence employs a

imaging is 80 msec. This value optimizes the higher TE (~180 msec). By increasing the TE
contrast between substances of different bound value to this level, the transverse magnetization
water content, such as normal parenchymal of solid tissues with bound water decays signifi­
tissue and neoplasms, which typically harbor cantly, whereas free water maintains transverse
higher water content. The addition of fat magnetization (Fig. 1-32) (free water T2 = ~180
suppression augments tissue contrast by improv­ msec at 1.5 Tesla). Contrast between solid
ing the dynamic range, which increases the tissues with different bound water content
visible discrepancy between tissues with differ­ decays compared with the moderately
ent quantities of bound water (Fig. 1-31). The T2-weighted sequence, potentially obscuring
bound water specificity justifies the name bound solid lesions (prompting the name lesion sup-
water sequence. pression sequence). Because SNR depends
 Introduction to Body MRI  •  19

Interstitium:
Free OOP: micro fat Bound fibrosis,
water IP: susceptibility water inflammation

In/out Moderate
Localizer SSFSE Delayed
phase T2W

Paramagnetic: Arterial system Portal

blood, melanin, hypervascular system
protein tissue solid tissue

Pre Arterial Portal

Delay

Gadolinium
FIGURE 1-28.  Dynamic pulse sequence schematic. IP, in phase; OOP, out of phase; SSFSE, single-shot fast spin-echo.

A B

C D
FIGURE 1-29.  Precontrast imaging shows paramagnetic substance. A, The precontrast fat-suppressed (paramagnetic) image in a patient
with metastatic uveal melanoma shows multiple, variably hyperintense lesions (arrows) reflecting variable melanotic content. B, A para-
magnetic image in a patient with pelvic pain shows a large, irregularly shaped lesion with significant paramagnetism (arrow) due to
hemorrhage. C, Marked hypointensity on the T2-weighted image characterizes the concentrated blood products found in an endome-
trioma (arrow). D, A paramagnetic image in a different patient shows the paramagnetic effects of a small left renal hemorrhagic cyst
(thin arrow) and enzymatic proteins in the pancreas (thick arrows), causing these structures to be relatively hyperintense.
20  •  Fundamentals of Body MRI

A B

FIGURE 1-30.  Delayed postcontrast imaging shows interstitial

enhancement. A, The T2-weighted image reveals an unusual,
large hypointense lesion involving the anterior abdominal
wall (arrows). Marked gradual enhancement—based on com-
parison between early postcontrast (B) and delayed postcon-
trast (C)—reflects the large interstitial space in a desmoid
C
tumor with extensive fibrosis.

A B
FIGURE 1-31.  Moderately T2-weighted imaging shows bound water tissue contrast. A, The moderately T2-weighted image in a patient
with a hepatic schwannoma (arrow) expresses the high water content often seen in schwannomas. Note the relatively higher tissue water
content of the spleen compared with the liver—reflected by relative hyperintensity—serving as an indication of the tissue contrast of
the bound water sequence. B, Even the relatively unhydrated lymphomatous lesions (thin arrows) with periportal lymphadenopathy
(thick arrow) in a different patient with disseminated lymphoma are conspicuous on the bound water sequence owing to the high tissue
contrast.

on transverse magnetization, which decays isolating free water protons, this sequence
rapidly with increasing TE, the heavily deserves the title free water sequence.
T2-weighted sequence is relatively signal- Dramatically increasing the TE results in
starved. Consequently, this sequence usually extreme T2-weighting and T2 decay of all sub­
avoids fat-suppression—which has the second­ stances except free water protons—a water-
ary effect of decreasing SNR. By relatively only sequence. This technique is applied to
 Introduction to Body MRI  •  21

A B
FIGURE 1-32.  Heavily T2-weighted imaging shows free water. A and B, The heavily T2-weighted images depict free water protons pref-
erentially, at the expense of solid tissue contrast. Solid tissues with bound water molecules, such as the liver, lack signal, whereas structures
with free water exhibit marked hyperintensity proportional to their water content. Pure free water molecules found in cerebrospinal fluid
(arrows), gastrointestinal contents (thick arrows), gallbladder (open arrow), and simple renal and hepatic cysts define maximum signal
intensity, whereas lesions with intermediate free water content, such as hemangiomas (dashed arrows) appear moderately hyperintense.

imaging structures containing free water mole­ categories, based on the physical explanation
cules, such as the biliary system (MRCP) and the for the artifact encountered—view-to-view
urinary system (MRU). phase errors and within-view phase errors.13
The term view refers to echo and within-view
phase errors occur during the acquisition of the
OPTIMIZING BODY MRI
echo, whereas view-to-view phase errors arise
The torso poses many unique problems to the because of motion between the acquisition of
prospect of obtaining MR images. In addition to successive echoes.
artifacts encountered universally in MRI appli­ Within-view phase errors arise because a
cations, such as magnetic field heterogeneity, moving proton fails to be rephased by applied
chemical shift artifact, and Rf artifact, body gradients. Magnetic gradients in MR imaging are
MRI encounters additional obstacles. Unlike often applied in separate dephasing and rephas­
most other body parts, continuous physiologic ing lobes with a net phase shift of zero in order
motion, variable quantities of paramagnetic to reestablish spin phase coherence, as previ­
substances, and variable patient body habitus ously discussed. The unpredictable phase shift
frequently complicate the process. Addressing accumulated by the moving spin is not addressed
these issues greatly improves image quality. with this technique and the acquired phase shift
is assumed to have been induced by the phase-
encoding gradient and spatially mapped accord­
Motion
ingly (Figs. 1-33 and 1-34). View-to-view phase
Motion artifact is a layered topic complicating errors result from signal amplitude variations
every examination, especially in the abdomen. resulting from motion between echoes, which
Motion induces a phase shift in a proton during results from bulk motion (see Fig. 1-34). Consid­
the application of a magnetic field gradient. ering a single voxel, when the signal amplitude
There is no implicit correction algorithm in k varies from echo to echo because motion trans­
space or the Fourier transform for the phase ports different spins into the voxel between
shift induced by motion. Phase shift induced echoes view-to-view phase errors occur. This
by the phase-encoding gradient is indistinguish­ happens under the circumstances of direct
able from phase shift induced by motion. motion and pulsatile vascular flow. Physically
Consequently, the Fourier transform spatially replacing spins of different species explains the
misregisters moving protons. basis for this error in the case of direct motion.
Motion from bulk patient motion, cardiac pul­ The variable replacement of unpredictably satu­
sation, respiratory motion, bowel peristalsis, rated spins with inconstant velocity explains
and blood flow separates into two broad this problem in pulsatile vascular flow.
22  •  Fundamentals of Body MRI

TE Most of the strategies employed in body MRI

Rf
to correct motion artifact minimize acquisition
time. Acquisition time depends on multiple
parameters (Fig. 1-35) and is expressed in the
Dephasing form of the equation:
lobe
Gf
Rephasing TR × G p × NEX
lobe T=
ETL × R

Phase where T is the acquisition time, TR is the repeti­

Static spins tion time, Gp is the number of phase-encoding
steps, NEX is the number of excitations, ETL is
Moving spins the echo train length, and R is the acceleration
factor (in parallel imaging).14 The TR is usually
FIGURE 1-33.  Within-view motion artifact. Rf, radiofrequency; already minimized and optimized to the pulse
TE, time to excitation. sequence and not amenable to modification.
The NEX is usually already minimized. The other
parameters in the equation offer the most poten­
tial utility in minimizing acquisition time.
Because Gp contributes to acquisition time and
Gf does not, the smaller of the transverse axes

A B

D
C
FIGURE 1-34.  Motion artifact. A, The sagittal T2-weighted fat-suppressed image shows the effects of motion during image acquisition
with phase misregistration of protons in the iliac vessels (arrows) portrayed by periodic superimposition across the phase axis—ghosting.
B, The same phenomenon (thin arrows) occurs along the phase-encoding axis on the corresponding axial image, which is accompanied
by phase misregistration of bowel loops due to peristaltic motion (thick arrows). C, Occasionally, this artifact simulates a pathologic
lesion (arrow). The appearance of this pseudolesion (the pulsatile ghost of the aorta) on multiple contiguous images and absence on
other sequences resistant to artifact disclose the artifactual etiology. D, Bulk motion from breathing also causes phase-encoding errors
reflected by ghosting (arrows).
 Introduction to Body MRI  •  23

Motion artifact Parameter adjusted Tradeoffs

correction
Rectangular FOV Decreased phase FOV (less phase encoding Phase wraparound (see Fig. 1-37A)
steps acquired)
Phase encoding resolution Decreasing phase matrix (y and z axes– Decreased spatial resolution (decrease
z with 3D technique) phase FOV first)
Fast spin echo Increasing echo train length (more echoes Increased image blur
acquired per excitation pulse)
Parallel imaging Decreasing phase encoding (parallel imaging Decreased SNR, central wraparound
substitutes for phase encoding steps) (see Fig. 1-37C)
Respiratory triggering Segmenting acquisition according to Increased overall acquisition time
expiratory phase
Phase compensation Reordering the acquisition of echoes Decreased spatial resolution and fine
(ROPE) according to the phase encoding gradient detail
Navigator pulse Selective pulse targeting diaphragmatic Increased acquisition time
motion
Tissue saturation Spectral or inversion pulse (usually targeted Decreased SNR, slightly increased
to hyperintense fat) acquisition time
Signal averaging Increasing signal averages Increased acquisition time

Gradient moment nulling Frequency encoding gradient Increased acquisition time, increased TE

FIGURE 1-35.  Strategies to minimize motion artifact. FOV, field of view; ROPE, respiratory-ordered phase encoding; SNR, signal-to-noise
ratio; TE, time to excitation.

of the patient (usually anteroposterior) is imaging, the problem is exacerbated by the fact
assigned to the phase-encoding gradient. Careful that wraparound artifact plots centrally rather
attention to crop the phase-encoding FOV by than at the periphery of the image (see Fig.
reducing the phase-encoding matrix (number of 1-37). For this reason, parallel imaging demands
phase-encoding lines) and include only relevant greater attention to FOV considerations.
anatomy (and not air surrounding the patient) Although theoretically wraparound artifact also
yields dividends in image acquisition time. Elimi­ plagues the frequency-encoding axis when
nating phase-encoding steps covering air directly sampled frequencies outside the sampled range
reduces scan time (Fig. 1-36). Converting the are plotted into k space, digital filters eliminate
default square FOV (equal x and y dimensions) these unwanted frequencies, obviating this
to an asymmetrical phase-encoding minimized problem.
construct is termed rectangular FOV. Increasing the ETL also reduces scan time by
Overminimizing the FOV threatens the possi­ economizing the utility of each Rf excitation
bility of wraparound artifact, however (Fig. pulse. For each applied Rf excitation pulse, the
1-37).15 Spatial mapping of received MR signal ETL defines the number of echoes acquired.
plots along a periodic spectrum from 0° to 360° With increasing ETL, the pulse sequence repeti­
in the phase-encoding axis. Spins outside the tion decreases, resulting in decreased overall
prescribed phase FOV do not fall within the 0° scan time. The SSFSE sequence exemplifies the
to 360° phase range. Instead, consider these utility of this technique by acquiring all echoes
spins to have phases of either 360 + a° or 0 – b° after a single Rf excitation pulse.
phase, which plots to the 0 + a° and 360 – b° Image blur is a potential unwanted side effect
phase locations, respectively, at the upper of long echo-train imaging. Each successive
and lower margins of the image. Although echo sampled during an echo train possesses a
not problematic when wraparound artifact is progressively longer TE. When combined to
superimposed over superfluous anatomy, form a single image, the effect of the variable TE
superim­position over important structures is is suboptimal edge detection, or blur. The echo
clearly problematic. The solution is to increase with the weakest phase-encoding gradient
the phase FOV. When implementing parallel defines the effective TE (TEeff)—understandable,
24  •  Fundamentals of Body MRI

Square FOV
Rectangular FOV

Gp Gp

Gf

No wasted frequency encoding lines

↓
Gf
↑ Increased spatial resolution of
relevant anatomy
Wasted frequency encoding lines (no increased acquisition time)
↓
↓ Decreased spatial resolution of relevant anatomy
(no increased acquisition time)
↓ Decreased phase encoding lines
↓
↑ Increased acquisition time
Wasted phase encoding lines ↓
↓ ↓ Decreased motion artifacts
↑ Increased acquisition time
↓
↓ Decreased spatial resolution of relevant anatomy

FIGURE 1-36.  Rectangular field of view (FOV).

because the weakest gradient defines tissue The acceleration factor R applied to parallel
contrast. Acquiring echoes after the TEeff con­ imaging describes the proportion of phase-
tributes to blur. For this reason, ETL and TE encoding k-space lines filled per Rf excitation
adjustments follow one another proportionally pulse. So, an acceleration factor of 2 means that
to minimize blur artifact. only half of the phase-encoding lines of k space
Parallel imaging is the MR counterpart to must be filled using the echoes obtained from
multidetector-to-multidetector computed tomo­ the pulse sequence. R defines the theoretical
graphy (CT) technology (relative to single-slice upper limit by which acquisition time is reduced
CT) by maximizing the utility and functionality (practically speaking, the time saving is gener­
of the detector system. Parallel imaging uses ally significantly less).
the differential spatial profiles of the phased As a last resort, decreasing spatial resolution
array coil elements to reduce k space filling. in the slice and phase axes diminishes scan time.
Undersampled, aliasing k space is unwrapped By decreasing the image matrix in the phase-
with mathematical equations using the various encoding direction, fewer phase-encoding steps
spatially dependent coil element sensitivities. are acquired, decreasing acquisition time,
The relative amount of coil spatial sensitivity according to the previous equation. Obtaining
information replacing unwrapping aliased k fewer slices translates to adding the sum of the
space is expressed through the coefficient R. acquisition time equation together fewer times
Increasing R decreases SNR according to the (i.e., 15 slices instead of 20 means acquisition
following equation: time × 15 instead of 20).
Alternatively, using physiologic monitoring to
SNR = 1/ ( g × R ). determine relatively motionless phases of the
cardiac/respiratory cycles, pulse sequences are
The geometry factor, g, measures the acquired in fragments during these quiescent
aliasing unwrapping proficiency of the coil phases and subsequently spliced together. This
arrangement. technique involves cardiac or respiratory
 Introduction to Body MRI  •  25

A B

C D

0°
a°

Gz

360°

360° + a°

E F
FIGURE 1-37.  Wraparound artifact. A, The axial T2-weighted image focused on the kidneys demonstrates two-dimensional (2-D) wrap-
around artifact (thin arrows) because the prescribed field of view (FOV) excludes the anterior abdominal wall (not assigned 0°–360°
phase), causing it to alias—or wraparound—to an anatomically incorrect spatial location. However, the relevant finding—the left renal
cell carcinoma (RCC; thick arrow)—is not obscured by this artifact. B, Wraparound artifact occurs in any acquisition plane, exemplified
by the coronal image with right-to-left phase encoding and wraparound artifact (arrows). C, With parallel imaging, wraparound artifact
appears in the middle of the image (arrows), forcing prescription of larger FOVs. An apparent enhancing mass in the liver (arrow) on
the three-dimensional (3-D) postcontrast image (D) in a different patient resembles the transverse appearance of the kidney more infe-
riorly positioned (E). This example illustrates wraparound artifact occurring along the second phase-encoding axis in a 3-D acquisition—
the slice direction. F, Arrows outside the volume plotted on the coronal image correspond to tissue prone to 3-D aliasing.
26  •  Fundamentals of Body MRI

monitoring to trigger each phase of the acquisi­ when diaphragmatic motion is minimal (i.e.,
tion. 3-D MRCP and FSE T2-weighted and inver­ expiration).
sion recovery sequences occasionally employ Reducing the signal intensity of tissues con­
respiratory triggering (Fig. 1-38). Cardiac moni­ tributing to visible motion artifact is another
toring, although integral to chest and cardiac im­ viable strategy for minimizing motion artifact.
aging, is rarely employed in abdominal imaging. Spatially and spectrally selective saturation tech­
Methods of controlling for respiratory motion niques both accomplish this objective in differ­
include respiratory triggering using a bellows ent ways. Spatially selective Rf excitation pulse
(wrapped around the patient’s torso designed to applied to the vascular inflow outside the image
detect the inspiratory and expiratory phases) volume followed by a spoiler gradient inducing
and navigator pulse triggering. The respiratory dephasing eliminates signal from flowing blood,
bellows approach offers two possibilities. Either thereby eliminating ghost artifact. Spectrally
image acquisition is triggered to occur during selective saturation pulses generally target
the relatively quiescent expiratory phase only, hyperintense fat—especially copious in the
or phase encoding steps are arranged so that abdominal wall—potentially ghosting across the
central k-space steps are acquired during the phase-encoding axis.
quiescent expiratory phase and peripheral Another method of reducing signal intensity
k-space steps are acquired during inspiration– from tissues contributing to motion artifact
known as respiratory compensation or respira­ involves increasing the signal intensity of tissues
tory-ordered phase encoding (ROPE). Since relative to artifact. Although counterintuitive,
central k-space corresponds to image signal, per­ increasing the number of signal averages (NEX)
ceived motion artifact is reduced. increases the signal intensity of tissues relative
The navigatory system involves a “navigatory to motion artifact, which is not reproducible
pulse,” a vertically-oriented column of echoes and not equally intensified compared with body
targeted to the diaphragm to detect diaphrag­ tissues. Of course, while downsizing motion
matic motion. Practically speaking, this sequ­ artifact, this technique actually increases the
ence maps out diaphragmatic excursion so chances of motion artifact and increases the
that image acquisition is timed to occur only acquisition time.

A B

FIGURE 1-38.  Short tau inversion recovery (STIR) with

and without respiratory triggering. A, The rich tissue
contrast on the STIR image acquired with respiratory
triggering free of motion artifact justifies its use; a large
hemangioma occupies the posterior segment. B, A
STIR image in another patient with respiratory
motion preempted by triggering exemplifies another
etiology of motion artifact—bowel peristalsis—not
corrected by respiratory triggering. C, A STIR image
in a patient in whom respiratory triggering failed
shows the havoc wrought by uncorrected respiratory
C
motion.
 Introduction to Body MRI  •  27

Gradient moment nulling (GMN) addresses at rates based on the strength of the magnetic
within-view phase errors and involves manipula­ field, this magnetic field heterogeneity results in
tion of the magnetic gradient to result in suc­ unpredictably random precessional frequencies.
cessful rephasing of both static and moving Consequently, protons dephase (T2*) and signal
spins. Adding lobes to the standard unipolar loss ensues. Because the degree of this random
dephasing and rephasing lobes of the frequency dephasing process is proportional to the time
encoding gradient increases the chances of elapsed before the echo, minimizing the echo
successful rephasing of static and moving spins time minimizes susceptibility artifact (Fig. 1-40).
(Fig. 1-39). The problem of susceptibility artifact poses the
greatest challenge in the context of surgical hard­
ware and embolization coils (see Fig. 1-27). Surgi­
Susceptibility Artifact
cal clips are generally not highly ferromagnetic
Decreasing scan time dovetails with a problem and susceptibility artifact is not prohibitively
often arising in body MRI—susceptibility severe. Whereas all pulse sequences experience
artifact—managed by decreasing scan time. susceptibility artifact in some measure, the
Because most body tissues are diagmagnetic dynamic sequence is most amenable to corrective
(not very magnetizeable), proximity to sub­ measures. The FSE and SSFSE sequences inher­
stances with highly magnetic properties— ently address susceptibility artifact through the
ferromagnetic—induces susceptibility artifact. application of multiple 180° refocusing pulses.
Susceptibility artifact in MRI is defined as signal The in- and out-of-phase sequence is not subject
incoherence generated by the intermingling of to corrective measures because the approach to
substances with discrepant capacities to be mag­ the susceptibility problem centers on lowering
netized (measured by χ, susceptibility). In the the TE (otherwise the desired chemical shift
setting of the diagmagnetic human body with properties are sacrificed). The shorter the TE,
little to no inherent magnetism to distort the the less time elapses during which spin dephasing
magnetic field, highly magnetic substances with occurs owing to magnetic susceptibility.
induced magnetic fields of their own corrupt Whereas the dynamic sequence TE is usually
the homogeneity of B0. Because protons precess set to minimum, a number of adjustments lower
the potential minimum TE. For example, frac­
tional echo sampling decreases the time during
which the echo reception occurs, decreasing
the TE by that incremental amount (Fig. 1-41).
Gf
This involves sampling slightly more than half
of the echo, thereby filling slightly more than
half of k space in the frequency dimension.
Because of the symmetry of k space, the
Static spins TE remainder is interpolated. The time saving is
Phase counterbalanced by a reduction in SNR (usually
not problematic in inherently SNR-rich 3-D
Moving spins acquisitions). In order to take advantage of this
technique, another competing parameter
FIGURE 1-39.  Gradient moment nulling. TE, time to excitation. modification must be disabled—partial Fourier

Parameter adjusted Effect

Minimize TE Less time for susceptibility artifact to occur

Fractional echo sampling Decreased TE, decreased SNR

Increased receiver bandwidth Faster echo sampling → decreased TE, decreased SNR

Eliminate fat saturation Preclude variable fat saturation

FIGURE 1-40.  Strategies to minimize susceptibility artifact. SNR, signal-to-noise ratio; TE, time to excitation.
28  •  Fundamentals of Body MRI

TE ↑ Bandwidth

Rf
Faster
Full echo sampling sampling
Signal ↓ SNR
Gf
↓ Bandwidth
TE
Slower
Rf Noise sampling
↑ SNR
Fractional echo sampling Signal

Gf
FIGURE 1-42.  Receiver bandwidth. SNR, signal-to-noise ratio.

FIGURE 1-41.  Fractional echo sampling. Rf, radiofrequency; TE, Potential problems arise from the magnetic
time to excitation. field, the cryogens, the gradient coils, the Rf
transmitter, contrast agents, and the configura­
acquisition. Whereas fractional echo sampling tion of the MR system itself—claustrophobia
involves filling k space partially in the frequency (Fig. 1-43). In order to preempt at least most
domain, partial Fourier acquisition involves of these problems, careful screening must
partial k-space filling in the phase domain. These be undertaken. Ideally, screening begins at the
techniques are generally mutually exclusive referring physician’s office. Realistically, this
owing to SNR reduction. never happens. Redundancy of screening at the
Another method to minimize TE and suscepti­ time of scheduling, registration, and immedi­
bility artifact accomplishes the same feat of ately before scanning minimizes the risk of
decreased echo sampling time—increasing the complications. Documenting and guiding the
receiver (or receiver) bandwidth. The receiver execution of the screening process with a
bandwidth defines the rate at which the echo is screening form are critical (Fig. 1-44).
sampled by the receiver. Increased receiver Patient safety concerns arising from the mag­
bandwidth samples faster with a greater range of netic field are twofold—complications arising
sampled frequencies, which includes more noise from the static magnetic field and from induced
and less relevant signal-generated frequencies. time-varying magnetic fields.16,17 According to
So, although time is saved, thereby decreasing the latest guidelines generated by the U.S. Food
the TE, SNR is compromised (generally not pro­ and Drug Administration (FDA), clinical MR
hibitively with 3-D sequences) (Fig. 1-42). systems with static magnetic fields up to 8 Tesla
By altering spin precessional frequencies, sus­ pose no significant biologic effects to adults. MR
ceptibility artifact also wreaks havoc on spec­ systems in routine clinical practice range up to
trally selective Rf pulses, such as fat saturation 3 Tesla.
(in addition to inducing signal loss due to spin The most prevalent threat due to the static
dephasing). Therefore, consider eliminating fat magnetic field is the attractive force on ferro­
suppression on the dynamic sequence in the magnetic objects. B0 in a 1.5-Tesla magnet is
setting of susceptibility artifact. The fat suppres­ 15,000 times as strong as the earth’s magnetic
sion Rf excitation pulse depends on reliably force. The attraction to ferromagnetic objects is
predictable precessional fat proton frequency. proportionally stronger and metallic objects
Variable precessional frequencies result in experience projectile behavior in proximity to
incomplete fat proton excitation and subse­ B0. The attractive force increases exponentially
quently incomplete dephasing by the ensuing with proximity to B0—half the distance quadru­
spoiler gradient. ples the attractive force. The likelihood of this
phenomenon is a function of the fringe field,
extending centrifugally away from the bore of
MRI SAFETY
the magnet (Fig. 1-45). The fringe field does not
MRI incurs a number of potential hazards to respect normal structural elements, such as ceil­
patients and employees if proper care and adher­ ings, walls, and doors, and the fringe field must
ence to established guidelines is not considered. be contained by passive and/or active shielding.
 Introduction to Body MRI  •  29

Static Gradient Radiofrequency Cryogens Contrast Patient

Magnetic Coil Transmitter Agents Factors
Field System System
Projectile Acoustic Energy Quenching Nephrogenic Claustro-
effect noise deposition systemic phobia
(SAR) fibrosis
Implanted Peripheral Conduction Contrast- Discomfort
device stimulation effects induced
failure nephropathy
(rare)
Implanted Visual Acute reactions
device stimulatory
torque effects

FIGURE 1-43.  MRI safety issues.

The goal of shielding is to minimize the fringe implants. Recently implanted devices, such as
field so that the perimeter of potential harmful vascular stents, deserve caution and exposure to
effects is reduced. Passive shielding involves the magnetic field is generally delayed for 6
enveloping the magnet within material that weeks to allow for the ingrowth of granulation
counteracts B0; active shielding passes current tissue to prevent deflection and migration.
through coils on the exterior of the magnet, Whereas almost all of these artificial devices
generating a magnetic field that opposes B0. By pose no health risk, most induce at least some
containing the fringe field, shielding eliminates degree of susceptibility artifact and appropriate
the interference with devices such as pace­ measures address this problem, as previously
makers and video monitors, which safely discussed.
operate below field strengths of 0.5 mT and The gradient coils, used to generate the mag­
0.1 mT, respectively. Accordingly, access below netic field gradients for spatial localization,
the fringe field strength at 0.5 mT, or 5 gauss (1 engender time-varying magnetic fields (TVMFs).
Tesla = 104 gauss), must be vigilantly guarded TVMFs induce electric current in conductive
to prevent untoward accidents (see Fig. 1-45). media, according to Faraday’s Law of
The term 5-gauss line communicates the pres­ Induction. The potential clinical manifestations
ence of this invisible barrier that MR personnel reflect peripheral nerve stimulation—including
observe to protect patients (with pacemakers) muscular contractions and cutaneous sensory
from magnetic field effects. The American disturbances—and retinal phosphene stimula­
College of Radiology (ACR) promotes the tion, inducing visual disturbances. FDA limits
concept of static field safety zones.18 Zones TVMFs to 6 T/sec and sequences with the fastest
1 through 4 describe increased levels of vigi­ gradient-switching needs, such as echo planar
lance and stringency to access in order to imaging, incur the greatest risk.
prevent inadvertent exposure to the fringe field TVMFs pose another serious risk—burns. Con­
(Fig. 1-46). ducting materials, such as monitoring cables,
Because of the number of devices that are permit the flow of current induced by TVMFs,
potentially incompatible with a strong magnetic which is facilitated in the setting of a loop con­
field, vigilance is warranted (for a comprehen­ figuration (which increases inductance and
sive MRI compatibility, see “The List” at therefore current). Ohmic heating—the dissipa­
www.mrisafety.com). Generally contraindi­ tion of heat by a conductor transmitting current—
cated devices include pacemakers, cochlear ensues, potentially resulting in burns. All looped
implants, and intraorbital metallic foreign devices—including leg crossing—must be elimi­
bodies. Most other artificially implanted or nated to minimize the risk of this complication.
inserted devices or objects usually incur no risk The other side effect of passing current
from the static magnetic field, including fre­ through the gradient coils is acoustic noise.19
quently encountered shrapnel, heart valves, Rapid gradient switching in the presence of a
inferior vena cava filters, and orthopedic strong magnetic field generates the loud noise
30  •  Fundamentals of Body MRI

FIGURE 1-44.  MRI screening form.

 Introduction to Body MRI  •  31

FIGURE 1-44, cont’d 

32  •  Fundamentals of Body MRI

experienced by the patient during scanning. Ear membrane rupture (due to pressure effects),
plugs or MR-compatible earphones mitigate this and hypothermia.
problem. Intravenous gadolinium formulations (Fig.
The deposition of energy by the transmitted 1-47)20 pose potentially harmful—even lethal—
Rf energy (i.e., Rf excitation pulse, refocusing effects, albeit extremely rare (Fig. 1-48). Minor
pulse) potentially imposes harmful biologic complications include headaches, nausea,
effects. This quantity is measured by specific vomiting, rash, and hypotension. The overall
absorption rate (SAR), expressed in Watts/ incidence of adverse reactions approximates
kilogram. Patient weight and pulse sequence 0.2%.21–23 Most reactions fall into the acute cate­
parameters figure most prominently into this gory and the vast majority are minor and treated
calculation. The FDA imposes SAR limits based conservatively with observation. Chronic reac­
on an increase of 1°C in core body temperature tions include contrast-induced nephropathy
(e.g., 4 W/kg for whole body exposure), and (CIN) and nephrogenic systemic fibrosis (NSF).
most modern MR systems calculate SAR before CIN occurs much less commonly after gado­
each pulse sequence, avoiding excessive SAR linium administration than with iodinated con­
levels. trast materials. Risk factors for CIN include
One of the most potentially lethal risks in MRI diabetes mellitus, renal insufficiency, intravascu­
is quenching. Quenching refers to the abrupt lar volume depletion, reduced cardiac output,
heating of the cryogen, converting from liquid and concomitant nephrotoxins.
to gaseous form. Helium in gaseous form sup­ Between 200 and 300 cases of NSF have been
plants oxygen, threatening suffocation, and criti­ reported worldwide. Originally dubbed “neph­
cally elevates pressure, potentially preventing rogenic fibrosing dermopathy” (NFD) in the
entrance to the magnet room. Quenching risks 1990s, skeletal muscle, lung, myocardium, and
to the patient include asphyxiation, tympanic liver involvement superimposed on preeminent
skin manifestations prompted the name change
to NSF. More cases of NSF have been reported
after the use of gadodiamide (Omniscan) and
gadoversetamide (OptiMARK) compared with
B0 other contrast agents, and the use of newer
agents, such as gadoxetate disodium (Eovist)
and gadobenate dimeglumine (Multihance),
with greater relaxivity and decreased dosing
5 gauss line
potentially reduces the risk of NSF. The calcu­
lated glomerular filtration rate (GFR) establishes
the risk category of gadolinium administration—
normal: GFR > 60 mL/min/1.73 m2 = no risk;
mild-moderate renal insufficiency: 30 < GFR <
60 mL/min/1.73 m2 = minimal if any risk; severe
FIGURE 1-45.  The fringe field. renal insufficiency: GFR < 30 mL/min/1.73 m2 =

Zone Access Environment Details

1 General public Outside MR facility

2 Patients undergoing Reception, patient Supervised by MR

screening, paperwork, dressing and personnel; interception
etc. holding areas, etc. of ferromagnetic objects;
venue for patient screening
3 MR personnel and Control room, Restricted access;
screened patients computer room, includes all areas with
etc. fringe field >5 gauss
4 MR personnel and Scanner room Labeled as
screened patients hazardous

FIGURE 1-46.  American College of Radiology (ACR) magnetic resonance (MR) safety zones.
 Introduction to Body MRI  •  33

Brand Chemical Structure Ionicity Clearance, Relaxivity

Name Name T½ (hours)

Magnevist Gadopentetate Linear Ionic Renal, 1.6 4.3

dimeglumine
(Gd-DTPA)
Prohance Gadoteridol Macro- Non-ionic Renal, 1.57 4.4
(Gd-HP-DO3A) cyclic

Omniscan Gadodiamide Linear Non-ionic Renal, 1.3 4.6

(Gd-DTPA-BMA)

OptiMARK Gadoversetamide Linear Non-ionic Renal, 1.73 5.2

(Gd-DTPA-BMEA)

Multihance Gadobenate Linear Non-ionic Renal (96%)/ 6.7

dimeglumine hepatic (4%),
(Gd-BOPTA) up to 2 hrs
Eovist Gadoxetate Linear Ionic Renal (50%)/ 8.7
disodium hepatic (50%),
(Gd-EOB-DTPA) 0.95
FIGURE 1-47.  Gadolinium formulations.

Mild Moderate Severe

• Nausea • Generalized or diffuse • Laryngeal edema
• Vomiting erythema • Unresponsiveness
• Cough • Dyspnea • Cardiopulmonary
• Warmth • Bronchospasm arrest
• Headache • Wheezing • Convulsions
• Dizziness • Mild hypotension/ • Profound
A • Shaking hypertension hypotension
c • Taste alteration • Tachycardia/bradycardia • Arrhythmias
u • Itching
t • Pallor
e • Flushing
• Chills C
• Sweats h
r • Contrast-induced nephropathy (CIN)
• Rash/hives o
• Nasal n • Nephrogenic systemic fibrosis (NSF)
congestion i
• Eye/face c
swelling FIGURE 1-48.  Adverse reactions to gadolinium
• Anxiety
agents.

potential risk. Based on this scheme, gadolinium to electromagnetic fields prompts circumspec­
aversion in patients with GFR less than 30 is tion, especially during the first trimester. The
recommended. decision to scan a pregnant patient reduces to
Another circumstance in which gadolinium a risk-benefit analysis. Whereas the risk is
administration is not recommended is preg­ unknown and theoretical, the benefit should be
nancy.24 Gadolinium passes across the placenta, tangible to justify the study. For example, in
entering the fetal circulation, and is excreted by cases of suspected appendicitis, MRI threatens
the fetal kidneys into the amniotic fluid, where less fetal harm than the effects of ionizing radia­
it potentially dissociates threatening harmful tion incurred during CT scanning, justifying the
effects. However, the risk to the fetus/embryo use of MRI in this potentially life-threatening
is unknown, relegating gadolinium use in preg­ circumstance.25
nancy to the class C drug category. The (theo­
retical) risk-benefit ratio recommends gadolinium
SUMMARY
abstinence during pregnancy.
MRI imposes no known biologic effects on Although MRI avoids ionizing radiation present
the fetus. However, the theoretical risk of sub­ in other imaging modalities and employs
jecting dividing cells undergoing organogenesis contrast media with less risk of serious
34  •  Fundamentals of Body MRI

compli­cations, a finite risk of complications 2. Pavlicek W. MR instrumentation and image formation.

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unnecessary exposure to patients at elevated cepts. Radiographics 7:579–596, 1987.
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The process of obtaining images in MRI ders, 2004.
6. Brown MA, Semelka RC. MRI Basic Principles and Appli­
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ate dimeglumine: Experience with 32,659 injections.
MRI into this brief synopsis inevitably trivializes AJR Am J Roentgenol 194:430–434, 2010.
its complexity and the time and effort required 22. Hunt CH, Hartman RP, Hesley GK. Frequency and sever­
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Fundamental physics of MR imaging. Radiographics
25:1087–1099, 2005.
 chapter two 

MRI of the Liver

INTRODUCTION
distance from the patient and ROI. Most torso
Magnetic resonance imaging (MRI) is the coils afford the use of parallel imaging (MRI’s
most comprehensive and definitive noninvasive counterpart to multidetector computed tomog-
modality for evaluating the liver. A combination raphy [CT]) to further lower acquisition times.
of enhancement characteristics and exquisite Acquisition times drop in proportion to the par-
tissue contrast allows for characterization of allel imaging factor—a measure of the degree of
liver lesions. Unique artifacts—such as suscepti- parallel imaging incorporated into the pulse
bility and chemical shift—allow for sensitive sequence—facilitating breathholding (although
detection of hepatic iron and lipid deposition, SNR also drops).
respectively. Common indications for liver MRI Intravenous gadolinium is routinely admini­
include liver lesion characterization, hepatic stered unless contraindicated by a previously
steatosis quantification and surveillance, liver documented reaction to gadolinium or a signifi-
surveillance in patients with risk factors for cant risk of nephrogenic systemic fibrosis (NSF)
hepatocellular carcinoma (HCC), metastatic in cases of severe renal failure (glomerular
workup in patients diagnosed with cancer, and filtration rate [GFR] < 30 mL/min). With lesser
further investigation for patients with abnormal degrees of renal insufficiency (GFR 30–60 mL/
liver enzymes of unknown etiology (Table 2-1). min), gadolinium formulations with higher
relaxivity permit a lower dose, theoretically
minimizing the risk of NSF (Table 2-2). The stan-
dard dose is 0.1 mmol/kg; smaller doses (0.5–
TECHNIQUE
0.7 mmol/kg) of agents with greater relaxivity
The need to achieve high spatial resolution are administered in patients with renal
promptly—within a breathhold—demands insufficiency.
rapid imaging capabilities. Because signal-to- Dynamic imaging—repetitive imaging of the
noise ratio (SNR) is the rate-limiting step, scan- same ROI before and repeatedly after
ners yielding more SNR scan faster. Because SNR gadolinium—depicts the duality of hepatic
increases roughly proportionally to magnetic blood supply and detects underlying lesions
field strength, high-field systems are capable of with aberrant blood supply. Dynamic imaging
shorter acquisition times compared with their relies on reproducible, rapid contrast delivery
low-field counterparts, minimizing motion arti- best achieved by power injecting (2–3 mL/sec).
fact while preserving SNR. Practically speaking, Timing the acquisition of the arterial phase
1.0 Tesla defines the threshold below which images is critical and multiple techniques serve
abdominal imaging suffers from prohibitively to gauge the arrival of contrast into the arterial
low SNR and long acquisition times promoting system to accurately time the arterial phase of
(breathing) motion artifact (Fig. 2-1). With the examination (Fig. 2-3). The timing bolus is
diminishing field strength, image quality declines the time-tested and least technically sensitive
generally below acceptable levels (Fig. 2-2; see method. After an injection of a small volume of
also Fig. 2-1). contrast (2–3 mL), a T1-weighted gradient-echo
A quality examination demands a coil dedi- (GE) image is obtained at the level of the abdo­
cated to the region of interest (ROI)—an abdo­ minal aorta until enhancement is detected—
minal phased array torso coil, which is wrapped defining the onset of the arterial phase. The
around the abdomen. The body coil built into application of superior and inferior saturation
the gantry of the magnetic resonance (MR) pulses removes pseudoenhancement of the
system is a suboptimal alternative yielding less aorta and inferior vena cava (IVC), respectively,
signal commensurate with the increased due to the inflow effect.
35
36  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-1.  Liver magnetic resonance imaging (MRI) obtained on a 0.3-Tesla system. Axial in-phase (A) and out-of-phase (B) images
display relatively markedly diminished signal throughout the liver on the out-of-phase image compared with the in-phase image, indicat-
ing fatty infiltration. The axial T2-weighted image (C) reveals a small hyperintense lesion (arrow in C and D), which enhances as seen
on the delayed T1-weighted gradient echo image (D), degraded by low signal-to-noise ratio and breathing motion artifact.
 MRI of the Liver  •  37

E F
FIGURE 2-1, cont’d  Axial T2-weighted image obtained on a different patient on a 0.3-Tesla system (E) demonstrates prohibitive artifact
distorting the image beyond diagnostic utility compared with the corresponding image (F) from a follow-up study performed on a 1.5-
Tesla short-bore, open-configuration system.

TABLE 2-1.  Common Indications for Liver Magnetic Resonance Imaging

Indication Imaging Objective Details

Liver lesion Definitive lesion diagnosis (usually detected on CT, US)

characterization
Known or suspected Exclude or detect metastases from gastrointestinal, pancreatic breast, melanoma, or other primary
metastasis tumors
Elevated LFTs Exclude or detect biliary obstruction and potential obstructing mass or stones, parenchymal
disease due to inflammation or underlying lesions
Chronic liver disease/ Exclude or detect hepatocellular carcinoma, evaluate vascular structures for patency, assess for
cirrhosis portal hypertension, assess degree of cirrhosis
Portal venous patency Identify normal enhancement and absence of filling defect, recanalization or collateralization Consider ⇑ dose gadolinium,
SSFP
Hepatic steatosis Quantify degree of steatosis, assess for development of cirrhosis Consider spectroscopy
Iron deposition Liver iron quantification; involvement of pancreas, spleen, bone marrow, myocardium Specific protocol for Fe
quantification
Response to treatment Identification of residual/recurrent viable tumor after percutaneous, intra-arterial, or systemic
therapy
Hepatocellular Assess size, multifocality and vascular invasion Correlate with alpha-
carcinoma fetoprotein levels
Cholangiocarcinoma Assess size, extent of biliary involvement, lobar atrophy, lymphadenopathy, vascular invasion
CT, computed tomography; LFTs, liver function tests; SSFP, steady state free precession; US, ultrasound.
38  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 2-2.  Liver MRI obtained on a 1.5-Tesla system. In-phase (A) and out-of-phase (B) images demonstrate steatosis reflected by rela-
tive signal loss on the out-of-phase image. Axial T2-weighted single-shot fast spin-echo (SSFSE) image (C) reveals a small hyperintense
lesion (arrow) in the posterior segment of the liver. The axial arterial (D) and delayed (E) images show initial clumped, peripheral,
discontinuous enhancement with uniform, persistent enhancement (arrow). Note the higher signal-to-noise (SNR) and improved image
quality compared with Figure 2-1A–D.
 MRI of the Liver  •  39

A B

C D
FIGURE 2-3.  Example of BolusTrack timing sequence to initiate the dynamic acquisition. Selected serial coronal large field-of-view
gradient-echo images obtained immediately after the intravenous administration of gadolinium (A–D) reveal the inflow of gadolinium
into the superior vena cava (SVC; A), the right ventricle (B), through the pulmonary outflow tract and into the pulmonary arterial
system (C), and into the thoracic aorta, down the abdominal aorta (D).

TABLE 2-2.  Gadolinium Formulations

Brand Name Generic Name Chemical Structure Charge Elimination Cases of NSF

Omniscan Gadodiamide Linear Nonionic Kidney Yes

OptiMARK Gadoversetamid Linear Nonionic Kidney Yes
Magnevist Gadopentetic acid Linear Ionic Kidney Yes
MultiHance Gadobenic acid Linear Ionic 97% kidney/3% bile Yes
Primovist Gadoxetic acid Linear Ionic 50% kidney/50% bile No
Vasovist Gadofosveset Linear Ionic 91% kidney/9% bile No
Eovist Gadoxetic acid disodium Linear Ionic 50% kidney/50% bile No
ProHance Gadoteridol Cyclic Nonionic Kidney No
Gadovist Gadobutrol Cyclic Nonionic Kidney No
Dotarem Gadoteric acid Cyclic Ionic Kidney No
NSF, nephrogenic systemic fibrosis.
40  •  Fundamentals of Body MRI

TABLE 2-3.  Protocol with Sequence Parameters

Sequence Planes TR/TE Slice Thickness Details

Steady-state Three-plane, axial or coronal min/min 6×0

Heavily T2-weighted Coronal and/or axial NA/180 5×0
In-/out-of-phase Axial min/2.2, 4.4 7×1
Dynamic 3D Axial min/min 4-5 (interpolated ⇒ 2–2.5)
Moderately T2-weighted Axial 3000/80 7 × 0.5
Delayed (3D) Axial min/min 4–5 (interpolated ⇒ 2–2.5)
Delayed (2D) Axial 20/min 5×0
MRCP (2D) Radial NA/∼850 40
MRCP (3D) Coronal 1300/680 2 (interpolated ⇒ 1) Respiration triggered
Diffusion (B = 20) Axial min/min 8×1 Breathhold
Diffusion (B = 500) Axial min/min 8×1 Respiration triggered
MRCP, magnetic resonance cholangiopancreatography; NA, not applicable; 3D, three-dimensional; TE, time to excitation; TR, time to repetition;
2D, two-dimensional.

Real-time viewing of contrast transit (Bolus- wall in order to boost spatial resolution, as long
Track, Philips; CARE Bolus, Siemens; SmartPrep, as wraparound artifact does not obscure the
GE; VisualPrep, Toshiba) involves careful moni- ROI. Assign phase encoding to the anteroposte-
toring by the technologist of serial large field-of- rior (AP) axis and customize the phase FOV to
view (FOV) GE images after administration of the AP dimension of the patient because most
the entire bolus of contrast (see Fig. 2-3). Transit patients are narrower in the AP dimension.
of gadolinium through the superior vena cava Phase encoding costs time, according to the
(SVC) into the right heart through the pulmo- equation: acquisition time = TR × number of
nary circulation and from the left heart into the phase encoding steps × number of signal aver-
aorta is portrayed on the monitor cinegraphi- ages. Therefore, decreasing phase-encoding
cally. With impending arrival of contrast into the FOV commensurate with patient size in the AP
abdominal aorta, the technologist instructs the dimension saves time by eliminating phase-
patient to suspend respiration in preparation to encoding steps (Fig. 2-5) (see Chapter 1).
acquire the arterial phase images. Portal phase The standard protocol includes moderately
images are subsequently obtained after allowing and heavily T2-weighted, in- and out-of-phase
the patient to breathe after the arterial phase GE, dynamic gadolinium-enhanced, and delayed
acquisition. postcontrast T1-weighted images (see Table
Practical demands prioritize throughput, 2-3). Add MRCP (magnetic resonance cholangio-
necessitating economy of pulse sequences and pancreatography) sequences if indicated. The
mandating a rational approach to designing the SSFSE conventionally serves as the heavily
MR protocol (Table 2-3). Begin the examination T2-weighted sequence. Heavy T2-weighting
with a large FOV (~34 cm) T2-weighted (single- means designing the sequence to favor signal
shot fast spin-echo [SSFSE], GE; HASTE, Siemens; from substances with long T2 values (e.g., free
SSH-TSE, Philips; FASE, Toshiba; SSFSE, Hitachi) unbound water—bile, urine). Sequence para­
or balanced GE sequence (balanced FFE, Philips; meters include prolonged TE (time to excita-
true-FISP, Siemens; True SSFP, Toshiba; FIESTA, tion; 180–200 msec) and TR (time to repetition)
GE). Each is a rapid sequence serving as an ana- values. SSFSE sequences are obtained with a
tomic overview. Assess proper coil placement— single excitation pulse followed by a rapid series
maximal signal should originate from the of 180° pulses, each refocusing an echo until all
ROI—the center of the abdomen. Needless to of the k space data for a single slice are acquired.
say, the entire ROI should be visible with ade- So, technically, TR is nonexistent or infinite,
quate SNR (Fig. 2-4). because the excitation pulse is not repeated.
Thereafter, spatial resolution needs and acqui- Although relatively signal-starved (because of
sition time constraints determine FOV. Keeping the single excitation pulse), the SSFSE sequence
the matrix constant (between 256 and 320 in resists motion and susceptibility artifact (Fig.
the frequency axis), adapt the FOV to the 2-6). The rapid acquisition protects against
patient’s size in order to maximize spatial resolu- motion artifact and the multiple refocusing
tion. Sacrifice visualization of the abdominal pulses repeatedly undo or correct for
 MRI of the Liver  •  41

A B
FIGURE 2-4.  Assessing coil placement. A, Coronal localizing SSFSE T2-weighted image reveals maximal signal emanating from the lower
abdomen, instead of the upper abdomen. B, Coronal localizing SSFSE T2-weighted image of a different patient reveals a mildly hyper-
intense exophytic lesion (arrow) arising from the lateral segment of the liver, which is well visualized because of optimal coil placement
yielding superior signal over the region of interest.

susceptibility artifact. Heavy T2-weighting opti-

TABLE 2-4.  In- and Out-of-Phase Times to
mizes tissue contrast for visualizing fluid-filled
Excitation by Magnetic Field Strength
structures, such as the gallbladder and biliary
tree—sort of a “poor man’s MRCP.” Magnetic Field Out-of-Phase In-Phase
Strength (T) (msec) (msec)
In- and out-of-phase images are T1-weighted
GE images with TE values timed to coincide 0.3 11.3 22.6
with fat and water molecules precessing in-phase 0.7 4.8 9.2
1.0 3.4 6.8
and out-of-phase, respectively. On most scan- 1.5 2.2 4.4
ners, these images are obtained simultaneously 3.0 1.1 2.2
as a double-echo sequence in a single breath-
hold; at each slice, one image with an in-phase
TE and one image with an out-of-phase TE are sequence, which boosts SNR compared with
obtained concurrently. TE values are fixed by two-dimensional (2-D) counterparts (allowing
magnetic field strength according to the Larmor for smaller voxels). The increased SNR also
equation (Table 2-4). These images provide permits the use of parallel imaging (which costs
T1-weighting and the ability to detect fat deposi- SNR), reducing acquisition time and breathhold
tion (among other things, which are discussed duration. A set of images preceding the injection
in the forthcoming section). functions as the unenhanced images. The next
The examination revolves around the dyna­­ set of images with identical parameters synchro-
mic gadolinium-enhanced sequence. Dynamic nized with the arrival of gadolinium in the arte-
refers to the temporal sense of the word— rial system (as previously discussed) constitutes
obtaining views at the same location repetitively the arterial phase images. Following a short
after contrast. Since gadolinium is a T1-shortening delay to allow the patient to breathe, a third set
agent, detection of gadolinium enhancement of images with the same parameters is acquired—
necessitates a T1-weighted sequence. Improved the portal phase images.
dynamic range afforded by fat suppression At this point, only moderately T2-weighted and
further improves enhancement conspicuity. delayed enhanced images remain to complete
High spatial resolution requirements recom- the examination. Deferral of the delayed
mend the use of a three-dimensional (3-D) pulse enhanced images until after acquiring
42  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-5.  Rectangular field of view. Axial T1-weighted enhanced images (A and B) performed on a 3-Tesla system with a relatively
large square field of view—adding time-consuming phase-encoding steps to cover air over the patient—in a patient with primary scleros-
ing cholangitis reveal irregular beaded biliary ductal dilatation and structuring as corroborated on the corresponding magnetic resonance
cholangiopancreatography (MRCP) images (C and D).
 MRI of the Liver  •  43

E F

G
FIGURE 2-5, cont’d  The axial postcontrast image in a patient with a patent transjugular intrahepatic portosystemic shunt (TIPS) (arrow
in E) exemplifies the use of rectangular field of view, which results in prominent wraparound of the anterior and posterior abdominal
wall without obscuring the relevant visceral structures. Arterial phase (F) and delayed postcontrast (G) images in a different patient show
a lesser degree of wraparound of the posterior abdominal wall also not interfering with the assessment of the liver and hypervascular
lesion (arrow) with delayed washout—typical features of hepatocellular carcinoma.
44  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 2-6.  SSFSE images minimizing susceptibility artifact. Coronal (A) and axial (B) T2-weighted SSFSE images in a patient with
embolization coils in gastrohepatic collaterals corresponding to susceptibility artifact (arrow in A-F) in the epigastrium, which is mini-
mized compared with the axial steady-state image (C)—an alternative localizer—the fat-suppressed T2-weighted fast spin-echo (FSE;
D), the in-phase (E) and the fat-suppressed arterial phase (F) gradient-echo images. Note the clear depiction of loops of small and large
bowel on the coronal SSFSE image.
 MRI of the Liver  •  45

the moderately T2-weighted images achieves

TABLE 2-5.  Magnetic Resonance Imaging
a reasonable delay. Moderately T2-weighted
Liver Checklist
images possess better tissue contrast compared
with their heavily T2-weighed counterpart and Technical
Magnetic field strength
the presence of intravenous gadolinium confers Coil position
even higher conspicuity for solid liver lesions Signal ⇒ maximal signal arising from liver
compared with normal parenchyma.1 Normal Enhancement ⇒ note amount and type of contrast administered
Arterial phase adequacy
tissue retains more gadolinium and the associ- Artifacts
ated magnetization transfer effects diminish Susceptibility ⇒ surgical hardware, embolization coils, TIPS, bowel
parenchymal signal, resulting in greater lesion- gas, etc.
Motion ⇒ bulk motion, respiratory motion, vascular flow artifacts
to-liver contrast-to-noise ratio (CNR). Fat sup- Conductivity/dielectric effects ⇒ focal signal loss (⇑ at 3 T)
pression conveys greater tissue contrast by
improving dynamic range. Moderate T2-weighting Signal
Fat ⇒ loss of signal on out-of-phase
requires TE values on the order of 80 msec and Diffuse versus segmental versus focal
the fast spin-echo (FSE)—or turbo spin-echo Fatty sparing
(TSE)—sequence adapts best to this parameter Iron ⇒ loss of signal on in-phase
Pancreatic signal loss
requirement within the constraints of a breath- Splenic signal loss
hold. Whereas the FSE sequence rapidly fills k Bone marrow signal loss
space enabling breathhold imaging, the relatively Fibrosis ⇒ reticular versus confluent
longer acquisition time compared with other Morphology
sequences (such as the SSFSE), especially on Atrophy/hypertrophy
older systems, challenges breathholding. Respi- Nodularity
Capsular retraction
ratory triggering circumvents this problem.
The delayed (or interstitial or equilibrium) Vascular
phase images depict the eventual passage of Portal system
Portal vein and branches
contrast into the extravascular space, perfusing Superior mesenteric vein
the interstitial tissues. Either 3-D or 2-D Splenic vein
T1-weighted fat-suppressed GE sequences Hepatic veins
Arterial system
suffice. Three-dimensional pulse sequences Celiac axis
potentially suffer more from breathing motion Stenosis
artifact—obviated on the 2-D sequence, when Variant anatomy
Left hepatic artery from left gastric artery
fragmented into multiple breathholds. A delay Common hepatic artery from SMA
of up to 7 minutes has been proposed, defined Replaced or accessory right hepatic artery from SMA
by the time enhancement occurs in cholangio- Hepatic artery
Occlusion or stenosis after liver transplantation
carcinoma. Practically, this is rarely achieved in
order to maximize throughput. Focal Lesions
Cystic versus solid
Solitary versus multiple
SMA, superior mesenteric artery; TIPS, transjugular intrahepatic
INTERPRETATION portosystemic shunt.

An effective search pattern acknowledges the

specific utility of each pulse sequence (Tables precontrast fat-saturated sequence is T1-
2-5 and 2-6). The multiplicity of arcanely named weighted with sensitivity to blood, protein, and
pulse sequences is simplified according to a melanin (paramagnetic substances). The post-
basic T1-weighting versus T2-weighting scheme. contrast dynamic T1-weighted sequences are
T1-weighted images include the in- and out-of- T1-weighted with sensitivity to solid tissue
phase, dynamic, and delayed T1-weighted GE (enhancement) and vascular structures.
pulse sequences. In addition to the inherent T1 Enhancement on the delayed T1-weighted
contrast inherent to all of these pulse sequences, sequence represents a map of extracellular
each possesses unique properties. The out-of- spaces, because conventional gadolinium agents
phase sequence is T1-weighted with sensitivity are extracellular agents. With time, gadolinium
to microscopic fat. The in-phase sequence is eventually travels throughout the extracellular
T1-weighted with sensitivity to susceptibility space (including the vascular space and intersti-
artifact or iron (practically speaking). The tium). Substances with large extracellular
46  •  Fundamentals of Body MRI

showcasing fluid and cystic lesions—the water-

TABLE 2-6.  Pulse Sequence Scheme
specific (or free water) sequence. The moder-
T2-Weighted Sequences ately T2-weighted sequence depicts subtle
• Moderately T2-weighted sequence = water-sensitive sequence = bound
water sequence differences in bound water (found in solid
TE ≈ 80 msec, usually fat-suppressed tissue), sensitive to the increased bound water
Superior tissue contrast ⇒ subtle differences in bound water in malignant lesions—the water-sensitive (or
Sensitive for solid lesions
Depicts lymph nodes bound water) sequence. The MRCP sequence
• Heavily T2-weighted sequence = water-specific sequence = free water receives signal only from free water protons—
sequence the (free) water-only sequence.
TE ≈ 180 msec, usually performed with single-shot technique
Depicts free water with benefit of anatomic detail The individual properties of each sequence
Lacks tissue contrast dictate the approach to that particular set of
Rapid ⇒ motion insensitive images. For example, heavily T2-weighted SSFSE
Resistant to susceptibility artifact (⇑⇑ 180° refocusing pulses)
• MRCP sequence = water-only sequence images are grant conspicuity to fluid-filled
TE > 500–750 msec, 2D and 3D techniques objects and are resistant to motion and suscep-
Renders only free water protons due to ⇑⇑ TE tibility artifact—optimally adapting them to
Perform after intravenous gadolinium to eliminate signal from
collecting systems evaluate the gallbladder, hepatobiliary tree, pan-
• Steady-state sequence = fluid-solid tissue sequence creatic duct, and gastrointestinal tract (minimiz-
T2/T1-weighted sequence but functionally T2-weighted ing peristaltic motion artifact and gas-related
Dephasing of moving spins refocused ⇒ vessels yield signal
Accessory vascular sequence susceptibility artifact) (Fig. 2-7). Cystic lesions
(such as simple cysts and hemangiomas)—as
T1-Weighted Sequences opposed to solid lesions—and other fluid-filled
• Out-of-phase sequence = microscopic fat sequence
TE = 2.2 msec (at 1.5T), usually performed with in-phase as one
structures (such as the renal collecting system)
pulse sequence are clearly depicted on these images.
Shows microscopic fat as hypointensity compared with in-phase Steady-state images exploit T2/T1 contrast
Phase cancellation artifact ⇒ signal void at fat/water interfaces
(“India ink” artifact)
and portray superior fluid-to-solid tissue con-
• In-phase sequence = susceptibility sequence trast. Practically, the chief diagnostic utility of
TE = 4.4 msec (at 1.5T), usually performed with out-of-phase as one these sequences is the evaluation of fluid-filled
pulse sequence
Shows ferromagnetic substances (iron, surgical clips, metallic objects)
structures and blood vessels (and heart) (Fig.
as susceptibility artifact (or signal void more prominent compared 2-8). Susceptibility artifact plagues these sequ­
with out-of-phase) ences, limiting utility for evaluating bowel.
• Precontrast fat-suppressed sequence = paramagnetic sequence
Precontrast phase of dynamic sequence, usually performed with 3D
In- and out-of-phase sequences yield multi­
technique faceted diagnostic information (Fig. 2-9). Use
Only paramagnetic sequences yield signal ⇒ hemorrhage, protein, the T1-weighted microscopic fat sequence (out-
melanin, etc.
• Dynamic postcontrast sequences = solid tissue (and vascular)
of-phase) by comparing signal intensity of the
sequences opposed-phase images with the in-phase images.
Each phase after contrast offers specificity for different solid lesions Signal loss on opposed-phase images indicates
and vascular structures
3D sequences ⇒ better SNR, thinner contiguous slices, prone to
microscopic fat. Use the T1-weighted suscepti-
saturation bility sequence (in-phase) to detect susceptibil-
2D sequences ⇒ lower SNR, thicker noncontiguous slices, avoid ity artifact and iron by comparing signal intensity
saturation
Time-of-flight effect ⇒ inflow of fresh protons in vessels yields signal
between in-phase and opposed phase images;
• Delayed postcontrast sequence = interstitial phase sequence loss of signal on the in-phase image suggests
Same parameters as dynamic sequence susceptibility artifact (e.g., cholecystectomy
Substances with large extracellular spaces gradually enhance most
avidly on delayed images
clips, iron deposition in the liver and/or spleen
or pancreas). In addition to the unique attri-
MRCP, magnetic resonance cholangiopancreatography; SNR, signal-
to-noise ratio; 2D, two-dimensional; 3D, three-dimensional; TE,
butes of these images, their T1 contrast lends
time to excitation. conspicuity to blood, melanin, and (macro-
scopic) fat. Search the kidneys for hemorrhagic
spaces, such as fibrosis and inflammation, often cysts; the liver for dysplastic nodules (in the
enhance most avidly on the delayed sequence— appropriate clinical setting of cirrhosis); the
the interstitial phase sequence. liver, spleen, and kidneys for subcapsular hema-
T2-weighted images include the moderately tomas (in the appropriate clinical setting); and
and heavily T2-weighted (and steady-state) and the liver for melanotic melanoma or hemor-
MRCP images. The heavily T2-weighted rhagic metastases (in the setting of a known
sequence is specific for free water molecules, primary malignancy).
 MRI of the Liver  •  47

A B
FIGURE 2-7.  SSFSE image resistance to motion and susceptibility artifact and utility for fluid-filled structures. Coronal (A) and axial (B)
heavily T2-weighted SSFSE images depict fluid-filled structures, such as the stone-containing gallbladder (arrow) and loops of bowel,
with great detail and clarity and absence of susceptibility and motion artifact.

A B
FIGURE 2-8.  Steady-state images. A, Coronal steady-state image in the same patient depicted in Figure 2-4B demonstrates robust fluid–to–
solid tissue contrast, with exquisite depiction of the imaged cardiac chambers, gallbladder (arrow), and intrahepatic vessels and bile ducts.
B, A sagittal steady-state image in a different patient with cirrhosis shows hyperintensity of the cerebrospinal fluid and cardiac chambers
and a tortuous hyperintense structure (arrow) extending to the umbilicus—a paraumbilical portosystemic collateral.

However, the fat-suppressed precontrast pancreatic parenchyma become far more

T1-weighted sequence is the paramount conspicuous.
T1-weighted blood (paramagnetic) sequence Change in signal on the postcontrast images
(Fig. 2-10). By spectrally eliminating macro- compared with the precontrast images equals
scopic fat signal and dramatically improving enhancement, which occurs in solid lesions and
dynamic range, methemoglobin in hematomas, vascular structures—hence, the designation
hemorrhagic cysts, hemorrhagic metastases, T1-weighted images for solid and vascular
melanoma in melanotic metastases, copper in lesions. The multiphasic nature of the dynamic
dysplastic nodules and protein in normal sequence furnishes layered, multifaceted
48  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-9.  In- and out-of-phase images. Axial out-of-phase (A) and in-phase (B) images in a patient with severe steatosis show marked
reduction in signal on the out-of-phase image and similar signal drop in a left adrenal adenoma (arrow). Axial out-of-phase (C) and
in-phase (D) images in a different patient with hemosiderosis portray the opposite pattern with relative signal loss on the in-phase image
as a consequence of susceptibility artifact.

A B
FIGURE 2-10.  T1-weighted fat-suppressed image. The T2-weighted fat-suppressed image (A) reveals multiple nonspecific hyperintense
lesions, many of which appear hyperintense on the T1-weighted fat-suppressed image (B) due to their melanotic content in a patient
with metastatic uveal melanoma.
 MRI of the Liver  •  49

information that requires careful attention to T2-weighted images discriminate fluid-filled

technique. Compare the arterial phase images lesions, such as cysts and hemangiomas, from
for technical adequacy—the signal intensity of liver parenchyma, solid masses and lesions
the hepatic parenchyma on the arterial phase approximate normal parenchymal signal. Con-
images should approximate the signal on the ceptually, most pathologic conditions, although
unenhanced images (because the liver is largely not cystic, generally harbor more water protons
perfused by the portal vein under normal cir- compared with normal tissue. Whereas long TE
cumstances) (Fig. 2-11). Arterially enhancing values—in heavily T2-weighted images—target
lesions (such as focal nodular hyperplasia [FNH], substances with very long T2 values and fail to
adenoma, vascular shunts, hypervascular meta­ discriminate subtle differences in tissue water
stases, and HCC) brightly contrast with the content, moderately T2-weighted images retain
relatively dark, unenhanced background liver sensitivity to slight differences in tissue water
parenchyma. On portal phase images, hypo­ content (Fig. 2-12). Moderately T2-weighted
vascular liver lesions gain conspicuity as the image contrast is designed to detect solid
background parenchyma enhances—cysts and lesions with slightly greater water content from
hypovascular metastases are relatively dark. normal liver parenchyma (Fig. 2-13). Malignant
Identify arterial stenoses and aberrant arterial lesions generally contain slightly greater water
anatomy on the arterial phase images and venous content and appear mildly hyperintense com-
occlusion and anatomic anomalies on the portal pared with liver parenchyma. Outside the liver,
venous images. lymph nodes, pancreatic parenchymal lesions
Moderately T2-weighted images (the T2 and peripancreatic inflammation, pericholecys-
solid lesion images) supplement the dynamic tic inflammation, and other pathology are con-
sequence in identifying and characterizing liver spicuous as a consequence of increased water
lesions and, generically speaking, serve as a resulting in hyperintensity (especially with fat
“pathology sequence.” Whereas heavily saturation).

A B

FIGURE 2-11.  Technically adequate enhancement. The signal

intensity of the liver parenchyma on the arterial phase image
(B) more closely approximates the liver signal on the precon-
trast image (A) compared with the portal phase image (C) in
a hepatitis B patient with a hypervascular lesion simulating
HCC (which turned out to be a perivascular epithelioid cell
tumor, or PEComa—a tumor of uncertain malignant
C
potential).
50  •  Fundamentals of Body MRI

Delayed images confirm absence of enhance- In summary, simplify the myriad potentially
ment in cystic lesions and delayed enhancement confusing pulse sequences into a few basic cat-
in specific lesions, such as hemangiomas, chol- egories (see Table 2-6). The three T2-weighted
angiocarcinoma, and fibrous lesions (scarring). pulse sequences include (1) water-sensitive
Inspect venous structures again for potential T2-weighted images—the heavily T2-weighted
anatomic anomalies and/or occlusion. Use SSFSE sequence; (2) pathology-sensitive images,
delayed enhancement as a potential indication or moderately T2-weighted images; and (3)
of inflammation, which becomes more conspic- water-only images—MRCP images. The T1-
uous as gadolinium accumulates in the expanded weighted images also enjoy uniquely different
interstitial space associated with inflammation properties. Out-of-phase images are T1-weighted
and edema. images with sensitivity to microscopic fat.
In-phase images are T1-weighted images with
sensitivity to susceptibility artifact, such as iron
deposition and artifact arising from surgical
↑ T2
relaxation clips or clumps of calcium. Precontrast fat-
suppressed images are T1-weighted images with
Signal

sensitivity to hemorrhage, melanin, and protein.

↑ Tissue
contrast Postcontrast dynamic images are T1-weighted
↓ T2
relaxation
images with sensitivity to viable tumor and vas-
↓ Tissue cular anatomy.
contrast

NORMAL FEATURES
Moderate Heavy
T2 weighting T2 weighting Morphology, signal, and texture are the cur-
TE rency used to describe the MRI appearance of
FIGURE 2-12.  T2 relaxation curves show heavily versus moder- the liver. The normal liver is usually described
ately T2-weighted contrast. TE, time to excitation. from a negative reference point—“lack of

A B

FIGURE 2-13.  Moderately T2-weighted image. The axial

heavily T2-weighted SSFSE image (A) demonstrates multiple
subtle hepatic and splenic lesions, which are much more 
conspicuous on the moderately T2-weighted fat-suppressed
image (B). The lesions are also relatively inconspicuous on the
postcontrast image (C). Note the typical peripheral enhance-
C
ment in the lateral segmental lesion (arrow).
 MRI of the Liver  •  51

Signal characteristics generally supplement

IVC enhancement data in assessing liver lesions.
I
Gadolinium enhancement is a biphasic phenom-
II enon in the liver as a consequence of dual blood
supply. The portal vein delivers 75% of blood
VII IVa
VIII
III flow to the liver, with the hepatic artery account-
ing for the rest. Four discrete phases describe
IVb the transit of intravenous contrast through the
liver: the hepatic artery–only phase (HAOP),
V the hepatic artery–dominant phase (HADP;
VI
PV also known as the capillary phase), the portal
venous phase (PVP; also known as the early
hepatic venous phase), and the hepatic venous
FIGURE 2-14.  Liver segments. IVC, inferior vena cava; PV, portal phase (HVP; otherwise known as the interstitial
vein. phase) (Fig. 2-15).
Liver imaging relies heavily on the HADP.
HADP image acquisition begins approximately
15 seconds after contrast administration. Modest
nodularity” or “no atrophy/hypertrophy enhancement, or relative T1 hyperintensity
pattern.” Normal liver texture is smooth, compared with unenhanced images, and con-
reflected by an absence of both surface nodular- trast within the hepatic arteries and portal veins
ity and an underlying reticular appearance. The characterize the HADP in which the paren-
liver occupies most of the right upper quadrant chyma has been perfused by the hepatic arterial
and global morphology varies. Mentally decon- circulation (Fig. 2-16). Arterial contrast preced-
struct the liver into segments—right lobe, ing parenchymal and portal venous enhance-
medial segment, lateral segment, and caudate ment corresponds to the HAOP, preceding the
lobe—to establish the basis for normal and mor- HADP. Successful acquisition of an HADP phase
phologic derangements associated with cirrho- permits lesion enhancement stratification into
sis (the former two atrophy and the latter two four categories relative to liver parenchyma:
hypertrophy) (Fig. 2-14). hypervascular (more arterial perfusion), isovas-
Further deconstruct the liver spatially into cular, hypovascular, and avascular (Fig. 2-17).
segments according to the Couinaud system in Correlating this information with data from sub-
order to facilitate communication with referring sequent timepoints often yields specific diagnos-
physicians and specifically locate lesions and tic information. Before making this assessment,
pathology. Each Couinaud segment functions corroborate adequate timing of the intended
independently with unique vascular inflow, HADP; early or delayed timing potentially
outflow, and biliary drainage; the central portal obscures hypervascular lesions.
vein, hepatic artery, and bile duct define the PVP acquisition time begins approximately 45
segment. Consequently, each segment is inde- to 60 seconds after contrast administration and
pendently resectable without affecting neigh- corresponds to peak parenchymal enhance-
boring liver tissue. The horizontal plane of the ment. All vessels, including hepatic veins, are
portal vein bifurcation transects the vertical enhanced. Liver features during the HVP resem-
planes of the hepatic veins to delineate the ble the PVP and underlying lesion enhancement
Couinaud segments. changes, such as washout, may be more
Relatively low water content accounts for conspicuous with time. PVP timing constraints
hepatic parenchymal signal characteristics— are less rigorous and may be obtained between
relative T1 hyper- and T2 hypointensity. Hepatic 90 seconds and 5 minutes after contrast
T1 signal nearly matches pancreatic T1 hyperin- administration.
tensity, and most tumors contain more water
and appear relatively T1 hypointense and T2
FOCAL LESIONS
hyperintense to normal liver. Isointensity
between in- and out-of-phase images reflects an Exquisite tissue contrast and enhancement
absence of fat and iron deposition under normal conspicuity distinguish MRI as the definitive
circumstances. noninvasive diagnostic authority on liver lesions.
 Precontrast
HAOP

HA

PV HADP
IVC

PVP
Interstitial phase

HA = Hepatic artery HAOP = HA only phase

PV = Portal vein HADP = HA dominant phase
FIGURE 2-15.  Dynamic enhancement IVC = Inferior vena cava PVP = PV phase
phases with schematic representations.

A B

C D
FIGURE 2-16.  Hepatic artery–dominant phase (HADP). Notice the relatively similar intensity of the liver parenchyma on the (hepatic
artery–dominant) arterial phase image (A) compared with the unenhanced image (B) and hypointensity compared with the portal phase
image (C), indicating a lack of portal perfusion despite gadolinium in the main portal vein. Note the focal nodular hyperplasia (FNH)
in the medial segment (arrow in A) enhancing avidly in the arterial phase. Compare the HADP image (A) with a prematurely obtained
hepatic artery–only phase image (D), which shows lack of parenchymal enhancement with isolated enhancement of arterial structures
without portal venous enhancement in a different patient with an aortic aneurysm (arrow in D) responsible for slow flow.
 MRI of the Liver  •  53

Precontrast

Contrast administration

Avascular Hypovascular Isovascular Hypervascular

(i.e., cyst) (i.e., metastasis)

FIGURE 2-17.  Liver lesion enhancement

scheme based on hepatic artery–
Washout Fading Persistent
(i.e., HCC) (i.e., FNH) hyperintensity dominant phase (HADP) findings.
(i.e., flash-filling FNH, focal nodular hyperplasia; HCC,
hemangioma) hepatocellular carcinoma.

Cystic Lesions
Like ultrasound, MRI unequivocally discrimi-
nates solid from cystic lesions and, like CT, Establish cystic lesion character using heavily
incorporates enhancement characteristics into T2-weighted images and pre- and postcontrast
the diagnostic analysis. T2 values differentiate images. As T2-weighting increases, signal decays
cystic (almost always benign) from solid (benign from everything but unbound water protons
or malignant) lesions with virtually no overlap. and free fluid. Consequently, on heavily
Review the heavily T2-weighted images to iden- T2-weighted images, all hyperintense lesions are
tify cystic lesions; visibility on these images con- effectively cystic. Cystic designation effectively
notes predominantly fluid content and excludes connotes benign etiology. Simple cysts and
solid masses. Cysts, biliary hamartomas, and biliary hamartomas define the highest end of the
hemangiomas—all benign lesions—dominate T2 signal intensity spectrum as purely fluid-filled
this category, referred to as cystic lesions, for structures (Fig. 2-18). Hemangiomas are slightly
the purposes of this discussion. Inflammatory less intense and frame the lower limit of signal
lesions, such as echinococcal cysts and abscesses, intensity for fluid-intensive liver lesions. Echino-
enter the differential only in the appropriate coccal cysts are generally similar in intensity to
clinical setting. In the neoplastic category, only simple cysts, but might be complicated with
the exceedingly rare biliary cystadenoma (and wall thickening, septation (pericyst), (daughter
cystadenocarcinoma) breaches the cystic liver cyst), and/or internal debris (matrix, hydatid
lesion differential and only when characteristic sand). Fungal and pyogenic abscesses are usually
features coexist. Whereas cystic or necrotic not technically cystic and are more accurately
metastases feature cystic components, periph- described as “liquefying,” but for the purposes
eral solid tissue excludes true cystic etiology. of our discussion, they are included in the cystic
Enhancement indicates solid tissue excluding category. The only neoplastic lesion—biliary
cystic etiologies and serves as the basis for solid cystadenoma/cystadenocarcinoma—is predomi-
versus cystic lesion classification and diagnosis nantly cystic with variable septation and scant
(supplemented by T2 characteristics). solid tissue (unless rarely flagrantly malignant).
54  •  Fundamentals of Body MRI

Cyst these complications, lack of enhancement is

otherwise maintained.
Of course, the probability of complications
Pseudocyst increases with an increased number of cysts.
With more than 10 cysts, the possibility of poly-
T2 signal

Abscess cystic liver disease (PCLD) should be considered

Cystic
neoplasms (see Fig. 2-19). PCLD is in the family of fibro-
FNH
polycystic liver diseases that include bile duct
hamartoma, Caroli’s disease, congenital hepatic
Hemangioma
fibrosis, and choledochal cysts. Imaging features
HCC do not distinguish these cysts from simple
hepatic cysts and histology is identical. Although
Fluid content commonly associated with polycystic kidney
FIGURE 2-18.  T2 signal lesion graph. Normal liver tissue plots to
disease, PCLD also occurs in isolation.
the same point as FNH on the graph. FNH, focal nodular hyper-
plasia; HCC, hepatocellular carcinoma. Bile Duct Hamartoma
The bile duct hamartoma (von Meyenburg
complex) is another liver lesion that is usually
Developmental Lesions cystic. It is a focal cluster of disorganized
bile ducts and ductules surrounded by
Simple Hepatic Cyst fibrous stroma. Bile duct hamartomas are inci-
Simple hepatic (bile duct) cysts are benign dental developmental lesions of uncertain
incidental lesions not communicating with the pathogenesis—possibly ischemia, inflammation,
biliary tree,2 although lined with biliary endothe- or genetic anomalies. Although present in 3% of
lium. They arise from a defect in bile duct forma- autopsy specimens,4,5 more than half evade
tion. Hepatic cyst prevalence has been reported detection on imaging studies. Lesion size ranges
in the 2.5% range,3 although anecdotal experi- from 2 to 15 mm, and they tend to be peripher-
ence suggests a higher prevalence. These lesions ally distributed. The MRI appearance is defined
are almost always incidental, unless associated by a spectrum extending from simple fluid with
with an inherited polycystic syndrome. no enhancement on one end to solid, enhancing
The water content of cysts dictates the imaging tissue (fibrous stroma) on the other. The simple
appearance—uniform T2 hyperintensity and T1 fluid appearance dominates, simulating a hepatic
hypointensity equivalent to cerebrospinal fluid cyst, although a thin, peripheral rim of enhance-
(Fig. 2-19). No solid tissue complicates the ment occasionally coexists (Fig. 2-20). When
appearance and the wall is imperceptible. Size solid, these lesions exhibit intermediate signal
ranges from a few millimeters to (usually) less intensity on T2-weighed images and generally
than 10 cm. Occasional thin (essentially unmea- gradually solidly enhance. Progressive enhance-
surable) septa are present. Simple cysts maintain ment of the fibrous tissue simulates metastases
maximum signal intensity even on heavily and follow-up imaging to confirm stability or
T2-weighted images, whereas other relatively biopsy ensues.
high fluid content substances (such as hemangi-
oms) lose signal compared with moderately Caroli’s Disease
T2-weighted images. The absence of solid tissue Caroli’s disease (or “congenital communicating
is confirmed when contrast enhances the back- cavernous ectasia of the biliary tract,” if you
ground liver parenchyma and the water-filled prefer—less mellifluous but descriptive) simu-
cyst remains a T1 signal void. Complications lates other polycystic liver diseases—PCLD, mul-
explain aberrancy in the monotonous appear- tiple simple (biliary) hepatic cysts, and biliary
ance of simple cysts and include infection, hamartomas. Many of these cystic diseases
rupture, and hemorrhage. Infected cysts may (except the biliary cyst) derive from primordial
contain septa and debris, which changes the ductal plate disorders.6,7 Caroli’s disease repre-
internal signal profile. Hemorrhagic cysts usually sents one of the family of fibrocystic ductal plate
exhibit T1 hyperintense internal contents with diseases to which the following diseases also
possible fluid-fluid levels. Although minimal belong: autosomal recessive polycystic kidney
reactive rim enhancement may accompany disease, congenital hepatic fibrosis, autosomal
 MRI of the Liver  •  55

A B

FIGURE 2-19.  Polycystic liver disease. Axial (A) and coronal (B)
heavily T2-weighted images show hepatomegaly with replace-
ment of the hepatic parenchyma with cysts with involvement
of the kidneys (arrows in A) in a patient with polycystic liver
(and kidney) disease. C, The T1-weighted fat-suppressed
image shows septation (thin arrow) and hemorrhage (thick
C
arrows) complicating scattered cysts.

inflammation and stricturing alternating with

TABLE 2-7.  Fibrocystic Ductal Plate Diseases
saccular and fusiform dilatation of the involved
Congenital hepatic fibrosis
Autosomal recessive polycystic kidney disease
ducts results.
Autosomal dominant polycystic kidney disease MRI reveals innumerable round and/or tubular
Autosomal dominant polycystic liver disease fluid collections within the liver measuring up
Caroli’s disease
Choledochal cysts
to 5 cm in Caroli’s disease. Although the pres-
Biliary hamartomas ence of multiple cystic intrahepatic foci simu-
lates PCLD or biliary hamartomas, communication
with the biliary tree discriminates Caroli’s
dominant polycystic kidney disease, biliary ham- disease from these entities. An additional dis-
artomas, and mesenchymal hamartomas (Table criminating feature—the central dot sign8—seen
2-7). The ductal plate represents the anlage of on enhanced images, reflects the portal vein
the intrahepatic biliary system. Ductal plate re- branch within the dilated biliary radicle.
modeling into the mature intrahepatic biliary Intraductal/intracystic filling defects (usually
dilatation follows a complex series of precisely bilirubin stones) may also differentiate Caroli’s
timed events. In the case of Caroli’s disease, disease from the other cystic liver disorders and
arrest in ductal plate remodeling involves the are best visualized on fluid-sensitive sequences—
larger bile ducts (interlobular and more central); either heavily T2-weighted or MRCP images.
Caroli’s syndrome affects the smaller, peripheral Other diseases to consider in the differential
intrahepatic ducts, which undergo remodeling diagnosis include primary sclerosing cholangitis
later in embryonic life and manifest with co­ (PSC) and recurrent pyogenic cholangitis (RPC).
existent hepatic fibrosis. A pattern of segmental Ductal dilatation is less severe and more
56  •  Fundamentals of Body MRI

A B

FIGURE 2-20.  Biliary hamartoma. The coronal heavily

T2-weighted (A) and fat-suppressed moderately T2-weighted
(B) images reveal multiple small fluid-intensity lesions scat-
tered throughout the liver. The maximal intensity projec-
tional image from a three-dimensional (3-D) MRCP sequence
(C) confirms high fluid content isointense to bile. Note the
mild hyperintensity of the breast implants, typical of silicone
C
and less intense than saline.

cylindrical (as opposed to saccular) in PSC and Cavernous Hemangioma

RPC compared with Caroli’s disease. Involve- Hemangiomas (cavernous hemangiomas) are
ment of the extrahepatic duct often character- classified as cystic for the purposes of this dis-
izes PSC and RPC and excludes Caroli’s disease. cussion because of the high fluid content and
Complications in Caroli’s disease occur as a con- MR signal characteristics similar to fluid—even
sequence of bile stagnation and include stones, though the internal contents are blood, instead
cholangitis, hepatic abscesses, postinflamma- of water, or serous fluid. Blood flowing slowly
tory strictures, and secondary biliary cirrhosis. enough to avoid flow artifacts and/or flow voids
Cholangiocarcinoma develops in 7% of patients. accounts for the signal characteristics; a single
 MRI of the Liver  •  57

A B

C D
FIGURE 2-21.  Hemangioma. A, The hemangioma with a characteristic lobulated border demonstrates moderately high hyperintensity on
the heavily T2-weighted image (A), but less than the adjacent fluid-filled gallbladder. The arterial phase image (B) demonstrates the
typical clumped, discontinuous peripheral enhancement, which gradually progresses centripetally to complete uniform hyperintensity,
as seen (arrow in D) on the portal phase (C) and delayed (D) images in a different patient.

layer of endothelial lining suspended by fibrous 2; Fig. 2-22). Relatively smaller and larger
stroma constitutes the only solid component. hemangiomas have a predilection for variant
Hemangiomas are almost invariably incidental enhancement patterns. Small hemangiomas
lesions representing a collection of dilated vas- (<2 cm) more often demonstrate uniform early
cular channels replacing hepatic parenchyma. and persistent hyperenhancement (type 1; Fig.
Hemangiomas are found in 7% of patients with 2-23). Early hyperenhancement also character-
a slight female predominance (1.5 : 1). Multiple izes other benign and malignant lesions, such
hemangiomas are present in up to 50% of as FNH, adenoma, HCC, and hypervascular
patients. metastases. Marked T2 hyperintensity and
Hemangiomas range in size from a few milli- persistent hyperenhancement single out the
meters to well over 10 cm and complexity is so-called flash-filling hemangioma from the
generally proportional to size. The prototypic other hypervascular lesions (none of which
hemangioma exhibits homogeneous near- exhibit marked T2 hyperintensity and all of
isointensity to simple fluid (cyst) on heavily which either washout or fade on delayed
T2-weighted images with well-defined, lobu- images). Perilesional perfusional alterations
lated borders and exhibits a unique enhance- most commonly accompany the smaller flash-
ment pattern. Early peripheral, nodular, filling hemangiomas (see Fig. 2-23). Segmental
discontinuous enhancement centripetally pro- or nodular hyperattenuation (usually peripheral
gressively fills in on successive delayed images to the lesion) on HADP images fades to isoin-
until uniform hyperattenuation (relative to tensity on delayed images and reflects either
hepatic parenchyma) is achieved (Fig. 2-21). increased arterial inflow or arterioportal shunt-
The aforementioned imaging features define ing resulting in contrast overflow into perile-
the standard appearance of hemangiomas (type sional sinusoids.9–11
58  •  Fundamentals of Body MRI

Giant hemangiomas often display complex central variably shaped “scar” (linear, round,
imaging features. The definition of giant hem- oval, cleftlike, or irregular) conforms to cystic
angioma varies from 4 to 10 or 12 cm, depend- degeneration, liquefaction, or myxoid change
ing on the source (4 cm is the conventional size and usually appears relatively T1 hypo- and T2
cutoff).12–16 The enhancement pattern of the hyperintense to the surrounding lesion (Fig.
giant hemangioma often reiterates the typical 2-24). Although other liver lesions possess
pattern with peripheral, nodular, discontinuous central scars, such as FNH, fibrolamellar HCC,
centripetal propagation, except for the pres- and cholangiocarcinoma, these scars usually
ence of a central nonenhancing “scar.” The enhance late and overall lesion enhancement
features are distinctly different (FNH and fibro­
Precontrast Early phase Delayed phase lamellar HCC hyperenhance then washout,
whereas rim enhancement with patchy, irregu-
lar progression typifies cholangiocarcinoma).
Type 1
Less common features complicate the MR
appearance of hemangiomas, such as peduncu-
lation, calcification, capsular retraction, and hya-
Type 2 linization or thrombosis (Fig. 2-25). Whereas
torsion and/or ischemia may complicate the
appearance of an exophytic or pedunculated
hemangioma, the appearance is otherwise
Type 3 typical—just be aware that pedunculation rarely
occurs. Reported prevalence of calcification
varies from 1% to 20%, and anecdotally, the
FIGURE 2-22.  Hemangioma enhancement types.

A B

FIGURE 2-23.  Flash-filling hemangioma with perfusional

perilesional enhancement. A, Moderately T2-weighted fat-
suppressed image shows a small ovoid hyperintense lesion at
the periphery of the anterior segment (thin arrow) adjacent to
a punctate simple cyst (thick arrow). Avid enhancement of the
lesion (thin arrow) on the arterial phase image (B) is partially
obscured by perilesional enhancement (thick arrow), which
fades on the portal phase image (C), whereas the hemangioma
C
retains contrast remaining hyperintense (arrow).
 MRI of the Liver  •  59

A B

FIGURE 2-24.  Giant hemangioma with cystic degeneration.

A, The axial heavily T2-weighted image reveals a large hem-
angioma in the posterior segment with central hyperintensity.
Whereas the periphery of the hemangioma exhibits the typical
early nodular peripheral enhancement (B) with complete
fill-in on the delayed image (C), the central cystic focus fails
C
to enhance.

A B
FIGURE 2-25.  Complex hemangioma. The stellate central hypointensity (arrow in A) within the hyperintense hemangioma on the
moderately T2-weighted image (A) fails to enhance on the delayed image (B).

actual prevalence seems to be closer to the peripheral, fibrosis associated with a hemangi-
lower end of the range, or even lower.17,18 Cal- oma potentially results in capsular retraction.
cification in a hemangioma corresponds to The other focal hepatic lesion known to induce
phleboliths and/or dystrophic changes in areas capsular retraction is cholangiocarcinoma,
of fibrosis and thrombosis. Practically speaking, which should not present diagnostic difficulty.
calcification rarely, if ever, confounds the MR Hyalinization indicates hemangioma involution
appearance of hemangiomas, and if present, and histologically corresponds to thrombosis
most likely manifests as a signal void. When of vascular channels.12,19 T2 signal decreases
60  •  Fundamentals of Body MRI

remaining relatively hyperintense to liver and platelets causing thrombocytopenia. Consump-

enhancement is variably absent with as little as tion of clotting factors ensues, leading to
minimal peripheral delayed enhancement. disseminated intravascular coagulation (DIC).
A few parting thoughts about hemangiomas Unless associated with KMS or DIC, for which
are worth mentioning. Although usually static, surgical resection may be warranted, no treat-
hemangiomas have been shown to grow on ment or follow-up is necessary.
occasion (sometimes with exogenous estro- Hemangiomatosis refers to diffuse replace-
gens), and conversely, they are usually eradi- ment of hepatic parenchyma by multiple, often
cated in the setting of cirrhosis. Malignant innumerable, ill-defined hemangiomas. Diffuse
transformation has never been described and enlargement of the liver with multiple lesions
spontaneous rupture is exceedingly rare (~30 with signal and enhancement characteristics
cases have been reported).20 There is no known typical of hemangiomas—albeit frequently with
association with other tumors or other diseases, ill-defined margins—often profoundly disfigures
except Kasabach-Merritt syndrome (KMS). KMS the liver, rendering it virtually unrecognizable
involves a vascular tumor—such as a hemangi- (Fig. 2-26). Although commonly resulting in
oma or hemangioendothelioma—sequestering high-output cardiac failure and mortality in

A B

C D
FIGURE 2-26.  Hemangiomatosis. Replacement of the normal hepatic parenchyma by ill-defined, near–fluid hyperintensity on the axial
T2-weighted image (A) with gross hepatomegaly evident on the precontrast T1-weighted image (B). Following the administration of
intravenous gadolinium, multifocal nodular enhancement on the arterial phase image (C) progresses to near-complete enhancement on
the delayed image (D), reminiscent of a hemangioma.
 MRI of the Liver  •  61

infants, hemangiomatosis usually symptomati- confounders. Septal and mural calcification

cally spares adults—only potentially generating best visualized on CT usually evades detection
diagnostic uncertainty on imaging studies. on MRI. Communication with the biliary tree—
albeit rare and more likely noted on endo-
Unlike the previously discussed lesions, scopic retrograde cholangiopancreatography
the remaining cystic liver lesions—biliary (ERCP) than MRCP—does not exclude biliary
cysta­­denoma/cystadenocarcinoma and infec- cystadenoma/cystadenocarcinoma.24
tious lesions—exhibit more complexity and Nonneoplastic cystic lesions dominate the dif-
variability. Multilocularity and wall thickening ferential diagnostic possibilities. Echinococcal
are common features, and these lesions rarely cyst, pyogenic abscess, and complicated (hem-
simulate the other simple cystic lesions already orrhagic) bile duct cyst most frequently approxi-
discussed. Clinical factors assume a greater role mate the MR appearance of biliary cystadenoma.
in diagnosis, which is important because all of Rare cystic HCC and cystic metastases are worth
these lesions require further treatment. considering in the differential, but usually mani-
fest a greater solid component, irregular margins,
and suggestive clinical features.
Neoplastic Lesions
Biliary Cystadenoma
Infectious Lesions
(-adenocarcinoma)
Biliary cystadenomas and cystadenocarcinomas Echinococcal Cyst
require surgical resection for treatment and Inflammatory cystic lesions rarely afflict the liver
potential cure. These lesions arise from bile duct and definitive diagnosis usually relies on clinical
epithelium—constituted from mucin-secreting information, such as concurrent infection in the
epithelial cells. Approximately 85% arise from gastrointestinal tract or demographic data in the
intrahepatic bile ducts (as opposed to extra­ case of echinococcal cyst—endemic in certain
hepatic bile ducts and gallbladder).21 Most parts of the world (Table 2-8). Echinococcal
commonly affecting middle-aged females, cysts are a manifestation of hydatid disease,
two histologic subtypes—with or without which encompasses infestation by either of two
ovarian stroma (accounting for the female different species of parasites—Echinococcus
preponderance)—confer different prognostic granulosus and Echinococcus multilocularis.
outcomes. Lesions with ovarian stroma exhibit Dogs, sheep, and cattle serve as (definitive and
a more indolent course compared with lesions intermediate) host organisms for these parasites.
with absent ovarian stroma.22 Differentiating Ingestion of food contaminated with embryo-
benign (cystadenoma) from malignant (cystad- nated eggs (in feces) leads to human infestation.
enocarcinoma) is less relevant than discriminat- Ingested organisms penetrate the intestinal wall
ing neoplasm from nonneoplastic etiologies, and migrate hematogenously (usually) to the
because of the treatment implications—biopsy
and ultimately resection. In any event, no
imaging features reliably discriminate benign TABLE 2-8.  Inflammatory Cystic Liver Lesions
from malignant. Lesion Pathogen Imaging
To put things in perspective, these lesions
Pyogenic abscess Clostridium Variable liquefaction
reportedly constitute less than 5% of cystic liver Gram-negative Cluster sign
lesions23 and empirically far less than that. Size organisms Reactive enhancement
ranges from a few centimeters to up to 40 cm Nonpyogenic abscess
  Amebic abscess Entamoeba Well-defined
and, when detected on imaging studies, these histolytica Peripheral right lobe
lesions are usually fairly large (Fig. 2-27). Extrahepatic findings
Although occasionally unilocular, multilocular-   Fungal abscess Candida <1 cm
albicans Peripheral
ity, septation, and nodularity distinguish these Prominent T2 hyperintensity
lesions from other cystic liver lesions. Variable Splenic, renal involvement
  Mycobacterial Mycobacterium Possibly T2 hypointense
signal intensity of internal contents depends on abscess tuberculosis Calcification
mucin content and occasional hemorrhage. Lymphadenopathy
Whereas mild wall thickening is common and   Echinococcal cyst Echinococcus Daughter cysts
granulosus Hypointense pericyst
nonspecific, associated T2 hypointensity from Internal debris, membranes
hemorrhage excludes many other potential
62  •  Fundamentals of Body MRI

A B

FIGURE 2-27.  Biliary cystadenoma. The coronal (A) and axial

(B) heavily T2-weighted images reveal a large, septated cystic
lesion and the corresponding enhanced T1-weighted fat-
suppressed image (C) confirms an absence of solid, enhancing
C
components, suggesting benignity.

liver and lungs (but not exclusively)—liver 63%, Understanding the mature hydatid cyst struc-
lungs 25%, muscles (5%), bones (3%), kidneys ture and life cycle facilitates appreciation of the
(2%), brain (1%), and spleen (1%). In the target imaging appearance. Mature hydatid cystic tri-
organ, the parasite develops into a cyst. Internal laminar cyst wall structure encompasses the
daughter cysts and protoscolices proliferate. outer pericyst (the fibrous host response layer),
Notwithstanding the respective names, E. the middle laminated membrane (i.e., ectocyst,
granulosus exhibits a multiloculated imaging transmitting the passage of nutrients), and the
appearance contrasted with the infiltrative inner germinal layer (endocyst), from which the
pattern typified by E. multilocularis. Although laminated membrane and larvae (scolices) are
neither is endemic in the United States, E. gran- produced. Scolices spawned from the endocyst
ulosus cases outnumber E. multilocularis in the are contained within daughter cysts (“brood
United States, with approximately 1 per 1 capsules”) within the cyst. Over time, the
million inhabitants. Endemic areas include the hydatid cyst degenerates and progressively calci-
Middle East, southern South America, southern fies (Fig. 2-28).
Africa, the Mediterranean region, Australia, and The imaging appearance corresponds to the
New Zealand. Increasing size and pressure phase of the life cycle and the presence/absence
effects lead to symptoms such as abdominal of complications. In fact, a radiologic classifica-
pain, jaundice, cough, pleuritic chest pain, and tion system expresses this fact visually (see Fig.
dyspnea. 2-28).25 The hydatid cyst generally progresses
 MRI of the Liver  •  63

Type 1 Type 2 Type 3

Unilocular Daughter Ca++

cyst cysts

Infection
rupture

Type 4
FIGURE 2-28.  Hydatid cyst evolution and structure.

scheme describes three categories: contained,

communicating, and direct.27 Contained
rupture connotes endocyst rupture with peri-
cyst integrity with the detached endocyst
reflected by “floating membranes,” a contracted
serpiginous intraluminal hypointensity. Com-
municating rupture happens when cyst con-
tents pass into biliary radicles incorporated into
the pericyst. Direct rupture involves both the
endocyst and the pericyst with spillage into the
peritoneal cavity. Communicating and direct
rupture result in cyst deflation and focal loss of
integrity of the hypointense pericyst, although
interruption of the hypointense rim is often
FIGURE 2-29.  Echinococcal cyst. Except for a mildly irregular
contour, the thin hypointense rim is the only finding complicat-
difficult to visualize. Communicating and direct
ing the large echinococcal cyst in the right lobe—daughter cysts ruptures permit intracystic passage of bacteria
would seal the diagnosis. and superinfection. Poorly defined margins,
increasing complexity, a solid appearance, and
from a simple unilocular cyst (type I) (Fig. 2-29) intraluminal gas suggest infection.
to a multilocular cyst with internal, peripherally The differential diagnosis of uncomplicated
arrayed daughter cysts (type II), to wall calcifica- hydatid cysts includes simple hepatic (bile duct)
tion to complete calcification at the end of the cysts and biliary cystadenoma—biliary hamarto-
cycle (type III). Cyst complication with rupture mas are generally smaller although similar
and/or infection is the type IV hydatid cyst. The in appearance. Pyogenic abscess, biliary
fibrous pericyst accounts for the commonly cystadenoma/cystadenocarcinoma, and cystic
observed T2 hypointense rim, a characteristic metastases share common imaging features with
finding in hydatid disease.26 Developing daughter complicated echinococcal cysts. Inclusion of
cysts contain fluid with simple features com- hydatid cyst in the differential hopefully pre-
pared with surrounding endocystic fluid, which cludes inadvertent spillage of cyst contents
is generally more T1 hyperintense and T2 hypoin- during attempted biopsy or aspiration, which
tense. Endocystic internal contents are further potentially incites an anaphylactic response.
complicated by collapsed parasitic membranes— Recognition of the typical features of echinococ-
twisted curvilinear hypointensities representing cus eliminates this risk and directs the clinician
detached, involuted daughter cysts. to the appropriate workup—serology. Medical
Imaging occasionally discloses cyst rupture or therapy (antihelminthics, e.g., albendazole) is
infection—the primary complications of hepatic the first-line treatment; surgical resection gener-
hydatid disease. The cyst rupture classification ally follows failure of medical therapy.
64  •  Fundamentals of Body MRI

Pyogenic Abscess describes the characteristic coalescence of small

Clinical history and demographic factors usually abscess cavities thought to represent an early
distinguish other infectious lesions from hydatid step in the development of a large multiseptated
cysts. Pyogenic, amebic, and fungal types con- abscess cavity (Fig. 2-31; see also Fig. 2-30).28
stitute the different varieties of liver abscesses Solid components, including the abscess wall
encountered in clinical practice. An identifiable and septa, enhance dramatically on arterial
source is established in 40% to 50% of cases of phase images and remain hyperintense on
pyogenic, or bacterial, abscesses. Ascending delayed images. Circumferential or triangular
biliary infection and hematogenous spread via edema extending peripherally from the lesion
the portal system account for most cases of pyo- arising from sinusoidal congestion appears
genic abscesses; with the advent of antibiotics, hyperintense on T2-weighted images and usually
biliary transmission has surpassed portal venous enhances avidly, although less than solid com-
hematogenous spread. Other etiologies include ponents of the abscess.
hematogenous spread via the hepatic arterial Without suggestive clinical and laboratory
circulation (in the setting of septicemia), direct findings, pyogenic abscess is not a straightfor-
extension from intraperitoneal infection, and ward diagnosis. Hydatid cyst, amebic abscess,
posttraumatic or postprocedural causes. In con- cystic metastases, and biliary cystadenoma/
tradistinction to echinococcal cysts, aspiration— cystadenocarcinoma share common features.
for the purposes of diagnosis and treatment/ The presence of (usually curvilinear) calcifica-
drainage—is routine in the case of pyogenic tion occasionally seen in echinococcal cysts
abscess. Mixed pathogens are cultured 50% of (predominantly on CT) excludes the possibility
the time and common organisms include Esch- of pyogenic abscess; internal, peripherally
erichia coli (associated with biliary infection arrayed daughter cysts conceivably simulate the
and pylephlebitis from hematogenous portal cluster sign—but encapsulation within, rather
venous transmission), gram-positive cocci (in than coalescence to contrive a dominant cyst,
the setting of sepsis), and others, such as clos- distinguishes daughter cysts from the cluster
tridium, proteus, klebsiella, and bacteroides. sign, respectively. Whereas the enhancement
The temporal evolution of pyogenic abscess pattern of the amebic abscess mimics the
explains the protean appearance. In the first of pyogenic abscess enhancement pattern,29 the
three phases—the acute phase—spanning the amebic abscess is usually solitary (85%) and well
first 10 days, parenchymal necrosis and liquefac- defined. Cystic, or necrotic, metastases closely
tion begin to develop. The subacute phase— simulate the appearance of pyogenic abscesses,
days 10 to 15—entails ongoing liquefaction and lacking only the cluster sign. The biliary cystad-
resorption of debris. The chronic phase— enoma fails to exhibit surrounding inflammatory
beyond day 15—is heralded by the development changes and multiplicity. Intralesional gas—
of a thick fibrous wall enveloping the central perhaps the most specific sign—reflected by
necrotic material (Fig. 2-30). Consequently, the uniform punctate hypointensities with suscepti-
MRI appearance depends on the phase of evolu- bility artifact excludes other etiologies, although
tion along this time course—the degree of present only 20% of the time.
liquefaction and encapsulation increases with
chronicity. Although occasionally unilocular Amebic Abscess
and solitary, pyogenic abscesses are usually Although Entamoeba histolytica—the caus-
multilocular and multiple. The “cluster” sign ative parasite in amebic liver abscess—colonizes

Acute phase Subacute phase Chronic phase

Early liquefaction Clustered coalescing Thick fibrous wall with

cavities central necrotic debris
FIGURE 2-30.  Pyogenic liver abscess evolution.
 MRI of the Liver  •  65

A B

C D

FIGURE 2-31.  Pyogenic abscess. A, A large hyperintense lesion

in the posterior segment on the moderately T2-weighted
image contains intralesional cystic foci (arrow). Note the per-
ilesional hyperintensity indicating edema with corresponding
enhancement on the arterial phase image (B), which equili-
brates on the delayed image (C). Solid, enhancing compo-
nents are more visible on the delayed image. Hyperintensity
on the diffusion-weighted image (D) with hypointensity on
the apparent diffusion coefficient (ADC) map (E) indicates
E
restricted diffusion.

the large bowel in 12% of the world population, Amebic abscess MRI features are not highly
the amebic hepatic abscess is a rare entity in the specific. Right lobe predominance most likely
United States (<3000 reported to the Centers for reflects mesenteric laminar flow—the superior
Disease Control and Prevention [CDC] in 1994). mesenteric vein (SMV), which drains the colo-
The highest rates of infestation are observed in nized colon flows toward the right hepatic
Mexico, Central and South America, India, and lobe. Peripheral location presumably also
tropical areas of Asia and Africa. Ingesting the reflects hematogenous origin. Whereas sharper
larval, cystic form of the organism in feces leads margins distinguish the amebic abscess from
to colonization of the cecum, where trophozo- the pyogenic abscess, enhancement and signal
ites penetrate the mucosa, initiating symptom- characteristics overlap.30 A high prevalence of
atic infection and potentially mesenteric venous extrahepatic manifestations—right pleural
dissemination to the liver (the right lobe in effusion, perihepatic fluid collections, and
~75% of cases). gastric and/or colonic involvement—potentially
66  •  Fundamentals of Body MRI

discriminates the amebic abscess from other parameters and absence of splenic involvement,
etiologies. generally separate metastases from hepatic can-
Serologic testing identifying antibodies spe- didiasis. Although hepatic lymphomatous infil-
cific for E. histolytica clinches the diagnosis. tration often involves the spleen, larger, less
Amebicidal medical therapy (metronidazole) numerous lesions with more infiltrative margins
eradicates liver infestation. Aspiration is avoided differentiate the imaging appearance from can-
unless (1) medical therapy fails in 5 to 7 days, didiasis. The solid variant of biliary hamartomas
(2) impending rupture is imminent, (3) pyo- closely simulates the appearance of hepatic can-
genic abscess is not definitively excluded, and didiasis; absence of clinical findings, stability
(4) the left lobe is involved (associated with confirmed on prior imaging studies, and periph-
greater mortality and potential peritoneal and eral distribution hopefully suggest the diagnosis
pericardial spread). and exclude candidiasis. Other infectious/
inflammatory lesions beyond the scope of this
Fungal Abscess text potentially simulate the imaging appear-
Fungal abscesses are distinguished by the clini- ance of hepatic candidiasis, including hepatic
cal scenario—neutropenia—and the characteris- tuberculosis and hepatic sarcoidosis.
tic imaging appearance. Usually caused by the
fungus Candida albicans and otherwise known
Traumatic Lesions
as hepatic candidiasis, fungal abscesses spread
in immunocompromised patients with hemato- Traumatic lesions of the liver—hematoma and
poietic malignancies, intensive chemotherapy, biloma—rarely warrant MRI. Nonetheless, mis-
and acquired immunodeficiency syndrome diagnosis because of lack of familiarity with
(AIDS). Bowel wall trauma in the immunosup- imaging features and failure to suggest the
pressed state permits transmural migration of appropriate diagnosis potentially leads to mor-
the organism and hematogenous dissemination. bidity and a brief discussion of these lesions will
Subsequent clinical symptoms and abscess for- hopefully help prevent that.
mation often signify the onset of recovery from
neutropenia with a mounting immune response. Hematoma
Small size (<1 cm) and diffuse, random distri- Liver hemorrhage most commonly follows
bution throughout the liver (and spleen—rarely either blunt trauma or surgery. Bleeding com­
involving the kidneys) characterize candidiasis. plicating a solid liver mass—most notably
Slight T1 hypointensity, prominent T2 hyperin- adenoma—accounts for another mechanism.34
tensity, and hypointensity on enhanced images The most specific imaging features are associ-
typify these microabscesses before treatment.31 ated with the underlying etiology: rib fractures,
In the subacute phase after antimycotic treat- liver laceration, hemoperitoneum (e.g., in the
ment, signal characteristics convert to mild case of blunt trauma); spatial and temporal rela-
hyperintensity on T1-weighted, T2-weighted, tionships to the surgical plane and procedure in
and enhanced images; a peripheral hypointense the case of postoperative bleeding; and the
rim corresponds to hemosiderin-laden macro- presence of an underlying lesion in the case of
phages surrounding the granulomas.32 neoplastic etiology. The T1 hyperintensity of
Whereas the clinical features strongly suggest methemoglobin in the acute-subacute phase
the diagnosis in the appropriate setting, MRI implicates hemorrhage (Fig. 2-32); after 10 days
plays a role in the diagnosis.33 MRI sensitivity or so, signal intensity approximates simple fluid.
and specificity exceed other diagnostic imaging
studies, and harvesting organisms from either Biloma
blood cultures or biopsy samples is difficult. Rupture of the biliary system leading to the for-
Despite its diagnostic utility, MRI features of mation of a biloma is usually either traumatic or
candidiasis may raise the specter of alternative iatrogenic in etiology. Location near the proce-
diagnoses, such as pyogenic abscesses, metasta- dural site and often abutting the porta hepatis
ses, lymphomatous infiltration, and biliary ham- or gallbladder fossa is characteristic. Other fea-
artomas. Clustering, larger size, more extensive tures, such as relatively sharply defined margins,
cystic/necrotic features, and lack of splenic relative absence of complexity, and bland signal
involvement favor pyogenic abscesses. Larger characteristics, are otherwise nonspecific (Fig.
size and smaller number, along with clinical 2-33). Further analysis needs to substantiate
 MRI of the Liver  •  67

whether hepatocyte-specific agents with

Solid (and Pseudosolid) Lesions
biliary excretion confirming biliary origin con-
tribute to the diagnosis (i.e., mangofodipir Enhancement connotes solid (and pseudosolid)
trisodium [Teslascan]—now unavailable—and tissue in MRI and indicates viability (in ablated
cholescintigraphy). lesions), with one exception—lesions of lipid
content (i.e., angiomyolipoma and lipoma).
Whereas a precise cut-off between cystic or
necrotic solid lesions and complex cystic lesions
eludes imaging capabilities, differentiation is
usually possible. Solid lesions with secondary
cystic or necrotic degeneration usually exhibit
a cavitated appearance—the central cystic
component appears excavated, a defect in an
otherwise solid lesion—whereas primary cystic
lesions generally exhibit more outwardly
expansile cystic components.
Solid lesions fall into two main groups defined
by their enhancement pattern compared with
normal liver parenchyma—hypervascular and
hypovascular (avascular ablated lesions are rele­
gated to the hypovascular category, and discus-
sion of rare isovascular lesions is deferred in the
interest of brevity) (see Fig. 2-17). On arterial
FIGURE 2-32.  Hematoma. Axial T1-weighted fat-suppressed phase images, hypervascular lesions enhance
image after a liver biopsy reveals tandem small hyperintense more, and hypovascular lesions less, than
hematomas in the posterior segment (arrows). hepatic parenchyma, respectively. Attenuation

A B

FIGURE 2-33.  Infected biloma. Relatively homogeneous hyper-

intensity on the moderately T2-weighted image (A) and
hypointensity on the T1-weighted fat-suppressed image (B)
is nonspecific. C, Internal complexity and an enhancing reac-
tive rim (thin arrows) with reactive hyperemia (thick arrows)
C
on the delayed image raises the suspicion of infection.
68  •  Fundamentals of Body MRI

pattern on subsequent timepoints further sub- Hepatic Adenoma

classifies lesions within each category (see Fig. Hepatocellular adenoma (or, simply, adenoma)
2-17). Signal and morphologic features add ancil- represents a cluster of hepatocytes lacking the
lary information; clinical information and under- normal hepatic architecture, biliary ductal
lying liver pathology and clinical conditions system, and functional Kupffer cells. Dilated
(e.g., chronic hepatitis, cirrhosis) help predict sinusoids perfused by arterial feeding vessels
the likelihood of malignancy. separate sheets of hepatocytes. The absence of
a coexistent portal venous system accounts for
Hypervascular Lesions the arterial enhancement. Adenoma cells often
Hypervascular liver lesions include a wide range contain large amounts of glycogen and lipid.35 A
of lesions ranging from benign, incidental devel- pseudocapsule of compressed parenchyma and/
opmental lesions (such as FNH) to aggressive or fibrosis often incompletely encircles the
malignant lesions (such as HCC and hypervas­ lesion.
cular metastases). Accurate characterization Adenomas afflict two major population
demands stepwise analysis of intensity on suc- groups: (1) patients using estrogen- or androgen-
cessive timepoints (see Fig. 2-17). Hypervas­ containing steroids and (2) patients with type
cularity on the arterial phase connotes I glycogen storage disease. Whereas 70% to
hypervascularity. Signal intensity on delayed 80% of adenoma cases are solitary, extreme
images discriminates benign from malignant multiplicity defines a third recently described
with diagnostic confidence. Hypervascularity category, adenomatosis, characterized by the
followed by delayed hyperintensity or fading presence of multiple (usually > 10) adenomas.
(isointensity to liver parenchyma) connotes These patients lack the conventional risk
benign etiology—flash-filling hemangioma or factors (e.g., steroids, glycogen storage disease)
FNH, vascular shunt and adenoma, respectively. and suffer from progressive symptomatic
Hypervascularity followed by delayed hypoin- disease, impaired liver function, hemorrhage,
tensity (to liver parenchyma) equals washout—a and occasionally malignant degeneration.36
malignant feature. Malignant hypervascular In all cases, malignant degeneration is a
lesions with washout include HCC and hyper- concern, although the risk estimates are vari-
vascular metastases. To be clear, a critical able. Thin-walled sinusoids subjected to the
semantic distinction deserves reiteration. In the high pressures of the feeding arteries explain
setting of hypervascularity, washout means the propensity of adenomas to bleed. Frequent
delayed signal intensity less than liver, whereas discontinuity of the pseudocapsule permits
fading refers to delayed signal intensity equal to transgression of hemorrhage, and proximity to
liver. Washout equals malignancy and fading the capsule predicts extrahepatic rupture and
equals benignity (Fig. 2-34). hemoperitoneum.
Delayed phase

Persistent
hyperintensity
Precontrast Arterial phase BENIGN

Fading
Hypervascular BENIGN
lesion

Washout
MALIGNANT
FIGURE 2-34.  Hypervascular lesion scheme.
 MRI of the Liver  •  69

Adenomas usually exhibit iso- to hyperinten- reverse pattern—hypovascularity with possible

sity on (in-phase) T1-weighted images due to delayed enhancement.
either hemorrhage (52%–93%) and/or lipid Without intralesional hemorrhage or fat, ade-
(36%–77%) (Fig. 2-35).35,37,38 Because intrale- nomas simulate other hypervascular lesions.
sional lipid usually manifests microscopically, as Imaging features often fail to discriminate
opposed to macroscopically, T1 hyperintensity hepatic adenoma from HCC, except for the
drops on out-of-phase more frequently than on absence of vascular invasion in adenomas and
fat-saturated images. T1 hyperintensity arising washout versus fading in HCC and adenoma,
from hemorrhage does not suppress on these respectively. Variable signal, hypervascularity,
pulse sequences. Intralesional hemorrhage and intralesional lipid and hemorrhage, and sur-
necrosis interrupt mild baseline T2 hyperinten- rounding pseudocapsule characterize both
sity. The pseudocapsule exhibits T1 hypointen- lesions. Discrepant clinical features suggest the
sity and variable T2 hyperintensity with roughly underlying diagnosis. Adenomas occur in young,
equal proportions of iso-, hypo-, and hyper­ otherwise healthy patients on oral contracep-
intense rims. Except where complicated by tives or steroids with normal α-fetoprotein (AFP)
hemorrhage and/or necrosis, adenomas enhance levels; HCC prevails in cirrhotic livers and often
avidly in the arterial phase and fade on delayed elicits AFP. Imaging features also overlap with
images. The pseudocapsule demonstrates the FNH. The presence of hemorrhage and/or fat

A B

C D
FIGURE 2-35.  Hepatic adenomas. Multiple liver lesions (thin arrows in A-D) demonstrate relative signal loss on the out-of-phase image
(A) compared with the in-phase image (B), indicating microscopic fat with corresponding hypervascularity on the arterial phase image
(C). D, On the portal phase image, the lesions become uncharacteristically hypointense. Note the exaggeration of the susceptibility
artifact from embolization coils (thick arrow in A and B) on the in-phase image compared with the out-of-phase image owing to the
longer time to excitation (TE).
70  •  Fundamentals of Body MRI

A B

FIGURE 2-36.  FNH enhancement pattern. FNH typifies the

usually benign hypervascular enhancement pattern of marked
hypervascularity—as demonstrated by the dramatic intensity
increase between the precontrast (A) and arterial phase (B)
images—followed by fading or isointensity to liver paren-
C
chyma on delayed images (C).

excludes FNH and a central scar suggests FNH, demonstrate the classic “central scar.” The
not being a characteristic of adenoma. central scar enhances gradually—exhibiting
delayed hyperenhancement (Fig. 2-37). Whereas
Focal Nodular Hyperplasia the lesion itself is nearly isointense on T1-
FNH deserves the designation “pseudosolid” weighted and T2-weighted images—minimally
because it is composed of elements of normal hypo- and hyperintense, respectively—the
liver tissue—hepatocytes, bile ducts, and arter- central scar exaggerates this pattern, conferring
ies embedded in fibrous septa. FNH is the greater conspicuity on unenhanced images.
second most common benign liver tumor (after Ancillary findings include relatively small size
hemangioma), representing a hyperplastic (85% < 5 cm), frequent subcapsular right lobe
response to a localized vascular malformation— distribution, and solitary and rare pedunculation
in other words, a hamartoma. Consequently, and multiplicity.
FNH is an incidental lesion with virtually no Other etiologies in the differential diagnosis
risk of complications (except exceedingly are eliminated with multiparametric analysis
rare rupture and hemorrhage39) requiring no including temporal enhancement pattern, clini-
treatment or follow-up, assuming adequate cal features, and ancillary signal characteristics.
characterization. Although hypervascular, HCC washes out and
FNH enhances avidly during the arterial phase usually arises in the setting of cirrhosis and/or
and fades on portal venous and delayed images chronic hepatitis. Fibrolamellar HCC more
(Fig. 2-36). Approximately one half of lesions closely simulates the imaging appearance of
 MRI of the Liver  •  71

A B

C D

FIGURE 2-37.  FNH with central scar. A, On the precontast

T1-weighted image, a massive FNH in the right lobe of the
liver is mostly mildly hypointense with a more focal central
moderate hypointensity corresponding to the scar (arrow).
B, During the arterial phase, the FNH experiences dramatic
enhancement, while the central scar remains unenhanced. On
the portal phase image (C), the FNH has nearly achieved
isointensity with continued hypointensity of the central scar,
which begins to enhance on the equilibrium phase image (D).
E, The moderately T2-weighted image shows the typical near
E
isointensity of the FNH and hyperintensity of the central scar.

FNH, but usually achieves much larger size and Occasionally, atypical features or diagnostic
heterogeneity and the central scar is usually T2 uncertainty demands additional testing to estab-
hypointense. Hypervascular metastases washout lish the diagnosis in cases of possible FNH. In
and exhibit multiplicity. Hypervascular heman- an effort to avoid an invasive diagnostic proce-
giomas demonstrating arterial hypervascularity dure, repeat MR examination with a hepatocyte-
remain hyperintense (without fading) and specific agent confirms the presence of
exhibit near-water attenuation on unenhanced hepatocytes on delayed enhanced images with
images. When not complicated by hemorrhage, lesion hyperintensity (Fig. 2-38).40 While the
lipid, or necrosis, hepatic adenoma closely agent has been channeled through the biliary
mimics FNH. Adenomas are usually less hyper- system, clearing the normal parenchyma, hepa-
vascular, lack a central scar, and may be associ- tocytes within the lesion imbibe the contrast
ated with oral contraceptive use, anabolic agent, but lack the organized biliary system for
steroids, and glycogen storage disease. excretion.
72  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-38.  FNH imaging with hepatocyte-specific agent. A, The precontrast image from the dynamic sequence reveals a subtly hypoin-
tense lesion (arrow) in the posterior segment abutting the right hepatic vein. Following the administration of Eovist (gadoxetate), avid
enhancement is observed during the arterial phase (B), followed by near isointensity during the portal phase (C), characteristic of FNH.
D, On the delayed T1-weighted fat-suppressed image obtained 20 minutes later, intralesional hyperintensity confirms the diagnosis
of FNH.

Focal Transient Hepatic (although small HCCs sometimes lack these

Intensity Difference imaging features). These lesions raise concern
Without the benefit of hepatocyte-specific in cirrhotic livers because of the higher preva-
imaging, transient hepatic intensity differences lence of HCC—also hypervascular. When small
(THIDs) mimic FNH.41,42 The duality of liver hypervascular lesions such as these so-called
blood supply explains the basis of this phenom- THIDs populate cirrhotic livers, follow-up
enon. Increased arterial flow compensates for imaging urgency increases in order to exclude a
compromised portal flow reflected by hyperin- small HCC.
tensity on the HADP with corresponding isoin-
tensity on delayed phases. THIDs exist with or Cirrhotic Nodules (Prehypervascular)
without underlying lesions and manifest variable Other small nodular lesions inhabit cirrhotic
appearances, depending on the etiology. Geo- livers, including regenerative nodules, siderotic
graphic distribution, triangular shape, and sharp, nodules, dysplastic nodules, and HCC. Whereas
linear borders commonly observed in these not all hypervascular, they deserve a collective
lesions reflect vascular anatomy—hepatic tissue discussion because of their strong etiologic con-
subtended by the affected vascular tree enhances nection (Fig. 2-41). For the purposes of our dis-
arterially (Fig. 2-39). cussion, the nonhypervascular lesions in this
The diagnostic dilemma arises in the case of group can be thought of as “prehypervascular.”
“pseudoglobular” THIDs. Blind vessels not Conceptually, these nodules represent an evolu-
reaching Glisson’s capsule defy the geographic tionary spectrum from regenerative nodule to
pattern and appear more nodular or round (Fig. dysplastic nodule to HCC. The term siderotic
2-40). Larger lesions (>1.5 cm) present no diag- applies to iron deposition in regenerative and
nostic difficulty because the absence of signal dysplastic nodules, which are indistinguishable.
changes and washout excludes HCC of this size With chronic inflammation, liver parenchyma is
 MRI of the Liver  •  73

A B

FIGURE 2-39.  Geographic THID. Only the arterial phase

image (B) reveals the enhancement of the geographic, wedge-
shaped THID—the precontrast (A) and portal phase (C)
C
images reveal isointensity with no trace of the THID.

destroyed and the liver’s natural ability to regen- by the effects of that damage—surrounding
erate yields regenerative nodules, which are fibrous septa. Regenerative nodular prolifera-
composed of normal liver cells. Dysplastic tion due to cirrhosis falls into two gross patho-
nodules harbor histologically abnormal cells logic categories: micronodular (i.e., Laennec’s
(e.g., nuclear crowding, increased nuclear :  cirrhosis, often synonymous with alcoholic cir-
cytoplasmic ratio) with variable neoplastic rhosis) and macronodular (usually viral), depend-
angiogenesis—pathologic arteries—replacing ing on the size of the regenerative nodules.
the normal portal triads.43,44 HCC represents the Micronodular nodules measure up to 3 mm and
final endpoint along the malignant degeneration macronodular nodules measure more than
pathway—most cases are associated with 3 mm and up to 5 cm. Whatever the pathologic
chronic liver disease. Whereas many histologic descriptor, nodules are delineated by bands of
subtypes exist, for our purposes, HCC simply T2 hyperintense, gradually enhancing fibrosis
connotes malignant hepatocytes with arterial (Fig. 2-42).
blood supply. Under normal circumstances, regenerative
Regenerative nodules reiterate normal liver nodules have no differential diagnosis. Rarely,
parenchymal signal and enhancement character- regenerative nodules enhance arterially, imper-
istics and differ only in their morphology and sonating HCC (at least on the arterial phase).45
surroundings (assuming the absence of iron Delayed enhancement of peripheral fibrosis
deposition). By definition, regenerative nodules conceivably mimics the late-enhancing capsule
inhabit a damaged hepatic environment, usually of an HCC. Corroboration with unenhanced and
cirrhosis, and are spatially and visually defined dynamic images confirms absence of signal
74  •  Fundamentals of Body MRI

A B

C
FIGURE 2-40.  Pseudoglobular transient hepatic intensity difference (THID). The arterial phase image (A) shows a round focus of arterial
enhancement (arrow in A) adjacent to the gallbladder, which fades on the portal phase image (B) and demonstrates no signal changes
on the precontrast image (C).

Regenerative Adenomatous Dysplastic HCC

nodule nodule nodule

T2

T1

HADP

FIGURE 2-41.  Pathogenesis of hepatocellular carcinoma (HCC). HADP, hepatic artery–dominant phase.
 MRI of the Liver  •  75

A B
FIGURE 2-42.  Regenerative nodules surrounded by fibrosis. A, Innumerable nodular islands of hepatic parenchyma are marginated by
bridging bands of hyperintensity on the moderately T2-weighted image in a very cirrhotic liver—the typical appearance of regenerative
nodules with intervening reticular fibrosis. B, Delayed enhancement of the fibrotic bands surrounding the relatively hypointense nodules
conjures a honeycomb appearance.

derangements—T1 hypo- and T2 hyper­­intensity— nodule (although actually 34% of high-grade and
and usually arterial enhancement, which would 4% of low-grade dysplastic nodules have been
otherwise suggest HCC. Rarely, diagnostic shown to enhance arterially47). High-grade dys-
imaging uncertainty provokes follow-up imaging plastic nodules also differ in signal characteris-
or biopsy. tics with isointensity on T2-weighted images
A dysplastic nodule is defined as a cluster of and iso- to hypointensity on T1-weighted images.
histologically atypical hepatocytes measuring The T1 hyperintensity of low-grade dysplastic
at least 1 cm not meeting histologic criteria nodules should not be confused with (micro-
for malignancy.46 Dysplastic nodules afflict 15% scopic or macroscopic) fat. The T1 hyperin­
to 25% of cirrhotic livers. Dysplastic nodules tensity in dysplastic nodules (which is not
display greater variability and less commonality attributable to fat) does not suppress on out-of-
with normal liver parenchymal MR characteris- phase or fat-suppressed images. Hemorrhage or
tics. Although the signal profile varies, proto- protein complicating an underlying cyst or
typically, dysplastic nodules are hyperintense solid lesion lacks the enhancement seen in dys-
on T1-weighted images and hypointense on plastic nodules (check subtracted images).
T2-weighted images (compared with liver) (Fig. Whereas the signal characteristics of melanotic
2-43). The paramagnetic effects of glycogen and hemorrhagic metastases overlap with T1
and/or copper explains the T1 hyperintensity. hyperintense dysplastic nodules, metastases
T2 hypointensity, at least occasionally attribut- washout on delayed images and rarely invade
able to iron content, is virtually always present. the cirrhotic liver (the obligate home of the
Although sporting unpaired arteries (not part of dysplastic nodule).
a portal triad), dysplastic nodules typically High-grade dysplastic nodules show consider-
enhance commensurate with normal liver tissue able overlap in imaging features with HCC. A
and fail to enhance during the arterial phase few features compel consideration of HCC over
(prehypervascular). With precontrast T1 hyper- dysplastic nodule. T2 hyperintensity is not a
intensity, enhancement is difficult to perceive; feature of dysplastic nodules and at least two
subtraction images remove the intrinsic hyper- thirds of HCCs exhibit T2 hyperintensity.48
intensity and display the change from baseline Washout after arterial enhancement also favors
(i.e., enhancement). HCC over dysplastic nodule. Finally, the pres-
With further evolution or dedifferentiation— ence of a late-enhancing capsule also preempts
depending on your perspective—the term pre- the diagnosis of dysplastic nodule in favor of
hypervascular becomes prophetic and the HCC. Size considerations also weigh in on the
dysplastic nodule enhances arterially and usually management of these lesions, because over 95%
fades (isointense to liver on delayed images). of dysplastic nodules are less than 2 cm. Lesion
Conceptually, this enhancement pattern distin- diameter of 2 cm or more or growth in a lesion
guishes the high-grade dysplastic nodule from over 1 cm prompts consideration of ablation
the prehypervascular low-grade dysplastic and the presumptive diagnosis of HCC.
76  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 2-43.  Dysplastic nodule. The opposed phase (A) and in-phase (B) images reveal a hyperintense nodular lesion (arrow in A) at
the periphery of the posterior segment in a diffusely nodular, cirrhotic liver. C, The fat-saturated T1-weighted unenhanced image excludes
T1 hyperintense fat. The T1-weighted fat-saturated image (D) in a different patient shows a similar hyperintense lesion (arrow in D
and E) with lack of enhancement confirmed on the subtracted arterial phase image (E).

The earliest definitive sign of dysplastic focus of T2 hyperintensity—corresponding to

nodule dedifferentiation is the “nodule within HCC—within a T2 hypointense dysplastic
a nodule” phenomenon, which also nodule (Fig. 2-44). Associated HCC enhance-
prompts (usually invasive) action. The nodule ment characteristics increase diagnostic
within a nodule appearance describes a confidence.
 MRI of the Liver  •  77

A B

D
FIGURE 2-44.  Nodule within a nodule. The axial fat-suppressed unenhanced T1-weighted image (A) reveals a hyperintense lesion (arrow
in A) in the lateral segment of a cirrhotic liver characteristic of a dysplastic nodule, which is hypointense on the moderately T2-weighted
image (arrow in B) with a punctate intralesional hyperintensity. C, The arterial phase image demonstrates corresponding ill-defined
central enhancement (arrow) suspicious for HCC. D, A magnified axial moderately T2-weighted image in a different patient with severe
cirrhosis reveals a dominant hypointense nodule (thin arrow) with intralesional hyperintensity (thick arrow) exemplifying the nodule-
within-a-nodule appearance of early HCC.

Hepatocellular Carcinoma are vital. Annual screening (with MRI or other

The discussion so far has been a preamble for modalities, depending on the institution) in cor-
the topic of HCC. HCC (or “hepatoma”) is the roboration with AFP helps detect these lesions
most common primary hepatic malignancy, at an early phase and preserves the hopes of
although secondary malignancies (metastases) liver transplantation (LT), if planned. Consider-
outnumber HCCs. Most cases evolve along the ing HCC doubling time of approximately 2 to 3
aforementioned dedifferentiation pathway in months50 and high MR detection rate51 virtually
the cirrhotic liver in the setting of chronic hepa- reaching 100% with increasing lesion size
titis B (HBV) or C virus (HCV) or alcoholism. (>1.5 cm), an annual screening scheme gener-
Because of the dismal long-term survival of ally guarantees early HCC detection before viola-
untreated HCC (<5% 5-year survival rate49), sur- tion of transplantation size rules.
veillance in the appropriate high-risk popula- Screening high-risk patients with chronic liver
tion, prompt diagnosis, and treatment planning disease for the purpose of early HCC detection
78  •  Fundamentals of Body MRI

presence of HCC manifests as a pseudocapsule

TABLE 2-9.  The Milan Criteria
of inflammatory and stromal cells and bile ducts,
One tumor < 5 cm or
Up to three tumors ≤ 3 cm thought to reflect an attempt to contain the
lesion and/or passive centrifugal compression of
liver parenchyma (Fig. 2-47).53 Although malig-
nant angiogenesis recruits unpaired arteries—
TABLE 2-10.  Tumor-Node-Metastasis Staging the dominant HCC blood supply—hepatic and
of Hepatocellular Carcinoma portal veins proliferate around the lesion and
Tumor Node Metastasis provide a portal for metastatic spread.
Stage (T) (N) (M) Although imperfect, the classic dogma of HCC
I T1 N0 M0 MRI features—T2 hyperintensity, (heteroge-
II T2 N0 M0 neous) hypervascularity, and washout—applies
IIIA T3 N0 M0
IIIB T1 N1 M0
to most lesions (see Figs. 2-46 and 2-47).
T2 N1 M0 Although not unanimously present (more often
T3 N1 M0 in larger lesions), the late-enhancing pseudocap-
IVA T4 Any N M0
IVB Any T Any N M1
sule further clinches the diagnosis (Fig. 2-48).
Portal or hepatic venous invasion—rarely
Primary Tumor (T) observed in other tumors—also confirms the
T1 = Solitary tumor ≤ 2 cm without vascular invasion
T2 = Solitary tumor ≤ 2 cm with vascular invasion
diagnosis of HCC. Ancillary factors further ele-
Multiple tumors limited to one lobe all ≤ 2 cm without vating the diagnostic confidence level include
vascular invasion elevated AFP, cirrhosis, and HBV infection (even
Solitary tumor > 2 cm without vascular invasion
T3 = Solitary tumor > 2 cm with vascular invasion
without cirrhosis).
Multiple tumors limited to one lobe all ≤ 2 cm with vascular The classic HCC imaging features become
invasion more vividly depicted with increasing size.
Multiple tumors limited to one lobe any > 2 cm with or
without vascular invasion
HCCs less than 2 cm often enhance more homo-
T4 = Multiple tumors in more than one lobe geneously in the arterial phase and 10% to 15%
Tumor involvement of major portal or hepatic venous branch(es) simulate arterioportal shunts with relative incon-
Regional Lymph Nodes (N)
spicuity on unenhanced and delayed images
N0 = No regional lymph node metastases (Fig. 2-49).54 (Most HCCs generally exhibit
N1 = Regional lymph node metastases hypointensity on T1-weighted images and hyper-
Distant Metastases (M)
intensity on T2-weighted images, as previously
M0 = No distant metastases discussed.) In fact, although arterial enhance-
M1 = Distant metastases ment is virtually the sine qua non of HCC, before
the onset of increased arterial flow, portal
venous flow begins to wane and relative hypo­
and treatment is driven by the Milan Criteria intensity on arterial and portal phase images
(Table 2-9)—the universally adopted rules gov- results.55 With larger lesion size and dedifferen-
erning LT. The Milan Criteria is based on tiation, variegated arterial enhancement devel-
research showing improved survival rates when ops as a consequence of larger sinusoidal spaces
restricting LT to patients with early HCC— exaggerating arterial enhancement punctuated
defined as T1 and T2 tumors, according to the by hypo- or avascular foci representing necrosis,
TNM (tumor-node-metastasis) staging system hemorrhage, and/or fat (Fig. 2-50). Perilesional
(Table 2-10). edema and enhancement derangements (THIDs
Three dominant patterns describe HCC or hypovascular regions) reflect vascular inva-
growth: solitary, multifocal or nodular, and sion and usually correspond to the vascular
diffuse (“cirrhotomimetic”; Fig. 2-45). The soli- territory subtended by the vessel invaded by
tary form predominates at least 50% of the time. the mass (i.e., the HCC defines the apex of the
The nodular form follows in prevalence, and vascular derangement induced by the vascular
the diffuse form accounts for approximately invasion).
10%.52 Soft, fleshy HCCs have a propensity for HCC more frequently invades the portal veins
hemorrhage and necrosis and increased levels of than the hepatic veins.56 Vascular invasion con-
fat and glycogen observed in the cytoplasm also notes a poorer prognosis and higher likelihood
occasionally affects the MR appearance of these of metastatic spread. The lack of vascular inva-
lesions (Fig. 2-46). The host reaction to the sion also helps predict the success of surgical
 MRI of the Liver  •  79

A B

C D
FIGURE 2-45.  Infiltrative HCC with portal venous thrombosis. The heavily T2-weighted (A) and arterial phase (B) images show nodular
infiltrative hyperintensity and enhancement throughout the posterior segment with thrombus in the right portal vein (arrow in B). The
out-of-phase (C) and in-phase (D) images demonstrate punctate hyperintense foci of hemorrhage (thin arrows) and a large focus of
microscopic fat (thick arrow).

excision, along with the absence of extrahepatic diagnoses. Although in isolation, imaging fea-
metastases, baseline liver function, and size of tures overlap very closely, extraneous factors
the residual liver. Occasionally, vascular inva- differentiate hypervascular metastases from
sion heralds an underlying occult HCC. Detect- HCCs using a commonsense approach. Cirrhosis
ing tumor thrombus (as opposed to bland predicts HCC over hypervascular metastases for
thrombus) requires establishing thrombus two reasons: (1) cirrhosis predisposes to HCC
enhancement—most easily appreciated on sub- and (2) metastases rarely spread to the cirrhotic
tracted images (Fig. 2-51). liver. Elevated AFP and an absence of known
Extrahepatic sites of spread include lymph primary malignancy further boost diagnostic
nodes, lungs, bones, adrenal glands, and confidence. Metastatic lesion enhancement
peritoneum/omentum.57 In addition to vascular patterns simulate HCC patterns with uniform
invasion, extrahepatic involvement (>stage II) homogeneous enhancement, ring enhance-
precludes surgical treatment and the hopes of ment, and heterogeneous enhancement pat-
transplantation. Regional lymphadenopathy is terns. Frequent hypervascular shunts and rare
ambiguous; hepatic inflammation—ubiquitous hypervascular dysplastic nodules account for
in this population—and metastatic spread incite most of the rest of the hypervascular lesions
regional lymphadenopathy. Most commonly encountered in the cirrhotic liver. FNH and
observed metastatic lymph node distributions flash-filling hemangioma declare themselves on
include periceliac, porta hepatis, para-aortic, delayed images as discussed (with fading and
portocaval, peripancreatic, aortocaval, and ret- persistent hyperintensity, respectively), differ-
rocaval (Fig. 2-52). entiating themselves from HCC.
Hypervascular metastases and other cirrhosis- Despite high diagnostic accuracy, equivocal
related lesions dominate the list of differential cases require a consistent approach to
80  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-46.  HCC with microscopic fat. The in-phase image (A) of a nodular, cirrhotic liver shows a heterogeneous lesion at the bulging
posterior contour (arrow in A) with faint hyperintensity, which drops in signal on the out-of-phase image (B). Avid arterial enhancement
(C) followed by washout on delayed images (D) and a late-enhancing capsule typify HCC.

A B
FIGURE 2-47.  HCC pseudocapsule. A, Hypervascularity is evident in the lesion in the right lobe of the liver (arrow) on the arterial phase
image. B, Enhancement of the pseudocapsule (arrows) develops on the delayed image.
 MRI of the Liver  •  81

T2 T1

Cirrhotic morphology
(not necessary in HBV)

HADP Delayed

HA
Pseudocapsule
PV
IVC
Vascular invasion
FIGURE 2-48.  Hepatocellular carcinoma (HCC) schematic diagram. HA, hepatic artery; HADP, hepatic artery–dominant phase; HBV,
hepatitis B virus, IVC, inferior vena cava; PV, portal vein.

A B

C
FIGURE 2-49.  Small HCC. A, The arterial phase image shows a heterogeneously enhancing lesion in the medial aspect of the posterior
segment (thin arrow) and a homogeneously enhancing lesion in the posterior aspect to the posterior segment (thick arrow). B, On the
delayed image, the medial lesion washes out (arrow) betraying its malignant etiology—HCC—whereas the posterior lesion has faded,
characteristic of a THID or benign vascular shunt. C, Note the HCC hyperintensity (arrow) on the T2-weighted steady-state image.
82  •  Fundamentals of Body MRI

A B

C
FIGURE 2-50.  Large complex HCC. A, The moderately T2-weighted image shows a large heterogeneously hyperintense lesion (arrow)
bulging the liver capsule. The arterial phase (B) and delayed (C) images show variegated enhancement, often seen in large lesions.

A B
FIGURE 2-51.  HCC with tumor thrombus. A, The arterial phase image reveals an infiltrative hypervascular lesion (thin arrows) with portal
venous thrombus (thick arrows). B, The portal venous phase image shows lesion washout and exemplifies the difference between tumor
thrombus (thin arrows)—which is relatively more intense and enhancing—compared with bland thrombus (thick arrows).
 MRI of the Liver  •  83

A B

C
FIGURE 2-52.  HCC with metastatic lymphadenopathy. A and B, The moderately T2-weighted images show enlarged lymph nodes in
periportal (arrow in A) and celiac distributions (arrow in B) and heterogeneous hyperintensity throughout the lateral segment corre-
sponding to a large HCC. C, The large, mildly hypervascular, necrotic HCC (arrow) replacing the lateral segment is evident on the
arterial phase image.

consistency in diagnosis and management and

TABLE 2-11.  Liver Imaging and Reporting
eliminate the potential for perceived lack of
Data System
departmental cohesiveness and consensus by
LIRADS 0 = Insufficient data
LIRADS 1 = No evidence of HCC
referring clinicians.
LIRADS 2 = Focal unequivocally benign lesions (e.g., cyst, hemangioma)
LIRADS 3 = Indeterminate nodule Fibrolamellar Carcinoma
LIRADS 4 = Intermediate suspicion for HCC
LIRADS 5 = High suspicion for HCC
A variant of HCC inhabits the normal liver in
LIRADS 6 = Histologically confirmed HCC younger, healthy patients—fibrolamellar carci-
noma (FLC)—and accounts for less than 10%
HCC, hepatocellular carcinoma; LIRADS, Liver Imaging and Report-
ing Data System. and potentially as little as 1% of HCCs overall.
The lesion is named for its microscopic appear-
ance of malignant cells arranged in sheets sepa-
management. In an effort to manage equivoca- rated by fibrous bands, or lamellae. The typical
tion consistently, classification schemes are demographic, biochemical, and serologic fea-
being devised to stratify liver lesions into catego- tures are the exact opposite of HCC: (1) no
ries based on the likelihood of HCC. The Liver history of underlying cirrhosis or chronic hepa-
Cancer Group collaborates on the LIRADS titis, (2) younger age (median age 33 compared
system (Liver Imaging and Reporting Data with 66 for HCC), and (3) normal AFP (at least
System) (Table 2-11). An initiative in our own 85% of the time).
department, termed the Lesion Characterization A large (mean size ≤ 13 cm), lobulated
in Diffuse Liver Disease System, stratifies lesions mildly T1 hypointense, mildly T2 hyperintense
into five categories based on the risk estimate of heterogeneously hypervascular mass with a uni-
HCC (Table 2-12). These schemes promote formly hypointense, nonenhancing central scar
84  •  Fundamentals of Body MRI

TABLE 2-12.  TJU Lesion Characterization in TABLE 2-13.  Hypervascular Metastases

Chronic Liver Disease RCC
Neuroendocrine tumors
Category 1: No Focal Lesion Suspicious for HCC   Carcinoid tumors
(Risk Estimate < 5%) Thyroid carcinoma
(Note: Because these features are not clinically significant, they do not Uveal melanoma
necessarily have to be mentioned in the report.) Choriocarcinoma
Leiomyosarcoma
Imaging Features Breast (occasionally)
No lesion demonstrated. Ovary (occasionally)
<1 cm, transient arterial enhancing, and seen on the arterial phase Pancreas (occasionally)
images only.
<1 cm, T1 hyperintense, and enhances similar to background liver. RCC, renal cell carcinoma.
<1 cm nodular area of focal fatty or iron sparing without arterial
enhancement in the setting of diffuse fatty liver.
describes the typical MR appearance of FLC
Suggested Management
Continue routine surveillance. (Fig. 2-53). Intensity becomes more homoge-
nous and equilibrates with or slightly drops
Category 2: Probably Benign Lesion   compared with normal parenchyma. Chief dif-
(Risk Estimate 5–20%)
Imaging Features ferential considerations include HCC, FNH, and
Round transient arterial enhancing, 1–2 cm, and not visible on other adenoma. The absence of cirrhosis and chronic
sequences. liver disease and presence of a central scar favor
Round, 1–2 cm, hypointense on delayed images, and isointense on other
images. FLC, but HCC still figures prominently in
New, <1 cm T1 hyperintense, and enhances similar to background liver. the differential because of the much higher
incidence. Although the central scar and
Suggested Management
Short-term (3-mo) follow-up, possibly with Eovist. hyper­vascularity are reminiscent of FNH, the
heterogeneous enhancement, signal alterations
Category 3: Indeterminate Lesion   on unenhanced images, and specific features of
(Risk Estimate 21–70%)
Imaging Features the central scar point away from FNH. The central
>2 cm, T1 hyperintense, and enhances similar to background liver. scar of an FLC demonstrates hypointensity on
both T1-weighted and T2-weighted images and
Suggested Management
Short-term follow-up, biopsy or alternative imaging (e.g., angiography, usually fails to enhance even on delayed images.
US, Eovist-MRI). FLC and adenoma share the common features of
Indeterminate lesion should not be considered a diagnosis of HCC. hypervascularity and heterogeneous enhance-
Category 4: Probable HCC (Risk Estimate 71–95%) ment. Adenoma visibility on unenhanced images
Imaging Features derives from the presence of fat and/or hemor-
As in category 5. Suboptimal image quality or other factors, at rhage, both of which uncommonly affect FLC—in
radiologist’s discretion, may decrease confidence.
fact, intratumoral fat has never been reported.58
Suggested Management
Treat, biopsy, or transplant. Consider alternative imaging (e.g., Metastases
angiography, US, Eovist-MRI).
Metastases are the most common malignant
Category 5: HCC (Risk Estimate >95%) lesion in the liver, and the liver follows lymph
Imaging Features nodes as the most common sites of metastatic
Hyperenhancement with either washout, T2 brightness, or a delayed
enhancing capsule. spread in the human body. Multiple routes of
A solid round mass that is T2 bright. The presence of any additional spread provide tumor emboli access to the liver:
feature (e.g., enhancing capsule, washout, or enhancement) increases the hepatic artery, portal vein, lymphatics, and
confidence that this is not confluent fibrosis.
Note that many HCCs have washout and other HCC features, but not T2 peritoneal ascitic flow. Established metastases
brightness. T2 brightness is specific but not extremely sensitive. recruit arterial blood supply, whether hyper- or
Multinodular texture (nodules-in-nodule) is an important confirmatory hypovascular. Hypervascular metastases arise
finding of HCC.
from hypervascular primary tumors, such as
Management renal cell carcinoma, islet cell/neuroendocrine
Treat or transplant. Biopsy is not needed. tumor, thyroid carcinoma, carcinoid, breast car-
HCC, hepatocellular carcinoma; MRI, magnetic resonance imaging; cinoma, and melanoma (predominantly ocular,
TJU, Thomas Jefferson University; US, ultrasound. as opposed to dermal) (Table 2-13).
Detecting metastases dictates potential treat-
ment course, prognosis, and response to treat-
ment. Ten percent of metastases are solitary and
 MRI of the Liver  •  85

A B

C D

E
FIGURE 2-53.  Fibrolamellar HCC. The large hypervascular mass has a central hypointense scar on the precontrast image (A), enhances
on the arterial phase image (B) with the exception of the central scar (thin arrow in B-D). Washout is progressively evident on the portal
phase image (C) compared with the delayed image (D), as is the late-enhancing capsule (thick arrows in D). E, Hyperintensity is evident
on the moderately T2-weighted image. Note the lack of cirrhotic features.

77% inhabit both lobes; variable size reflects dif- with hypointensity of the peripheral rim and
ferent lesion age and ongoing embolic delivery. relative central hyperintensity as the intersti-
Hypervascular metastases typically enhance as tium gradually perfuses with contrast.61 These
avidly as the pancreas and enhancement pattern enhancement characteristics reflect the tumor’s
varies (Fig. 2-54). Smaller lesions tend to be ability to induce angiogenesis peripherally with
more homogeneous in enhancement with het- relative central hypovascularity ultimately trend-
erogeneity increasing with lesion size. Whether ing to central fibrosis and/or necrosis as it out-
hyper- or hypovascular, metastases commonly grows its blood supply.
exhibit a continuous rim of enhancement.59,60 Signal intensity patterns on unenhanced
The peripheral washout sign describes a delayed images vary but hover around the basic template
inversion of the arterial phase enhancement of T1 hypointensity and T2 hyperintensity,
86  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-54.  Hypervascular metastasis. The moderately T2-weighted image (A) shows a hyperintense uveal melanoma metastasis in the
right lobe of the liver (arrow in A), which is hypointense on the corresponding precontrast T1-weighted image (B), enhancing avidly
on the arterial phase image (C) and washing out on the delayed image (D).

reflecting increased intralesional water content still usually relatively hypointense to cystic
compared with liver parenchyma. Concentric lesions, including hemangioma.63 Heavily
variations of this pattern on both T1-weighted T2-weighted images confirm a relative signal
and T2-weighted images have earned the drop in metastatic lesions compared with hem-
descriptors “doughnut” sign and “lightbulb” angiomas and cysts.
sign, respectively.62 These signs are essentially T2 hypointensity is uncommon and usually
the pulse sequence counterpart of each other: accompanies T1 hyperintensity, indicating hem-
doughnut sign = mildly T1 hypointense rim orrhage or melanin. Preservation of T1 hyper­
surrounding markedly hypointense center; intensity on fat-suppressed images excludes fat
lightbulb sign = mildly T2 hyperintense rim and confirms a paramagnetic substance—either
surrounding markedly hyperintense center blood or melanin. Without a known history of
(Fig. 2-55). These signs conjure the notion of ocular melanoma, T1 hyperintensity most likely
viable tumor surrounding a nonviable central represents hemorrhage, most commonly arising
necrotic core. from renal, melanoma, breast, and choriocarci-
Aberrations in metastatic signal intensity tem- noma metastases in the hypervascular realm
plate emerge for a variety of reasons. Whereas (and lung, pancreatic, gastric, prostatic, and gall-
T2 values between benign lesions (i.e., cysts and bladder carcinoma in the hypovascular cate-
hemangiomas) and malignant lesions (i.e., gory).34 Melanoma metastases contain variable
metastases and HCCs) do not overlap, for all quantities of melanin, which facilitates T1 relax-
intents and purposes, some hypervascular ation, enhances T2 relaxation, and promotes T1
metastases demonstrate marked T2 hyperinten- hyperintensity and T2 hypointensity, respec-
sity. Hypervascularity, increased interstitial tively. Increasing melanin content equates with
water content, vascular lakes, and dilated vascu- increasing T1 and decreasing T2 signal.64
lar spaces (and mucin as in the case of colorectal Imaging features of hypervascular metastases
metastases—typically hypovascular) confer most closely overlap with (multifocal) HCCs,
higher signal on T2-weighted images, although multiple hepatic adenomas, and/or FNHs.
 MRI of the Liver  •  87

A B

FIGURE 2-55.  Doughnut and lightbulb signs in metastatic

disease. Colon carcinoma metastases display the doughnut
sign (thin arrows in A) on the T1-weighted fat-suppressed
image (A) and the lightbulb sign (thick arrows in B and C)
more vividly on the moderately T2-weighted fat-suppressed
(B) and inversion recovery (C) images. Increased lesion con-
spicuity and tissue contrast are inherent features of inversion
recovery images, which are magnified by the presence of hepa-
tocellular Eovist (gadoxetate disodium). Note the relatively
prominent hyperintensity on the fluid-sensitive sequences,
C
typical of mucinous metastases.

Lesion for lesion, HCCs and hypervascular Infection appropriately factors in the differen-
metastases are often indistinguishable— tial diagnosis in the absence of known primary
multiplicity, absence of chronic liver disease, malignancy in a suggestive clinical scenario.
normal AFP, and history of primary extrahe- During the liquefactive stage of pyogenic abscess
patic malignancy argue in favor of metastatic evolution, the hypervascular wall encapsulating
disease. T1 hyperintensity not attributable to central necrosis and debris mirrors the appear-
lipid is noncontributory; blood complicates ance of necrotic and cystic metastases. However,
HCCs and metastases and is not distinguishable primary cystic metastases are often hypovascu-
from melanin. T1 hyperintensity attributable to lar, such as mucinous cystadenocarcinoma (i.e.,
fat favors HCC—lipid-containing metastases colon, gastric, pancreatic, ovarian). The cluster-
(i.e., metastatic liposarcoma) are exceedingly ing sign and relatively prominent perilesional
rare. Vascular invasion is diagnostic of HCC reactive change favor pyogenic abscess, along
and excludes extrahepatic malignancy. The with suggestive signs of underlying infection—
presence of multiple adenomas theoretically including adjacent findings of right pleural effu-
echoes the appearance of hypervascular sion and basal atelectasis/consolidation.
metastases—albeit not entirely faithfully—
lacking washout and often containing lipid Hypovascular Lesions
and/or hemorrhage with suggestive demo- Hypointensity relative to liver on dynamic
graphic data. FNHs even less closely simulate images translates to hypovascularity; hypovascu-
hypervascular metastases owing to their rela- lar lesion conspicuity peaks on portal phase
tively homogeneous enhancement and invisi- images when the liver maximally enhances.
bility on unenhanced images. Metastases dominate this category of solid
88  •  Fundamentals of Body MRI

Hypovascular lesion

T2 signal

At least near fluid hyperintensity Moderate hyperintensity or less

Delayed enhancement Delayed enhancement

Heterogeneous enhancement
None Hyperintensity

Hypovascular metastases
Cyst Hemangioma Cholangiocarcinoma
Biliary hamartoma

FIGURE 2-56.  Hypovascular liver lesion diagnostic algorithm.

small fraction of hypovascular liver metastases).

TABLE 2-14.  Hypovascular Liver Lesions
Metastatic lesions restricted to the liver present
Developmental Potentially Malignant the opportunity for successful treatment, such
Bile duct cyst Ablated lesions
as chemotherapy, chemoembolization, radioem-
Biliary hamartoma
Malignant bolization, and immunoembolization. Metastatic
Inflammatory Peripheral cholangiocarcinoma disease frequently beyond the liver—pancreas,
Pyogenic abscess Metastases
Colon adenocarcinoma
breast, lung, and melanoma—is less amenable to
Echinococcal cyst
Fungal abscess Lung carcinoma these treatments. So, while cataloguing metasta-
Gastric adenocarcinoma ses on MRI studies of the liver seems academic
Neoplasms Breast carcinoma
and rote, the potential impact on treatment
Benign Pancreatic adenocarcinoma
Hemangioma (usually) Lymphoma course is real. Many of these schemes depend
Angiomyolipoma on RECIST (Response Evaluation Criteria in
Lipoma Solid Tumors) criteria (recommended by the
National Cancer Institute), which offers a stan-
dardized analytic method to stratify metastatic
lesions, distantly followed by treated (i.e., embo- disease into four categories: (1) complete
lized, ablated) malignancies, peripheral chol­ response (CR), (2) partial response (PR), (3)
angiocarcinoma, and miscellaneous assorted stable disease (SD), and (4) progressive disease
lesions (Table 2-14). The presence of solid tissue (PD). These assessments are based on the sum
exhibiting at least gradual enhancement usually of the index lesions—referred to as target
excludes consideration of simple cysts or cysts lesions—compared with baseline. An increase
complicated by hemorrhage or protein. Success- of 20% or more connotes PD, a decrease of 30%
fully ablated lesions lack enhancement and carry or more indicates PR, SD encompasses the
an underlying diagnosis, disclosing their true middle ground, and CR denotes complete regres-
identity (Fig. 2-56). sion of all lesions. Although clinical radiology
reporting demands more layered nuancing and
comprehensiveness, familiarity with this stratifi-
Metastases
cation scheme helps understand the imaging
Hypovascular hepatic metastases most com- impact on treatment decisions, especially in
monly originate from the colon and remainder clinical trials (Table 2-15).
of the gastrointestinal tract (see Table 2-14). The Whereas the arterial phase identifies hypervas-
portal venous system transports these tumor cular lesions, because of their marked con­
emboli to the liver, where they are either spicuity compared with adjacent tissue, the
obstructed by macrophages or filtered into the portal phase generally most clearly depicts
space of Disse, gaining a foothold for sustenance hypovascular metastases. Prominent parenchymal
and growth (peritoneal seeding accounts for a enhancement contrasts with the hypointensity
 MRI of the Liver  •  89

A B
FIGURE 2-57.  Hypovascular metastases. A and B, Urothelial metastases are characteristically hypovascular with an occasional rim (arrows)
on arterial phase images.

structures, such as hemangiomas (see Fig. 2-55).

TABLE 2-15.  Response Evaluation Criteria in
Conversely, colorectal carcinoma frequently
Solid Tumors Criteria
undergoes central coagulative necrosis and des-
Target Lesions moplasia accounting for central hypointensity in
Amenable to reproducible repeated measurements 50% of cases.65
Up to 5 target lesions
Up to 2 per organ Nonneoplastic cystic lesions, such as inciden-
Response = sum of long axis of non-nodal lesions and short axis of nodal tal hepatic cysts, biliary hamartomas, hemangio-
lesions mas, and pyogenic abscesses, share some
Nontarget Lesions imaging features (see Fig. 2-56). The complete
All other pathologic lesions absence of enhancement and uniform fluid
Nonmeasurable lesions content of simple hepatic cysts (and usually
Not measured: present, unequivocably progressed or resolved
biliary hamartomas) attest to the lack of solid,
Response Criteria metastatic tissue and endorse the benign etio­
Target Lesions logy. The uniformly peripheral distribution, con-
Complete response (CR) = disappearance of all target lesions (all nodes
<10 mm) sistently small size of biliary hamartomas and
Partial response (PR) = ≥30% decrease in the sum of diameters of target (usual) absence of solid components, excludes
lesions compared with baseline the diagnosis of metastases. The unique enhance-
Progressive disease (PD) = >20% increase in the sum of diameters of
target lesions above smallest size ment characteristics, including persistent hyper-
Stable disease (PD) = insufficient change to qualify for PR or PD attenuation of hemangiomas, differentiates them
from T2 hyperintense metastases. The liquefac-
Nontarget Lesions
Complete response (CR) = disappearance of all nontarget lesions (all tive stage of pyogenic abscesses resembles
nodes <10 mm) hypovascular metastases; clustering and second-
Non-CR/non-PD = persistence of ≥1 nontarget lesion(s) ary signs of infection, including right pleural
Progressive disease (PD) = unequivocal progression of nontarget lesions
or appearance of new lesion effusion and basal parenchymal changes, imply
an infectious etiology.

of the hypovascular metastases, which often

Lymphoma
gradually enhance over time and move toward
equilibration with liver parenchyma (Fig. 2-57). Lymphoma rarely involves the liver, and hepatic
Arterial phase images occasionally reveal a thin involvement is almost invariably secondary.
hypervascular rim. Hypovascular metastases Primary hepatic lymphoma prompts consider-
resemble their hypervascular counterparts on ation of underlying diseases, such as AIDS, other
unenhanced images with mild T2 hyper- and immune disorders, chronic HCV infection, and
T1 hypointensity. Mucin from mucinous metas- other liver diseases. Secondary hepatic involve-
tases (i.e., rectal, gastric, ovarian mucinous ment occurs with both Hodgkin’s disease (HD)
adenocarcinoma) magnifies T2 hyperintensity, and non-Hodgkin’s lymphoma (NHL). Histopatho­
approaching the signal of benign fluid-filled logically, secondary hepatic lymphoma entails
90  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-58.  Hepatic lymphoma. A, Axial moderately T2-weighted image shows uniformly hyperintense material extending along the
central portal tracts (arrow). Precontrast (B) and postcontrast (C) images depict associated enhancement, which is more conspicuous
with the advantage of subtraction (D).

Ablated Tumors
tumor deposits within the portal tracts, poten-
tially leading to visible periportal infiltration Ablated hepatic malignancies encompass a wide
reflected by T2 hyperintense infiltration along range of primary and secondary tumors treated
the portal tracts. Whereas this pattern is fairly with a variety of methods. A comprehensive
specific for lymphoma and is associated with review of this topic exceeds the scope of this
both secondary forms of lymphoma, HD more text, but a targeted discussion facilitates under-
consistently exhibits this pattern. Secondary standing MR findings in these patients. Thera-
hepatic NHL more frequently displays a multifo- peutic agent delivery options to liver lesions
cal nodular pattern. Lymphomatous deposits are include systemic, organ-specific, and lesion-
usually monotonously T2 hyperintense and specific. Systemic therapy is synonymous with
hypovascular with relative peripheral enhance- chemotherapy, for the purposes of this discus-
ment (Fig. 2-58). sion. Organ-specific therapy regimens include
The diagnosis generally relies on the underly- chemoembolization, immunoembolization, and
ing history of lymphoma and multifocality. Mul- radioembolization. Chemical (ethanol), thermal,
tifocal HCC usually invades a diseased liver with and cryoablation account for most of the (per-
a history of chronic liver disease and demon- cutaneous) lesion-specific ablation techniques
strates arterial enhancement. Multifocal cholan- (Table 2-16).
giocarcinoma exhibits hypovascularity, but Whatever the technique, the common objec-
often displays specific characteristic features, tive of destruction of solid tissue equates with
such as capsular retraction, biliary involvement, absence of enhancement on MR images.66 Thin,
and segmental or lobar atrophy. Hypovascular peripheral, reactive enhancement often sur-
metastases from another primary malignancy rounds percutaneously treated lesions and mea-
more closely mirror the appearance of hepatic sures a few millimeters in thickness (usually
lymphoma, and clinical history and/or tissue ≤3 mm) and persists up to 3 to 6 months
sampling ultimately establishes the etiology. (Fig. 2-59).67 Focal nodularity or thickening is
 MRI of the Liver  •  91

A B

FIGURE 2-59.  Reactive enhancement around ablated lesion.

Precontrast axial fat-suppressed image (A) shows a large hyper-
intense lesion (representing an ablated HCC with hemorrhage
and/or coagulative necrosis), around which there is a thin rim
of reactive enhancement (arrows in B) on the arterial phase
image (B) with no apparent central, intralesional enhance-
ment. C, Compare the appearance with the pre-embolized
C
arterial phase image showing hypervascularity.

complications is more practical. Systemic che-

TABLE 2-16.  Liver Lesion Ablation/Treatment
motherapy potentially induces hepatic steatosis
Methods
and pseudocirrhosis (hepatotoxic effects of the
Chemical Ablation Cold Deposition chemotherapy agent), in addition to the extra-
Ethanol injection Cryoablation hepatic side effects. Non–target organ delivery
Acetic acid injection
Arterial Delivery of   of embolization material is the main source of
Thermal Ablation Ablative Substances complications and most commonly affects the
Heat Deposition Chemoembolization lungs and celiac artery branches (to the pan-
Radiofrequency ablation Immunoembolization
Laser ablation creas, duodenum, stomach, gallbladder, and
Microwave ablation spleen). Liver infarction rarely occurs—probably
High-intensity focused ultrasound more likely with coexistent portal venous
occlusion—providing fertile ground for super-
imposed infection (Fig. 2-61). Subcapsular
a potential sign of residual or recurrent tumor, hematoma rarely complicates both percutane-
and short-term follow-up imaging or retreatment ous treatments and chemoembolization, espe-
is pursued (Fig. 2-60). Because many ablative cially after prior intervention (Fig. 2-62). Other
techniques result in coagulation, often manifest- complications have been reported, most of
ing with T1 shortening and hyperintensity, which result from the direct effects of image-
subtracted images more accurately impart the guided percutaneous intervention (e.g., perihe-
presence, nature, and degree of enhancement. patic abscess, biloma, hemorrhage).68
Size changes are less meaningful; in fact, a
desired ablative margin of 5 to 10 mm increases
Peripheral Cholangiocarcinoma
the measureable size of an image-guided ablated
lesion. Anatomic location classifies cholangiocarci-
The most realistic differential diagnosis is per- noma into three groups: peripheral cholangio-
sistent tumor, and a brief discussion of potential carcinoma (PCC—arising from intrahepatic
92  •  Fundamentals of Body MRI

A B

C
FIGURE 2-60.  Nodular enhancement of ablated lesion. Following ablation of the large hypervascular hepatocellular carcinoma in the right
lobe of the liver (arrow in A), gross nodular enhancement (arrow in B) on the arterial phase image (B) of a subsequent examination
indicates residual tumor, which contrasts with the thin, reactive rim surrounding the successfully ablated component of the tumor (arrows
in C) seen on the delayed image (C).

PCC is an adenocarcinoma originating from

TABLE 2-17.  Cholangiocarcinoma bile duct epithelium accounting for 5% to 30%
Classification of primary malignant hepatic tumors, and a
Intrahepatic (peripheral) cholangiocarcinoma (10%) distant second to HCC.69–71 Cholangiocarcinoma
Hilar cholangiocarcinoma (Klatskin’s tumor) (65%)
Extrahepatic cholangiocarcinoma (25%) predominates in the 6th and 7th decades with
predisposing factors promoting earlier onset,
such as PSC, choledochal cyst, Caroli’s disease,
hepatolithiasis, Clonorchis sinensis infection,
ducts distal to the second-order branches, 10%); and Thorotrast exposure.
hilar cholangiocarcinoma, or Klatskin’s tumor PCC exhibits three growth patterns, codified
(involving the first-order bile ducts or conflu- into a classification scheme by the Liver Cancer
ence, 60%); and extrahepatic cholangiocarci- Study Group of Japan72,73: mass-forming, periduc-
noma (originating from the common hepatic or tal infiltrating, and intraductal papillary types
common bile duct, 30%) (Table 2-17). Because (Fig. 2-63). PCC most commonly subscribes to
PCC imaging features more closely simulate the mass-forming variety and presents as a large
primary hepatic lesions, inclusion in the discus- (usually > 5 cm) lobulated mass. Large size is
sion of liver lesions is more relevant; distal attributable to the relative lack of symptoms
types of cholangiocarcinoma are deferred to because of the peripheral location and
Chapter 3. relative lack of biliary obstruction. Nonspecific
 MRI of the Liver  •  93

A B

C D
FIGURE 2-61.  Liver infarction/infection due to chemoembolization. A, The moderately T2-weighted image demonstrates a markedly
hyperintense, segmental roughly wedge-shaped lesion in the posterior segment of the liver with an adjacent tubular hyperintensity (arrow)
at its apex—the thrombosed portal venous branch. Hyperintensity persists on the heavily T2-weighted image (B) with corresponding
hypointensity on the T1-weighted in-phase image (C). D, Lack of enhancement of both the liver infarct and the thrombosed portal
venous branch (arrow) is depicted on the contrast-enhanced image.

hypointensity on T1-weighted images accompa- clearly distinguishes PCC from HCC, but poten-
nied by peripheral T2 hyperintensity and central tially overlaps with the appearance of a hypovas-
T2 hypointensity typifies the classic appearance cular metastasis. Capsular retraction, presumably
of mass-forming PCCs (Fig. 2-64).74 Peripheral induced by desmoplasia associated with PCC,
cellularity and central fibrosis explains the T2 stands in contradistinction to capsular bulging
signal characteristics. Enhancement characteris- exerted by other space-occupying masses in the
tics reiterate this centripetal architecture with liver (Fig. 2-65 and Table 2-18). Although not
hypovascular enhancement of the peripheral cel- commonly observed, biliary invasion excludes
lular zone followed by progressive enhancement other etiologies. Lobar or segmental atrophy due
of the central fibrotic/desmoplastic zone (see to (usually portal) venous encasement uniquely
Fig. 2-64). Foci of coagulative necrosis, also characterizes PCC.
hypointense on T2-weighted images, do not The presence of vascular invasion is an impor-
enhance. The relatively delayed enhancement of tant consideration in staging PCC and predicting
PCC differentiates it from the other most common resectability (Table 2-19).77 Other prognostic
primary hepatic malignancy, HCC,75,76 and justi- factors include: size (>2–3 cm confers poor
fies the acquisition of delayed enhanced images. prognosis), metastatic lymphadenopathy, and
Slowly, gradually increasing, progressively cen- multifocality.78,79 Unfortunately, PCC usually sur-
tripetal enhancement evolves over minutes. passes these parameters at the time of diagnosis,
Relative hypovascularity with progressive filling precluding surgical resection. In summary, PCC
94  •  Fundamentals of Body MRI

A B

C D

FIGURE 2-62.  Subcapsular hematoma after intervention.

A, The axial T2-weighted fat-suppressed image reveals an
extraparenchymal, subcapsular hyperintense collection along
the anterior segment of the liver. Diffuse hyperintensity on
the corresponding out-of-phase (B) and in-phase (C) images
indicates either macroscopic fat (which would exhibit periph-
eral phase cancellation or India ink artifact) or hemorrhage.
The fat-suppressed precontrast image (D) confirms the hem-
orrhagic content of the collection, which exhibits no enhance-
E
ment on the postcontrast image (E).

Mass-forming

Periductal infiltrating

Polypoid intraductal

FIGURE 2-63.  Cholangiocarcinoma growth patterns. (From Han JK, Choi BI, Kim AY, et al. Cholangiocarcinoma:
Pictorial essay of CT and cholangiographic findings. Radiographics 22:173–187, 2002.)
 MRI of the Liver  •  95

A B

C D

E
FIGURE 2-64.  Cholangiocarcinoma signal and enhancement patterns. Mild patchy enhancement of the central aspect of the large peripheral
cholangiocarcinoma on the arterial phase image (B) compared with the precontrast image (A) progresses on the serial delayed images
(C and D). E, Patchy central enhancement likely reflects a combination of coagulative necrosis and desmoplasia—both hypointense on
the moderately T2-weighted image. Note the classic peripheral hyperintensity, central hypointensity, and capsular retraction.

modes of spread explain some of its features and spread = proximal biliary dilatation and/or
propensity for metastatic spread: lymphatic abnormal wall thickening and enhancement.
spread = lymphadenopathy; vascular invasion = Parenthetically, cholangiocarcinoma also under-
(usually portal) venous obliteration and associ- goes perineural spread, which eludes MRI
ated segmental or lobar atrophy; and biliary capabilities.
96  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 2-65.  Cholangiocarcinoma with capsular retraction. Coronal (A) and axial (B) heavily T2-weighted and fat-suppressed moderately
T2-weighted (C) images show a large mildly hyperintense lesion bridging the right and left hepatic lobes with convexity of the outer
liver margin, indicating capsular retraction (arrow in A and B). Arterial phase (D) and delayed (E) images after contrast portray the
typical hypovascular enhancement pattern with delayed, centripetal progression.
 MRI of the Liver  •  97

a separate category that is more appropriately

TABLE 2-18.  Causes of Capsular Retraction
entitled lipid-rich lesions or lipid-dominant
Tumors lesions (so as not to confuse the issue by includ-
HCC
FLC
ing adenoma and HCC, which may harbor small
PCC quantities of fat). These lesions plot along a
Adenocarcinoma (colon, stomach, breast, lung, pancreas, GB) scale from solely microscopic fat (steatosis) to
HCC postembolization
Malignant tumor postchemotherapy
some macroscopic fat (angiomyolipoma) to
Hemangioma gross macroscopic fat (lipoma). The common
thread unifying these lesions is the presence of
Absent Tumor
Confluent hepatic fibrosis
fat—usually the diagnostic endpoint of these
Oriental cholangiohepatitis lesions.
Bile duct necrosis

Pseudoretraction
Hepatic Angiomyolipoma
Accessory fissure Hepatic angiomyolipoma (AML) is a benign ham-
Normal liver between protruding lesions artomatous lesion and the liver follows the
FLC, fibrolamellar carcinoma; GB, gallbladder; HCC, hepatocellular kidney in incidence. AMLs are associated with
carcinoma; PCC, peripheral cholangiocarcinoma. tuberous sclerosis, but also arise in isolation.
From Yang DM, Kim HS, Cho SW, et al. Pictorial review, various
causes of hepatic capsular retraction: CT and MR findings. Br J The name belies the histologic constituents of
Radiol 75:994–1002, 2002. the angiomyolipoma: blood vessels (angio-),
smooth muscle (-myo-) and fat (-lipoma). The
only variable is the relative quantity of each
TABLE 2-19.  Peripheral Cholangiocarcinoma component. The presence of fat generally estab-
Staging lishes the diagnosis and lipid content varies from
T Groups less than 10% to more than 90% of tumor
TX: Primary tumor cannot be assessed volume.
T0: No evidence of primary tumor A mixed signal pattern including macroscopic
T1: Single tumor (any size) with no vascular involvement
T2: Either single tumor (any size) with vascular involvement, or > 1 fat with T1 hyperintensity and suppression on
tumor with none > 5 cm fat-saturated images describes the typical MR
T3: Multiple tumors > 5 cm, or tumor involvement of major portal or appearance (Fig. 2-66). Voxels containing lipid
hepatic venous branch
T4: Direct invasion into adjacent organ (not including gallbladder), or and nonlipoid elements experience loss of signal
visceral peritoneal involvement on out-of-phase images. Angioid components or
tumoral vessels enhance avidly (and lend a
N Groups
NX: Regional lymph node cannot be assessed hypervascular quality to these lesions) and
N0: No regional lymph node involvement connect to a draining (hepatic) vein. Monoto-
N1: Regional lymph node involvement nous smooth muscle elements enhance blandly
M Groups and contribute no specific imaging features,
MX: Distant metastatic spread cannot be assessed tending to exaggerate heterogeneity and
M0: No distant metastatic spread increase nonspecificity.
M1: Spread to distant lymph nodes or organs
Stage I: T1, N0, M0 AML fat content raises the suspicion of HCC
Stage II: T2, M0, M0 and adenoma (in addition to the other usually
Stage IIIA: T3, N0, M0 incidental lesions—lipoma and nodular steato-
Stage IIIB: T4, N0, M0
Stage IIIC: Any T, N1, M0 sis). The absence of a capsule and the presence
Stage IV: Any T, Any N, M1 of tumoral vessels connecting to a draining vein
M, metastasis; N, node; T, tumor.
discriminate AML from HCC and adenoma.80
From American Joint Committee on Cancer (AJCC) Liver Cancer These features should be sought, because gross,
Staging (histologically insensitive: also applies to hepatocellular
carcinoma [HCC]). macroscopic fat alone suggests an alternative to
HCC and adenoma (either AML or lipoma), but
does not necessarily forestall biopsy. Other rare
Lipid-Based Lesions
fat-containing lesions to consider (on the boards
The dominant remaining hypovascular solid or in conference) include metastatic teratoma
lesions share a common feature—intralesional and liposarcoma; teratomas often calcify and
lipid—and include angiomyolipoma, lipoma, liposarcomas often contain significant solid,
and nodular steatosis. In a literal sense, these hypervascular tissue—both not features of AML.
lesions are not actually hypovascular and form Whereas otherwise incidental, large size confers
98  •  Fundamentals of Body MRI

A B

FIGURE 2-66.  Hepatic angiomyolipoma. The in-phase image (A)

of a patient with tuberous sclerosis shows a small hyperintense
lesion in the right lobe of the liver (arrow in A), which loses
signal on the out-of-phase image (B), indicating the presence
of fat. C, Relative hypointensity on the fat-suppressed postcon-
trast image reflects the combination of lack of enhancement
C
and fat-suppression signal loss.

risk of hemorrhage and/or rupture—the only characterizes hepatic lipoma (and all simple
reported complication, which may prompt sur- lipomas). The absence of vascular enhancement
gical resection or embolization. AMLs have no excludes AML, and lack of solid, enhancing com-
malignant potential. ponents excludes other lipid-containing lesions,
such as HCC and adenoma. Nodular steatosis
Hepatic Lipoma exemplifies microscopic fat signal with little to
Lipomas rarely affect the liver and present little no signal loss on out-of-phase images with no
diagnostic difficulty when they do. Uniform perceptible signal loss on fat-suppressed images,
macroscopic fat signal suppressed on fat- in contradistinction to lipomas. Lipomas incur
saturated images with no appreciable enhance- no risk of complications or need for further
ment or complexity pathognomonically evaluation.81
 MRI of the Liver  •  99

Focal Steatosis (Fatty Infiltration) artifact reflected by signal loss on out-of-phase

Hepatic steatosis manifests in various patterns: images, lack of mass effect (note normal vessels
diffuse, patchy, segmental or geographic, and coursing through the lesions), enhancement
focal or nodular.82 Steatosis signifies abnormal equivalent to liver parenchyma, stability over
accumulation of fat (i.e., triglycerides) in hepa- time, and relative inconspicuity on all other
tocytes and develops in underlying conditions images characterize focal fat.85 These features
such as alcoholism, medication effects or toxin discriminate multifocal steatosis from other
exposure, obesity, insulin resistance, and hyper- lesions in the differential diagnosis containing
triglyceridemia. Micro- and macrovesicular his- microscopic fat. Although HCC occasionally
topathologic types portend different disease contains microscopic lipid, focal intralesional
processes, and this classification scheme reflects inclusions are the norm and the heterogeneous
the size of the fat droplets within the hepato- visibility on unenhanced and arterial phase
cytes. Microvesicular steatosis involves deficient images, clear mass effect, and vascular invasion
hepatic β-oxidation of fatty acids and more fre- differentiate HCC from steatosis. Adenomas
quently accompanies severe hepatic dysfunc- also demonstrate mass effect and usually mani-
tion. Multifactorial causes lead to macrovesicular fest focal intralesional fat. Macroscopic fat
steatosis, including enhanced lipolysis of triglyc- indicates an alternative diagnosis, as previously
erides (associated with insulin resistance), lipo- discussed.
genesis promotion, and increased delivery and
secretion of lipids. Although these histopatho- Focal Fatty Sparing
logic designations confer different prognostic Focal fatty sparing simulates a T1 hyperintense
and disease specific information, the MR appear- pseudolesion (not to be confused with an
ance is identical, with relative loss of signal on adenoma, hemorrhagic or melanotic metastasis,
out-of-phase images. When focal or geographic, or dysplastic nodule in the cirrhotic liver) com-
steatosis often indicates underlying portal or sys- pared with the out-of-phase hypointensity of the
temic venous anomalous supply. background fatty liver. Actually, spared tissue is
The juxtaposition of intracellular fat vesicles the only normal part of hepatic parenchyma in
with cytoplasm, interstitial fluid, and any other steatosis. Anomalous venous circulation spares
free water protons in the same imaging voxel the affected parenchyma from fatty infiltration,
results in destructive interference on out-of- resulting in focal sparing.86 Periligamentous
phase images. The TE of out-of-phase images (around the falciform ligament and ligamentum
(2.2–2.3 msec at 1.5 Tesla) is timed to occur venosum), periportal, and pericholecystic
when fat and water have precessed 180° apart regions most often exhibit fatty sparing. Isoin-
from one another, which means that the signal tensity between in- and out-of-phase images
contributions of each respective proton—fat against the backdrop of generalized signal loss
and water—are subtractive. With increasing on out-of-phase images points to spared liver
hepatocytic lipid, parenchymal signal progres- parenchyma (Fig. 2-68). The key is to appreciate
sively darkens. Visual appreciation of this that the diffuse steatosis is the abnormality and
phenomenon suffices; comparison with a ref- not falsely identify relatively hyperintense zones
erence that is unlikely to harbor fat—such as on out-of-phase images as potential lesions.
the spleen—confirms a relative drop in signal
on out-of-phase images. More detailed analysis
GEOGRAPHIC OR
and quantification techniques are deferred
SEGMENTAL LESIONS
to the forthcoming discussion of diffuse
steatosis. Most liver pathology manifests either focally or
Common characteristic locations for focal ste- diffusely. Occasionally, abnormalities involving
atosis include the medial segment, periligamen- only a segment or territory of the liver defy focal
tous regions (i.e., adjacent to the falciform or diffuse spatial pattern classification. Mentally
ligament), around the gallbladder fossa and segregate these lesions into primary versus sec-
porta hepatic, and in subcapsular distributions ondary (to an occult lesion) abnormalities. Geo-
(Fig. 2-67).82–84 Generalized, multifocal steatosis graphic changes—especially enhancement—
potentially generates diagnostic ambiguity, often belie the presence of an underlying liver
especially when nodular or round, simulating mass and the presence of a segmental abnormal-
solid masses. In addition to the chemical shift ity demands further investigation to detect a
100  •  Fundamentals of Body MRI

A B

FIGURE 2-67.  Focal steatosis. The focally hyperintense foci on

the in-phase image (A) show markedly (thin arrow in A-C)
and mildly (thick arrow in A-C) decreased signal on the out-
of-phase image (B). C, Enhancement matches the normal
liver parenchyma—decreased signal on the enhanced image is
C
a consequence of fat suppression.

A B
FIGURE 2-68.  Focal fatty sparing. The out-of-phase image (A) shows a residual rim of hyperintensity in the periportal region (arrows in
A) against the backdrop of hypointense fatty infiltration, which becomes isointense on the in-phase image (B) where the surrounding
liver regains normal signal.

subtle underlying mass. Whereas geographic primarily signal changes versus primarily
signal changes often accompany an underlying enhancement changes (Fig. 2-69).
focal mass, signal abnormalities more frequently
signify a primary disorder, such as steatosis or
Primarily Enhancement Lesions
fibrosis. Enhancement tends to predominate
over signal changes in secondary lesions, Primarily enhancement lesions encompass
whereas signal predominates in primary lesions THIDs, macrovascular occlusion (usually portal
(although abnormal enhancement characterizes venous), and hepatic infarct—rarely seen as a
some lesions such as confluent fibrosis). Based consequence of dual hepatic blood supply.
on these general principles, consider a binary These lesions share the common theme of
approach to segmental lesions according to normal underlying hepatic parenchyma usually
 MRI of the Liver  •  101

GEOGRAPHIC LESIONS
Enhancement Lesions Signal Lesions
THID Geographic steatosis
Portal venous occlusion Confluent fibrosis
Hepatic infarct

Geographic steatosis

OOP IP

Arterial
phase
Confluent
fibrosis

T2

FIGURE 2-69.  Geographic lesions including diagram of secondary perfusion changes. IP, in phase; OOP, out of phase; THID, transient
hepatic intensity difference.

exhibiting fading (or isointensity) on delayed cholecystitis), and postprocedural changes (i.e.,
images. transcutaneous biopsy or ablation).

Geographic THID Other Geographic Vascular Lesions

THIDs originate for a variety of reasons, depend- Other vascular etiologies resemble THIDs, such
ing on the presence or absence of an underlying as hepatic infarct and portal venous occlusion.
lesion. The dual portal venous–hepatic arterial Hepatic infarcts are not incidental lesions and
blood supply allows increased arterial flow to usually accompany LT, laparoscopic cholecys-
compensate for a decrease in portal venous tectomy, vasculitis, and profound hypovole-
flow—the basic premise of a THID. Pathoge- mia.87 Temporal stability excludes infarct, which
netic mechanisms of primary lesions include atrophies, degenerates, and may undergo necro-
portal venous compression (due to portal branch sis. PVT also rarely manifests spontaneously and
compression or thrombosis), flow diversion usually accompanies inflammation (i.e., pancre-
(due to arterioportal shunt or anomalous blood atitis, peritonitis, diverticulitis) or malignancy.
supply), and effects of adjacent inflammation. Wedge-shaped morphology and hypervascular-
Secondary causes include siphoning (increase in ity often associated with portal venous occlu-
arterial flow), portal hypoperfusion (due to sion reiterate the appearance of a THID and only
compression or infiltration), portal venous direct visualization of a filling defect in a portal
thrombosis (PVT), and flow diversion (due to an venous branch excludes THID.
arterioportal shunt associated with an underly- Because of its rare occurrence and protective
ing lesion).41,42 dual hepatic perfusion, infarct should be realisti-
Sharp margins, arterial enhancement, and an cally entertained only in appropriate clinical set-
absence of signal changes on unenhanced tings (e.g., LT, laparoscopic cholecystectomy,
images usually characterize these lesions (see vascular intervention; see Figs. 2-61 and 2-70).
Fig. 2-39). Occlusion or truncation of vessels Signal changes develop gradually along with
proximal to the capsule and distal to the lesion atrophy and volume loss of the affected segment.
potentially results in a rounded appearance. In the acute phase, only the clinical scenario and
Nonsectorial or amorphous morphology results direct signs of arterial occlusion (lack of enhance-
from extrinsic compression (i.e., subcapsular ment of the hepatic artery or one of its branches)
collections), anomalous vascular supply, hyper- positively identify arterial infarction as the
emia due to adjacent inflammation (i.e., correct diagnosis.
102  •  Fundamentals of Body MRI

A B
FIGURE 2-70.  Liver infarct associated with malignant vascular invasion. The postcontrast image (A) shows a roughly wedge-shaped geo-
graphic nonenhancing lesion in the anterior and medial hepatic segments (arrows), thought to represent a liver infarct in a patient with
hilar cholangiocarcinoma, which is better seen on the T2-weighted image (arrows in B) at the confluence of the dilated intrahepatic
ducts.

Signal ± Enhancement Lesions

Many geographic liver lesions manifest primarily
with signal changes, with or without abnormal
enhancement. Geographic steatosis and iron
deposition constitute the segmental lesions
solely manifesting signal changes. Signal changes
arising from confluent fibrosis and segmental
biliary obstruction often experience abnormal
enhancement and a greater potential for diag-
nostic uncertainty.

FIGURE 2-71.  Portal venous thrombosis with filling defect. Portal Geographic Steatosis/Iron Deposition
venous phase contrast-enhanced image shows an avidly enhanc- Geographic steatosis (or fatty infiltration)
ing splenic vein (thin arrow) with an occlusive filling defect in exhibits the same signal characteristics as its
the main and right and left portal veins (thick arrows). Note the nodular counterpart (Fig. 2-72). Isolated loss of
ascites (open arrows) and susceptibility artifact arising from the signal on out-of-phase images with no mass
TIPS shunt in the posterior segment (circle).
effect on normal hepatic structures character-
izes steatosis. Whereas iron deposition also
lacks mass effect, the opposite signal loss
Portal venous occlusion also rarely arises pattern is observed—loss of signal on in-phase
spontaneously. Identification of segmental arte- images—reflecting increasing susceptibility
rial enhancement prompts inspection of the effects of iron as a consequence of the longer
regional portal venous branches in pursuit of a echo time (and iron deposition is usually
filling defect (Fig. 2-71). A history of visceral diffuse). Enhancement equivalent to hepatic
inflammation or malignancy (particularly HCC) parenchyma characterizes both entities.
increases the likelihood of portal venous occlu- Neither demonstrates profound signal changes
sion. In the absence of an underlying culprit on spin-echo (or FSE) images, however,
lesion—such as HCC—signal or morphologic because the 180° pulse(s) correct for phase
changes are usually absent. When associated changes (in the case of steatosis) and suscepti-
with malignancy, check for enhancement of the bility artifact (in the case of iron deposition).
filling defect, which indicates tumor thrombus, Spin-echo images generally brandish mild rela-
as opposed to bland thrombus (which does not tive hyperintensity due to fat and hypointen-
enhance). sity due to iron, respectively.
 MRI of the Liver  •  103

A B
FIGURE 2-72.  Geographic steatosis. A segmental wedge-shaped region of hypointensity (arrows in A) on the out-of-phase image (A) is
isointense to surrounding liver parenchyma on the in-phase image (B).

A B
FIGURE 2-73.  Confluent fibrosis. Two adjacent, peripheral, wedge-shaped lesions (arrows) with capsular retraction exhibit hyperintensity
on the T2-weighted, fat-suppressed image (A) and delayed enhancement on the corresponding interstitial phase T1-weighted image (B).

Confluent Fibrosis vascular structures and the extracellular dead

Confluent fibrosis connotes a segmental area space of fibrosis. Negative mass effect generally
of scarring or collagenous tissue forming in differentiates confluent fibrosis from most other
response to a hepatic insult, most commonly T2 hyperintense lesions, including neoplasms.
cirrhosis (although reticular fibrosis predomi- The enhancement pattern discriminates conflu-
nates in cirrhosis). Confluent fibrosis affects ent fibrosis from the hypervascularity of HCCs
approximately 14% of cirrhotic livers and usually and other hypervascular masses. Cholangiocar-
involves the medial and/or anterior segments.88 cinoma most closely approximates the appear-
Confluent fibrosis occasions hepatic parenchy- ance of confluent fibrosis, exhibiting similar
mal atrophy, and volume loss—reflected by cap- signal characteristics and enhancement pattern.
sular retraction—is a hallmark (Fig. 2-73). Lesion Lack of upstream ductal dilatation and other
margins are sharp and morphology is usually signs of mass effect and association with cirrho-
triangular or pyramidal with the vertex centrally sis favor confluent fibrosis.
positioned. Signal characteristics differ from
fibrosis arising in other body parts, which is Intrahepatic Cholestasis
globally hypointense. Although dark on Intrahepatic cholestasis is included in the cate-
T1-weighted images, confluent fibrosis demon- gory of parenchymal geographic lesions because
strates moderate hyperintensity on T2-weighted of the propensity to manifest signal changes—
images, probably reflecting a combination of specifically T1 hyperintensity.90 Still, T1 hyper-
edema and residual vascular spaces.89 Gradual, intensity affects a minority of cases of cholestasis
delayed enhancement reflects the presence of and its absence clearly does not exclude it.
104  •  Fundamentals of Body MRI

A B
FIGURE 2-74.  Intrahepatic cholestasis. A and B, Note the central tubular hypointensities within the peripheral triangular hyperintensity
(arrow in A) in the T1-weighted fat-suppressed image in the medial segment correspond to dilated biliary radicles.

Absent T2 signal changes and possibly arterial

TABLE 2-20.  Diffuse Liver Diseases
enhancement (possibly due to increased pres-
sures) are additional imaging features. Associ- Morphology Diseases Occult Diseases
ated dilatation of the biliary radicles and Cirrhosis Acute hepatitis
(Primary) sclerosing cholangitis Fulminant liver failure
characteristic T1 hyperintensity increase diag- (Primary) biliary cirrhosis Autoimmune hepatitis
nostic confidence (Fig. 2-74). Budd-Chiari syndrome Liver transplantation

Signal Diseases
Steatosis
Hemochromatosis
DIFFUSE ABNORMALITIES Hemosiderosis
Diffuse liver abnormalities fall loosely into two
broad imaging categories: morphology and
signal derangements (Table 2-20). Morphologic processes, respectively, and lack acute
conditions include cirrhosis, Budd-Chiari syn- symptomatology.
drome (BCS), and other lesions, such as biliary
cirrhosis and sclerosing cholangitis, which etio-
Occult (General Lack of Signal and
logically belong to the biliary classification.
Morphologic Changes) Processes
Signal abnormalities encompass some lesions
already covered and include steatosis, iron The occult category serves as an auspicious
deposition (hemochromatosis and hemosidero- starting point for the discussion of diffuse liver
sis), and rare conditions (beyond the scope of disease because the normal liver appearance is
this text) such as glycogen storage disease. A reiterated and the feared endpoint is cirrhosis—
third phantom, or occult, category includes dis- the preeminent diffuse liver disease. Most cases
eases with significant clinical findings often of acute hepatitis are attributable to viral hepa-
revealing no (obvious or specific) imaging titis and the most frequent culprits are hepatitis
abnormality: acute hepatitis/fulminant liver A through E viruses. Although acute hepatitis
failure, chronic hepatitis, and autoimmune hep- manifests histologically with hepatocytic
atitis (AIH). Conceptually, the occult disorders damage and scattered necrosis, the imaging fea-
present acutely and the disorders involving mor- tures are nonspecific and often absent. Imaging
phologic and signal derangements represent the accomplishes the objective of excluding other
effects of longstanding disease and depositional potential etiologies that simulate the clinical and
 MRI of the Liver  •  105

A B
FIGURE 2-75.  Hepatic inflammation. Periportal edema (arrows in A) and patchy, multifocal parenchymal hyperintensity on the heavily
T2-weighted image (A) corresponding to inflammation and edema in a patient with acute fulminant liver failure demonstrate enhance-
ment on the delayed image (B).

biochemical derangements, such as cholestasis,

TABLE 2-21.  Etiologies of Acute Hepatic
metastatic disease, and chronic liver disease.31
Inflammation
Imaging studies generally lack positive findings,
and when present, they are usually nonspecific— Viral Etiologies Toxins
hepatomegaly, periportal lymphadenopathy, Hepatitis A Amanita toxin (mushrooms)
Hepatitis B Carbon tetrachloride
and periportal edema indicate hepatic inflamma- Hepatitis C
tion. Periportal T2 hyperintensity and delayed, Hepatitis D Drugs
gradual enhancement correspond to edema and Hepatitis E Amoxicillin
Ebstein-Barr virus Minocycline
inflammatory infiltrate (Fig. 2-75). Extrahepatic Cytomegalovirus Antituberculous agents
secondary inflammatory changes, such as edem- Adenovirus
atous gallbladder wall thickening and ascites, Autoimmune Etiologies
Bacterial Etiologies Systemic lupus erythematosus
are also nonspecific.
Persistence of hepatic inflammation continu- Parasitic Etiologies Metabolic Diseases
ing for at least 6 months qualifies as chronic Toxoplasma Wilson’s disease
Q fever
hepatitis. HBV and HCV are the usual suspects. Leptospira Other
Periportal lymphadenopathy may or may not Rocky Mountain spotted fever Alcohol
persist with ongoing inflammation, which pro- Pregnancy
gresses temporally unpredictably to cirrhosis (to
be discussed in the section on “Primarily Mor- apply to AIH, and lymphadenopathy is relatively
phology Diseases,” later). uncommon. Diagnosis relies on a scoring system
Many other pathogens and idiopathic phe- based on clinical, serologic, and histologic find-
nomena afflict the liver, triggering the acute ings (and not on imaging findings) devised
hepatitis pattern. In addition to viruses, nonviral by the International Autoimmune Hepatitis
pathogens (such as toxoplasma and leptospiro- Group.91,92 Autoantibodies, an association with
sis), alcohol and other toxins, medications, met- other autoimmune diseases (such as thyroiditis,
abolic diseases (such as Wilson’s disease), and ulcerative colitis, rheumatoid arthritis, and
autoimmune conditions cause acute hepatitis celiac disease), and overlap syndromic patho­
(Table 2-21). logy (i.e., coexistence with primary biliary cir-
AIH accounts for a small fraction of acute rhosis [PBC] and PSC) provide the only potential
hepatitis cases, but deserves recognition because specific or suggestive diagnostic data.
of the frequent progression to chronic liver
disease and cirrhosis and the unique treatment
Primarily Signal Processes
scheme. Although up to 80% of patients initially
respond to corticosteroid and immunosuppres- Fatty Liver Disease
sive treatment, most relapse and AIH accounts Fatty liver disease subdivides into two basic cate­
for nearly 20% of cases of chronic liver disease gories: steatosis alone and steatosis with necro-
overall. The same nonspecific imaging findings inflammatory activity (steatohepatitis), which
106  •  Fundamentals of Body MRI

Hepatic steatosis

Alcohol

No Yes

Nonalcoholic liver disease Alcoholic steatosis

Necroinflammatory changes Primary Secondary

Insulin Drugs Surgical Miscellaneous

resistant procedures
Yes No syndromes

DM type II Corticosteroids Gastropexy TPN with

glucose
NASH Nonalcoholic
steatosis Obesity Synthetic Jejunoileal Environmental
estrogens bypass toxins

Hyperlipidemia Amiodarone Extensive bowel Small bowel

resection diverticulosis

Nifedipine Biliopancreatic A-hypolipoproteinemia

diversion

FIGURE 2-76.  Classification of steatosis syndromes. DM, diabetes mellitus; NASH, nonalcoholic steatohepatitis; TPN, total parenteral
nutrition.

encompasses alcoholic and nonalcoholic steato- with or without using the spleen as a reference
hepatitis (NASH) (Fig. 2-76). When not associ- standard:
ated with alcoholism, steatosis is termed
nonalcoholic fatty liver disease (NAFLD), ( liver IP − liver OP ) /( liver ×100 ) : uncorrected
which is an evolving concept afflicting a large [( liver IP / spleen IP ) − ( liver OP / spleen OP )]
segment of the population (≤15%), and up to /( liver IP / spleen IP ×100) : spleen-corrected
10% have steatohepatitis.93 NALFD is the hepatic
component of the systemic metabolic syndrome where IP = in-phase and OP = out-of-phase.
of obesity, type II diabetes mellitus, insulin resis- Ultimately, the diagnosis of NAFLD/NASH
tance, dyslipidemia, and hypertension. Predict- depends on histologic findings and an absence
ing the onset and progression of steatohepatitis of alcohol intake. MR findings of pronounced
eludes current diagnostic modalities. Obesity signal loss on out-of-phase images—reflecting
and insulin resistance reportedly promote microscopic fat—corroborates the diagnosis.
hepatic inflammation, and fibrogenesis and Development of MR features of cirrhosis con-
genetic factors likely play a role. Treatment firms chronic inflammation after it is already too
focuses on minimizing risk factors, such as late. NASH and alcoholic steatohepatitis present
obesity, and pharmacologic therapy attempting no unique imaging findings, until fibrosis and
to improve insulin sensitivity, treat dyslipid- morphologic hallmarks of cirrhosis set in.
emia, and protect hepatocytes. Monitoring treat- Despite the presence of inflammation, reactive
ment effects requires accurate assessment of lymphadenopathy is typically absent.
lipid content. Liver biopsy had been considered
the gold standard for lipid quantification, but Iron Depositional Disease
recent work in MR and specifically MR spectros- Iron depositional diseases account for the other
copy, challenges that assumption.94 Calculations major category of diffuse hepatic signal abnor-
based on in- and out-of-phase imaging also yields malities and consist of two disease entities:
accurate quantification of intrahepatocellular (primary) hemochromatosis and hemosiderosis
lipid content. Fat quantification is calculated (secondary hemochromatosis) (Fig. 2-77).
 MRI of the Liver  •  107

Primary hemochromatosis liver signal intensity is significantly less than the

OOP IP out-of-phase liver signal intensity, susceptibility
artifact is at work, which is almost always attrib-
Liver Spleen utable to iron (Figs. 2-78 and 2-79).
Pancreas Using the same approach, assess the spleen
and pancreas for the same signal loss phenome-
non. Pancreatic signal loss signifies parenchymal,
Secondary hemochromatosis (“hemosiderosis”) or primary, hemochromatosis and splenic signal
OOP IP loss indicates RES, or secondary, hemochromato-
sis (see Figs. 2-78 and 2-79). This diagnostic
approach is useful not because iron can be
detected only on the in- and out-of-phase images,
but because this sequence is obtained whether
or not iron is suspected and because the out-of-
FIGURE 2-77.  Hemochromatosis and hemosiderosis. IP, in phase; phase serves as a baseline or reference standard.
OOP, out of phase. Difficulty arises when coexistent steatosis
decreases hepatic signal on the out-of-phase
images. In that case, obtaining a longer series of
Primary hemochromatosis is an autosomally in- and out-of-phase images reveals oscillating
recessive inherited disease of gastrointestinal signal between in- and out-of-phase images with
iron absorption resulting in parenchymal depo- a pronounced downward trend due to the sus-
sition of iron. Hemosiderosis connotes iron ceptibility of iron. Exaggerated signal loss on the
overload of the reticuloendothelial system (RES), standard SSFSE or FSE T2-weighted images is a
usually from repeated blood transfusions or more subjective means of detecting iron, which
ineffective erythropoiesis (i.e., thalassemia is not subject to the presence of lipid.
major, sideroblastic anemia). Parenchymal—or Because of the deleterious effects of paren­
primary—hemochromatosis involves the pan- chymal iron, chelation therapy is administered
creas and liver (and myocardium), and RES—or to hopefully stave off the onset of cirrhosis.
secondary—hemochromatosis involves the Assessment of response to therapy involves T2
spleen and liver (and bone marrow). Toxic (spin-echo) and T2*(GE) mapping, which
parenchymal iron incites fibrosis in primary involves ROI measurement on multiple sets of
hemochromatosis whereas RES cells accumulate T2-weighted and T2*-weighted images. In fact, an
iron in secondary hemochromatosis, sparing on-line calculation algorithm generated by the
hepatocytes and avoiding fibrogenesis. Conse- University of Rennes provides a useful, accessi-
quently, primary hemochromatosis leads to cir- ble calculation method (http://www.radio.
rhosis and secondary hemochromatosis usually univ-rennes1.fr/Sources/EN/Hemo.html). ROI
does not (see Fig. 2-77). measurements and adherence to specific proto-
Despite the different histology and cellular col parameters are required (Table 2-22).
deposition of iron in primary and secondary No realistic differential diagnosis is worth con-
hemochromatosis, the MR appearance of iron sidering in the case of diffuse hepatic suscepti-
deposition in the two diseases is the same. Visu- bility or signal loss. Punctate or focal signal loss
alization of iron is a reflection of its strong sus- signifies calcified granulomas, siderotic nodules
ceptibility relative to surrounding tissues, which in the liver, or Gamna-Gandy bodies in the
locally distorts the magnetic field resulting in spleen. Segmental signal loss on T1-weighted
signal loss. Because the 180° refocusing pulses images without a TE-dependent increase charac-
in spin-echo pulse sequences correct for suscep- terizes confluent fibrosis, which also demon-
tibility, GE sequences are much more sensitive strates T2 hyperintensity (as opposed to relative
to this phenomenon. Increasing the TE increases T2 hypointensity in iron deposition).
the duration of the distortion with proportion-
ally greater signal loss. Therefore, GE sequences
Primarily Morphology Diseases
with longer TE are more sensitive to the pres-
ence of iron. Using the out-of-phase as a base- Broadly speaking, morphologic derangements
line, compare the liver signal on the in-phase of the liver parenchyma signify chronic or
image, which has twice the TE. If the in-phase advanced disease and define the endpoint of
108  •  Fundamentals of Body MRI

A B

C D
FIGURE 2-78.  Primary hemochromatosis. The pancreas (thin arrow in A and B) and liver (thick arrow in A and B) drop in signal between
the out-of-phase (A) and the in-phase (B) images, reflecting susceptibility artifact. C, The heavily T2-weighted image shows the char-
acteristic nodular atrophy-hypertrophy pattern of cirrhosis (arrow). D, Note the tubular signal voids (arrows), which enhance on the
delayed postcontrast image and correspond to massively enlarged portosystemic splenorenal collaterals (due to portal hypertension).

A B
FIGURE 2-79.  Secondary hemochromatosis (hemosiderosis). Gradient-echo images with short TE (A, ~1 msec) and long TE (B, ~7 msec)
exemplify iron deposited in the liver and spleen with susceptibility artifact more severely affecting the spleen.
 MRI of the Liver  •  109

TABLE 2-22.  Liver Iron Quantification Instructions

T2 Mapping ⇒ GRASE
T2* Mapping ⇒ multi-echo GRE
Use dual GRE (in-/out-of-phase) to assess for superimposed steatosis
Sample Template Dictation
Exam Type: «Order Procedure Description»
Exam Date and Time: «Order Observation End Time»
Indication: «Clinical information» [Additional available history…]
Comparison: [<None>].
Impression:
1. [<No evidence of>] [<mild>] [<moderate>] [<severe>] [<secondary>] iron overload in the [<heart>] [<with an estimated cardiac iron concentration>]
[<of [ ] mg/g>]. [<Normal left ventricular wall motion>].
2. [<No evidence of>] [<mild>] [<moderate>] [<severe>] [<secondary>] iron overload in the [<liver>], [<spleen>] & [<bone marrow>]. The estimated
liver iron concentrations is [ ] mg/g. [<Findings likely represent iron overload consistent with the patient’s history of>] [<transfusional siderosis>]
[<thalassemia >] [<primary hemochromatosis>].
3. [<No evidence of iron overload >] [<iron overload >] involving the pancreas.

Procedure:
Non contrast MRI of the abdomen was performed on a [1.0/1.5/3.0] Tesla [open-bore] scanner. Image quality is [<good>] [<satisfactory>] [<degraded by
motion>].

Liver Iron Quantification:

1. A total of 16 breathhold multiecho gradient echo images were obtained at multiple TE time points to calculate the T2* value in the liver. From this value, an
iron concentration was generated based on data in an article from the European Heart Journal, December 2001, pages 2171–2179. An ROI was placed in the
liver on 2 separate series. The calculated liver T2* on 2 separate measurements is [ ] and [ ]. This corresponds to a liver iron concentration of [ ] and [ ]
mg/g respectively.
2. A total of 5 GRASE images were obtained to calculate the T2 value in the liver. From this value, an iron concentration was generated based on data in an
article from Blood Journal, January 2005, pages 855–861. An ROI was placed in the liver on two separate series. The calculated liver T2 on 2 separate
measurements is [ ] and [ ]. This corresponds to a liver iron concentration of [ ] and [ ] mg/g respectively.
3. The liver iron concentration was estimated at [ ] (±50) µmol/g (normal < 36 µmol/g) using a calculator (http://www.radio.univ-rennes1.fr/Sources/EN/
HemoCalc15.html). This calculation takes into account the MRI signal intensity in three separate regions of interest in the liver measuring [ ], [ ], and [ ]
and two separate regions of interest in the paraspinal muscles measuring [ ] and [ ]. These values were obtained with GRE images (TE 4.6 msec/Flip angle
20 degrees), using the built-in body coil to ensure a homogeneous signal profile.

Cardiac Iron Quantification:

1. Cardiac gated, short axis multiecho gradient echo images were obtained for cardiac iron mapping. From this, an ROI was placed in the interventricular
septum and a T2* value of the myocardium was obtained to calculate a cardiac iron concentration based on data in an article from the European Heart
Journal, December 2001, pages 2171–2179.

Findings:
Liver: There is [<no>] fatty infiltration. No liver mass is demonstrated.
Spleen: [<Within normal limits>]. [<No evidence of>] [<mild>] [<moderate>] [<severe>] [<secondary>] iron overload.
Heart: Cine cardiac imaging demonstrates normal heart size and cardiac function. [<No pericardial effusion >]. The calculated T2* in the interventricular
septum is [ ].
Pancreas: [<The pancreas and pancreatic duct are normal>]. [<The pancreatic parenchyma has normal signal intensity>]. [<No evidence of iron overload>].
[<The main pancreatic duct is normal>].
There is [<no>] ascites. Abdominal Vessels: [<The superior mesenteric vein, portal vein, splenic vein, and hepatic veins are grossly patent. There is standard
hepatic arterial anatomy. The proximal celiac artery, superior mesenteric artery, and inferior mesenteric artery are patent.>]
Biliary system: [<No biliary ductal dilatation>]. Gallbladder is [<within normal limits>].
Adrenal glands: [<Within normal limits>].
Kidneys: [<Within normal limits>].
Lymph nodes: [<No lymphadenopathy>].
Bones: [<Within normal limits>]. [<No evidence of iron overload>].
Lung bases: [<Within normal limits>].
GRASE, gradient and spin echo; GRE, gradient-recalled echo; MRI, magnetic resonance imaging; ROI, region of interest; TE, time to excitation.

many of the previously discussed disorders. BCS exhibits a protean appearance depending
Whereas cirrhosis dominates this category, dif- on the temporal phase, ultimately demonstrat-
ferent patterns of cirrhosis typify different ing morphologic abnormalities in the chronic
disease processes. For example, sclerosing chol- phase. LT represents a morphologic derange-
angitis characteristically exhibits a macrono­ ment with reference to the patient’s native liver
dular cirrhotic pattern, whereas many other and is relegated to this category by default (see
etiologies demonstrate a micronodular pattern. Table 2-20).
110  •  Fundamentals of Body MRI

Cirrhosis adequate portal flow, typically reflected by

Cirrhosis is the common endpoint of chronic caudate hypertrophy.
liver diseases undergoing parenchymal necrosis Multiple imaging signs announcing these mor-
and fibrosis with ongoing regeneration. Whereas phologic derangements have been described
parenchymal injury induces scarring or fibrosis, (Fig. 2-81). Enlargement of the hilar periportal
the unique ability of the liver to regenerate space (between the anterior wall of the right
mani­fests in the form of intervening islands—or portal vein and the posterior edge of the medial
nodules—of hepatocytes. The macroscopic segment of the liver) beyond 10 mm is observed
result is a patchwork quilt of bridging bands of with atrophy of the medial segment (see Fig.
fibrosis surrounding regenerative nodules. In 2-80).95,96 The “expanded gallbladder fossa”
addition to nodularity, global morphologic fea- sign reflects a combination of trophic phenom-
tures usually develop as a function of differences ena: (1) medial segment atrophy, (2) caudate
in portal venous circulation. A sectorial atrophy-
hypertrophy pattern reflects relative portal
venous supply. Compromised portal venous
flow starves the affected parenchyma resulting
in atrophy, with hypertrophy of the tissue enjoy-
ing more robust portal flow (Fig. 2-80). Conse-
quently, the right lobe atrophies owing to the
long, tenuous intrahepatic course of the right
portal vein through a scarred, cirrhotic liver
compromising portal blood flow. Although the
protective course of the left portal vein in the
falciform ligament explains the lateral segmental
hypertrophy, factors uniquely affecting the
medial segment counteract this protective phe-
nomenon, resulting in medial segmental atrophy.
FIGURE 2-80.  Atrophy-hypertrophy pattern in cirrhosis. The axial
The helical portal venous flow pattern directs
heavily T2-weighted image of a cirrhotic liver shows the typical
flow away from the medial segment and concur- atrophy-hypertrophy pattern resulting in the hepatic notch sign
rent blood flow from the gastric, cystic, peribili- (angled lines) due to right lobe atrophy and caudate hypertrophy
ary, and capsular veins throttle portal venous and prominence of the periportal space (arrows) due to medial
inflow. The short intrahepatic course of the segment atrophy. Note the nodularity and lateral segmental
portal venous supply to the caudate ensures hypertrophy.

3 4

1. Right lobe atrophy

2 2. Caudate lobe hypertrophy
3. Medial segment atrophy
4. Lateral segment hypertrophy

Widened
periportal
space
Diffuse parenchymal nodularity

Right posterior notch sign

FIGURE 2-81.  Imaging signs of cirrhosis.

 MRI of the Liver  •  111

hypertrophy, (3) right lobe atophy, and (4) regeneration manifests with nodules of regener-
lateral segment hypertrophy.97 The “right poste- ating parenchyma with surrounding fibrosis rep-
rior notch” sign describes the appearance of the resenting the byproduct of hepatotoxic effects.
posterior margin of the liver on axial images.98,99 MR images portray this as parenchymal nodular-
Concurrent right lobe atrophy and caudate ity with interdigitating fibrotic bands (Fig. 2-83).
hypertrophy invert the normal smoothly convex
posterior liver margin, eventually forming an
angular concave margin—the “right posterior
notch sign.”
A measurement scheme has been devised to
detect early cirrhosis before these signs develop.
The (modified) caudate–right lobe ratio reflects
the hypertrophy-atrophy pattern by comparing
the size of the caudate lobe—defined laterally
by the lateral wall of the right portal vein and A: 89.8mm
medially by the medial extent of the caudate— A
C
with the size of the right lobe—defined medially C: 75.7mm
by the right portal vein and laterally by the
capsular surface (Fig. 2-82). A ratio of greater
than 0.90 predicts cirrhosis with a sensitivity,
specificity, and accuracy of 72%, 77% and FIGURE 2-82.  Modified caudate–to–right lobe ratio. The axial
74%, respectively.100 enhanced image of a nodular, cirrhotic liver with the character-
Along with the global morphologic changes, istic atrophy-hypertrophy pattern exemplifies the elevated modi-
textural changes develop. Parenchymal fied caudate–to–right lobe ratio.

A B

C D
FIGURE 2-83.  Parenchymal nodularity with bridging bands of fibrosis. The axial moderately T2-weighted fat-suppressed images at baseline
(A) and follow-up (B) portray advanced cirrhosis reflected by diffuse nodularity with intervening reticular hyperintensity corresponding
to fibrosis with worsening ascites. Comparing the out-of-phase (C) with the in-phase (D) images reveals susceptibility artifact arising
from the parenchymal (siderotic) nodules due to their iron content.
112  •  Fundamentals of Body MRI

Nodular parenchymal signal intensity and routine use in this capacity and morphologic
enhancement do not differ from noncirrhotic descriptors are the mainstay.
parenchyma. Reticular fibrosis appearing as Assessing the degree of cirrhosis with atten-
bridging bands of fibrosis between islands of tion to the risk of developing HCC and other
nodular parenchyma is the more common mani- complications—such as portal venous occlusion
festation of fibrosis; confluent fibrosis occurs and portal hypertension with collaterals—
less frequently and often coexists with reticular assumes prime importance in cirrhosis surveil-
fibrosis (see Fig. 2-73). As previously discussed lance. As an aside, remember that cirrhosis is
in reference to confluent fibrosis, signal charac- not a prerequisite for the development of HCC
teristics typically reflect edema and vascular in chronic HBV infection (unlike HCV). In addi-
spaces with T2 hyperintensity (and T1 hypoin- tion to assessing the degree of cirrhosis, evalu-
tensity). Delayed enhancement is also character- ate the portal circulation to ensure patency for
istic. Therefore, moderately T2-weighted and transplant technical considerations. Whereas
delayed images most clearly depict fibrosis. occlusion of the portal vein and/or SMV histori-
Novel methods are being tested to increase the cally precluded transplantation, innovative
sensitivity of MR for fibrosis, including diffusion- technical methods—such as thrombectomy or
weighted imaging. Increased connective tissue interposition grafting—must be employed to cir-
(fibrosis), distorted sinusoids, decreased blood cumvent the compromised circulation. Note the
flow, and possibly other factors restrict diffusion presence of portosystemic collaterals signifying
in the cirrhotic liver, reflected by diminished portal hypertension with attendant risks, such
apparent diffusion coefficient (ADC) values as upper gastrointestinal bleeding. The common
compared with normal liver.101 Quantifying portosystemic collateral pathways include (1)
fibrosis as a marker for disease severity, tradi- paraumbilical vein (contributing to the caput
tionally achieved with liver biopsy, influences medusa), (2) left gastric vein feeding submu­
treatment (i.e., antiviral therapy for HBV and cosal esophageal and paraesophageal varices,
HCV). Although potentially useful, diffusion- (3) splenorenal shunting, (4) retroperitoneal
weighted imaging has not been established for varices, and (5) mesorectal collaterals (Figs. 2-84

1. Paraumbilical vein
2. Para- and esophageal varices
3. Splenorenal shunt
IVC 4. Retroperitoneal varices
2 5. Mesorectal varices

LGV

PV
3
SV
IVC = Inferior vena cava
PV = Portal vein
LRV LGV = Left gastric vein
SMV SV = Splenic vein
1 LRV = Left renal vein
4 IMV
IMV = Inferior mesenteric vein
SMV = Superior mesenteric vein
CIV = Common iliac vein
CIV
Rectum
5

FIGURE 2-84.  Portosystemic collateral pathways.

 MRI of the Liver  •  113

and 2-85).102 Other signs of portal hypertension

TABLE 2-23.  Etiologies of Cirrhosis
include splenomegaly, ascites, and enlargement
of the cisterna chyli (>6 mm) (Fig. 2-86).103 Most Common Causes of Cirrhosis (in the United States)
Hepatitis C (26%)
Ascites grading ranges from mesenteric edema, Alcoholic liver disease (21%)
constituting the forme fruste of ascites, to Hepatitis C plus alcoholic liver disease (15%)
severe when fluid volume exceeds visceral Cryptogenic causes (18%)
Hepatitis B, which may be coincident with hepatitis D (15%)
volume. The cisterna chyli courses cephalad Miscellaneous (5%)
along the right side of the aorta appearing as a
mildly tortuous, fluid-filled structure exhibiting Miscellaneous Causes of Chronic Liver Disease  
and Cirrhosis
delayed enhancement (usually enhancing a Autoimmune hepatitis
few minutes after gadolinium administration). Primary biliary cirrhosis
Recent work suggests that a diameter greater Secondary biliary cirrhosis (associated with chronic extrahepatic bile duct
obstruction)
than 6 mm predicts uncompensated cirrhosis. Primary sclerosing cholangitis
Few cirrhotic etiologies demonstrate specific Hemochromatosis
findings. Most cases of cirrhosis develop from Wilson’s disease
Alpha1-antitrypsin deficiency
chronic hepatitis (HBV and HCV) and alcoholic Granulomatous disease (e.g., sarcoidosis)
liver disease. Among the myriad other etiologies Type IV glycogen storage disease
of cirrhosis, the most commonly encountered Drug-induced liver disease (e.g., methotrexate, alpha methyldopa,
amiodarone)
include PSC, primary and secondary biliary cir- Venous outflow obstruction (e.g., Budd-Chiari syndrome, veno-occlusive
rhosis, hemochromatosis, AIH, and vascular eti- disease)
ologies, such as BCS (Table 2-23). Few specific Chronic right-sided heart failure
Tricuspid regurgitation

A B

C D
FIGURE 2-85.  Portosystemic collateral vessels. A, A large paraumbilical collateral vessel (arrows) courses through the left lobe in the region
of the falciform ligament. B, Paraesophageal varices (thin arrow) and submucosal esophageal varices (thick arrow) in a different patient.
C, Markedly enlarged splenorenal varices in the periportal region eventually channel caudally and drain into the left renal vein (not
shown). D, A coronal image in a different patient shows clustered splenorenal varices (thin arrows) draining into the left renal vein (thick
arrow).
114  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 2-86.  Signs of portal hypertension. A, Coronal heavily T2-weighted image shows the extent of marked generalized ascites and a
cirrhotic liver. The axial T2-weighted image (B) at the level of the aortic hiatus shows a hyperintense fluid-filled structure (arrow in B
and C), which enhances on the delayed image (C), characteristic of a lymphatic structure and in the expected location of the cisterna
chyli—in this case, enlarged due to portal hypertension. D, Delayed postcontrast image in a different patient with portal hypertension
reveals portosystemic collateral channels, including a large paraumbilical portosystemic collateral vessel (thin arrow) and paraesophageal
varices (thick arrow). E, A different patient with cirrhosis exemplifies features of portal hypertension—splenomegaly with a splenic infarct
(thin arrow), ascites (thick arrows), and nonocclusive portal venous thrombus (open arrow).
 MRI of the Liver  •  115

A B
FIGURE 2-87.  Cirrhosis in primary biliary cirrhosis (PBC). Parenchymal macronodularity with interdigitating reticular fibrosis character-
izes PBC.

features distinguish these disorders, with some resulting in nonspecific cirrhosis. Occasionally,
exceptions. Chronic viral hepatitis and alcoholic relative macronodularity with reticulated fibro-
liver disease present no specific features and are sis develops (Fig. 2-87). Despite the biliary
indistinguishable, accounting for the vast major- nature of the disease, biliary findings are absent.
ity of cases. Many other etiologies also lack spe- During the course of inflammation, two imaging
cific features, but a few characteristic findings features occasionally suggest the diagnosis—
potentially identify some etiologies. prominent periportal lymph nodes104 and
peripheral, periportal hypointensities (“the
Autoimmune Hepatitis periportal halo sign,” referring to 5- to
AIH is often a diagnosis of exclusion character- 10-mm hypointensities encircling portal triads)
ized by chronic hepatocellular inflammation and (Fig. 2-88).105
necrosis. AIH classically afflicts young women
and frequently follows the typical cirrhotic Primary Sclerosing Cholangitis
pattern—distinguished by a frequent coexis- PSC is another inflammatory chronic cholestatic
tence with other autoimmune disease, such as disease that affects large and extrahepatic ducts.
inflammatory bowel disease, PBC and PSC Unlike its inflammatory counterparts, specific
among others. A composite score incorporating imaging features confirm the diagnosis. The
clinical, serologic, and histologic findings pre- diagnostic criteria include (1) typical (MR or
dicts the probability of the diagnosis.91 Note the endoscopic) cholangiographic abnormalities;
lack of imaging findings included in the diagnos- (2) suggestive clinical, biochemical, and histo-
tic algorithm. logic findings; and (3) the absence of secondary
causes of sclerosing cholangitis.106 Although also
Primary Biliary Cirrhosis associated with other inflammatory diseases—
Although PBC is a chronic cholestatic liver most notably inflammatory bowel disease—the
disease targeting the small and medium-sized demographics differ in that young males are
bile ducts, the primary imaging manifestations most commonly affected and 71% are associated
are parenchymal. Demographic features are with inflammatory bowel disease.
similar to AIH and other autoimmune diseases— The imaging appearance evolves over time. In
such as autoimmune thyroiditis, CREST (calcino- the early phase, relatively circumferential short
sis cutis, Raynaud’s phenomenon, esophageal segmental strictures usually located at biliary
dysfunction, sclerodactyly, and telangiectasia) ductal bifurcations alternate with mildly dilated
syndrome, and sicca syndrome—frequently segments yielding the “beaded” appearance
coexist. The diagnosis relies on combination of characteristic of PSC (Fig. 2-89). Progressive
clinical, biochemical, histologic, and serologic biliary ductal inflammation leads to the charac-
features—antimitochondrial antibodies are teristic imaging appearance with multifocal
considered the hallmark of the disease. PBC strictures, segmental ectasia, ductal wall thick-
often progresses to chronic disease frequently ening and enhancement, and irregular ductal
116  •  Fundamentals of Body MRI

A B
FIGURE 2-88.  Periportal halo sign in PBC. Numerous hypointensities (thin arrows in A and B) surround central portal hyperintensities
on the axial moderately T2-weighted fat-suppressed image (A) and enhanced image (B). Note the paraesophageal varices (thick arrow
in B).

B C
FIGURE 2-89.  Beaded ductal appearance in primary sclerosing cholangitis (PSC). A, Mild changes are apparent on the 2D MRCP radial
slab image with mild stricturing (thin arrows) and upstream ectasia (thick arrows). Another 2D MRCP image (B) showcases more
advanced biliary stricturing (thin arrows in B and C) and ectasia (thick arrows in B and C), also shown on the corresponding enhanced
image (C), revealing direct signs of inflammation in the form of periductal enhancement (open arrows in C).

beading.107 Peripheral ducts are eventually oblit- accounting for relative underdistention proxi-
erated, resulting in the “pruned tree” appear- mal to PSC strictures.
ance, and biliary branching becomes more Idiosyncratic parenchymal changes also
obtusely angulated. Inflammation and fibrosis typify PSC. Relatively early peripheral ductal
presumably restricts upstream dilatation, involvement ultimately generates a peripheral
 MRI of the Liver  •  117

A B

FIGURE 2-90.  Peripheral atrophy–central hypertrophy pattern

in PSC. A–C, Irregular ductal dilatation throughout the atro-
phic periphery contrasts with the hypertrophic central caudate
lobe on the axial heavily T2-weighted image (A). The atrophic
peripheral right lobe appears characteristically hyperintense on
the fat-suppressed T2-weighted image (B). The peripheral
predilection is strikingly portrayed on the MRCP image (C)
showing peripheral markedly irregularly dilated biliary ducts
C
displaced centrifugally by the central hypertrophy.

atrophy–central hypertrophy pattern (Fig. PSC, although rarely present with the diffuse
2-90). Macronodular cirrhosis (nodules meas­ involvement seen in PSC. However, the rare seg-
uring at least 3 cm)—with central nodular mental form of PSC simulates the periductal
predominance—commonly ensues, in contra- infiltrating form of cholangiocarcinoma. Signs of
distinction to most other etiologies, which more an underlying mass (e.g., enhancing tissue, mass
typically develop micronodular cirrhosis.108 effect), bile wall thickening greater than 4 mm,
Although PSC findings are described as classic and relatively greater progressive upstream dila-
and diagnostic, a differential diagnosis exists. tation predict cholangiocarcinoma. Remember
Secondary causes of sclerosing cholangitis that cholangiocarcinoma complicates PSC with
include drug side effects, recurrent pyogenic a frequency of 13%. The other feared complica-
cholangitis, AIDS, cholangiopathy, ischemic tion of PSC is HCC, with an incidence rate of
cholangiopathy, and posttraumatic/postsurgical 1.5%/yr.109
bile duct injury. Clinical history differentiates
these etiologies from PSC. Cirrhosis due to other Budd-Chiari Syndrome
etiologies deforms the biliary ducts, simulating BCS is the final disease in the diffuse morpho-
the appearance of PSC on MRCP and ERCP logic category. The morphologic derangement
images, but generally lacks the suggestive clini- develops as a consequence of hepatic venous
cal findings, macronodularity and the classic occlusion. Occlusion at any point from the small
peripheral atrophy–central hypertrophy pattern hepatic veins through the suprahepatic IVC
of PSC. Tumors invading the biliary tree, particu- leads to centrilobular congestion, sinusoidal
larly cholangiocarcinoma, occasionally mimic dilatation, and ultimately, hepatocellular
118  •  Fundamentals of Body MRI

necrosis and fibrosis. Not surprisingly, underly-

TABLE 2-24.  Etiologies of Budd-Chiari
ing thrombotic diatheses are usually blamed for
Syndrome
the development of this disease, although no
etiology is discovered in one third of patients. Hematologic Disorders
Polycythemia rubra vera
Common causative etiologies include hemato- Paroxysmal nocturnal hemoglobinuria
logic disorders (e.g., polycythemia vera, myelo- Unspecified myeloproliferative disorder
proliferative disorders, essential thrombocytosis, Antiphospholipid antibody syndrome
Essential thrombocytosis
antiphospholipid antibody syndrome), inherited
thrombotic diseases (e.g., protein C deficiency, Inherited Thrombotic Diathesis
protein S deficiency, Factor V Leiden deficiency, Protein C deficiency
Protein S deficiency
antithrombin III deficiency), pregnancy, oral Antithrombin III deficiency
contraceptives, chronic infections and inflam- Factor V Leiden deficiency
matory conditions, malignancies (especially
Pregnancy and Postpartum
HCC and renal cell carcinoma), and intravascu-
lar webs (Table 2-24).110 Membranous Webs
Untreated BCS usually progresses and medi­­
Oral Contraceptives
cal therapy (anticoagulation, antithrombotic
therapy, and management of ascites), intravas- Chronic Infections
cular intervention (angioplasty or TIPS), and Hydatid cysts
Aspergillosis
surgical treatments (vascular decompression Amebic abscess
and transplant) become necessary to preserve Syphilis
life; medical therapy alone incurs an 80% to 85% Tuberculosis
2-year mortality rate. Four clinical syndromes Chronic Inflammatory Diseases
are observed: (1) acute liver disease, (2) sub- Behçet’s disease
acute liver disease, (3) fulminant liver disease, Inflammatory bowel disease
Sarcoidosis
and (4) liver failure. Portal hypertension fre- Systemic lupus erythematosus
quently complicates the disease process. Sjögren’s syndrome
MRI features depend on the temporal phase Mixed connective-tissue disease
of the process. The direct finding of hepatic Tumors
venous thrombosis becomes less prevalent with Hepatocellular carcinoma
chronicity and is more likely visualized in the Renal cell carcinoma
Leiomyosarcoma
acute or subacute setting, whereas intrahepatic Adrenal carcinoma
and extrahepatic collaterals are more conspicu- Wilms’ tumor
ous in the chronic phase (Fig. 2-91). Because Right atrial myxoma
dense contrast enhancement of (hepatic) veins Miscellaneous
cannot be directly timed and contrast is invari- Alpha1-antitrypsin deficiency
ably diluted at the time of venous enhancement, Trauma
Dacarbazine
consider using double-dose gadolinium to evalu- Urethane
ate the hepatic veins and IVC in potential cases
of BCS. Also incorporate steady-state images, Idiopathic
which possess intrinsic fluid–to–solid tissue
contrast and do not rely on time-of-flight or T1
shortening from gadolinium to display vascular reflect the edema and increased tissue pressure,
anatomy. “Comma-shaped” intrahepatic collat- respectively (see Figs. 2-91 and 2-92). The pro-
eral veins are reportedly specific for BCS. Sono- tected caudate lobe enlarges and demonstrates
graphically demonstrated large caudate veins relatively increased enhancement. Centripetal
(>3 mm) in the appropriate clinical setting signal changes fade with time, and regenerative
strongly suggest the diagnosis of BCS.111 Narrow- nodules begin to proliferate.
ing or obliteration of the hepatic veins and/or Regenerative nodules in BCS represent
IVC develops over time. Acute parenchymal regions of the liver with relatively preserved
changes reflect the differential venous drainage blood flow. BCS nodules range in size from 0.5
between the peripheral and the central (caudate to 4 cm and are hyperintense on T1-weighted
lobe, primarily) portions of the liver. Peripheral images because of the hypointensity of the
T2 hyperintensity and diminished enhancement edematous surrounding tissue and/or increased
 MRI of the Liver  •  119

A B

FIGURE 2-91.  Budd-Chiari syndrome. A, The portal phase

image reveals a filling defect in right hepatic venous branches
(arrows). The delayed image (B) shows a filling defect in a
middle hepatic venous branch (arrow in B) and hyperintensity
of the central liver parenchyma with corresponding hyperin-
tense, edematous changes in the periphery on the T2-weighted
C
image (C).

A B

FIGURE 2-92.  Signal characteristics of Budd-Chiari syndrome.

There is patchy hyperintensity in the periphery of the liver on
the heavily T2-weighted image (A) with corresponding
hypointensity on the precontrast T1-weighted image (B)
reflecting edema and congestion with diminished enhance-
ment on the postcontrast image (C) compared with the avidly
C
enhancing central portion of the liver.
120  •  Fundamentals of Body MRI

A B
FIGURE 2-93.  Passive hepatic congestion. In a patient with congestive failure, the arterial phase image (A) reveals heterogeneous enhance-
ment reiterated on the portal phase image (B), highlighted by a reticulated network of curvilinear hypointensities (arrows in B).

copper content. T2 isointensity to mild hypoin- Liver Transplantation

tensity is the norm in BCS regenerative nodules. LT involves replacement of a failed recipient
Hyperintensity on T2-weighted images proba- liver with a healthy cadaveric (orthotopic liver
bly reflects infarction, which is a risk given the transplantation [OLT]) or part of a living
precarious hepatic venous drainage. Regenera- donor’s liver (living donor liver transplantation
tive nodule hypervascularity reflects arterial [LDLT]). LT treats end-stage hepatic parenchy-
supply with persistent hyperintensity on portal mal disease, such as cirrhosis, portal hyperten-
phase images. Unfortunately, this appearance sion, and unresectable localized tumors (i.e.,
overlaps significantly with the appearance of HCC). Serial MR examinations in patients with
HCC in BCS (which has an annual occurrence chronic liver disease and HBV and HCV are
rate reported at 4%,112 similar to other chronic ordered to screen the liver and exclude HCC
liver diseases). In addition, the typical HCC that would violate transplant criteria. Most
washout pattern on delayed images yields low transplant centers adhere to the Milan Criteria—
sensitivity in BCS—most HCCs (in BCS) remain solitary HCC less than 5 cm or up to three
hyperintense. Because specific HCC imaging lesions less than 3 cm—shown to guarantee
features are forfeited in BCS, greater reliance over 70% 5-year survival.114 Pretransplant
on AFP is necessary. A central scar reminiscent imaging guides treatment of small, early HCC
of FNH is an occasional feature of benign, lesions with ablation to obviate transplant con-
regenerative BCS nodules and not characteristic traindication. Posttransplant imaging focuses
of HCC. on tumor surveillance (in the case of chronic
Differentiating the chronic form of BCS from HBV or HCV infection) and posttransplant com-
cirrhosis is often problematic. Nodularity and plications, such as post- fluid collections, biliary
diffuse derangement of the hepatic morphol- strictures, and vascular complications. Biliary
ogy with intervening fibrosis characterize both and vascular complications arise from the mul-
clinical entities. Coexistent portal hyperten- tiple anastomoses involved in transplantation:
sion complicates both diseases. Definitive (1) common bile duct, (2) hepatic artery, (3)
identification of hepatic venous and/or caval portal vein, (4) suprahepatic IVC, and (5) infra-
thrombosis or occlusion establishes the diag- hepatic IVC (Fig. 2-94).
nosis of BCS. Passive hepatic congestion Expected perihepatic findings usually out-
produces a heterogeneous, reticulated enhance- number parenchymal findings after LT. A small
ment pattern with curvilinear hypovascular amount of (usually not encapsulated or local-
regions corresponding to relative hepatic ized) perihepatic, interlobar fissural and right
venous hypertension (Fig. 2-93) and potentially pleural fluid resolves within weeks (Fig. 2-95).115
confused with BCS.113 In contradistinction to Expect susceptibility at the IVC anastomotic site
BCS, the hepatic veins and IVC are abnormally (particularly the suprahepatic anastomosis).
distended and evidence of either right heart Mild portal venous narrowing at the porta
failure or constrictive pericarditis is usually hepatic (probably due to extrinsic compression
forthcoming. by edematous liver) and anastomotic site (due
 MRI of the Liver  •  121

Anastomoses

Complications
Vascular
HA thrombosis and stenosis
PV thrombosis and stenosis
IVC thrombosis and stenosis

Biliary
CBD stenosis

Fluid collections
Biloma
Hematoma
Seroma
HA
PV Malignancy
Recurrent HCC
IVC
PTLD
CBD
FIGURE 2-94.  Diagram of liver transplantation and complications. CBD, common bile duct; HA, hepatic artery; HCC, hepatocellular
carcinoma; IVC, inferior vena cava; PTLD, posttransplant lymphoproliferative disorder; PV, portal vein.

often presents within 4 weeks with graft failure,

biliary stricturing or leak (due to ischemia), or
liver abscess or sepsis (arising from infracted
parenchyma). HAT demands urgent surgical
intervention with revascularization techniques
or retransplantation.117 MR angiography images
provide the most detailed assessment of the
hepatic arterial anatomy and require little modi-
fication of the standard abdominal protocol.
Consider increasing the gadolinium dose (for
increased vascular conspicuity, including venous
structures, which are also at risk), increasing the
flip angle to increase T1-weighting enhancing
FIGURE 2-95.  Perihepatic fluid after liver transplant. The heavily vascular structures, and increasing the spatial
T2-weighted sequence in a patient with a recently placed ortho- resolution (at the expense of coverage, which
topic liver transplant shows a perihepatic fluid collection along is probably expendable in this setting). If sub-
the posterior margin of the liver dome (arrow). stantial susceptibility artifact arises from surgical
clips around the hepatic artery, consider invok-
to discrepancy in size between recipient and ing metal minimization strategies (minimal TE
donor portal vein) is frequently observed. Peri- with fractional echo sampling afforded by using
portal edema peaks in the postoperative period 1 NEX [number of excitations] instead of partial
as a consequence of lack of lymphatic drainage k-space filling, increasing the bandwidth to
(Fig. 2-96). Reactive periportal and portocaval drive down the TE, and eliminating fat suppres-
nodes are only worrisome when enlarged and sion). Look for occlusion at the anastomotic site,
detected in the posttransplant lymphoprolifera- where it usually occurs. Stenosis, the second
tive disorder (PTLD) window—4 to 12 months most common vascular complication (~5% inci-
after transplantation. dence) also develops at the anastomotic site
The most obvious transplant complication— and leads to similar complications—biliary
rejection—has no reliable MRI correlate.116 Vas- ischemia and stricturing and infection—evolving
cular insufficiency, biliary abnormalities, fluid over a longer timecourse. Other arterial
collections, and malignancy constitute the main complications—pseudoaneurysm and arteriove-
complications confronted by imaging. Hepatic nous fistula—occur in less than 5% of cases.
artery thrombosis (HAT), the most common vas- Pseudoaneurysms potentially form at the anasto-
cular complication, occurs in up to 9% of motic site or at the ligated gastroduodenal artery
patients and has declined in incidence. HAT site. Intraparenchymal arteriovenous fistulae
122  •  Fundamentals of Body MRI

A B

FIGURE 2-96.  Periportal edema after liver transplant. Periportal

edema (arrows in A-C) appears as hyperintensity surrounding
the central portal structures on the moderately T2-weighted
C
image (A), enhancing on delayed 2D (B) and 3D (C) images.

and pseudoaneurysms complicate biopsy, biliary potentially confound or obscure the portal vein.
interventions, and other procedures. Parenchymal changes have not been extensively
Portal venous complications occur less com- reported, but probably manifest predominantly
monly. Portal venous stenosis (PVS) threatens on dynamic imaging with compensatory arterial
the onset of portal hypertension, graft failure, enhancement. IVC stenosis and/or thrombosis
and progression to PVT, which further elevates occurs in less than 2% of patients (Fig. 2-98). IVC
the risk of these complications. Surgical techni- complications predispose to BCS, lower extre­
cal factors and hypercoagulable states are the mity edema, ascites, and diminished hepatic
major risk factors for portal venous complica- venous outflow with hepatomegaly. Employ the
tions. PVS usually occurs at the anastomotic site same imaging strategy as in the case of portal
and PVT usually involves the extrahepatic main venous complications.
portal vein (Fig. 2-97). When portal venous com- Parenchymal infarcts resulting from vascular
plications are suspected, consider using a higher insufficiency—usually arterial—must be differ-
dose of gadolinium (up to twice the standard entiated from other parenchymal complica-
dose) and rely mostly on portal phase and tions, such as abscess and biloma. Although
delayed images, using either direct coronal occasionally peripheral, geographic, and
acquisition or coronally reformatted images to wedge-shaped and respecting vascular anatomy
assess the portal vein for stenosis or thrombosis. (see Fig. 2-61), hepatic infarcts also demon-
If available, use steady-state images to supple- strate ill-defined and round morphology (Fig.
ment the gadolinium-enhanced images, with 2-99). Absent enhancement with relative fluid
the caveat that adjacent fluid-filled structures signal potentially overlaps with the appearance
(common bile duct and hepatic artery) of abscess and biloma, but relative preservation
 MRI of the Liver  •  123

A B

FIGURE 2-97.  Portal venous stenosis/thrombosis. Anastomotic

narrowing of the portal vein (arrow in A and B) is clearly
depicted on the steady-state (A) and enhanced (B) images.
C, By eliminating surrounding tissues, the maximal intensity
projectional image portrays the anastomotic stenosis (arrow)
C
more vividly.

of hepatic architecture and portal triads However, be circumspect regarding fluid

excludes other diagnoses. collections because they may belie serious com-
Postoperative fluid collections are either plications. Biloma and abscess are the fluid col-
expected and incidental or potentially problem- lections prompting serious concern. Although
atic and requiring treatment or intervention. occasionally intraparenchymal, bilomas usually
Incidental fluid collections include right pleural inhabit the porta hepatis or gallbladder fossa
effusion and small perihepatic hematomas/ and exhibit uniform T2 hyperintensity with
seromas. Typical locations include the gallblad- variable, but homogeneous T1 signal.118 Con-
der fossa and hepatorenal space, and most inci- sider substituting a hepatocyte-specific gadolin-
dental perihepatic fluid collections measure a ium agent with delayed imaging if biloma is
few centimeters. These collections usually dem- suspected; continuity with the biliary system
onstrate simple fluid characteristics with T2 associated with progressive accumulation of
hyperintensity—T1 hyperintensity indicating contrast indicates biliary origin. Although bile
methemoglobin may be present, depending on incites an inflammatory reaction reflected
the timecourse. Remember that right adrenal pathologically by a pseudocapsule, no rim is
hemorrhage occasionally follows LT due to usually perceived on MRI. Identification of an
either ligation complicating caval resection or enhancing rim raises the suspicion of an abscess
coagulopathy associated with underlying liver (see Fig. 2-33). Identification of internal
disease. Small intraparenchymal collections are complexity and septation elevates the suspi-
also incidental and include contusions, hemato- cion (see the section on “Cystic Lesions,”
mas, and small, incidental bilomas. earlier).
124  •  Fundamentals of Body MRI

A B

FIGURE 2-98.  Inferior vena cava (IVC) stenosis. A large complex

posttransplant fluid collection abuts the IVC (arrow in A) on
the T2-weighted image (A) and encircles and narrows the IVC
(arrows in B) on the coronal enhanced image (B). C, The axial
C
enhanced image corroborates the IVC stenosis (arrow).

A B
FIGURE 2-99.  Hepatic infarct. The T2-weighted fat-saturated image (A) shows a round, subcapsular hyperintensity (arrow), which lacks
enhancement on the postcontrast image (arrow in B), corresponding to an infarct in a transplanted liver. The susceptibility artifact arises
from embolization coils in esophageal varices.

Biliary complications arise from technical dif- Anastomotic technique depends on the type of
ficulties or ischemia (the native biliary tree is surgery. OLT involves primary, end-to-end cho-
collateralized by the gastroduodenal artery, ledochocholedochostomy, and LDLT cases often
unlike the transplanted biliary system, which involve hepatojejunostomy. Anastomotic stric-
is solely reliant on the hepatic artery). tures are technical or ischemic in etiology.
 MRI of the Liver  •  125

Nonanastomotic strictures represent arterial involvement is the hallmark of PTLD, and the
insufficiency and most severely affect the hilum liver is the most frequent site of abdominal
and progress peripherally. MRCP images supple- involvement. Multifocal parenchymal lesions or
mented by heavily T2-weighted images provide periportal infiltration constitutes the dominant
the best overview of the biliary system to iden- forms of hepatic PTLD. PTLD is problematic
tify biliary stenoses. Waisting with relative nar- because treatment involves counterproductive
rowing often characterizes the anastomotic site; measures—reduction or cessation of immuno-
in the absence of a physiologically significant suppressive therapy instituted for the sake of
stenosis, no proximal, upstream biliary dilata- the allograft. Anti–B-cell therapy regimens
tion is present. Three-dimensional gadolinium- follow inadequate response to discontinuation
enhanced images supplement fluid-sensitive of immunosuppressive therapy.120
sequences in evaluating the biliary system with
Figures 2-100 to 2-103 are available online on
the advantage of high spatial resolution and
Expert Consult at www.expertconsult.com
negative contrast effect (the bile ducts appear
dark against enhanced parenchyma). Hepatocyte-
specific gadolinium agents provide an additional
means of evaluating the biliary tree. References
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infection predating or during transplantation tomas (Von Meyenburg complexes): Value of MR
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Polymorphic diffuse B-cell hyperplasia enhancing hepatic cavernous hemangiomas: High
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 CHAPTER THREE 

MRI of the Pancreaticobiliary

System
Sandeep Deshmukh and Christopher G. Roth

PANCREAS pancreas increases on fat-suppressed T1-

weighted images owing to the increased
Anatomy and Function
dynamic range (see Fig. 3-2B). Normal pancreas
The pancreas is a nonencapsulated organ of the is slightly hyperintense to muscle on T2-weighted
digestive system located within the retroperito- imaging (Fig. 3-3A). With the addition of fat-
neum, posterior to the stomach and anterior to suppression, there is minimal contrast between
the spine. The pancreas is approximately 2 normal pancreatic parenchyma and the sur-
inches wide and 6 to 8 inches in length. The rounding suppressed fat (see Fig. 3-3B).1,2
pancreas can be subdivided into the head, unci- Owing to the highly vascular nature of the
nate process, neck, body, and tail (Fig. 3-1). The pancreas, the normal pancreatic parenchyma
head and uncinate process are cradled by the demonstrates a homogeneous blush shortly
duodenum. The body sits posterior to the body after the arrival of gadolinium in the abdominal
of the stomach. The tail of the pancreas tickles aorta. Because the liver receives the majority of
the hilum of the spleen. its blood flow via the portal system, the pan-
The pancreas possesses exocrine and endo- creas is hyperintense to liver and fat during the
crine function. The exocrine tissues of the arterial phase (Fig. 3-4).3,4
pancreas (acinar cells) constitute approximately
95% of the pancreatic tissue and are made up of
Imaging Techniques
acinar cells. The acinar cells produce pancreatic
enzymes, which flow through the pancreatic Optimal imaging of the pancreas demands high-
duct and enter the duodenum via the ampulla field-strength systems with an adequate fat-water
of Vater (at the major papilla) to aid in digestion. frequency shift for chemically selective fat
(In a minority of patients, the minor papilla, suppression (≥1 Tesla) and high-performance
situated slightly cephalad to the major papilla, gradients that enable the use of fast magnetic
also transmits digestive fluids into the duodenal resonance (MR) sequences.1 Protocols should
lumen.) The remaining 5% of the pancreatic include axial T1-weighted imaging with and
tissue is responsible for the endocrine function without fat suppression (either breathhold gra-
of the gland and is made up of small clusters dient recalled-echo or breathing signal-averaged
of cells throughout the gland, called islets of spin-echo sequences). T1-weighted images with
Langerhans. The endocrine tissues produce hor- fat suppression are ideal for depicting the extent
mones that are released into the bloodstream. of extrapancreatic involvement of inflammatory
and neoplastic processes (i.e., vascular encase-
ment).1,5 As discussed previously, fat suppres-
Normal Appearance
sion increases the dynamic range and improves
The normal pancreas has the highest signal the detection of small pancreatic lesions by
intensity of the abdominal organs on in-phase providing the greatest contrast between normal
T1-weighted gradient recalled-echo images and abnormal pancreatic tissues. Fat-suppressed
(except in the presence of hepatic steatosis) T2-weighted imaging is useful for depicting
owing to the aqueous proteins in the glandular ductal anatomy, cystic pancreatic lesions, islet
elements, intracellular paramagnetic substances cell tumors, peripancreatic fluid collections, and
(like manganese), and abundant endoplasmic hepatic metastases.5
reticulum in the pancreatic exocrine cells Two-dimensional (2-D) or three-dimensional
(Fig. 3-2A).1,2 The relative signal intensity of the (3-D) dynamic postgadolinium fat-suppressed
129
130  •  Fundamentals of Body MRI

T1-weighted gradient recalled-echo sequences parenchymal and the peripancreatic vascular

aid in the characterization of pancreatic masses, phases. In general, this can be accomplished by
diffuse inflammatory pancreatic processes, and imaging at 15 seconds and 35 to 45 seconds
vascular involvement. Postcontrast imaging after the arrival of gadolinium in the abdominal
involves imaging of both the pancreatic aorta.6

Congenital/Developmental
Anomalies of the Pancreas
During normal development, the ventral and
dorsal pancreatic buds rotate about the duode-
num and fuse. The ventral pancreatic bud con-
stitutes the posteroinferior pancreatic head as
well as the uncinate process. The dorsal pancre-
atic bud constitutes the anterior head, body, and
tail. Following rotation and fusion of the ventral
and dorsal pancreatic buds, there is fusion of
the main pancreatic duct (Wirsung) and the
Tail accessory pancreatic duct (Santorini) (Fig. 3-5).
Neck (in splenophrenic Migrational disturbances result in a variety of
(straddles SMV/SMA) ligament congenital lesions marked by different structural
deformities in pancreatic anatomy.

Pancreatic Annular Pancreas

head Annular pancreas is a rare congenital anomaly
that results when there is abnormal migration
Body
(anterior to and rotation of the ventral bud of the pancreas
lesser sca) resulting in a ring of pancreatic tissue that com-
Uncinate process pletely or partially encircles the duodenum (Fig.
(posterior to SMV/SMA) 3-6). The majority of patients with annular pan-
FIGURE 3-1.  Anatomy of the pancreas. creas present with gastric outlet obstruction

A B
FIGURE 3-2.  Normal appearance of the pancreas on T1-weighted images. A, In-phase T1-weighted image of the pancreas demonstrates
the highest signal intensity of the abdominal organs secondary to aqueous proteins, paramagnetic substances, and endoplasmic reticulum.
B, Relative increased signal intensity of the pancreas after fat suppression due to increased dynamic range.
 MRI of the Pancreaticobiliary System  •  131

A B
FIGURE 3-3.  Normal appearance of the pancreas on T2-weighted images. Slightly increased T2-weighted signal intensity of the pancreas
when compared with muscle (A), which is brought out after the addition of fat-suppression (B).

Pancreas– Pattern of Contrast Enhancement

Precontrast Arterial Delayed

Normal

FIGURE 3-4.  Pancreatic enhancement patterns. The normal pancreas (top row) is T1 hyperintense to the liver (middle row) with greater
arterial enhancement (middle column) The bottom row represents the pancreas in the setting of (acute or chronic) pancreatitis.

PANCREAS – NORMAL DUCT EMBRYOLOGY during infancy. Infants with symptomatic

Duodenum
annular pancreas also tend to have associated
anomalies, such as trisomy 21, duodenal atresia,
Ventral and tracheoesophageal fistula. Adults with
Dorsal
pancreas pancreas annular pancreas present with peptic ulcer
disease and pancreatitis.
At imaging, annular pancreas demonstrates a
ring of normal pancreatic parenchyma (high
T1-weighted signal intensity) about the duode-
num and an aberrant pancreatic duct encircling
the duodenum and joining the main pancreatic
duct (best seen on magnetic resonance cholan-
FIGURE 3-5.  Pancreatic duct embryology. giopancreatography [MRCP]).7
132  •  Fundamentals of Body MRI

A B

C
FIGURE 3-6.  Annular pancreas. T1-weighted in-phase (A), T2-weighted (B), and fat-suppressed T1-weighted postcontrast (C) images
demonstrate pancreas and aberrant duct of Santorini (arrowhead) encircling the duodenum (arrow) in this patient with annular
pancreas.

Pancreas Divisum benefit from endoscopic or surgical drainage of

Pancreas divisum is the most common congeni- the minor papilla.7
tal variant of the pancreatic duct, representing Variation in pancreatic ductal anatomy poten-
the failure of fusion of the ducts of the ventral tially simulates pancreas divisum (Fig. 3-8).
and dorsal pancreatic buds (Fig. 3-7). The clini- Aberrations in embryologic fusion of the pancre-
cal significance of this congenital variant is atic anlage result in different pancreatic ductal
controversial because most patients are asymp- configurations and potential persistent patency
tomatic. However, in a subset of these patients of the duct of Santorini through the minor
with recurrent pancreatitis or abdominal pain, papilla.
functional stenosis of the minor papilla with
resultant obstruction of the exocrine juices
causing increased intraductal pressure, ductal Agenesis
distention, and recurrent pancreatitis is believed Complete agenesis of the pancreas is a very rare
to be the pathogenesis. These patients often condition and incompatible with life. Partial
 MRI of the Pancreaticobiliary System  •  133

A B

C D
FIGURE 3-7.  Pancreas divisum. Fat-suppressed T1-weighted gradient recalled-echo (A) and T2-weighted (B) images depict the drainage
of the accessory duct of Santorini into the second portion of the duodenum (arrows). Thick-slab three-dimensional (3-D) magnetic reso-
nance cholangiopancreatography (MRCP) and coned down views (C and D, respectively) show the classic crossed-duct appearance of
the pancreatic accessory duct of Santorini and the common bile duct (CBD).

agenesis is rare, with either the ventral or the and present with exocrine insufficiency and
dorsal segment of the pancreas failing to normal endocrine function.
develop. Partial agenesis of the pancreas is asso-
ciated with polysplenia and intrathoracic abnor-
Diffuse Pancreatic Disorders
malities. Patients with agenesis of the dorsal bud
or hypoplasia are more common, but also rare. Lipomatosis
Agenesis of the dorsal bud is related to a muta- Severe pancreatic lipomatous depositions can
tion in the gene for insulin promoter factor-1 occur in adult patients with severe obesity,
(IPF-1). Patients with pancreatic hypoplasia gen- senile atrophy, or cystic fibrosis. The pancreatic
erally have a normal development of the pan- parenchyma demonstrates some degree of
creas, but later in life, they have replacement of atrophy with preservation of the pancreatic
the normal glandular elements with fatty tissue margins and normal lobulations.
134  •  Fundamentals of Body MRI

As such, the imaging appearance is varied

ranging from normal homogeneous T1 hyper­
intensity to heterogeneous T1 hypointensity
with glandular enlargement, heterogeneous
enhancement, and loss of the normal pancreatic
Standard pancreatic contours with thickening of the left anterior
ductal anatomy pararenal fascia (see Fig. 3-10).9–11
With pancreatic inflammation, the gland
focally or diffusely enlarges. Associated peripan-
creatic fluid is best detected on fat-suppressed
T2-weighted images with even trace T2-
Patent
hyperintense peripancreatic fluid standing out
accessory from the intermediate to low T2-weighted signal
duct intensity of the pancreatic parenchyma and the
signal suppressed peripancreatic fat. As the
severity of pancreatitis increases, there is
decreased T1-weighted parenchymal signal
intensity with blunted heterogeneous early
phase contrast enhancement (Fig. 3-11).9–11
In the majority of severe cases of pancreatitis,
there is a reaction to the pancreatic inflamma-
Patent tory process resulting in the development of
accessory
duct fluid collections within the pancreatic paren-
chyma, peripancreatic tissues, lesser sac, and
paracolic gutters. The majority of these fluid
Pancreas divisum
collections are resorbed in 4 to 6 weeks;
however, approximately 10% of these collec-
tions develop a capsule and eventually become
FIGURE 3-8.  Variations in pancreatic ductal anatomy. pseudocysts (Fig. 3-12).12
Pancreatic necrosis is a complication of severe
pancreatitis in which there is either focal or
Pancreatitis diffuse nonviable pancreatic parenchyma (Fig.
Pancreatitis is the most common benign disease 3-13). Absent enhancement, superimposed on
of the pancreas. The majority of cases are caused findings of acute pancreatitis, indicates necrosis.
by cholelithiasis or alcohol abuse (~80% of Pancreatic necrosis tends to involve the body
cases), but a wide variety of uncommon etio- and tail of the pancreas and spare the head
logic factors have been identified (Fig. 3-9).8 The owing to its abundant vascular supply.13 The
diagnosis of pancreatitis is clinical, based on potential for abscess development and the high
laboratory abnormalities and clinical presenta- morbidity of pancreatic necrosis usually neces-
tion. The role of magnetic resonance imaging sitate percutaneous drainage or surgical débride-
(MRI) is to identify possible etiologies (e.g., ment.10,13 When 75% or more of the gland is
choledocholithiasis) or complications (necro­­ necrotic or there is progression of pancreatic
sis, peripancreatic inflammation and fluid col- necrosis on serial examinations, necrosectomy
lections, pseudocysts, hemorrhage, abscess, is generally performed owing to the high
pseudoaneurysm, and/or venous thrombosis). morbidity.13
However, when the cause of abdominal pain is Leakage of pancreatic enzymes from the
unclear, imaging findings help establish the diag- inflamed pancreas can result in autodigestion of
nosis of pancreatitis. the arterial wall with subsequent pseudoaneu-
rysm formation (Fig. 3-14). The most commonly
Acute Pancreatitis.  Acute pancreatitis involved artery is the splenic artery followed by
encompasses a wide spectrum from mild inflam- the pancreaticoduodenal and gastroduodenal
mation of the pancreatic parenchyma to severe arteries.14
disease possibly including hemorrhage, necro- The most common vascular complication of
sis, and/or superimposed infection (Fig. 3-10). pancreatitis is venous thrombosis. The close
 MRI of the Pancreaticobiliary System  •  135

Drugs Infectious Inherited Mechanical Metabolic Toxins Other

Furosemide Coxsackie B Autosomal Gallstones Hypertrigliceridemia Alcohol Pregnancy

dominant
PRSS1
mutation
Azathioprine CMV Cystic ERCP Hypercalcemia Methanol Post renal
fibrosis transplant

Asparaginase Mumps Pancreatic or Tropical

ampullary pancreatitis
carcinoma

Pentamidine Salmonella Pancreas Ischemia (i.e.,

divisum hypotension)

Valproate Sphincter of Groove

Oddi stenosis pancreatitis

Sulfa drugs Choledochal Pancreatic

cyst cancer

ACE
inhibitors

FIGURE 3-9.  Etiologies of pancreatitis. ACE = angiotensin-converting enzyme; CMV = cytomegalovirus; ERCP = endoscopic retrograde
cholangiopancreatography.

proximity of the splenic vein to the body and feature of chronic pancreatitis is parenchymal
tail of the pancreas renders it the most suscep- calcification; however, this occurs late in the
tible to thrombosis. However, the superior mes- disease process and is best seen on computed
enteric vein and portal confluence can also be tomography (CT) (Fig. 3-16).
involved.15
Autoimmune Pancreatitis.  Autoimmune
Chronic Pancreatitis.  Chronic pancreatitis pancreatitis (AIP, also known as lymphoplasma-
is a progressive inflammatory disease of the pan- cytic sclerosing pancreatitis) is a rare form of
creas with irreversible morphologic changes of chronic pancreatitis. The autoimmune inflamma-
the pancreatic parenchyma eventually resulting tory process is marked by a lack of classic acute
in loss of endocrine and exocrine function of attacks of pancreatitis with a predilection for
the gland.16 older males (over 50 years of age). Because of the
Imaging stigmata of this disease process uniquely dramatic response to steroids, consider
include decreased T1-weighted signal intensity AIP in the appropriate clinical setting.
of the gland owing to decreased protein content Imaging findings also differ from other forms
due to glandular atrophy and fibrosis (also con- of pancreatitis. AIP tends to be mass-forming
tributing to T1 hypointensity). Furthermore, the with either focal or diffuse pancreatic enlarge-
fibrotic changes of the parenchyma result in ment with minimal peripancreatic inflammation
attenuation of the vascular supply reflected by and an absence of vascular encasement or calci-
decreased enhancement on immediate postg- fication. Diffuse irregular narrowing of the main
adolinium images.17 The spectrum of changes in pancreatic duct and a peripancreatic hypoin-
the pancreatic duct are broad including dilata- tense hypovascular rind are characteristic fea-
tion, stricture, stenosis, intraductal calculi, occa- tures. These imaging features occasionally
sionally side branch duct dilatation (“chain of simulate the appearance of pancreatic carci-
lakes” or “string of pearls” appearance) (Fig. noma (Fig. 3-17).19,20 An abrupt ductal caliber
3-15).18 The most pathognomonic imaging Text continued p. 144
136  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 3-10.  Acute hemorrhagic pancreatitis. Out-of-phase T1-weighted gradient recalled-echo (A and B), fat-suppressed T2-weighted
(C and D), and fat-suppressed T1-weighted gradient recalled-echo (E and F) images demonstrate marked acute pancreatitis with increased
T1-weighted signal intensity and corresponding decreased T2-weighted signal intensity related to hemorrhage, as well as marked peri-
pancreatic inflammation.
 MRI of the Pancreaticobiliary System  •  137

A B

C D

E F

FIGURE 3-11.  Magnetic resonance imaging (MRI) appearance

of acute pancreatitis on different pulse sequences. Patient
with acute pancreatitis, heterogeneity of the pancreas related
to parenchymal edema and hemorrhage, is best seen on the
in- and out-of-phase T1-weighted (A and B, respectively) and
fat-suppressed T1-weighted precontrast images (D). Minimal
peripancreatic edema is seen on the T2-weighted image (C),
but more pronounced with fat-suppression (G). Furthermore,
delayed parenchymal enhancement is demonstrated on the
early and late arterial phase postcontrast fat-suppressed
T1-weighted gradient recalled echo images (E and F,
G
respectively).
138  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-12.  Pancreatic pseudocysts. A, Heavily T2-weighted image shows an irregularly shaped, septated pseudocyst in the pancreatic
tail (arrow), which is surrounded by edema (arrowheads). B, The postcontrast image demonstrates absent enhancement in the locules
(arrows). In a different patient with pancreatitis, the heavily T2-weighted (C) and postcontrast (D) images reveal a large, complex,
multiloculated pseudocyst (arrow) abutting the lesser curvature of the stomach. Mild surrounding edema and inflammation (arrowheads)
and a history of pancreatitis help confirm the etiology and exclude neoplastic lesions.
 MRI of the Pancreaticobiliary System  •  139

A B

C D
FIGURE 3-13.  Pancreatic necrosis. A, The heavily T2-weighted image shows extensive peripancreatic inflammation (arrows) surrounding
an ill-defined pancreatic body and neck with relative hypointensity in the setting of acute inflammation. B, Marked parenchymal hyper-
intensity on the fat-suppressed T1-weighted image signifies hemorrhage. The relative hypointensity on the postcontrast image (C) reflects
the preferential enhancement of surrounding structures, and the pancreatic signal void (arrows) on the subtracted image (D) confirms
necrosis.
140  •  Fundamentals of Body MRI

A B

C
FIGURE 3-14.  Arterial pseudoaneurysm complicating pancreatitis. A, Heavily T2-weighted image in a patient with acute or chronic
pancreatitis reflected by peripancreatic inflammation and irregular ductal dilatation, respectively, shows a near–fluid-intensity lesion in
the pancreatic head (arrow). B, Following intravenous contrast, the lesional enhancement (arrow) is equivalent to arterial enhancement,
indicating arterial etiology and, specifically, a pseudoaneurysm arising from the gastroduodenal artery. C, The image from the celiac axis
injection showed prompt enhancement (arrow) and confirmed direct continuity with the gastroduodenal artery.
 MRI of the Pancreaticobiliary System  •  141

A B

C D

E F
FIGURE 3-15.  Chronic pancreatitis. A, The in-phase (T1-weighted) image through a chronically inflamed pancreas (arrows) reveals relative
parenchymal hypointensity and irregular beaded ductal dilatation. B, The early phase postcontrast image shows the extent of ductal dila-
tation (arrows) in the pancreatic body and heterogeneously decreased enhancement. C, The MRCP image isolates the pancreatic duct
(arrows) from the parenchyma and surrounding tissues, depicting the irregular pancreatic ductal and side branch dilatation (arrowheads).
D, The T1-weighted fat-suppressed image in a different patient with chronic pancreatitis exemplifies the typical heterogeneous decrease
in parenchymal signal intensity (arrows). The heavily T2-weighted (E) and MRCP (F) images show the associated ductal changes, typify-
ing the “chain of lakes” or “string of pearls” appearance.
142  •  Fundamentals of Body MRI

A B

C D

E F

G H
FIGURE 3-16.  Chronic calcific pancreatitis. Out-of-phase (A) and in-phase (B) T1-weighted gradient recalled-echo images demonstrate
atrophy of the glandular pancreatic parenchyma with blooming on the in-phase (B) image related to pancreatic calcifications. T2-weighted
(C) and fat-suppressed T2-weighted (D) images of the pancreas reveal multiple areas of pancreatic duct stricturing and dilatation. Pre-
contrast (E), arterial (F), and delayed (G) fat-suppressed T1-weighted gradient recalled-echo images depict the decreased T1-weighted
pancreatic signal intensity with mottled early enhancement and homogeneous delayed enhancement. Enhanced computed tomography
(CT; H) image better depicts the extent of pancreatic parenchymal calcification.
 A B

C D

E F
FIGURE 3-17.  Autoimmune pancreatitis. In-phase (A) and out-of-phase (B) T1-weighted and T2-weighted (C) images of the pancreas
demonstrate decreased T1-weighted signal intensity, a smooth contour, and focal duct dilatation in a patient with autoimmune pancre-
atitis. Precontrast (D), arterial (E), and delayed (F) fat-suppressed T1-weighted gradient recalled-echo images of the same patient
demonstrate delayed pancreatic parenchymal enhancement.
144  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-18.  Groove pancreatitis. Out-of-phase (A) and in-phase (B) T1-weighted gradient recalled-echo images demonstrate decreased
T1-weighted signal intensity in the pancreaticoduodenal groove with corresponding increased signal intensity on T2-weighted (C) and
fat-suppressed T2-weighted (D) images (arrows) as well as retroperitoneal edema in a patient with groove pancreatitis.

change with upstream dilatation and glandular and widening of the space between the distal
atrophy and vascular encasement favor pancre- common bile/pancreatic ducts and the duode-
atic carcinoma. Elevated IgG and autoantibody nal lumen (best seen on MRCP) (Fig. 3-19).21
levels and clinical response to corticosteroids
favor AIP. Hereditary Pancreatitis.  Hereditary pan-
creatitis is a rare autosomal dominant disease
Groove Pancreatitis.  Groove pancreatitis with variable penetrance leading to exocrine
is a form of segmental pancreatitis occurring dysfunction. This disease arises from mutations
between the pancreatic head, the common bile in the trypsinogen gene. The natural history is
duct, and the duodenum. Although usually very similar to that of chronic alcoholic pancre-
occurring in young men with a history of alcohol atitis; however, symptom onset occurs at an
abuse, the etiology and pathogenesis of groove earlier age and there is a higher prevalence of
pancreatitis remain unknown. The imaging is pseudocyst formation. There is an elevated risk
similar to that of acute pancreatitis; however, for the development of pancreatic adenocarci-
the focal nature of this process makes differen- noma (~50–60 times) with smoking increasing
tiation from a periampullary tumor difficult the risk and lowering the age of onset. Promi-
(Figs. 3-18 and 3-19).21 The characteristic MRI nent pancreatic duct calcifications are a hall-
findings include a sheetlike mass between the mark of this disease and are similar to those seen
second segment of the duodenum and the pan- in chronic alcoholic pancreatitis; however,
creatic head often with superimposed cysts (fre- affliction of a much younger age group distin-
quently in the duodenal wall), duodenal stenosis, guishes hereditary pancreatitis (Fig. 3-20).22
 MRI of the Pancreaticobiliary System  •  145

A B
FIGURE 3-19.  Cystic groove pancreatitis. A, The heavily T2-weighted image portrays a large, complex cystic lesion (closed arrow) in the
pancreaticoduodenal groove between the duodenum (arrowhead) and the pancreatic head, displacing the main pancreatic duct (open
arrow). B, The maximal intensity projection reconstructed from a 3-D MRCP shows the cystic lesion (arrows) between the distal CBD
and the pancreatic duct and duodenum.

parenchymal signal intensity (lower than skeletal

Genetic Disorders
muscle) due to the paramagnetic effects of iron.
Cystic Fibrosis These paramagnetic effects are exaggerated on
Cystic fibrosis is an autosomal recessive disease gradient recalled-echo images with increasing
characterized by secretory dysfunction of the echo times; therefore, on the in-phase
exocrine pancreas. Impaired mucociliary trans- T1-weighted images, the pancreas will lose signal
port results in mucous plugging of the exocrine when compared with the out-of-phase images
glands. MRI findings encompass a spectrum of (Fig. 3-22).25,26
imaging appearances including pancreatic
enlargement with complete fatty replacement Von Hippel–Lindau Disease
with or without loss of the normal lobulated Von Hippel–Lindau disease is an autosomal
contour, pancreatic atrophy with partial fatty dominant condition with variable penetration
replacement, and diffuse atrophy of the pan- (see Chapter 4). This condition is character-
creas without fatty replacement.23,24 Superim- ized by cerebellar, spinal cord, renal, and
posed pancreatic cysts secondary to duct retinal hemangioblastomas and is associated
obstruction are another manifestation of cystic with renal angioma, renal cell carcinoma, and
fibrosis.24 Enlargement of the pancreas with pheochromocytoma.
complete fatty replacement is the most common Pancreatic lesions include single or multiple
imaging appearance (Fig. 3-21).23 Fatty replace- cysts, cystic replacement of the pancreas, micro-
ment imitates the appearance of retroperitoneal cystic adenomas, and islet cell tumors. Cysts are
(macroscopic) fat with uniform T1 hyperinten- the most common pancreatic manifestation
sity and signal loss on fat-suppressed images. (Fig. 3-23).27

Primary (Idiopathic) Hemochromatosis Schwachman-Diamond Syndrome

Primary (idiopathic or genetic) hemochromato- Schwachman-Diamond syndrome is a rare con-
sis is an autosomal recessive disease caused by genital disorder of pancreatic insufficiency,
a mutation that results in excessive iron absorp- growth retardation, and other congenital abnor-
tion from the gastrointestinal tract with deposi- malities. Imaging demonstrates exten­­sive
tion of iron in the liver, heart, anterior pituitary, replacement of the pancreatic tissue with fat.
pancreas, joints, and skin (see Chapter 2).
Cardiac and pan­creatic deposition progresses Johanson-Blizzard Syndrome
over time. The presence of iron deposition in Johanson-Blizzard syndrome is an autosomal
the pancreas correlates with irreversible changes recessive disorder of ectodermal dysplasia with
of cirrhosis in the liver. both endocrine and exocrine insufficiency. The
MR images demonstrate decreased T1- primary defect is in the acinar cells with fatty
weighted and T2-weighted pancreatic replacement occurring over time.
146  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 3-20.  Hereditary pancreatitis. Four in-phase T1-weighted gradient recalled echo (A–D) and coronal thick-slab maximal intensity
projectional MRCP (E) images through the pancreas demonstrate blooming within the head and proximal body of an atrophic pancreas
with decreased T1-weighted signal intensity related to ductal calcification (arrows), better seen on the fluoroscopic spot radiograph (F),
in a patient with hereditary pancreatitis.
 MRI of the Pancreaticobiliary System  •  147

A B

C D

E
FIGURE 3-21.  Cystic fibrosis. T2-weighted (A), fat-suppressed T2-weighted (B), venous phase (C), and delayed phase (D) postcontrast
fat-suppressed T1-weighted gradient recalled-echo images and unenhanced CT image (E) demonstrate complete fatty replacement of
the pancreas in a patient with cystic fibrosis.
148  •  Fundamentals of Body MRI

A B

FIGURE 3-22.  Hemochromatosis. Out-of-phase (A, time to

excitation [TE] = 2.3 msec), in-phase (B, TE = 4.6 msec), and
long echo (C, TE = 9.4 msec) T1-weighted gradient recalled-
echo images demonstrate decreased signal intensity of the
C
liver, spleen, and pancreas with increasing echo times.

Both Schwachman-Diamond and Johanson- tissue. Marked hyperintensity on T2-weighted

Blizzard syndromes have preserved ductal sequences, indicating free water protons, char-
output of fluid and electrolyes. acterizes cystic lesions. Postcontrast images
bear binary information: enhancement = solid
(enhancement) versus cystic (absent enhance-
Focal Pancreatic Lesions
ment). The discrimination between lesions
Focal pancreatic lesions stratify into two basic within cystic and solid categories becomes
categories: cystic and solid (Fig. 3-24). The more difficult. Specific features within each
distinction helps lower the suspicion of category (discussed later) narrow the differen-
malignancy—solidity usually implies malig- tial diagnosis.
nancy. Solid tissue raises the specter of pan-
creatic adenocarcinoma—the diagnosis of Solid Pancreatic Lesions
exclusion. Cystic etiology incurs a better prog- The two most common solid pancreatic neo-
nosis but still threatens malignancy in the form plasms are adenocarcinoma and neuroendo-
of intraductal papillary mucinous neoplasm crine tumors. These lesions have drastically
(IPMN), cystic metastases, and other condi- different enhancement patterns and establish
tions. T2-weighted sequences and postcontrast the archetypal enhancement categories—
imaging collude to establish cystic versus solid hypovascular and hypervascular, respectively.
 MRI of the Pancreaticobiliary System  •  149

A B

C D
FIGURE 3-23.  von Hippel–Lindau disease. T2-weighted (A), fat-suppressed T2-weighted (B), in-phase T1-weighted (C), and out-of-phase
T1-weighted (D) images of cystic pancreatic replacement in a patient with von Hippel–Lindau disease.

Pancreatic lesion

Solid Cystic

Intrapancreatic Retroperitoneal Neoplastic Non-

neoplastic

Primary Metastases Lymphoma (Pre) Benign Simple cyst

Mesenchymal tumors malignant Inherited
Nerve sheath tumor syndromes

Adenocarcinoma Macrocystic Microcystic

Other epithelial tumors tumor tumor
Islet cell tumors IMPN SPEN
Others
FIGURE 3-24.  Focal pancreatic lesion scheme. IMPN = intraductal mucinous papillary neoplasm; SPEN = solid-cystic papillary epithelial
neoplasm.
150  •  Fundamentals of Body MRI

Pancreas – T1 Appearance of Solid Lesions

Precontrast Arterial Delayed

Normal
FIGURE 3-25.  Pancreatic lesion enhance-
ment patterns. Top, In the normal pan-
Islet cell
creas, most solid lesions appear relatively tumor(s)
hypointense on T1-weighted images.
Pancreatic
Middle, Because of the normal avid pan-
adenocarcinoma
creatic arterial enhancement, most solid
lesions are relatively hypovascular, with
the notable exception of islet cell tumors.
Bottom, The T1 hypointensity associated
with pancreatitis often renders lesions less
conspicuous. Pancreatitis

These designations depend on comparison with the head of the pancreas and presents with
the background pancreatic parenchyma (Fig. either jaundice, weight loss, pain, or nausea.
3-25). Under normal circumstances, the pancre- Carbohydrate antigen 19-9 (CA 19-9) has been
atic parenchyma avidly enhances, approximat- shown to be an effective diagnostic serum
ing the hypervascularity of islet cell tumors tumor marker with good sensitivity and
and significantly out-enhancing hypovascular specificity.28,29
pancreatic adenocarcinoma. However, with Pancreatic adenocarcinoma is typically
coexistent pancreatitis, pancreatic parenchymal hypointense compared with the normal pancre-
enhancement (and precontrast signal intensity) atic parenchyma on T1-weighted imaging (Fig.
drops, closely simulating adenocarcinoma. For 3-26; see also Fig. 3-25). Fat suppression
this reason, the pancreatic lesion assessment increases lesion conspicuity by increasing the
depends on the status of the background pan- dynamic range between the low signal intensity
creatic parenchyma. tumor and the higher signal intensity of the
normal parenchyma. Tumors have variable
Pancreatic Adenocarcinoma.  Pancreatic signal intensity on T2-weighted imaging depend-
adenocarcinoma is the most common pancre- ing on the degree of hemorrhage, necrosis, and
atic malignancy, accounting for approximately inflammatory changes. In general, T2-weighted
95% of all pancreatic malignant tumors. Based imaging is less helpful than T1-weighted imaging
on incidence rates from 2004 to 2006, approxi- because of the poor contrast between the mass
mately 1.4% of all men and women born today and the normal pancreas. Pancreatic adenocar-
will be diagnosed with pancreatic adenocarci- cinoma is usually hypovascular to the normal
noma at some time during their lifetime. Pancre- glandular tissue on arterial phase imaging fol-
atic adenocarcinoma is the fifth leading cause of lowed by gradual enhancement on delayed
cancer death in the United States, mainly attrib- imaging, related to its desmoplastic content
utable to the extremely poor survival: less than (see Fig. 3-25). Immediate contrast-enhanced
20% of newly diagnosed patients survive the imaging is the most sensitive for detecting pan-
first year. There is an overall dismal prognosis creatic adenocarcinoma, especially in lesions
with 5-year survival rates between 4.5% and 6%. that are small or do not deform the contour of
Patients with localized disease at diagnosis have the normal pancreas (Fig. 3-27). Obstruction of
improved survival rates relative to those with the main pancreatic duct is one of the most
advanced disease at diagnosis (22% 5-year sur- common findings in pancreatic adenocarcinoma
vival for those with localized disease vs. 2% for (Fig. 3-28). Contiguous obstruction of the pan-
those with distant metastases). Pancreatic ade- creatic and common bile ducts due to the pres-
nocarcinoma predominantly affects the elderly ence of a pancreatic head mass is known as the
population, with 80% of patients diagnosed “double duct” sign and is highly suggestive of
older than 60 years, with the median age at malignancy (Fig. 3-29).30–32 Because pancreatic
diagnosis being 72 years. The majority of cases adenocarcinomas frequently progress unde-
of pancreatic adenocarcinoma occurs within tected until inciting symptoms, distal gland
 MRI of the Pancreaticobiliary System  •  151

A B

C
FIGURE 3-26.  Pancreatic adenocarcinoma. A, The in-phase (T1-weighted) image in a patient with pancreatic adenocarcinoma in the
pancreatic head (arrow) shows relative hypointensity compared with normal parenchyma (arrowhead). B, The T2-weighted image
exemplifies the usual hypointensity (arrow) with little contrast between normal tissue and neoplasm. C, The enhanced image bears the
highest tissue contrast between the lesion (arrow) and normal pancreatic tissue (arrowhead).

atrophy is often associated with the aforemen- metastases and local spread account for most
tioned duct dilatation.33 cases (40% each). Because the pancreas lacks a
In the setting of underlying pancreatitis, capsule to obstruct neoplastic spread and
detecting underlying adenocarcinoma is prob- because most lesions arise in the pancreatic
lematic because both the tumor and the sur- head densely surrounded by adjacent structures,
rounding pancreas demonstrate similar T1 regional spread proceeds rapidly (Fig. 3-31).
hypointensity. However, immediate contrast- Pancreatic continuity with the superior mesen-
enhanced images better delineate the size and teric vessels promotes vascular encasement of
extent of pancreatic adenocarcinomas, which these vessels, which also precludes curative sur-
tend to enhance less than adjacent inflamed pan- gical resection. Vessel enhancement of 180°
creatic parenchyma (see Fig. 3-25).33 However, constitutes vascular encasement (see Fig. 3-31).
focal pancreatitis presents diagnostic difficulty Metastatic spread progresses from regional
because focal pancreatic enlargement, distor- lymph nodes to the liver and, uncommonly, to
tion of the normal glandular contour, ductal dila- the lungs. In addition to direct invasion of adja-
tation, and abnormal enhancement simulate cent structures, such as the duodenum and
pancreatic adenocarcinoma. Short-term follow- stomach, spread to any peritoneal surface is at
up imaging after resolution of the acute illness risk from peritoneal dissemination.
hopefully eliminates equivocation.
For the majority of cases, the diagnosis of pan- Pancreatic Neuroendocrine (Islet Cell)
creatic adenocarcinoma is straightforward and Tumors.  Neuroendocrine (islet cell) tumors
the role of imaging is to determine resectability are uncommon, slow-growing pancreatic or
(Fig. 3-30).34 Among the factors preempting peripancreatic masses that may result in
respectability and surgical cure, distant symptomatic hormonal overproduction (and,
Text continued p. 156
152  •  Fundamentals of Body MRI

A B

C D

E F
 MRI of the Pancreaticobiliary System  •  153

FIGURE 3-27.  Pancreatic adenocarcinoma—arterial phase imaging. Infiltrative mass enlarges the body of the pancreas (arrows), which can
be seen on the in-phase T1-weighted (A) and the precontrast fat-suppressed T1-weighted gradient recalled-echo (D) images in contrast
to the normal pancreatic parenchyma in the head of the pancreas. This mass demonstrates mildly increased signal intensity on
T2-weighted imaging (B), which is pronounced on fat-suppressed T2-weighted imaging (C). In addition, distal gland atrophy and duct
dilatation (arrowheads) can be seen on the T2-weighted (B) and fat-suppressed T2-weighted (C) images. Furthermore, this mass dem-
onstrates decreased enhancement when compared with the normal pancreas, most pronounced on early arterial phase fat-suppressed
T1-weighted gradient recalled-echo imaging (E), with gradual enhancement on delayed phase fat-suppressed T1-weighted gradient
recalled-echo imaging (F) related to desmoplastic content.

Pancreas – Using the Pancreatic Duct

Normal

“3, 2, 1 Rule” IPMN

Main duct

Pancreatic IPMN
adenocarcinoma Branch duct

“Double duct” Pancreatic

ductal dilatation

CBD dilatation

FIGURE 3-28.  The pancreatic duct differential. The normal pancreatic duct measures 3 mm in the head of the pancreas, tapering to 2 mm
in the body. The normal accessory duct of Santorini measures 1 mm. In the setting of pancreatic adenocarcinoma, there is dilatation of
the duct and possibly its side branches, upstream from the lesion. Intraductal papillary mucinous neoplasms (IPMNs) secrete mucin
and, therefore, have downstream duct dilatation. Main duct IPMN harbors a higher malignant potential; concern for development of
adenocarcinoma within these lesions should increase when there are papillary projections/internal architecture and/or enhancement. In
contradistinction to IPMN, dilatation occurs proximal to the lesion in pancreatic adenocarcinoma. The pattern of pancreatic and/or
common bile duct (CBD) dilatation in pancreatic adenocarcinoma depends on the location of the lesion. Three basic patterns include
(1) the “double duct sign,” referring to dilatation of both the CBD and the pancreatic duct, (2) pancreatic ductal dilatation, and (3)
isolated CBD dilatation.
154  •  Fundamentals of Body MRI

A B

C
FIGURE 3-29.  Pancreatic adenocarcinoma—the double duct sign. A, The MRCP image shows marked biliary (closed arrows) and pancreatic
(arrowheads) dilatation, abruptly terminating at the level of the pancreatic head, where there is a cystic lesion (open arrow). The fat-
suppressed T2-weighted (B) and postcontrast (C) images reveal the obstructing pancreatic head mass (arrow) with central necrosis,
accounting for the cystic lesion on the MRCP image.

Liver metastases
Vascular encasement (180°)
Peritoneal implants
Peripancreatic spread
Size >3 cm
Adenopathy
• Retroperitoneal
• Mesenteric

FIGURE 3-30.  Factors predisposing to unresectability in pancreatic cancer.

FIGURE 3-31.  Pancreatic adenocarcinoma—regional and metastatic spread. A, The T2-weighted image shows an ill-defined hypointense
lesion (closed arrow) inducing upstream pancreatic ductal dilatation (arrowhead) and confluent peripancreatic tissue indicating local
spread (open arrow). B, The early phase postcontrast image depicts the hypovascularity of the pancreatic mass (arrow) with encasement
of the superior mesenteric artery (arrowheads). T2-weighted (C), in-phase T1-weighted (D), and arterial phase postcontrast (E) images
show a large, mildly hyperintense mass (arrow) in a different patient with pancreatic adenocarcinoma, which causes upstream pancreatic
ductal dilatation (arrow), demonstrated on the MIP image (F) from a 3-D MRCP. Multiple T2-hyperintense, hypovascular metastases
are visible on the T2-weighted (G) and postcontrast (H) images.
 MRI of the Pancreaticobiliary System  •  155

A B

C D

E F

G H
156  •  Fundamentals of Body MRI

ISLET CELL TUMORS

Tumor Cell Malignancy Clinical Imaging

rate
Insulinoma Beta 10% Hypoglycemia Small, solitary

Gastrinoma Alpha-1 60% Zollinger-Ellison Small, may be

syndrome multiple, ectopic
Glucagonoma Alpha-2 80% Diabetes mellitus Larger, usually body
and tail
VIPoma Delta-1 50% Watery diarrhea, Large, usually body
hypokalemia, and tail
achlorhydria (WDHA)
syndrome
Somatostatinoma Delta 67% Diarrhea, weight loss Large, usually head

Non-functioning Usually Abdominal pain, Very large

jaundice

FIGURE 3-32.  Islet cell tumor types.

therefore, are called functional) or elicit no enhancement with dynamic imaging (Fig.
clinical findings of hormone production (and, 3-34).36
therefore, called nonfunctional). Incidence of
pancreatic neuroendocrine tumors is 1 to 1.5 Gastrinomas.  Gastrinomas are the second
per 100,000 in the general population. Func- most common functional neuroendocrine
tioning neuroendocrine tumors manifest earlier tumor. Increased gastrin secretion results in a
owing to symptoms of hormone overproduction fulminant peptic ulcer disease known as
and are named according to the hormone they Zollinger-Ellison syndrome. Approximately
produce (Fig. 3-32). 75% of gastrinomas are sporadic, with the
Neuroendocrine tumors are well depicted on remaining 25% occurring as part of the multiple
MRI because of the high contrast between the endocrine neoplasia (MEN)-I syndrome. Tumors
high T1-weighted signal intensity of the normal are generally less than 4 cm in size. Most gastri-
pancreatic parenchyma and the low T1-weighted nomas are located within the “gastrinoma tri-
signal intensity of the tumor, and potentially angle,” which is bounded by the cystic duct,
because of their typical hypervascular enhance- second and third portion of the duodenum, and
ment.35 Fat-suppressed T2-weighted images the pancreatic neck. Approximately 60% to 80%
often demonstrate high signal intensity compo- of gastrinomas are malignant but follow a pro-
nents within the tumor compared with the adja- tracted or indolent course.
cent pan­creatic parenchyma.36 Less frequently, Gastrinomas typically demonstrate decreased
tumors may demonstrate hypointense or isoin- T1-weighted signal intensity on T1-weighted
tense T2-weighted signal intensity to the adja- images, increased signal intensity on T2-weighted
cent pancreas secondary to increased fibrous images, and smooth rim enhancement after con-
tissue content (Fig. 3-33).35 trast administration.36

Insulinomas.  Insulinomas are the most Glucagonomas, VIPomas, and Somato­

common functional neuroendocrine tumors and statinomas.  Glucagonomas, VIPomas, and
often present with symptomatic hypoglycemia somatostatinomas are functional neuroendo-
secondary to insulin oversecretion. These crine tumors that are not frequently detected
tumors are frequently benign, are usually soli- until later in the disease course because
tary, are less than 2 cm in size, and occur equally the clinical findings related to hormonal over-
throughout all parts of the pancreas. production are nonspecific. As such, they are
At imaging, insulinomas demonstrate decreased frequently larger (3–5 cm) at the time of
T1-weighted signal intensity on T1-weighted diagnosis. The majority of these less
images with homogeneously increased T2- com­­mon functional neuroendocrine tumors
weighted signal intensity and marked contrast are malignant.
 MRI of the Pancreaticobiliary System  •  157

A B

C D

E F
FIGURE 3-33.  Islet cell tumor. T2-weighted (A), fat-suppressed T2-weighted (B), and dynamic precontrast (D), early arterial phase (E),
and late arterial phase (F) 3-D fat-suppressed T1-weighted gradient recalled-echo images demonstrate two arterial enhancing lesions in
the pancreas. The solid lesion (arrow) is best appreciated on the early arterial phase image (E), and the cystic lesion (arrowhead) is best
identified on the fat-suppressed T2-weighted image (B). These lesions in a patient with a pituitary adenoma (identified on the sagittal
T1-weighted image [C] of the brain [arrow]) and a known parathyroid adenoma are solid and cystic islet cell tumors in the setting of
multiple endocrine neoplasia (MEN)-I or Wermer’s syndrome.
158  •  Fundamentals of Body MRI

A B

C
FIGURE 3-34.  Insulinoma. A, The precontrast T1-weighted fat-suppressed image in a patient with hyperinsulinemia reveals a small
hypointense lesion (arrow) in the uncinate process behind the superior mesenteric vessels (arrowhead). The T2-weighted image
(B) shows mild lesional hyperintensity (arrow) and the postcontrast image (C) demonstrates the hypervascularity typical of an insulinoma
(arrow).

At imaging, all three of these less common Pancreatic Metastases.  Metastatic disease
functional neuroendocrine tumors demonstrate to the pancreas is uncommon, occasionally
decreased T1-weighted signal intensity, in­­ arising from tumors with hematogenous spread,
creased T2-weighted signal intensity, and het- such as renal cell carcinoma, lung carcinoma,
erogeneous solid enhancement after contrast breast carcinoma, colon carcinoma, and
administration.36 melanoma.
Differentiation of metastatic disease to the
Nonfunctioning Islet Cell Tumors.  Non- pancreas from pancreatic adenocarcinoma is
functioning islet cell tumors may be discovered important because metastases portend a better
incidentally or when abdominal pain is induced prognosis. Metastases in general are hypoin-
by mass effect or metastatic disease (Fig. 3-35). tense in signal intensity on T1-weighted images
Nonfunctioning tumors are typically large and relative to the normal pancreatic parenchyma;
have foci of cystic degeneration and necrosis however, unlike pancreatic adenocarcinoma,
on T2-weighted imaging with associated het- metastases tend to demonstrate homogeneous
erogeneous enhancement (see Fig. 3-35).37 or heterogeneous enhancement compared with
More than 50% of nonfunctioning tumors are the hypovascularity of pancreatic adenocarci-
malignant, demonstrating local invasion and noma.38 Furthermore, certain metastases may be
distant metastatic disease; therefore, they have diagnosed based on their imaging characteris-
poor prognosis compared with functioning tics, which are similar to the primary tumor.
tumors. For example, melanomas metastases may
 MRI of the Pancreaticobiliary System  •  159

A B

C D

E
FIGURE 3-35.  Nonfunctioning islet cell tumors. A, The T2-weighted image shows a small polypoid lesion in the ampullary region (arrow)
obstructing the CBD and pancreatic duct (arrowheads). Precontrast (B) and postcontrast (C) images demonstrate corresponding lesional
T1 hypointensity and hypovascularity (arrow) in this small nonfunctional islet cell tumor presenting with biliary obstruction. A large
nonfunctional islet cell tumor in the pancreatic head (arrow) in a different patient demonstrates marked hyperintensity on the
T2-weighted image (D) and absent enhancement on the postcontrast image (E).
160  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-36.  Pancreatic melanotic melanoma metastases. In-phase (A) and out-of-phase (B) T1-weighted gradient recalled-echo,
T2-weighted (C) and fat-suppressed T2-weighted (D), and precontrast (E), arterial (F), and delayed (G) fat-suppressed T1-weighted
gradient recalled-echo images of two pancreatic melanoma metastases. One of these metastases contains more melanin (straight arrow),
increasing its T1-weighted signal intensity compared with the other lesion (curved arrow). Both metastases are slightly hyperintense to
the pancreas on the T2-weighted images (more pronounced with fat suppression owing to increased dynamic range). The metastases
demonstrate varied enhancement on postcontrast imaging.

demonstrate elevated T1-weighted signal inten- Imaging findings are nonspecific and vary
sity secondary to intratumoral hemorrhage or from a large mass with an enhancing capsule
the paramagnetic properties of melanin (Fig. and areas of necrosis to a hyperenhancing mass
3-36). Clear cell type renal cell carcinoma metas- similar to a neuroendocrine tumor.38
tases potentially harbor microscopic lipid, mir-
roring the primary lesion (Fig. 3-37). Lymphoma.  Primary pancreatic lymphoma
is very rare. However, secondary involvement
Other Solid Pancreatic Lesions of the pancreas occurs in approximately 30% of
Acinar Cell Carcinoma.  Although acinar non-Hodgkin’s lymphoma involving peripancre-
cells constitute approximately 80% of the pan- atic and para-aortic lymph nodes.
creatic parenchyma, acinar cell carcinoma of the Imaging findings typically include lymphade-
pancreas is a rare malignancy, accounting for 1% nopathy with direct extension and infiltration of
of pancreatic exocrine tumors and occurs pri- the pancreas. The pancreatic infiltration and
marily in men. This neoplasm is occasionally lymph nodes have similar imaging characteris-
associated with a syndrome of subcutaneous tics, including low T1-weighted signal inten­­
and intraosseous fat necrosis and polyarthralgia sity, variable T2-weighted signal intensity, and
due to the release of lipase. decreased enhancement in comparison with the
 MRI of the Pancreaticobiliary System  •  161

E F

G
FIGURE 3-36, cont’d 

normal pancreatic parenchyma (Fig. 3-38). kidney disease, von Hippel–Lindau disease, and
Whereas pancreatic lymphoma potentially cystic fibrosis.40
causes duct dilatation, the degree of duct dilata-
tion is generally less than expected for a pancre- Pseudocysts.  Pseudocysts evolve during
atic mass of similar size.39 the course of pancreatitis within areas of necro-
sis or exudate developing a surrounding wall of
Cystic Pancreatic Lesions granulation tissue without an epithelial lining.
Cystic pancreatic lesions have a broad differen- The contents of pseudocysts include pancreatic
tial diagnosis; however, morphology of the debris, pancreatic excretion, or blood products.
cystic component and connectivity with the As such, the imaging appearance varies consid-
pancreatic duct are the main factors in narrow- erably (see Fig. 3-12). The center typically shows
ing the differential (Fig. 3-39). Fluid hyperinten- low T1-weighted signal intensity and high
sity on T2-weighted images and absent T2-weighted signal intensity. Sludge and hemor-
enhancement (optimally confirmed with sub- rhagic components cause lower T2-weighted
tracted images) establish cystic etiology. signal intensity.40–42

Cysts Von Hippel–Lindau Disease.  As discussed

True Cysts.  True cysts of the pancreas are previously, multiple true pancreatic cysts are
very rare and thought to be congenital in origin. the most common manifestation of von
These cysts are lined by epithelial cells, gener- Hippel–Lindau disease (see Fig. 3-23) (see
ally multiple, and seen with adult polycystic Chapter 4).
162  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-37.  Pancreatic renal cell carcinoma metastases. The in-phase image (A) in a patient with metastatic clear cell renal cell carcinoma
shows a large lesion in the pancreatic body (arrow), which loses signal on the out-of-phase image (B). Central cystic necrosis and periph-
eral hypervascularity on the T2-weighted (C) and subtracted arterial phase (D) images reiterate the typical appearance of this type of
tumor (arrow).

Neoplasms typically more common in males and occur

Intraductal Papillary Mucinous Neo- during the sixth to eighth decades of life.
plasms.  IPMNs are a spectrum of neoplasms Main pancreatic duct IPMNs can be difficult
composed of proliferation of pancreatic ductal to distinguish from chronic pancreatitis. The
epithelium lining the main pancreatic duct or main duct is either diffusely or segmentally
side branch ducts (see Fig. 3-28). The mucin- involved with progressive duct dilatation and
filled dilated ducts demonstrate high T2-weighted parenchymal atrophy. At the time of diagnosis,
signal intensity and variable T1-weighted signal 30% to 40% of patients with main duct IPMNs
intensity depending on the hydration of the have invasive malignancy and the remainder
mucin (Fig. 3-40). Low signal intensity filling have cellular atypia, dysplasia, or carcinoma in
defects represent papillary projections or situ; therefore, these lesions should be resected.46
mural nodules. The presence of these lesions Features that suggest malignancy include: papil-
can be more accurately assessed after contrast lary projections, mural nodules, size greater
administration because the papillary projections than 3 cm, interval growth, or main pancreatic
or mural nodules demonstrate enhancement duct dilatation greater than 7 mm is suspicious
whereas mucin does not.43–45 IPMNs are for malignancy (Fig. 3-41).47

FIGURE 3-38.  Pancreatic lymphoma. Hypointense T1-weighted (axial in-phase [A], out-of-phase [B], and precontrast [F]) and slightly
hyperintense T2-weighted (axial single-shot fast spin-echo [SSFSE; C], axial fat-suppressed T2-weighted [D], and coronal SSFSE [E])
pancreatic lesions (arrows) with mild enhancement on early (G) and delayed (H) postcontrast images in a 19-year-old female with
pathologically proven primary pancreatic lymphoma.
A B

C D

G
 Pancreas – Cystic Lesions

Cyst Pseudocyst Serous Mucinous cystic

Cystadenoma neoplasm

FIGURE 3-39.  Pancreatic cystic lesions.

IPMN = intraductal papillary mucinous IPMN IPMN
neoplasm. Branch duct Main duct

A B

C D
FIGURE 3-40.  IPMN, main duct type. A, An MRCP image in a patient with a small main duct IPMN at the level of the pancreatic
head/neck (arrow) is associated with mild downstream dilatation (arrowhead). B, An MRCP image in a different patient with main
duct IPMN in the tail (arrow) shows continuity with the adjacent duct, which is not dilated. The T2-weighted (C) and postcontrast
(D) images exclude malignant features.

FIGURE 3-41.  IPMN with malignant features. Fat-suppressed T2-weighted (A) and coronal thick slab maximal intensity projectional
MRCP (B) images demonstrating a large cystic lesion in the pancreatic head (arrows). Precontrast (C), early arterial phase (D), late
arterial phase (E), and delayed phase (F) fat-suppressed T1-weighted gradient recalled-echo images demonstrate enhancement of internal
papillary projections and proximity to the main pancreatic duct, in keeping with a side branch intraductal papillary mucinous neoplasm
which has undergone malignant degeneration.
A B

C D

E F
166  •  Fundamentals of Body MRI

A B
FIGURE 3-42.  IPMN side branch type. The coronal T2-weighted image (A) shows a simple-appearing cystic lesion in the pancreatic
head (arrow). The corresponding MRCP image (B) depicts the connection with the main pancreatic duct and characteristic downstream
dilatation (arrow).

Side branch IPMNs appear as oval-shaped with abundant, thick gelatinous mucin and have
cystic masses in proximity to the main duct. a predilection for the pancreatic tail. The indi-
These lesions may have a cluster of grapes vidual cysts are generally larger than 20 mm and
appearance, and identifying a communication to may have papillary projections. These lesions do
the main pancreatic duct allows differentiation not communicate with the main pancreatic duct
from serous cystadenoma.48 Branch duct IPMNs and may have peripheral calcification (Fig. 3-44).
most commonly occur in the uncinate process These lesions occur primarily in women (6 : 1)
or pancreatic head but can also involve the body in the fourth to sixth decades of life. Seventy to
and tail (Fig. 3-42). 90% of mucinous cystic neoplasms occur in the
distal pancreatic body or tail. The mucin may
Serous Cystadenoma.  Serous cystadenoma have high T1-weighted and high T2-weighted
is a benign tumor occurring in older, predomi- signal intensity. When these lesions are multi-
nantly female, patients characterized by a cluster locular, they tend to have thick septations
of greater than six cysts—all less than 20 mm in (Fig. 3-45).49–51
diameter. Parenthetically, serous cystadenoma is
seen with increased frequency in patients with Cystic Neuroendocrine (Islet Cell)
von Hippel–Lindau disease. These tumors have Tumor.  As neuroendocrine tumors (see discus-
a slight predilection for the pancreatic head. sion under “Solid Lesions”) grow, they may
The tumor septations and cyst walls demon- develop a cystic appearance secondary to degen-
strate minimal enhancement (Fig. 3-43). The eration and necrosis (see Figs. 3-33 and 3-35).
tumor may contain a central scar that demon- Therefore, it is important to consider islet cell
strates low T1-weighted signal intensity with tumors in the differential of cystic lesions. The
variable contrast enhancement. The central scar central cystic component typically demonstrates
occasionally calcifies (better depicted on moderately T1-weighted and T2-weighted signal
CT).40–42 Although similar in appearance to intensity. The T1-weighted increased signal is a
branch duct IPMN, lack of connection with the nonspecific finding as can be seen in pseudo-
main pancreatic duct excludes this diagnosis. cysts and solid and papillary epithelial neo-
plasms (SPENs) with hemorrhage and mucinous
Mucinous Cystic Neoplasm.  Mucinous neoplasms. Cystic islet cell tumors have an irreg-
cystic neoplasm is an uncommon neoplasm ular thick wall that demonstrates avid enhance-
with malignant potential, prompting surgical ment after the administration of gadolinium,
resection. They are characterized by the forma- helping to differentiate them from other cystic
tion of unilocular or multilocular cysts filled lesions.42
 MRI of the Pancreaticobiliary System  •  167

A B

C D
FIGURE 3-43.  Pancreatic serous cystadenoma. Axial (A) and coronal (B) T2-weighted, coronal thick-slab MRCP (C), and dynamic pre-
contrast (D), early arterial (E), late arterial (F), and delayed (G) 3-D fat-suppressed T1-weighted gradient recalled-echo images depict
a large multiloculated cystic lesion in the distal body of the pancreas with minimal enhancement of the septations, in keeping with a
pancreatic serous cystadenoma.
168  •  Fundamentals of Body MRI

E F

G
FIGURE 3-43, cont’d 

Mucinous Cystic Neoplasm

Few large locules
Often > 2cm
Possible pancreatic tail
No connective duct

FIGURE 3-44.  Pancreatic cystic neoplasms.

IPMN = intraductal papillary mucinous IPMN Serous
neoplasm. Branch duct Cystadenoma
 MRI of the Pancreaticobiliary System  •  169

A B

C D
FIGURE 3-45.  Mucinous cystic neoplasm. Mucinous cystic neoplasm of the pancreatic tail in a 47-year-old woman. T2-weighted (A),
T1-weighted gradient recalled-echo (B), fat-suppressed T2-weighted (C), coronal thick-slab MIP MRCP (D), dynamic precontrast, early
arterial phase (E), and late phase 3-D fat-suppressed T1-weighted gradient recalled echo (F and G), and coronal T2-weighted (H) images
demonstrate a large cystic mass in the tail of the pancreas separate from the main pancreatic duct, with increased T1-weighted signal
intensity (related to the mucin content) and minimal internal enhancement.
170  •  Fundamentals of Body MRI

E F

G H
FIGURE 3-45, cont’d 

Solid-Cystic Papillary Epithelial Neo- demonstrates low T1-weighted and T2-weighted

plasm.  SPENs are lesions with low-grade malig- signal intensity. The most common imaging
nant potential. SPENs occur frequently in appearance is mixed solid and cystic lesion with
females between 20 and 30 years of age, typi- areas of hemorrhagic necrosis.52,53
cally of African American or Asian descent (Fig.
3-46). The imaging appearance is a large, well- GALLBLADDER
encapsulated mass with variable internal archi-
Anatomy
tecture (from solid to solid and cystic to a
thick-walled cyst), with focal signal voids (due The gallbladder is an ovoid cystic organ along
to calcification) and regions of hemorrhagic the undersurface of the liver at the interlobar
degeneration. Although these lesions occur fissure between the right and the left lobes of
throughout the pancreas, the most common the liver. Although the size and shape of the
location is the pancreatic tail. The hemorrhagic gallbladder vary with fasting state, it is approxi-
portion of the tumor may demonstrate high mately 10 cm long and 3 to 5 cm in diameter.
T1-weighted signal intensity and variable The normal capacity of the gallbladder is app­
T2-weighted signal intensity with or without roximately 50 mL. The normal gallbladder wall
a fluid-debris level. The fibrous capsule is 2 to 3 mm in thickness and composed of
 MRI of the Pancreaticobiliary System  •  171

A B

C D
FIGURE 3-46.  Solid-cystic papillary epithelial neoplasm (SPEN). In-phase (A) and out-of-phase (B) T1-weighted gradient recalled-echo,
fat-suppressed T2-weighted (C), and fat-suppressed T1-weighted gradient recalled-echo (D) images demonstrate a decreased T1-weighted
signal intensity, increased T2-weighted signal intensity mass, without upstream pancreatic duct dilatation, within the head of the pancreas
in this young female African American patient. Noncontrast (E), early arterial (F), late arterial (G), and delayed (H) CT images dem-
onstrate calcification and mild delayed enhancement of the same mass. These findings are characteristic of SPEN of the pancreas, which
was confirmed at surgery.

Normal Appearance
columnar epithelium. The gallbladder connects
with the biliary tree via the cystic duct, measur- The function of the gallbladder is to store and
ing 2 to 4 cm in length and 1 to 5 mm in caliber, concentrate bile. As such, the T1-weighted
characterized by prominent concentric folds, appearance of the gallbladder lumen varies
known as the spiral valves of Heister. The cystic with the concentration of the bile. In general,
duct usually joins the extrahepatic bile duct bile salts are of increased signal intensity on
halfway between the porta hepatis and the T1-weighted imaging in the fasting state;
ampulla of Vater. Variant anatomy, such as low however, the bile salt and protein concentration
medial cystic duct insertion, occurs approxi- affects the degree of the T1-weighted signal
mately 20% of the time. intensity. The gallbladder contents demonstrate
172  •  Fundamentals of Body MRI

E F

G H
FIGURE 3-46, cont’d 

increased signal on T2-weighted imaging as a

Congenital/Developmental
result of the static fluid content of bile.54
Abnormalities of the Gallbladder
Accessory Gallbladders, Ectopia,
Imaging Technique and Agenesis
MRI of the gallbladder should be performed in When there is aberrant branching of the fore­­
a manner similar to other abdominal imaging gut during development, gallbladder anomalies
protocols. When possible, the patient should potentially arise. Frequently, these anomalies
fast for at least 4 hours to promote adequate are part of a larger picture of heterotaxy syn-
gallbladder distention. In addition, the use drome with more significant anomalies (i.e.,
of newer contrast agents with increased cardiac and pulmonary). Congenital and devel-
hepatobiliary excretion can provide limited opmental anomalies of the gallbladder are often
information regarding gallbladder and biliary incidentally noted at autopsy; their only clinical
function. revelance is for presurgical planning (Fig. 3-47).
 MRI of the Pancreaticobiliary System  •  173

A B

C D
FIGURE 3-47.  Ectopic gallbladder. T2-weighted (A), fat-suppressed T2-weighted (B), postcontrast fat-suppressed T1-weighted gradient
recalled-echo (C), and coronal thick-slab MIP MRCP (D) images demonstrate an ectopic gallbladder in the fissure for the ligamentum
teres.

Cholelithiasis Diffuse Processes of

Cholelithiasis (or gallstones) is the most
the Gallbladder
common gallbladder disorder by a wide margin,
afflicting 10% of the population. Risk factors Cholecystitis
include obesity, pregnancy, rapid weight loss Acute.  Acute inflammation of the gallblad-
and estrogens and women are affected twice as der is caused by cystic duct obstruction in
often as men. While most often asymptomatic, the majority of cases. At imaging, gallstones
pain (or biliary colic) occasionally ensues. Cho- are identified in the gallbladder and/or cystic
lelithiasis is also the usual culprit in acute and duct as signal voids best visualized on
chronic cholecystitis. T2-weighted images. Associated findings
Gallstones appear as filling defects within the include mural thickening (>3  mm), mural
gallbladder lumen. The rigid internal structure hyperemia (as evidenced by hyperenhance-
of gallstones facilitates relaxation resulting in ment on postgadolinium images), and occa-
signal voids—best visualized against the bright sionally, transient adjacent hepatic hyperemia
background of fluid on T2-weighted images on immediate postgadolinium images (Fig.
(Fig. 3-48). The two dominant forms of gall- 3-49). Pericholecystic inflammatory changes
stones feature slightly different imaging find- and fluid are best appreciated on T2-
ings. Cholesterol stones—the more common weighted and postcontrast images (Fig.
variety (80%)—are hypointense signal voids on 3-50).54–57 Occasionally, abscesses form within
all pulse sequences. Pigmented stones are or outside the gallbladder wall (Fig. 3–51).
hypointense on T2-weighted images, but Acute acalculous cholecystitis accounts for
exhibit variable T1 signal depending on the the reminder of the cases of acute cholecysti-
degree of hydration. Regardless of the compo- tis and is often related to decreased gallblad-
sition, the sensitivity of MRI for detecting gall- der motility, decreased blood flow, or bacterial
stones approaches 100%. infection.54,55
174  •  Fundamentals of Body MRI

A B
FIGURE 3-48.  Cholelithiasis. The axial T2-weighted fat-suppressed image (A) through the gallbladder shows multiple intraluminal filling
defects corresponding to gallstones. In the in-phase image (B), the gallstones are conspicuous only because of the hyperintensity, sug-
gesting pigmented composition.

A B

C D

FIGURE 3-49.  Acute cholecystitis. In-phase (A) and out-of-phase (B) T1-weighted, T2-weighted (C), fat-suppressed T2-weighted (D),
and precontrast (E) and postcontrast (F) fat-suppressed T1-weighted gradient recalled-echo images demonstrate gallstones, mural thick-
ening, mural hyperemia, and adjacent hepatic hyperemia of acute cholecystitis caused by an obstructing T1 hyperintense gallstone within
the cystic duct (arrow in E).
 MRI of the Pancreaticobiliary System  •  175

E F
FIGURE 3-49, cont’d 

A B
FIGURE 3-50.  Acute cholecystitis with pericholecystic inflammatory changes. Coronal (A) and axial (B) T2-weighted images in a patient
with acute cholecystitis reveal wall thickening, gallstones, and pericholecystic inflammation and fluid (arrow).

A B
FIGURE 3-51.  Acute cholecystitis with intramural abscesses. Axial T2-weighted (A) and postcontrast (B) images in a patient with severe
acute cholecystitis show gallstones and mural thickening with intramural abscesses (arrows).
176  •  Fundamentals of Body MRI

A B

FIGURE 3-52.  Chronic cholecystitis. A, The T2-weighted

image in a patient with chronic cholecystitis depicts multiple
gallstones. The arterial phase (B) and delayed phase (C) post-
contrast images show progressively increasing mural enhance-
C
ment (arrows).

Chronic.  In chronic cholecystitis, mural hypoproteinemia, hypertension (both systemic

enhancement is mild and most prominent on and portal), and renal failure. The gallbladder
delayed postgadolinium images, related to fibro- wall demonstrates normal enhancement
sis within the gallbladder wall (Fig. 3-52). In with no hyperemia of the adjacent hepatic
addition, the gallbladder is often small and/or parenchyma.54,55
contracted with no adjacent hepatic hyperemia.
The gallbladder wall may calcify, resulting in a Adenomyomatosis
porcelain gallbladder.54,55 Gallbladder adenomyomatosis is a benign condi-
tion occurring either focally (most commonly at
Gangrenous.  Gangrenous or necrotizing the fundus), diffusely, or segmentally. There is
cholecystitis is a severe form of acute cholecys- hyperplasia of epithelial and muscular elements
titis with increased morbidity and mortality. resulting in mucosal outpouchings into a thick-
Older men with cardiovascular disease and dia- ened wall, forming intramural diverticula (also
betic patients are at increased risk for develop- known as Rokitansky-Aschoff sinuses) (Fig. 3-54).
ing gangrenous cholecystitis and are, therefore, Although there is no malignant potential, adeno-
more likely to require an open cholecystectomy. myomatosis and gallbladder carcinoma may have
Segmental absence of mucosal enhancement on similar presentations (gallbladder wall thicken-
postgadolinium images is suggestive of gangre- ing, intraluminal mass, and gallstones). There-
nous cholecystitis.54,55,58 fore, if diagnosis is equivocal, close follow-up or
cholecystectomy is recommended.59,60
Nonspecific Edema
Nonspecific edema manifests as diffuse gallblad-
Focal Processes of the Gallbladder
der wall thickening, in the setting of any of a
number of hepatic, pancreatic, and biliary dis- Polyp
eases. Common etiologies include cirrhosis The generic term, “gallbladder polyp” encom-
(Fig. 3-53)—which is the most common— passes a few distinctly different lesions that are
 MRI of the Pancreaticobiliary System  •  177

A B

FIGURE 3-53.  Gallbladder wall edema. T2-weighted (A), fat-

suppressed T2-weighted (B), and postcontrast fat-suppressed
T1-weighted gradient recalled-echo (C) images demonstrate
gallbladder wall edema in a patient with cirrhosis and portal
C Axial link
hypertension.

categorized according to their etiology and polypoid than sessile in morphology, the gall-
malignant potential. Polypoid mural-based bladder adenoma is usually composed of glandu-
lesions develop in the setting of the hyperplastic lar tissue with epithelial lining and an inner
cholecystoses (a term used to include a spec- fibrovascular core. Most lesions enhance and
trum of proliferative and degenerative changes measure less than 2 cm in diameter (Fig. 3-55).
involving the gallbladder wall and including Because adenomas are not reliably differentiated
cholesterosis and adenomyomatosis). These from the third category of polypoid lesions—
lesions, exemplified by the cholesterol polyp gallbladder carcinoma (except after aggressive
and adenomyoma, represent polypoid ingrowths features such as metastatic invasion or growth
of the hyperplastic epithelium, lack enhance- are evident)—follow-up (ultrasound) is war-
ment and harbor no malignant potential. In the ranted in lesions over 5 mm.61
case of the cholesterol polyp, signal loss on out-
of-phase images reflects intracytoplasmic lipid. Carcinoma
Polypoid lesions measuring less than 5 mm in Gallbladder carcinoma occurs primarily in the
size are almost always cholesterol polyps. sixth to seventh decade of life with a female
The adenoma is another benign, usually predominance (3 : 1). Early stage tumors are
incidental polypoid lesion. More frequently asymptomatic and often detected incidentally at
178  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-54.  Adenomyomatosis. T2-weighted (A), fat-suppressed T2-weighted (B), postcontrast fat-suppressed T1-weighted gradient
recalled-echo (C), and coronal thick-slab MIP MRCP (D) images demonstrate a cluster of cystic structures at the fundus of the gall­
bladder (arrow), corresponding to multiple intramural diverticula (Rokitansky-Aschoff sinuses) of adenomyomatosis.

surgery for benign disease. Advanced stage Metastases

disease often presents with anorexia, weight The gallbladder is infrequently involved by
loss, abdominal pain, and jaundice. MRI findings malignancies other than primary gallbladder car-
suggestive of gallbladder carcinoma include a cinoma. However, melanoma and breast cancer
mass protruding into the gallbladder lumen or metastasize to the gallbladder on rare occasions
replacing the lumen entirely, focal or diffuse (Fig. 3-58).64
gallbladder wall thickening (Fig. 3-56), and soft
tissue invasion of local organs (especially the BILIARY TREE
liver) (Fig. 3-57).62 Signal characteristics include
Anatomy and Normal Appearance
T1 hypointensity and T2 hyperintensity relative
to liver and heterogeneously hypovascular Intrahepatic biliary ducts follow the internal
enhancement.63 hepatic segmental anatomy; however, variations
 MRI of the Pancreaticobiliary System  •  179

A B
FIGURE 3-55.  Gallbladder adenoma. A sessile mural-based lesion (arrow) exhibits moderate enhancement comparing the precontrast image
(A) with the postcontrast image (B).

* *

A B
FIGURE 3-56.  Gallbladder carcinoma. A, Focal gallbladder fundal mural thickening focally obliterating the lumen (arrow) on the
T2-weighted fat-suppressed image corresponds to the primary tumor in a patient with gallbladder carcinoma (and a gallstone) with
metastatic lymphadenopathy (arrowheads). B, The postcontrast image shows heterogeneous hypovascular enhancement of both the
primary tumor (arrow) and the metastatic lymph nodes (arrowheads). Note the associated portal venous thrombosis (asterisk).

in the branching pattern commonly exist. Delin- congenital anomalies of the biliary tree, most
eation of peripheral branches is variable based commonly anomalies of the pancreaticobiliary
on patient factors, but the branches are visible junction and congenital cystic biliary disease.66
when dilated. Segmental intrahepatic ducts Biliary tree variants have become of increasing
commonly measure 3 to 4 mm in diameter. The importance as the role of laparoscopic surgery
extrahepatic bile duct (common hepatic duct has increased in hepaticobiliary disease.66
and common bile duct) commonly measures up As stated in the gallbladder section, bile salts are
to 7 mm (10 mm in postcholecystectomy hyperintense on T1-weighted imaging; however,
patients).65,66 this can be variable based on the concentration of
Pain, obstruction, and inflammatory condi- the bile. The fluid content of the bile also contrib-
tions involving the biliary tree may be related to utes to its T2-weighted increased signal.
180  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 3-57.  Gallbladder carcinoma with local invasion. Superior and inferior T2-weighted (A and B), fat-suppressed T2-weighted (C and
D), and postcontrast fat-suppressed T1-weighted gradient recalled-echo (E and F) images demonstrate an enhancing soft tissue mass at
the fundus of the gallbladder with direct invasion into the adjacent hepatic parenchyma, in keeping with gallbladder adenocarcinoma.
 MRI of the Pancreaticobiliary System  •  181

A B

C
FIGURE 3-58.  Gallbladder metastasis. T2-weighted (A), fat-suppressed T2-weighted (B), precontrast fat-suppressed T1-weighted (C), and
postcontrast fat-suppressed T1-weighted gradient recalled-echo (D) images demonstrate an enhancing mural nodule (arrow), in keeping
with a metastasis to the gallbladder wall.

and coronal planes, allowing separation from

Imaging Techniques
the adjacent fluid-filled bowel. Radial oblique
MRCP is a noninvasive imaging method for coronal images can provide additional informa-
imaging the biliary tree that complements tion in the evaluation of anatomic variants.
invasive endoscopic retrograde cholangiopan- Subsecond breathhold techniques are critical
creatography (ERCP) while avoiding its compli- in the acquisition of these images, eliminating
cations. Furthermore, MRI has nearly replaced respiratory motion and bowel peristalsis. Two-
ERCP in situations in which the anatomy has dimensional slab acquisition can provide an
been surgically altered, rendering ERCP difficult overview of the entire pancreaticobiliary tree;
or impossible to perform.65 however, these images also need to be com-
MRCP capitalizes on the T2-weighted contrast plemented by 3-D thin-section acquisition,
difference between the fluid-filled structures of which may require postprocessing to delineate
the biliary tree and the surrounding soft tissues. subtle biliary pathology and intraductal
Imaging is frequently performed in the axial pathology.
182  •  Fundamentals of Body MRI

For evaluation of the extraductal pathology, groups this protean entity into categories
T1-weighted pre- and postgadolinium images according to anatomic involvement (Fig. 3-59)
are crucial for evaluation of fibrosis and infiltrat- with type I choledochal cysts constituting
ing masses. 80-90% of all choledochal cysts. Postulated eti-
ologies include an anomalous junction between
the common bile and pancreatic ducts and con-
Choledochal Cyst
genital defects in bile duct wall formation. Proxi-
The term choledochal cyst comprises a spec- mal emptying of the pancreatic duct into the
trum of congenital biliary dilatation patterns common bile duct exposes the common bile
including the intrahepatic and extrahepatic duct to the damaging effects of the pancreatic
ducts. The Todani classification system nicely enzymes.
The majority of choledochal cysts are detected
in childhood. While not uniformly present, the
Type Appearance classic clinical triad includes right upper quad-
rant pain, jaundice and a palpable mass. Biliary
I Solitary fusiform extrahepatic stasis predisposes to gallstones, cholangitis and
II Saccular extrahepatic pancreatitis. The feared long-term complication
is cholangiocarcinoma.
III Choledochocele The imaging appearance depends on the ana-
IVa Fusiform intra- and extrahepatic
tomic involvement. Type I choledochal cysts
appear as fusiform dilatation of the common bile
IVb Multiple extrahepatic duct of variable degree, simulating the appear-
ance of mechanical biliary dilatation (i.e., by
V Caroli disease (multiple intrahepatic)
pancreatic adenocarcinoma or gallstones) (Fig.
3-60). The smooth, tapering distal margins of a
I II III choledochal cyst differ from either the irregular
or polypoid margins of a dilated duct in the
IVa IVb V setting of malignant obstruction or the menis-
coid margin of a dilated duct proximal to an
obstructing stone (Fig. 3-61). Benign biliary
strictures most closely simulate the appearance
FIGURE 3-59.  Todani classification of choledochal cysts. of type I choledochal cysts (see Fig. 3-61); a

A B
FIGURE 3-60.  Type I choledochal cyst. The MRCP image (A) shows moderate fusiform dilatation of the common bile duct (arrow)
without intrahepatic biliary dilatation tapering smoothly distally without evidence of an intraluminal filling defect or distal obstructing
mass. The maximal intensity projectional image from a 3D MRCP image (B) in a different patient with a type I choledochal cyst
(arrows) massively dilated—likely exacerbated by the gravid uterus (arrowheads) also inducing intrahepatic biliary dilatation (open
arrows).
 MRI of the Pancreaticobiliary System  •  183

A B

C D
FIGURE 3-61.  Differential diagnosis of type I choledochal cyst. The 3D MRCP image (A) reveals a dilated common bile duct with a distal
meniscoid configuration proximal to an obstructing stone (arrow). In a different patient, the coronal steady state (B) and MRCP (C)
images also show dilatation of the common bile duct with irregular distal margins at the level of a pancreatic head mass (arrow in B).
Note the mildly dilated pancreatic duct (arrow in C). The MRCP image in a patient with a benign biliary stricture (D) depicts common
bile duct dilatation with smooth distal tapering.

different clinical scenario—older patients with delayed images following injection of a hepato-
cholelithiasis, for example—and presence of cellular agent) differentiates the type II chole-
intrahepatic biliary dilatation favor a benign dochal cyst from a duodenal diverticulum or a
biliary stricture. pancreatic pseudocyst.
Type II choledochal cysts present diagnostic The type III choledochal cyst is synonymous
uncertainty either because of the difficulty in with choledochocele, or intraduodenal diver-
establishing an anatomic origin from the ticulum. The type III choledochal cyst arises
common bile duct or because of the rarity of the from the intraduodenal segment of the common
entity. A narrow channel connects the saccular bile duct and prolapses into the duodenal lumen
type II choledochal cyst with the common bile (Fig. 3-63). An intraduodenal cystic lesion at the
duct (Fig. 3-62). Careful attention to this feature level of the ampulla of Vater with continuity
(facilitated by using high-resolution MRCP with the common bile duct establishes the
images including 3D technique and potentially diagnosis.
184  •  Fundamentals of Body MRI

A B
FIGURE 3-62.  Type II choledochal cyst. A narrow channel (arrow) connecting the saccular type II choledochal cyst (arrowhead ) with the
common bile duct (open arrows) is better depicted on the thick-slab 2D MRCP image (A) compared with the coronal T2-weighted
SSFSE image (B) due to the relatively thinner slices and lack of orientation along the plane of the connecting channel.

A B
FIGURE 3-63.  Type III choledochal cyst. An intraduodenal cystic lesion (arrow) is apparent on the MRCP (A) and coronal T2-weighted
image (B), which is seen to be continuous with the common bile duct (arrowheads) consistent with a choledochocele. Note the waisting
at the level of the intraduodenal segment (open arrow).

The type IV (and V) designation connotes differentiate the type IV choledochal cysts
multiplicity. Type IVa involves the intra- and from mechanical biliary obstruction and dilata-
extrahepatic biliary tree, while the type IVb tion (Fig. 3-64). Extrahepatic involvement and
only involves the extrahepatic biliary tree. lack of the “central dot sign” excludes Caroli
Chief differential considerations include disease.
biliary dilatation from mechanical causes and Caroli disease is a congenital autosomal
Caroli disease (in the case of type IVa chole- recessive disorder characterized by “(congeni-
dochal cysts). Alternating segmental caliber tal) communicating cavernous ectasia of the
changes and lack of an obstructing lesion intrahepatic biliary tract” (see Chapter 2).
 MRI of the Pancreaticobiliary System  •  185

A B
FIGURE 3-64.  Type IVa choledochal cyst. The coronal steady-state image (A) shows marked fusiform dilatation of the common bile duct
(arrows) with abnormally dilated intrahepatic ducts (arrowheads). The extent of multifocal intrahepatic cystic dilatation is better appreci-
ated on the MIP image (B) from a 3D MRCP sequence.

A B
FIGURE 3-65.  Choledocholithiasis. A, The coronal heavily T2-weighted image shows three filling defects (arrows) in the dilated CBD.
B, The thick-slab MRCP image yields a more comprehensive appraisal of the biliary tree, showing choledocholithiasis (arrows) and the
full extent of intra- and extrahepatic biliary dilatation.

Choledocholithiasis Mirizzi’s Syndrome

Choledocholithiasis is the most common cause Mirizzi’s syndrome is the obstruction of the
of biliary obstruction. Patients with cholelithia- common hepatic duct secondary to impaction
sis who undergo laparoscopic cholecystectomy of a stone within the cystic duct near its conflu-
are at higher risk for choledocholithiasis. MRCP ence with the common hepatic duct (Fig. 3-66).
then becomes the best noninvasive tool for The role of imaging is to differentiate from other
determining which patients require endoscopic causes of obstructive jaundice. MRCP allows
stone extraction (Fig. 3-65). for noninvasive assessment of the level of
186  •  Fundamentals of Body MRI

A B
FIGURE 3-66.  Mirizzi’s syndrome. T2-weighted (A) and coronal thick-slab MIP MRCP (B) images demonstrate multiple stones in the
cystic duct causing extrinsic compression of the adjacent common hepatic duct in this patient with Mirizzi’s syndrome.

obstruction and the presence of associated gall- obvious solid or mass-like component (Fig.
bladder inflammatory changes.67,68 3-67). In addition, in the initial evaluation of
these lesions, the adjacent parenchyma can be
evaluated.52
BILIARY OBSTRUCTION
While measurement guidelines exist to help dis- Postoperative Biliary Strictures
criminate between unobstructed and obstructed Postoperative biliary complications include a
biliary systems (intrahepatic ducts <3mm and range of problems often coexisting and fre-
extrahepatic ducts <7-8 mm or <10 mm post- quently involving biliary dilatation and/or
cholecystectomy), biliary obstruction is truly a obstruction. These include retained stones,
physiologic state defined by a luminal caliber hemorrhage, hemobilia, biliary leak, bile duct
reduction impeding biliary flow reflected by ligation and stricturing. Postsurgical strictures
abnormal blood chemistry. Benign and malig- usually develop over months to years postopera-
nant etiologies include stone disease and iatro- tively and account for the majority of benign
genic, infectious/inflammatory and neoplastic biliary strictures. The rise of laparoscopic cho-
strictures (cholangiocarcinoma, pancreatic car- lecystectomy has increased the incidence of bile
cinoma and periampullary tumors). The goal of duct injury and stricturing (approximately 1% of
imaging is to identify the etiology and anatomy laparoscopic cholecystectomies). Regardless of
of the obstruction. the procedure, the imaging appearance is the
same—short segmental smooth narrowing with
or without mild concentric wall thickening and
Benign Etiologies
enhancement. The surgical approach to treat-
Stricturing of the biliary tree occurs in both ment depends on the length and location of
intra- and extrahepatic locations and is most injury and various classification systems have
commonly related to recurrent inflammatory been proposed to convey this information--most
change related to biliary stone disease. MRCP famously the Bismuth classification.
allows for assessment of length and location of MRI/MRCP affords the ability to investigate
these strictures. The imaging findings of benign surgically altered anatomy not amenable to
strictures generally differ from malignant stric- ERCP (i.e., hepaticojejunostomy). MRI/MRCP
tures in several ways: (1) mild, smooth concen- also proffers a wealth of information in liver
tric wall biliary wall thickening with mild transplant patients in whom a host of potential
enhancement, (2) relative short segment of complications arise, including anastomotic and
involvement (≤1-2 cm) and (3) absence of an nonanastomotic stenoses (see Chapter 2).
 MRI of the Pancreaticobiliary System  •  187

A B
FIGURE 3-67.  Benign strictures. The MRCP image in a patient with intra- and extrahepatic biliary dilatation and proximal and distal
CBD strictures (arrows in A) exemplifies the smooth, short segmental involvement typical of benign biliary strictures. In a different
patient with a distal CBD stricture (arrow in B) postcholecystectomy, the same features are evident, including dilatation of the cystic
duct remnant (arrowhead ).

INFLAMMATORY ETIOLOGIES wall. With disease progression, the normally

acute angles at bile duct intersections become
Cholangitis
gradually more obtuse approaching right angular
Primary Sclerosing Cholangitis configuration. T1-weighted, T2-weighted and
Primary sclerosing cholangitis (PSC) is a chronic postcontrast images complement MRCP images
idiopathic disease of the intra- and extrahepatic by depicting the biliary/peribiliary wall thicken-
biliary ducts with progressive fibrosis ultimately ing and enhancement, periportal edema, as well
resulting in biliary ductal obliteration and biliary as the reactive periportal lymphadeno­pathy
cirrhosis. PSC is frequently associated with commonly observed in PSC. as well as the reac-
inflammatory bowel disease (70%) and incurs tive periportal lymphadenopathy (commonly
an increased risk for development of cholangio- observed in PSC).69,70 Cirrhosis generally ensues
carcinoma. PSC more frequently afflicts males approximately a decade after decade onset and
with peak incidence in the third and fourth because of preferential involvement peripher-
decades of life. ally, end-stage PSC exhibits a characteristic
The PSC imaging features evolve over time. peripheral atrophy–central hypertrophy pattern
Early in the disease process, imaging frequently (see Fig. 3-68).71
reveals randomly distributed short annular struc-
tures (1-2 mm) of the intrahepatic ducts alter-
nating with normal or mildly dilated segments, Infectious Cholangitis
creating the classic beaded appearance (Fig. Infectious cholangitis (also known as ascending
3-68). With continued progression of disease or bacterial cholangitis) is a clinical syndrome of
and destruction of peripheral ducts related to biliary obstruction seeded with infection
chronic inflammation, destruction, and fibrosis, arising from the gastrointestinal tract. Central
the peripheral ducts will not be visible, causing intrahepatic biliary dilatation is the rule--the
a pruned appearance of the biliary tree. Relative opposite of PSC. Smooth, circumferential
lack of upstream biliary dilatation reflects ductal wall thickening and enhancement
decreased compliance of the inflamed bile duct reflects underlying inflammation. Superimposed
188  •  Fundamentals of Body MRI

A B

C D
FIGURE 3-68.  Primary sclerosing cholangitis (PSC). A, Delayed postcontrast image in a patient with mild, early PSC reveals periportal
enhancement with irregular biliary ductal dilatation (arrows). B, The corresponding fat-suppressed T2-weighted image shows markedly
enlarged reactive periportal lymph nodes (arrows). More extensive irregular, beaded ductal dilatation and stricturing is exemplified in
patients with more advanced PSC on the MRCP (C) and coronal T2-weighted (D) images. Marked irregular ductal dilatation and
stricturing peripherally with a characteristic central hypertrophy–peripheral atrophy pattern typifies end-stage PSC, as seen in this case
on the heavily T2-weighted (E), fat-suppressed steady-state (F), and MRCP (G) images.

parenchymal inflammatory changes include Chapter 2), (2) hilar (Klatskin) tumors involving
avidly enhancing, geographic, wedge-shaped the right and/or left first order bile ducts and/or
T2-hyperintense segments of inflamed tissue their confluence and (3) extrahepatic tumors.
and potentially parenchymal abscesses (see While generally exhibiting infiltrative growth
Chapter 2).72 dissecting along tissue planes, on a macro-
scopic/imaging level, three distinct growth
patterns are observed: (1) mass-forming, (2)
MALIGNANT ETIOLOGIES periductal-infiltrating and (3) intraductal-grow-
ing or polypoid (Fig. 3-69).
Cholangiocarcinoma
Central/hilar lesions classically follow the
Cholangiocarcinoma is a tumor arising from periductal-infiltrative growth pattern and the
intra- or extrahepatic biliary epithelium (90% subtle periductal signal alteration and enhance-
adenocarcinoma and 10% squamous cell carci- ment is often perceived only after the upstream
noma) affecting men and women in equal pro- biliary dilatation is noted and traced to the point
portions. Increased risk exists in patients with of obstruction (Figs. 3-70 and 3-71).
PSC, recurrent pyogenic cholangitis, and con- Occasionally, extrahepatic cholangiocarci-
genital cystic biliary disease. noma follows an intraductal masslike growth
Cholangiocarcinoma stratifies into three ana- pattern, which simulates choledocholithiasis
tomic categories: (1) peripheral tumors (see on MRCP images (Fig. 3-72). There may be
 MRI of the Pancreaticobiliary System  •  189

E F

G
FIGURE 3-68, cont’d 

Mass-forming

Periductal-infiltrating

Intraductal-polypoid

FIGURE 3-69.  Cholangiocarcinoma growth patterns.

190  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 3-70.  Hilar cholangiocarcinoma. T2-weighted (A), fat-suppressed T2-weighted (B), coronal thick-slab MIP MRCP (C), and
precontrast (D), early arterial phase (E), and delayed phase (F) fat-suppressed T1-weighted gradient recalled-echo images demonstrate
a mildly T2 hyperintense, gradually enhancing, intrahepatic, infiltrative mass with peripheral biliary radical dilatation.
 MRI of the Pancreaticobiliary System  •  191

A B

C D
FIGURE 3-71.  Cholangiocarcinoma with periductal-infiltrating growth pattern. T2-weighted (A), fat-suppressed T2-weighted (B), in-phase
T1-weighted (C), coronal thick-slab MIP MRCP (D), and precontrast (E), early arterial phase (F), and delayed phase (G) fat-suppressed
T1-weighted gradient recalled-echo images demonstrate gradually enhancing soft tissue about the extraheptic bile duct causing intra­
hepatic biliary ductal dilatation in keeping with cholangiocarcinoma.
192  •  Fundamentals of Body MRI

E F

G
FIGURE 3-71, cont’d 
 MRI of the Pancreaticobiliary System  •  193

A B

C D
FIGURE 3-72.  Cholangiocarcinoma with intraductal growth pattern. The coronal (A) and axial (B) heavily T2-weighted images depict
hypointense irregular filling defects in the CBD (arrows) with enhancement revealed on the postcontrast image (C), indicating solid
tissue in this uncommon case of extrahepatic, intraductal, mass-forming cholangiocarcinoma (arrow). D, MRCP shows stricturing of
the CBD with upstream biliary dilatation (arrows).

intrahepatic duct crowding in the setting of More commonly seen in males, an association
ipsilateral hepatic lobar atrophy related to with familial adenomatous polyposis has been
central duct obstruction or portal vein documented. Most patients present secondary
occlusion.73,74 to biliary obstruction or gastrointestinal
bleeding.
At imaging, these patients have biliary and
AMPULLARY CARCINOMA
pancreatic duct dilatation (with or without side
Ampullary carcinoma is a neoplasm developing branch dilatation), and the ampullary lesion is
from either ductal epithelium within the ampulla frequ­ently not visualized. Under these circum-
(i.e., ampullary CBD, ampullary pancreatic duct stances, it is impossible to distinguish between
or the common ampullary channel) or the ampullary carcinoma and a benign ampullary
duodenal papillary epithelium. Ampullary carci- stricture. When the ampullary lesion is visual-
noma generally portends a favorable prognosis ized, imaging features include a nodular or
because of the early presentation provoked by infiltrative mass, low signal intensity on T1-
either biliary obstruction or gastrointenstinal weighted and T2-weighted images with homo-
bleeding. geneous early enhancement and variable rim
194  •  Fundamentals of Body MRI

A B

C D

FIGURE 3-73.  Ampullary carcinoma. T2-weighted (A), coronal

thick-slab MIP MRCP (B), and precontrast (C), early arterial
phase (D), and delayed phase (E) fat-suppressed T1-weighted
gradient recalled-echo images demonstrate an enhancing 
T1 hypointense mass at the ampulla (arrow) causing mild
bile duct dilatation. Biopsy revealed invasive ampullary
E
adenocarcinoma.
 MRI of the Pancreaticobiliary System  •  195

A B

FIGURE 3-74.  Ampullary carcinoma. A, A polypoid

hypointense lesion (arrows) medial to the distal CBD
causes biliary dilatation. B, The T1-weighted fat-
suppressed image near the confluence of the distal CBD
and pancreatic ducts (arrows) shows the hypointense
lesion (arrowhead), subsequently proven to be ampullary
carcinoma. C, Marked biliary and pancreatic ductal dila-
C
tation is apparent on the MRCP image.

enhancement on delayed images with papillary

CBD bulging (Figs. 3-73 and 3-74). The ductal dilata-
Common tion pattern depends on the anatomy of the
channel inter­section of the pancreatic and common bile
uct
ducts—which is variable—either demonstrat-
ea tic d ing iso­­­­lated biliary dilatation or dilatation of
P ancr
both the biliary and pancreatic ducts (double
Papilla duct sign).75,76 However, establishing a specific
Duodenum histologic diagnosis in the setting of a suspected
Pancreatic head
“periampullary mass” is problematic because of
Periampullary carcinomas the multiplicity of lesions originating from the
Common Duodenum Pancreatic CBD ampullary region and overlap in imaging find-
channel head ings (Fig. 3-75). The term “periampullary mass”
Ampullary Duodenal Pancreatic Cholangio- serves to convey the fact that an obstructing
carcinoma adeno- adeno- carcinoma mass requiring further investigation (ERCP) is
carcinoma carcinoma warranted without potentially erroneously
FIGURE 3-75.  The periampullary region. assigning a tissue diagnosis.

Additional images for this chapter are

available online on Expert Consult at
www.expertconsult.com.
196  •  Fundamentals of Body MRI

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 chapter four 

MRI of the Kidneys

and Adrenal Glands
adrenal imaging. Adrenal adenomas and clear
INTRODUCTION
cell type renal cell carcinomas (RCCs) distin-
The tissue contrast and spectroscopic proper- guish themselves from other lesions (such as
ties of magnetic resonance imaging (MRI) rec- adrenal metastases and renal angiomyolipomas—
ommend its use as a problem solver for renal AMLs) by the presence of intralesional micro-
and adrenal imaging. The unsurpassed ability to scopic fat. In adrenal imaging, supplemental
discriminate cystic from solid lesions and higher three-dimensional (3-D) in- and out-of-phase se-
sensitivity to solid, neoplastic elements explains quences with thinner slices (and potentially
the superiority of MRI compared with other smaller field of view [FOV] and voxel size)
imaging modalities in renal imaging. Extreme better assess small adrenal lesions—often in­
sensitivity to the microscopic lipid—present adequately evaluated with standard two-
in the form of cholesterol compounds in dimensional (2-D) sequences (see Fig. 4-1).
adenomas—explains the utility in adrenal Rigorous dynamic contrast-enhanced imaging
imaging. Typical indications for MRI in renal and is less vital in renal and adrenal imaging, com-
adrenal imaging include indeterminate adrenal pared with liver and pancreatic imaging, because
lesion evaluation, endocrinologic workup for the issue of enhancement generally reduces to
potential adrenal adenoma or pheochromocy- a binary question of presence versus absence of
toma, indeterminate renal lesion, and posttreat- enhancement. The temporal nature of lesion
ment follow-up of renal neoplasms (Table 4-1). enhancement matters less (although adrenal
lesion characterization supplementally depends
on early versus delayed enhancement). None-
theless, the information gleaned by dynamic
TECHNIQUE
imaging, including solid lesion enhancement
Technical considerations in renal and adrenal characteristics (used to differentiate between
MRI are essentially the same as for other abdomi- different malignant lesions), adequacy of renal
nal indications (see Chapter 2, “Technique”), parenchymal enhancement/perfusion, and arte-
with a few occasional modifications. rial anatomic depiction, validates the effort. The
Hardware considerations—for example, high- choice of imaging planes depends on lesion
field imaging, dedicated torso coil, power location relative to organ of origin. For example,
injection—deserve equal priority in renal and in the case of a renal lesion arising from the
adrenal imaging. Although a standard liver pro- posterior aspect of the kidney, the axial plane
tocol may suffice for most renal and adrenal in- displays the lesion-kidney interface better than
dications, certain considerations recommend the coronal plane, which shows it en face tan-
protocol deviations and/or modifications (Fig. gentially. Conversely, in the case of an exo-
4-1). Steady-state localizer images are useful for phytic lesion arising from the upper or lower
the same reason in renal and adrenal imaging— pole of the kidney, the coronal plane better
for example, identification of cystic lesions, vas- depicts the lesion-kidney interface.
cular patency. Heavily T2-weighted images (or Subtracted images (precontrast from post­
single-shot images), usually obtained in coronal contrast images) serve a central role in differ­
and axial planes, provide an anatomic roadmap entiating benign from malignant in renal
and serve to discriminate cystic from solid lesions. Certain common features—such as
lesions and to detect potential solid components modest enhancement and precontrast T1
of cystic lesions. The ability to detect and quan- hyperintensity—challenge the human eye to
titate microscopic fat through in- and out-of- detect or exclude enhancement. Subtractions
phase images is indispensable in renal and eliminate precontrast hyperintensity and
199
200  •  Fundamentals of Body MRI

Sequence Planes TR/TE Slice thickness Details

Steady-state 3-plane min/min 6×0

Heavily T2-weighted Coronal, axial NA/180 5×0

In-/out-of-phase (2-D) Axial min/2.2, 4.4 7×1 Obtained as 1 sequence

In-/out-of-phase* Axial min/2.2, 4.4 3 (interpolated to 1.5) No fat saturation

Dynamic 3-D Axial or coronal min/min 4 (interpolated to 2) Fat saturation

Moderately T2-weighted Axial 3000/80 7 × 0.5

Delayed 3-D Axial or coronal min/min 4 (interpolated to 2) Fat saturation

2-D T2-weighted MRU Radial below NA/≈850 40 Same as MRCP sequence

each kidney before IV gadolinium

3-D T2 weighted MRU Coronal 1300/680 2 (interpolated to 1) Same as MRCP sequence

respiratory triggered
before IV gadolinium

3-D T1 weighted MRU Coronal min/min £4 (interpolated) Flip angle 15° and 40°

* Optional: use for characterization of small adrenal lesions (<1.5 cm)

MRU sequences are in italics
FIGURE 4-1.  Renal and adrenal MRI protocols. MRCP, magnetic resonance cholangiopancreatography; MRU, magnetic resonance
urography; NA, not applicable; TR, time to repetition; TE, time to excitation; 2-D, two-dimensional; 3-D, three-dimensional.

coronal plane as a modification of the dynamic

TABLE 4-1.  Common Indications for Renal and sequence (see Fig. 4-1). 2-D and 3-D T2-weighted
Adrenal Magnetic Resonance Imaging sequences are performed before contrast admini­
Adrenal stration; otherwise, excreted gadolinium in the
Indeterminate adrenal lesion (adenoma vs. other) collecting systems shortens the T2 of urine,
Endocrinologic workup (adrenal adenoma or pheochromocytoma)
precluding signal on heavily T2-weighted
Kidney images. The 2-D and 3-D MRU sequences are the
Indeterminate renal lesions magnetic resonance cholangiopancreatography
Follow-up likely benign renal lesions
Characterization of renal lesions in renal insufficiency (MRCP) sequences targeted to the collecting
Surveillance posttreatment RCC systems and ureters; instead of centering on the
common bile duct, the slices are oriented to the
Collecting System/Ureter
Surveillance posttreatment TCC renal collecting systems and ureters.
Collecting system and/or ureteral abnormality
RCC, renal cell carcinoma; TCC, transitional cell carcinoma.

INTERPRETATION
improve dynamic range to detect subtle Each MRI pulse sequence uniquely possesses
enhancement. specificity for certain tissues, and search pat-
Another protocol consideration includes terns must acknowledge this fact to be useful.
the decision whether to include urographic Steady-state images highlight fluid—whether
sequences—usually performed in the setting moving or static—against solid tissue. Use them
of transitional cell carcinoma or potential both as a vascular sequence and to assess cystic
collecting system or ureteral abnormality (see lesions. Heavily T2-weighted images are specific
Table 4-1). Lasix administration before imaging for only static fluid and eliminate many of the
augments the excretion of gadolinium and artifacts observed in steady-state imaging. These
collecting system distention. Magnetic reso- images permit more detailed evaluation of cystic
nance urography (MRU) sequences include lesions and mural nodules, septations, and other
T1-weighted and T2-weighted varieties. T1- solid components.
weighted sequences are obtained after contrast Moderately T2-weighted images also depict
during the excretory phase, usually in the cystic lesions and underlying complexity. The
 MRI of the Kidneys and Adrenal Glands   •  201

A B
FIGURE 4-2.  T1-weighted image of the kidneys shows corticomedullary differentiation. The axial in-phase image (A) in a patient with
normal renal function shows greater contrast between the hypointense renal medulla (thin arrow in A) and relatively hyperintense renal
cortex (thick arrow in A) compared with the axial in-phase image (B) in a patient with severely depressed renal function (glomerular
filtration rate 14).

improved tissue contrast supplemented by elim- the presence of gadolinium, which is confined
ination of signal from fat confers a high sensitiv- to the extracellular space (intravascular space
ity to lymphadenopathy, which appears bright and interstitial space). This means that blood
against the dark background of retroperitoneal vessels (assuming patency) and solid tissues
fat. Macrosopic fat in AMLs and myelolipomas (except for fat) will enhance. Because of the
loses signal, generally clinching the diagnosis. extreme sensitivity to enhancement, MRI is the
In- and out-of-phase images serve many pur- ultimate arbiter of indeterminate renal lesions to
poses. Inspect the parenchyma for corticome- differentiate solid masses (treated surgically)
dullary differentiation (relatively hypointense from nonneoplastic cystic lesions (treated
medulla), which connotes functional tissue (Fig. expectantly).
4-2). T1-weighting confers sensitivity to protein Difficulty in assessing enhancement arises in
and hemorrhage, which appear bright on these the case of the T1 hyperintense lesion (such as
images. Of course, macroscopic fat appears hemorrhagic cysts). Precontrast hyperintensity
equally bright on in- and out-of-phase images, plus even more signal (from enhancement) is
and microscopic fat (occasionally present in difficult for the human eye to detect. Subtracted
clear cell type RCC) appears dark on out-of- images negate precontrast hyperintensity,
phase images relative to in-phase images. Mac- showing only changes in signal intensity
roscopic fat (present in renal AMLs and adrenal between the precontrast and the postcontrast
myelolipomas), hyperintense on in- and out-of- image by literally subtracting the signal from
phase images, loses signal on the T1-weighted each pixel on the precontrast image from each
fat suppressed sequence—the paramagnetic pixel on the postcontrast image. All that
sequence (the precontrast phase of the dynamic remains is a map of contrast enhancement
sequence). (assuming no intervening patient motion
In addition to establishing the presence of causing misregistration).
macroscopic fat through signal suppression, If subtractions are not available, comparing
the paramagnetic sequence (precontrast T1- the region of interest (ROI) with a reference
weighted fat-suppressed) showcases hemor- standard establishes or excludes enhancement.
rhage and other paramagnetic substances, such As a rule of thumb, normal muscle enhances
as protein, and other molecules, such as melanin. 15%, which serves as a lower limit threshold for
This sequence is optimized to receive signal renal mass enhancement; most renal tumors
solely from (nonfat) substances with very short enhance avidly, but relatively hypovascular
T1 values—usually hemorrhage in the realm of papillary renal cell carcinomas tend to enhance
renal and adrenal imaging. approximately 15%. Compare the ROI signal
The postcontrast dynamic phases share the intensity values of the pre- and postcontrast
same attributes as the precontrast phase, supple- renal lesion with ROI values of normal muscle
mented by the addition of intravenous gadolin- (e.g., psoas, longissimus). An equal or greater
ium. Signal augmentation (i.e., enhancement) increase compared with muscle indicates
compared with the precontrast images indicates enhancement and solid tissue (Fig. 4-3).
202  •  Fundamentals of Body MRI

77.61 mean, 9.7 sd 191.53 mean, 46.4 sd

13.567 cm2 15.575 cm2

88.57 mean, 7.0 sd 94.64 mean, 6.9 sd

4.4302 cm2 3.3918 cm2
A B

33.36 mean, 6.5 sd

1.8793 cm2

40.79 mean, 3.3 sd

E F 2.5580 cm2

47.27 mean, 5.5 sd 54.79 mean, 7.7 sd

1.3051 cm2 1.8793 cm2

45.20 mean, 3.4 sd 51.18 mean, 4.6 sd

G 2.5580 cm2 H 3.3410 cm2
 MRI of the Kidneys and Adrenal Glands   •  203

FIGURE 4-3.  Solid renal enhancement demonstrated using region of interest (ROI) measurements. ROIs placed over a large right renal
lesion and left erector spinae muscles on the precontrast (A) and postcontrast (B) images reveal a much greater lesional increase in signal
intensity (from 77.61 to 191.53 = 113.92) compared with muscle (from 88.57 to 94.64 = 6.07). C, The corresponding subtracted image
confirms avid enhancement. In a different patient with a small T2 hypointense right renal lesion (arrow in D), enhancement is question-
able (arrow in E). Serial ROIs placed over the lesion and erector spinae muscles document relatively greater lesional signal change (from
33.36 to 47.27 to 54.79 = 21.43) compared with muscle (from 40.79 to 45.20 to 51.18 = 10.39), signaling mild enhancement—typical
of papillary-type RCC (subsequently confirmed at nephrectomy).

T12 T12

L1 L1

L2 L2

L3 L3

L4 L4

L5 L5
A B

C
FIGURE 4-4.  Normal kidneys and adrenal glands. Coronal T2-weighted images positioned through the posterior aspects (A) and midpor-
tions (B) of the kidneys show typical craniocaudal positioning and medial tilting. C, The axial fat-suppressed T1-weighted image
illustrates normal corticomedullary differentiation and orientation of the renal hila (arrows).

KIDNEYS fluid content in the medulla relatively to the

cortex (see Fig. 4-2).2 The kidneys enhance
Normal Features
avidly with earlier enhancement of the renal
Normal kidneys measure approximately 10 to cortex during the arterial phase, reiterating the
14 cm in length.1 Renal axes tilt medially at the corticomedullary pattern—renal cortical phase
upper poles with anteromedial rotation (accord- for our purposes. Within 60 to 90 seconds,
ing to the position of the hilum) and the kidneys contrast perfuses the medullary renal paren-
extend from the T12–L1 to the L3 levels (Fig. chyma, resulting in global renal parenchymal
4-4). The kidneys are cloaked in a sheath of enhancement—the parenchymal phase.
retroperitoneal fat with interdigitating fibrous The renal collecting system is generally bicon-
septa capped by the adrenal glands. A barely cave or flat and excreted urine demonstrates
perceptible linear hypointensity encircles the water signal. Occasional flow voids on T2-
retroperitoneal fat—Gerota’s fascia—an impor- weighted images sometimes simulate renal
tant landmark in staging RCC (Fig. 4-5). calculi. The collecting system urothelial lining
Normal kidneys exhibit corticomedullary dif- appears as inconspicuous linear hypointensity
ferentiation characterized by relatively greater exhibiting no discernible enhancement.
204  •  Fundamentals of Body MRI

Primary tumor (T) Regional lymph nodes Distant metastasis (M)

T0: no evidence of first-degree N0: no regional lymph node M0: no distant metastasis
tumor metastasis

T1: tumor ≤ 7 cm limited to kidney N1: metastasis in a single M1: distant metastasis
regional lymph node

T2: tumor > 7 cm limited to kidney N2: metastasis in > 1 regional

lymph node

T3: tumor extends into major

veins, invades adrenal gland or
perinephric tissues not beyond
Gerota’s fascia

T3a: tumor invades adrenal gland

or perinephric tissues not beyond
Gerota’s fascia
T3b: tumor extends into major
renal veins or IVC below
diaphragm

T3c: tumor extends into major

renal veins/IVC above diaphragm

T4: tumor invading beyond

Gerota’s fascia

Robson staging system American joint committee on cancer system

Stage I (T1 or 2, N0, M0): tumor confined to kidney Stage I: T1, N0, M0
Stage II (T3a, N0, M0): tumor spread to perinephric Stage II: T2, N0, M0
fat confined with renal fascia; possible ipsilateral Stage III: T1-2, N1, M0 or T3a-c, N0-1, M0
adrenal involvement Stage IV: T4 or any T, N2, M0 or any T, any N, M1
Stage IIIA (T3b-3c, N0, M0): tumor spread to renal vein,
IVC or both
Stage IIIB (T1-3a, N1-3, M0): tumor spread to local
lymph nodes
Stage IIIC (T3b-3c, N1-3, M0): tumor spread to local
vessels and lymph nodes
Stage IVA (T4, any N, M0): tumor spread to adjacent
organs (except ipsilateral adrenal gland)
Stage IVB (any T & N, M1): distant metastases
FIGURE 4-5.  RCC staging. IVC, inferior vena cava.

complex process following a series of steps nec-

TABLE 4-2.  Common Renal Developmental essary for the execution of subsequent develop-
Anomalies and Pseudolesions mental steps. Incomplete or absent interfacing
Inductional Fusion of the ureteric bud (primordial collecting system
Renal agenesis Horseshoe kidney and ureter) and metanephric blastema (primor-
Renal hypoplasia Crossed fused renal ectopia
Supernumerary kidney Pancake kidney dial renal parenchyma) results in renal agenesis
and/or a number of other potential parenchymal
Positional Structural and ureteral/collecting system anomalies.
Renal ectopia Fetal lobulation
Malrotation Prominent column of Bertin Positional anomalies include ectopia and mal-
Hilar lip rotation. Embryonic growth results in a relative
ascent of the kidneys during the fourth through
eighth week of gestation, ultimately positioned
between the first and the third lumbar verte-
Anomalies and Pseudolesions
brae. Underascent occurs far more commonly
A few common developmental anomalies and than overascent, and the ptotic kidney ranges in
pseudolesions (Table 4-2) are worth mentioning position from the true pelvis to the iliac fossa
before discussing pathologic renal lesions. Renal and anywhere below the expected location cen-
and collecting system embryogenesis is a tered at the L2 level (Fig. 4-6). Contralateral
 MRI of the Kidneys and Adrenal Glands   •  205

A B

C D
FIGURE 4-6.  Ptotic kidney. A, The axial T2-weighted image through the upper abdomen shows a normal right kidney with no visible
left kidney. B, The steady-state coronal localizing image with a large field of view (FOV) shows a reniform structure in the pelvis (arrow).
The postcontrast coronal image (C) corroborates the presence of a pelvic kidney (arrow) and the coronal maximal intensity projection
image (D) illustrates the relative positioning and orientation of the left (thin arrow in D) and right (thick arrow in D) kidneys.

renal anomalies, such as renal agenesis or ptosis, Renal fusion anomalies generally incur posi-
frequently coexist. tional and rotational derangements. Medial renal
Concomitant medial rotation along the longi- fusion results in a solitary discoid lump of renal
tudinal renal axis during ascent orients the ure- tissue in the pelvis, referred to as “pancake
teropelvic junction (UPJ) medially. Nonrotation kidney.” Crossed fused renal ectopia represents
or incomplete rotation leaves the UPJ facing the sequela of embryologic renal fusion with the
anteriorly, and renal calyces in the medial relatively normally positioned kidney dragging
segment of the kidney lie medial to the renal its fused counterpart across the midline, result-
pelvis (Fig. 4-7). Overrotation results in a poste- ing in a single ipsilateral S-shaped renal mass
riorly facing UPJ. with two separate moieties and normal bilateral
206  •  Fundamentals of Body MRI

47°
34°

A B
FIGURE 4-7.  Renal malrotation. Compare the orientation of the right renal hila on the steady-state images through the right renal hilum
(A) and the left renal hilum (B)—note the underrotation of the left kidney reflected by the incomplete medial rotation. Normal renal
rotation is approximately 30°.

A B

C D
FIGURE 4-8.  Crossed fused renal ectopia. A, Axial T2-weighted image through the upper abdomen reveals absence of the right kidney.
B, More caudally positioned axial T2-weighted image shows orientation of the left lower renal moiety (thin arrow) following the expected
rotation of the right kidney with the hilum facing laterally (thick arrow). C and D, Coronal postcontrast images show the fused con-
glomerate renal mass with separate hilar structures (arrow) and disparate orientation.

ureterovesical junctional positioning (Fig. 4-8). Coexistent anomalies, such as UPJ obstruction
Horseshoe kidney is the most common renal and duplication anomalies, conspire with the
anomaly reflecting midline fusion of the meta- geometric and rotational distortion and urinary
nephric blastema. Ascent is arrested at the level stasis to lead to complications, including stone
of the inferior mesenteric artery (Fig. 4-9). formation and infection.
 MRI of the Kidneys and Adrenal Glands   •  207

A B
FIGURE 4-9.  Horseshoe kidney. A, The axial T2-weighted image shows midline fusion of the lower renal poles (arrow) ventrally across
the midline, anterior to the aorta. B, The corresponding arterial phase postcontrast image depicts characteristic corticomedullary enhance-
ment of the fused renal mass.

Structural anomalies incur no risk of compli- components implies malignancy, which usually
cations and deserve mention only to prevent mandates surgical resection (Fig. 4-11).
misdiagnosis. Fetal lobulation persists in 5% of Most renal cysts are simple in appearance
adults with a smooth undulating outer renal with fluid signal characteristics (T2 hyperinten-
contour conforming to the position of the renal sity and T1 hypointensity), no enhancement,
pyramids. Smoothly marginated indentations septation, wall-thickening, or nodularity. Signal
conform to the edges of renal pyramids with alterations alone pose no risk of malignancy,
normal appearance and thickness of underlying although they often challenge interpretation.
parenchyma (≥14 mm), excluding the possi­ The most common signal alteration is due
bility of an underlying mass or scarring. The to hemorrhage, resulting in T1 hyperintensity
column of Bertin potentially simulates a renal and T2 hypointensity. Proteinaceous contents
mass, but represents invagination of normal induce a similar appearance.
renal cortical tissue into the renal sinus, usually Complex cystic lesions pose greater diagnos-
occurring at the upper polar/interpolar junction tic difficulty. Superimposed infection and
and averaging 3.5 cm in size (Fig. 4-10). The trauma induce reactive wall thickening, which
hilar lip represents fusion of medial renal lobes, overlaps with the appearance of cystic neo-
usually occurring in the upper pole and poten- plasms (especially RCC, clear cell type). These
tially protruding and distorting the renal sinus. neoplasms often harbor more complex features
Signal characteristics and enhancement identi- with mural nodularity and solid components. In
cal to adjacent renal parenchyma occurring in an effort to stratify renal lesions based on likeli-
the expected location confirm the presence of hood of malignancy, Bosniak5,6 developed a
normal functional renal tissue in cases of renal predictive classification system (for computed
anomalies. tomography [CT]) to guide management (Table
4-3). Although not specifically adapted for MRI,
this scheme illustrates the range of imaging
Focal Lesions
complexity of renal lesions and offers manage-
Focal renal lesions are encountered everyday in ment guidance.7 Although calcification escapes
clinical practice on cross-sectional imaging detection, the classification scheme applies to
studies—the vast majority of which are inciden- magnetic resonance (MR) findings, replacing
tal, and many indeterminate. Thirteen percent intensity changes for density changes.8
to 27% of abdominal imaging studies inciden- Solid lesions include benign and malignant
tally detect a renal lesion.3 Whereas many of neoplasms. Macroscopic fat is the only finding
these lesions are incompletely characterized, that connotes a benign etiology—AML. Although
the overwhelming majority of these lesions are renal infection and infarction and benign lesions
simple or minimally complex cysts with no ma- (such as oncocytoma) account for enhancing
lignant potential. Establishing true cystic lesions, for the most part, solid tissue (enhance-
etiology eliminates the need for further work­ ment) equals malignancy. Unless clinical find-
up and/or follow-up.4 The presence of solid ings raise the suspicion of inflammatory or
 A B

C D
FIGURE 4-10.  Column of Bertin. A, The axial T2-weighted image illustrates protrusion of solid tissue isointense to surrounding normal
renal parenchyma (arrow) and indenting the renal pelvis. B, The finding (arrow) is more pronounced on the axial steady-state image.
C, The sagittal steady-state image portrays this finding as an isointensity (thin arrow) dividing the upper polar calyces (thick arrow)
from the lower polar calyces (open arrow). D, The corresponding film from a retrograde pyelogram shows duplication of the renal col-
lecting system, which is separated by the column of Bertin (arrow).

Hemorrhage
No follow-up
or protein

Signal
changes Minimal Mild wall Sequela of previous
only septation thickening Infection or hemorrhage

Stability
Imaging
Uncertainty
follow-up
Progression

Simple
cyst
Multilocularity Focal Gross wall
nodularity thickening

Solid
Tumor Surgery
enhancement

FIGURE 4-11.  Focal renal lesion algorithm.

 MRI of the Kidneys and Adrenal Glands   •  209

Developmental Acquired
Simple cyst Hemorrhagic cyst
Calyceal diverticulum Infected cyst
Multicystic dysplastic kidney Hydatid cyst
Medullary sponge kidney Renal abscess
Hematoma
Acquired cystic kidney disease
Lithium
Hydronephrosis*

Inherited Neoplastic
Autosomal recessive polycystic kidney disease Renal cell carcinoma
Autosomal dominant polycystic kidney disease Multicystic locular nephroma
von Hippel–Lindau disease
Tuberous sclerosis
Medullary cystic kidney disease

FIGURE 4-12.  Differential diagnosis of renal cystic lesions.

TABLE 4-3.  Bosniak Classification Scheme for Cystic Renal Lesions

Bosniak
Category Imaging Features Management

I Thin wall; no septa, calcifications, or solid components, water features; no enhancement No follow-up
II Few thin septa with less than or minimal enhancement; fine calcification or focal thick calcification; No follow-up
homogeneous high-density sharply marginated lesion (<3 cm) with no enhancement
IIF Multiple thin septa with less than or minimal enhancement; thick or nodular calcification; no enhancing soft Observe
tissue components; high-density lesions (>3 cm) with no enhancement
III Thickened irregular or smooth walls or septa with enhancement Surgery
IV Same features as III also with enhancing soft tissue components Surgery

depict hemorrhagic cysts with variable hyper­

TABLE 4-4.  Management Scheme for Solid intensity, and postcontrast images exclude
Renal Lesions enhancement. Ninety percent of all renal cystic
Presumptive lesions are simple cysts (Fig. 4-12). Hemorrhage,
Size Diagnosis Management debris, and infection complicate renal cysts.
Large (>3 cm) RCC Surgery With an increasing number of cystic lesions (and
Small (1–3 cm) RCC Surgery renal enlargement), consider the possibility of
Minimal (<1 cm) RCC, AML, oncocytoma Observe up to 1 cm
polycystic disease. Cystic lesions prevail in other
AML, angiomyolipoma; RCC, renal cell carcinoma. inherited diseases, such as von Hippel–Lindau
(VHL) disease and tuberous sclerosis (TS) (with
assorted solid lesions, to be discussed later).
vascular etiology, the presumptive diagnosis is Developmental etiologies include multicystic
malignancy until proved otherwise. Because dysplastic kidney and calyceal diverticulum.
biopsy results are notoriously confusing, solid Acquired conditions, such as renal cystic disease
renal lesion management involves surgical of dialysis and lithium therapy, present with
pathologic diagnosis and treatment. Because renal cystic lesions. RCC (clear cell types) domi-
very small lesions (<1 cm) challenge the resolu- nates the cystic neoplastic category; consider
tion of imaging methods, limiting diagnostic multilocular cystic nephroma (MLCN) in the
confidence, imaging surveillance preempts appropriate demographic categories (young
potentially unnecessary surgery (Table 4-4). males and middle-aged females) with herniation
into the renal pelvis.
Cystic Lesions
Using the combination of heavily T2-weighted Simple Renal Cyst
images to detect fluid hyperintensity with post- The simple renal cyst is ubiquitous, with a pre­
contrast images to exclude enhancement con- valence of up to two thirds of the population,
firms cystic etiology. T1-weighted sequences and increasingly prevalent with age.9 Renal cysts
210  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 4-13.  Simple renal cyst. A large, exophytic simple cyst (arrow) arising from the left kidney exhibits typical features—simple fluid
T2-hyperintensity (A) and lack of enhancement (B)—based on the heavily T2-weighted (A) and the subtracted postcontrast (B) images.
A comparison of the moderately T2-weighted fat-saturated (C) with the heavily T2-weighted (D) images in a different patient with a
simple left renal cortical cyst (arrow) illustrates the effects of TE on free water (cyst) versus bound water (solid organs); free water
maintains signal with increasing TE whereas bound water loses signal. E, The postcontrast image confirms absent enhancement (arrow).

detach from the parent renal tubule and become wall is uniformly smooth with no perceptible
self-enclosed; continued fluid secretion distends enhancement on postcontrast images (Fig.
the cavity, resulting in an isolated cystic struc- 4-13). Size varies from millimeters to over 10 cm.
ture. Ongoing fluid secretion accounts for con- Cysts are stratified into different categories
tinued growth of simple renal cysts (≤5%/yr), based on location: exophytic, parenchymal, and
despite the lack of neoplastic or autonomously parapelvic (Figs. 4-14 and 4-15). Because most
regenerating cells.10 Therefore, careful attention renal cysts arise from the cortex (although some
to imaging features is paramount in excluding develop from the medulla), most renal cysts are
neoplasm. exophytic and/or intraparenchymal (see Figs.
The contents of the simple renal cyst—free 4-13 and 4-14).
water protons—account for its appearance: Renal cyst complexity assumes many forms,
extreme T2 hyperintensity and T1 hypointensity which fall into two major categories—
with no enhancement. If even visible, the cyst morphologic and signal-related. Morphologic
 MRI of the Kidneys and Adrenal Glands   •  211

derangements include deviation from simple layering hematocrit (Fig. 4-17)—a relatively
sphericity and/or septation; signal derange- infrequent manifestation of a hemorrhagic cyst.
ments deviate from simple fluid characteristics Signal alterations from hemorrhage present the
with evidence of hemorrhage or debris (Fig. greatest challenge to interpretation; precontrast
4-16). Occasional fluid-fluid levels depict hyperintensity limits the ability to detect aug-
mented T1 signal from enhancement (see Fig.
4-16). Fibrinous septations from previous infec-
tion generally measure less than 2 mm in thick-
Exophytic ness with no other evidence of complexity
to suggest neoplasm (Fig. 4-18).11 As long as
no enhancement beyond minimal linear septal
or wall enhancement is present, simple cystic
etiology is confirmed.
Parapelvic
Careful scrutiny of these features is critical,
Partially exophytic because a minority of clear cell RCC (~5%) is
Partially intraparenchymal mostly cystic. In Bosniak’s terms, the discrimina-
tion of type II and IIF lesions from understated
type III lesions bears close inspection. Usually,
a solid enhancing component differentiates
Intraparenchymal RCC from a nonneoplastic cyst—especially with
FIGURE 4-14.  Renal cyst classification by location. the benefit of subtractions. When subtractions

A B

FIGURE 4-15.  Parapelvic cysts. The coronal (A) and

axial (B) heavily T2-weighted images show bilateral
renal pelvic fluid signal intensity (arrows) potentially
representing hydronephrosis. C, The coronal post-
contrast image obtained during the pyelographic
phase excludes hydronephrosis by showing the
normal-caliber collecting system (thin arrows)
excreting contrast surrounded by the cystic
C
hyperintensities—parapelvic cysts (thick arrows).
212  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 4-16.  Hemorrhagic cyst with subtractions. Precontrast fat-suppressed image (A) shows an exophytic hyperintensity (arrow in A)
protruding from the upper pole of the left kidney. No apparent change in signal intensity is evident after intravenous contrast (arrow
in B), but subtle enhancement seems difficult to exclude. Subtracting the precontrast (A) from the postcontrast (B) image yields an
enhancement map image—subtraction (C)—that depicts a signal void corresponding to the lesion (arrow) in question, excluding
enhancement and confirming the diagnosis of a hemorrhagic cyst. D, Another lesion (arrow) in the same patient exhibits modest T1
hyperintensity, which is more equivocal. The postcontrast image (E) suggests absent enhancement (arrow), which is confirmed on the
subtracted image (F).

are not available and signal alterations limit multilo­cularity and when herniating into the
assessment of enhancement, rely on ROI mea- renal pelvis, consider MLCN in the appropriate
surements compared with a reference standard demographic settings (young males and middle-
(see Figs. 4-3 and 4-16). Other etiologies are aged females). Infectious cysts—renal abscess
not realistic considerations, except under and echinococcal cyst—require a suggestive
specific circumstances. For instance, with history.
 MRI of the Kidneys and Adrenal Glands   •  213

A B

FIGURE 4-17.  Hemorrhagic cyst with fluid-fluid level.

A, The T1-weighted out-of-phase image shows an exo-
phytic lesion with a fluid-fluid level (arrow) arising from
the left kidney. B, Fat suppression improves the dynamic
range, exaggerating the relative T1 hyperintensity, as seen
on the precontrast T1-weighted fat-suppressed image. 
C, On the T2-weighted fat suppressed image, note the
extreme T2 shortening of the layering blood products
C
(arrow) in the hemorrhagic cyst.

A B

FIGURE 4-18.  Simple septated cyst. A, An anterior partially

exophytic cyst in the anterior interpolar left kidney (thin
arrow) exhibits simple features, except for a thin, linear
septum (thick arrow) on the heavily T2-weighted image.
B, No septal enhancement is apparent on the postcontrast
image, confirming benign etiology (Bosniak II). C, The
coronal thick-slab magnetic resonance cholangiopancrea-
tography (MRCP) image provides an overview of the sep-
tated renal cyst (thin arrow) and a contralateral septated
C
cyst (thick arrow).
214  •  Fundamentals of Body MRI

Li MSK
MCKD
PCKD Simple cyst

Hemorrhagic cyst
Angiomyolipoma

Renal cell carcinoma

TS VHL

ADPKD

ARPKD

FIGURE 4-19.  Schematic representation of the renal polycystic diseases showing the distribution of cystic and solid lesions and relative
kidney size (with Li and MCKD representing normal-sized kidneys). ADPKD, autosomal dominant polycystic kidney disease; ARPKD,
autosomal recessive polycystic kidney disease; Li, lithium; MCKD, multicystic kidney disease; MSK, medullary sponge kidney; PCKD,
polycystic kidney disease; TS, tuberous sclerosis; VHL, von Hippel–Lindau.

Polycystic Diseases TABLE 4-5.  Diagnostic Criteria for Autosomal

Renal cystic bilaterality and multiplicity charac- Dominant Polycystic Kidney Disease
terize polycystic diseases (Fig. 4-19).11 Polycys-
tic kidney diseases fall into three categories: Age (yr) Criteria
inherited, developmental, and acquired. Inher- 15–39 ≥3 unilateral or bilateral cysts
ited diseases include autosomal recessive poly- 40–59 ≥2 cysts in each kidney
≥60 >4 cysts in each kidney or >6 cysts in women/>9 cysts
cystic kidney disease (ARPKD), autosomal in men (specifically based on MRI)
dominant polycystic kidney disease (ADPKD),
MRI, magnetic resonance imaging.
medullary cystic kidney disease (MCKD), and
the phakomatoses—TS and VHL. ARPKD and
ADPKD induce renal failure, but incur no risk Phakomatoses—such as TS and VHL—are dis-
of malignancy (Fig. 4-20). Solid renal lesions eases characterized by dysplasia and/or neopla-
complicate TS and VHL in addition to renal sia of organs arising from embryonic ectoderm
cysts. Clinical and demographic features sepa- (and often mesoderm and endoderm). TS and
rate ARPKD and ADPKD, whereas ARPKD pres- VHL feature a unique profile of extrarenal lesions
ents early in childhood with renal and/or liver (Fig. 4-21 and Table 4-6). The presence of solid
failure. ADPKD develops gradually over time, and/or noncystic lesions eliminates the possibil-
resulting in end-stage renal disease in middle ity of ADPKD from consideration. Macroscopic
age. Without the benefit of the genetic profile, fat arising from an AML suggests TS, and solid,
the early phase of ADPKD is indistinguishable enhancing lesion(s) favors VHL. MCKD is an
from incidental, noninherited simple renal inherited tubulointerstitial nephropathy charac-
cysts. Because renal cysts occur sporadically, terized by progressive renal failure and small
age-based numeric criteria have been generated cysts—usually less than 3 cm—predominating
to distinguish incidental sporadic cysts from at the corticomedullary junction in relatively
ADPKD (Table 4-5).12 In the adult general popu- normal-sized kidneys.14
lation (45- to 59-year-old age group), an average Although recognized as a developmental dis-
of two cysts are detectable at MRI (1.2 in order, the etiology of medullary sponge kidney
women and 2.9 in men).13 (MSK) is not fully understood. The burden of
 MRI of the Kidneys and Adrenal Glands   •  215

A B

C D
FIGURE 4-20.  ADPKD. A, The axial T2-weighted image reveals innumerable, mostly simple hyperintense renal cysts (arrows) replacing
renal parenchyma bilaterally in a patient with ADPKD in whom the liver is also involved. B, The coronal steady-state image shows the
polycystic liver and kidneys with upward displacement of the left kidney by a large pelvic lymphocele (arrow) complicating left iliac
fossa renal transplantation. C, The coronal T2-weighted image in a different patient shows multiple renal cysts bilaterally without liver
involvement. D, Hyperintensity complicating scattered cysts (arrows) on the in-phase image indicates hemorrhage.

evidence supports a disruption of the ureteral RCC constitutes a greater share of RCC in ACKD
bud–metanephric blastema interface. Cysts pre- compared with the general population (50%
dominate in the medullary pyramids and usually compared with 5%–7%), and is discussed further
measure less than 1 cm in size. The kidneys are in the upcoming section on “Solid Lesions.”
generally normal to mildly enlarged. Lithium nephropathy stratifies into three
Acquired renal cystic diseases include renal temporal categories: acute nephropathy, neph-
cystic disease of chronic renal insufficiency (or rogenic diabetes insipidus, and chronic nephro­
acquired cystic kidney disease [ACKD]) and pathy. Chronic lithium nephropathy is the cystic
lithium-induced renal cystic disease (see Fig. variety. Punctate cysts (a few millimeters)
4-19). Dilated renal tubules ultimately form cysts inhabit the cortex and medulla (Fig. 4-22; see
in failing kidneys, leading to ACKD. Hemorrhage also Fig. 4-19).
complicates cysts in 50% of patients with
ACKD,15 resulting in a combination of simple Unilateral renal cystic lesions include a variety
cystic and hemorrhagic cysts (see Fig. 4-19). The of additional rare developmental, infectious, and
appearance potentially simulates ADPKD and neoplastic lesions; hydronephrosis is added to
incidental sporadic cysts, but the history of the category of renal cystic lesions because of
underlying renal failure and visible renal atrophy the potential to simulate parapelvic cysts.
generally exclude these etiologies. Patients with Collecting system lesions—hydronephrosis and
ACKD incur an annual risk of 0.2% of developing calyceal diverticulum—are usually more easily
RCC—the feared complication—compared with differentiated from parapelvic cysts because of
0.005% in the general population. Papillary type (1) the ability to selectively image free water
216  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 4-21.  VHL and TS. A, The coronal postcontrast image in a patient with VHL disease shows multiple bilateral enhancing (thin
arrows) and nonenhancing cystic lesions (thick arrows). Axial T2-weighted (B) and enhanced (C) images in a different patient with VHL
reveal complex cystic lesions (thin arrows) in the right kidney (post left nephrectomy), including a cystic RCC (asterisk), and multiple
complex cystic pancreatic lesions (thick arrows). Two heterogeneous noncystic left renal lesions (arrows) on the coronal T2-weighted
image (D) in a different patient with TS fail to yield signal on the fat-suppressed image (E), and the corresponding fat-suppressed axial
image (F) shows a similar lesion in the right kidney (arrows in E and F) with eccentric vascular enhancement (thick arrows in F)—all
consistent with AMLs.
 MRI of the Kidneys and Adrenal Glands   •  217

TABLE 4-6.  Polycystic Kidney Diseases

Disease Renal Lesions Extrarenal Lesions

Polycystic Kidney Disease

ADPKD Cysts Liver, pancreatic, splenic, epididymal, seminal vesicular uterine, ovarian and thyroid
cysts; circle of Willis berry aneurysms; aortic dissection; cardiac valvular disease
ARPKD Cysts Portal hepatic fibrosis

Hereditary Malformation Syndromes

TS Cysts, AMLs Subependymal and cortical tubers, giant cell astrocytoma
RCC very rare
VHL Cysts, RCC, adenoma Cerebellar hemangioblastoma; lung cyst; cardiac rhabdomyoma; pancreatic islet cell
tumor, cyst, adenoma, microcystic adenoma; liver cyst and adenoma

Acquired Renal Cystic Disease

Dialysis Cysts, RCC N/A
Chronic renal insufficiency (without dialysis)
ADPKD, autosomal dominant polycystic disease; ARPKD, autosomal recessive polycystic disease; AML, angiomyolipoma; N/A, not applicable;
RCC, renal cell carcinoma; TS, tuberous sclerosis; VHL, von Hippel–Lindau.

A B

C
FIGURE 4-22.  Lithium cystic nephropathy. A, The coronal heavily T2-weighted image shows innumerable punctate simple cysts in the
cortex and medulla, most of which measure no more than a few millimeters. B, The postcontrast image confirms cystic etiology through
absent enhancement (arrows). C, The MRCP image portrays the multiplicity of punctate simple cysts in the left kidney (arrows) to
better advantage.
218  •  Fundamentals of Body MRI

confirms collecting system etiology, although

TABLE 4-7.  Etiologies of Hydronephrosis
increased pressure associated with high-grade
Ureter Functional obstruction delays urinary excretion and an
Intrinsic • Gram-negative infection
• Ureteropelvic junction stricture • Neurogenic bladder insufficient delay preempts enhancement. De­
• Ureterovesical junction layed collecting system enhancement excludes
obstruction Bladder the only differential diagnosis—parapelvic cysts
• Papillary necrosis Intrinsic
• Ureteral folds • Bladder carcinoma (see Fig. 4-15).
• Ureteral valves • Bladder calculi Although a full discussion of hydronephrotic
• Ureteral stricture (iatrogenic) • Bladder neck contracture obstructing lesions is beyond the scope of this
• Blood clot • Cystocele
• Benign fibroepithelial polyps • Primary bladder neck text, the most common obstructing lesion—
• Ureteral tumor hypertrophy renal calculus—deserves attention. The MR
• Fungus ball • Bladder diverticula appearance of renal calculi is basically the pho-
• Ureteral calculus
• Ureterocele Extrinsic tographic negative of the CT appearance. On all
• Endometriosis • Pelvic lipomatosis pulse sequences, renal calculi induce a signal
• Tuberculosis void owing to magnetic susceptibility (Fig.
• Retrocaval ureter Functional
• Neurogenic bladder 4-24). Hypointense renal calculi are most con-
Extrinsic • Vesicoureteral reflux spicuous when surrounded by hyperintense
• Retroperitoneal lymphoma urine on fluid-sensitive sequences. Although
• Retroperitoneal sarcoma Urethra
• Cervical cancer Intrinsic quoted as up to 97% sensitive for renal calculi,
• Prostate cancer • Urethral stricture anecdotally, MR sensitivity to renal stones is far
• Retroperitoneal fibrosis • Urethral valves lower.
• Aortic aneurysm • Urethral diverticula
• Inflammatory bowel disease • Urethral atresia
• Ovarian vein syndrome • Labial fusion Complex Cystic Lesions
• Retrocaval ureter For the purposes of our discussion, cystic com-
• Uterine prolapse Extrinsic
• Pregnancy • Benign prostatic hyperplasia plexity means wall thickening, peripheral nodu-
• Iatrogenic ureteral ligation and prostate cancer larity, septation, and/or enhancement—IIF or
• Ovarian cysts higher on the Bosniak scale. Using these fea-
• Diverticulitis
• Tubo-ovarian abscess tures to identify a category distinct from simple
• Retroperitoneal hemorrhage cystic (and solid) lesions defines our differential
• Lymphocele diagnostic scheme (Fig. 4-25). Complex cystic
lesions include infectious, posttraumatic, and
neoplastic etiologies.

(urine) and appreciate continuity with the col- Pyogenic Renal Abscess
lecting system and (2) exquisite sensitivity to One of the chief complex cystic infectious
enhancement by excreted gadolinium. lesions is the pyogenic renal abscess, which
accounts for approximately 2% of all renal
Hydronephrosis masses. Renal abscesses present 1 to 2 weeks
Hydronephrosis refers to the distention of the after the onset of infection and most commonly
collecting system with urine—obstructive (more complicate ascending urinary tract infection;
common) versus nonobstructive (Table 4-7). the minority arises hematogenously. Although
The imaging agenda is twofold: detecting hydro- the clinical features skew the differential diag-
nephrosis and identifying the etiology and point nosis toward an inflammatory etiology, circum-
of obstruction (if present). Heavily T2-weighted spection is warranted because of the shared
sequences depict hydronephrosis most clearly— imaging features with cystic neoplasms.
demonstrating collecting system and ureteral Internal contents are mildly relatively T1
continuity (Fig. 4-23). T2-weighted images help hyperintense and T2 hypointense compared
establish obstruction by demonstrating peri- with simple fluid with no enhancement (Fig.
nephric hyperintensity (shown to be present in 4-26).18 Rim enhancement with perilesional
cases of acute obstructive uropathy).16,17 Delayed enhancement and edema imply an inflammatory
postcontrast images with urine enhancement etiology. Obliteration of the adjacent renal sinus
by excreted gadolinium also depict collecting or perinephric fat, urothelial thickening and
system and ureteral anatomy and continuity. En- enhancement, thickening of Gerota’s fascia, and
hancement on delayed postcontrast images perinephric septa also advocate inflammation.19
 MRI of the Kidneys and Adrenal Glands   •  219

A B

E
FIGURE 4-23.  Hydronephrosis. A, The heavily T2-weighted magnetic resonance urography (MRU) image shows asymmetrical right-sided
collecting system (thin arrow) compared with the normal left-sided collecting system (thick arrow) in a patient with mild hydronephrosis.
The coronal heavily T2-weighted single-shot fast spin-echo (SSFSE) image (B) portrays an example of severe, longstanding left-sided
hydronephrosis (arrows), and the axial postcontrast image (C) shows the thinned, virtually obliterated, nonenhancing rim of nonfunc-
tioning enhancement (arrows). Mild to moderate right-sided hydronephrosis is apparent on the coronal T2-weighted image in a different
patient (D) due to the mass effect of the gravid uterus, as seen on a more caudally positioned T2-weighted image (arrows in E).
220  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-24.  Renal calculi. A, The coronal heavily T2-weighted image demonstrates a signal void in the collecting system of the upper
pole of the left kidney (arrow). Vague hypointensity (arrow in B) on the corresponding out-of-phase image (B), degraded by motion,
blooms on the in-phase image (arrow in C) due to susceptibility artifact, induced by the presence of calcium, as seen on the correspond-
ing computed tomography (CT) image (arrow in D).

Cystic Solid

Simple Complex Mass Infiltrative

Isolated Diffuse Infected cyst RCC Infarct

Echinococcal cyst TCC Pyelonephritis
Renal abscess Lymphoma
Hematoma Metastases
Simple cyst No solid ± solid MLCN
Hemorrhagic cyst lesions lesions RCC clear cell type
Calyceal diverticulum

ARPKD VHL
ADPKD TS
MCKD
MSK
Li nephropathy

FIGURE 4-25.  Kidney lesion diagnostic scheme. ADPKD, autosomal dominant polycystic kidney disease; ARPKD, autosomal recessive
polycystic kidney disease; Li, lithium; MCKD, multicystic kidney disease; MLCN, multilocular cystic nephroma; MSK, medullary sponge
kidney; RCC, renal cell carcinoma; TCC, transitional cell carcinoma; TS, tuberous sclerosis; VHL, von Hippel-Lindau.
 MRI of the Kidneys and Adrenal Glands   •  221

A B

C D
FIGURE 4-26.  Renal abscess. A, The axial fat-suppressed T2-weighted image shows a heterogeneously hyperintense lesion in the upper
pole of the left kidney (thin arrow in A and B) associated with perinephric edema (thick arrows in A and B). B, The corresponding
T2-weighted image without fat suppression exaggerates the internal complex hypointensity not typical of a simple or hemorrhagic cyst.
C, The postcontrast image reveals virtual absence of internal signal (minimal internal signal represents debris—also hyperintense on the
corresponding unenhanced image [not shown]). D, An axial T2-weighted image from a follow-up examination 1 month later establishes
involution and improvement after antibiotic treatment, confirming infectious (and non-neoplastic) etiology.

Although RCC is the main differential consider-

TABLE 4-8.  Renal Cell Carcinoma
ation, clinical and imaging signs of inflammation
Histologic Subtypes
and lack of enhancing solid tissue favor non-
Clear cell (65–70%)
neoplastic etiology. In addition to the clinical Papillary (15–20%)
features and surrounding inflammatory changes, Chromophobe (6–11%)
the main discriminating feature is the presence Multilocular cystic (<1%)
Collecting duct (<1%)
of hypervascular solid components. The mark- Medullary (<1%)
edly restricted diffusion of renal abscess con- Mucinous tubular and spindle cell (<1%)
tents also proposes the correct diagnosis.20
Based on Eble JN, Sauter G, Epstein JI, Sesterhenn IA, eds. Pathology
Differentiating renal abscess from an infected and Genetics of Tumours of the Urinary and Genital Organs. World
renal cyst may seem academic because both are Health Organization Classification of Tumours. International
Agency for Research on Cancer. 2004;12–43.
manifestations of infection, but treatment regi-
mens differ. Whereas both are treated with a
trial course of antibiotics, a lower success rate
with renal abscess prompts a lower threshold
for percutaneous drainage.21 Imaging features Cystic Renal Cell Carcinoma
overlap, but a greater degree of inflammatory RCC accounts for 90% of renal tumors with
changes, relatively poorer definition, and a protean clinical and imaging manifestations
shaggy inner wall favor abscess. depending on the subtype (Table 4-8).22,23 The
222  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-27.  Cystic RCC. The coronal T2-weighted (A) and enhanced (B) images show a cystic lesion (arrow) with mildly thickened
enhancing septa in a cystic clear cell RCC. Axial T2-weighted (C) and enhanced (D) images in a different patient reveal a clear cell RCC
(thin arrow) with even less complexity—mild wall thickening and a punctate mural nodule (thick arrow).

clear cell subtype accounts for most cystic Multilocular Cystic Nephroma
RCCs and 10% to 15% of clear cell RCCs are MLCN constitutes a potential confounder of
cystic. Even when predominantly cystic, cystic RCC in the appropriate demographic
careful inspection usually discloses a solid, categories. MLCN is a benign nonhereditary neo-
enhancing component. Solid components (of plasm arising from metanephric blastema with
clear cell RCCs) are usually hyperintense to a bimodal predilection for young males (3 mo–
renal parenchyma on T2-weighted images and 2 yr) and older females (fifth and sixth decades).
enhance avidly, although usually less than Classically, MLCN is a multiloculated cystic
renal parenchyma (Fig. 4-27). Motion artifact lesion with thin, septal enhancement, an absence
and lack of subtracted images hamper the of solid tissue, and herniation into the renal
ability to detect solid components, which are pelvis (putatively pathognomonic) (Fig. 4-28).
invariably present. Because most RCCs are Because most fall into the Bosniak III category,
predominantly solid, a more comprehensive excision is advocated. Also, imaging feature
review of RCC is deferred to the section on overlap with cystic and multilocular RCC force
“Solid Lesions.” circumspection and (at least) consideration of
Multilocular cystic RCC is the only consis- excision.
tently cystic subtype (see Table 4-8). Multilo­
cularity with thin septal enhancement and Renal Hematoma
occasional septal asymmetry characterize the Hematomas occur within the renal parenchyma,
typical appearance, which closely approximates within the renal capsule (subcapsular), and
MLCN. outside the capsule (perinephric). Blunt and
 MRI of the Kidneys and Adrenal Glands   •  223

A B

C D
FIGURE 4-28.  Multilocular cystic nephroma. The axial heavily T2-weighted (A) and postcontrast (B) images reveal a large multiloculated
cystic lesion in a 45-year-old woman. The coronal postcontrast image (C) portrays the size of the lesion and subtle medial protrusion
(arrows in C and D), corroborated on the coronal enhanced image (D), conforming to herniation into the renal pelvis at surgical
resection.

penetrating trauma and surgical and percutane- derangements of underlying renal parenchyma,
ous procedures account for the majority of renal morphology is preserved at the expense of
hematomas. Occasionally, underlying vascular signal and enhancement. These lesions tend to
disease, such as arteriovenous malformation manifest with either geographic or diffuse
(AVM) and vasculitis, induces hemorrhage. (signal and/or enhancement) findings, rather
Hemorrhage originating from an underlying than focal, masslike features—or the “bean”
renal mass is the diagnosis of exclusion and the versus “ball” renal lesion scheme (Fig. 4-30).
usual culprits are AML and RCC. The T1 hyper- Neoplastic masses expand more or less cen-
intensity of hemorrhage uniquely proclaims trifugally, conforming roughly to spheres, or
itself (Fig. 4-29), although underlying etiologies “balls.” In the process, the “bean” shape of the
must be entertained. Without an explanative eti- kidney is deformed. Meanwhile, other lesions
ology, RCC must be excluded with follow-up preserve the bean shape of the kidney by either
imaging. infiltrative neoplastic growth or nonneoplastic
affliction of a segment or entirety of the kidney
Solid Lesions (e.g., infection, infarction). This useful diagnos-
Solid renal lesions essentially equal malig­ tic scheme serves to frame differential diagno-
nancy. The rare exceptions are renal adenoma ses, not separate benign from malignant, because
and oncocytoma, which cannot be differenti- benign and malignant lesions fall into both
ated from malignant solid renal lesions. categories.
Pseudolesions—nonneoplastic lesions simulat-
ing neoplasms—confound the assessment of Renal Cell Carcinoma
solidity. These lesions include renal infarct, The quintessential (solid) ball lesion is RCC.
pyelonephritis, renal vein thrombosis (RVT), RCC represents over 90% of renal neoplasms.
and renal trauma. Because these lesions reflect For this reason, solidity generally equals RCC
224  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-29.  Renal hematoma. A large left perinephric collection (arrows in A) demonstrates heterogeneous hyperintensity on the
T2-weighted image (A) with corresponding hyperintensity on the T1-weighted fat-suppressed image (B). The postcontrast image (C)
shows mild intralesional hyperintensity not corresponding to enhancement, proven by the lack of signal on the subtracted image (D).

Round(-ish)
Expansile Non-deforming
Ball lesions Displaces Infiltrative Bean lesions
Cyst Well-defined Poorly defined Transitional cell carcinoma
Renal cell carcinoma Pyelonephritis
Angiomyolipoma Squamous cell carcinoma
Abscess Renal cell carcinoma
Metastases Lymphoma
Oncocytoma Metastases
Multilocular cystic nephroma Renal infarct
Lymphoma Renal medullary carcinoma
Collecting duct carcinoma

FIGURE 4-30.  Ball versus bean diagnostic approach.

 MRI of the Kidneys and Adrenal Glands   •  225

Syndrome Chromosomal RCC Other tumors

abnormality

VHL VHL gene (3p), Clear cell, bilateral and Pheochromocytoma,

autosomal dominant multifocal pancreatic cysts, islet cell
tumors, epidydymal
cystadenomas, others

Familial clear cell Chromosome 3 Clear cell, unilateral, Thyroid carcinoma

carcinoma bilateral solitary or
with translocation multifocal

Familial clear cell ? (absence of established Clear cell, solitary and None
carcinoma genetic source), ≥ 2 first- unilateral
degree relatives with RCC

Hereditary papillary renal 7q, autosomal dominant Papillary, multiple, bilateral Breast, lung, pancreatic,
cell carcinoma skin, gastric

Hereditary leiomyomatosis 1q, autosomal dominant Papillary, solitary and Uterine fibroids, cutaneous
and RCC unilateral (aggressive and leiomyomas
metastasize early)

Birt-Hogg-Dube 17p, autosomal dominant Oncocytomas, oncocytoma- Skin tumors, medullary thyroid
syndrome chromophobe hybrids, carcinoma, pulmonary cysts
chromophobe RCC, clear (spontaneous pneumothorax)
cell RCC, papillary RCC

Familial renal oncocytoma ? Oncocytomas, multiple Renal cysts

and bilateral

Tuberous sclerosis TSC gene 1 or 2 (9q), Clear cell, bilateral and Angiomyolipomas, adenoma
autosomal dominant multifocal (rarely reported) sebaceum, periungual fibromas,
cardiac rhabdomyomas, retinal
hamatomas, pulmonary
lymphangioleiomyomastosis,
giant cell astrocytomas, others

FIGURE 4-31.  Inherited renal cell carcinoma (RCC) syndromes. TSC, tuberous sclerosis complex; VHL, von Hippel–Lindau.

(until proved otherwise). RCC is a malignant cortex of the kidney. Hemorrhage, necrosis, and
neoplasm arising from renal tubular epithelium cyst formation frequently accompany tumor
with protean clinical and imaging manifesta- growth. The clear cell designation derives from
tions, according to the histologic subtype (see the microscopic appearance, attributable to
Table 4-8). Although all subtypes arise from the intracytoplasmic glycogen and lipid. Tumor
tubular epithelial cell, cytogenetic factors induce hypervascularity—thought to be related to inac-
wide variations in cell type and tumor growth tivation of tumor suppressor genes—is relative
patterns, reflected in the variable appearance of to other renal tumors; parenchymal enhance-
RCC on MR images. RCC cytogenetic analyses ment usually exceeds tumoral enhancement
have elucidated a number of inherited RCC syn- (Fig. 4-32). Intracytoplasmic lipid often induces
dromes (Fig. 4-31), which account for 4% of loss of signal on out-of-phase images (Fig.
RCCs.24 The imaging approach to RCC most 4-33).25,26 Whereas measureable loss of signal on
rationally focuses on histologic subtypes, which opposed-phase images is substantiated in up to
usually dictates imaging appearance. The most 60% of clear cell tumors, visibly detectable
common subtypes—clear cell and papillary— signal loss prevails far less commonly.
tend to differ dramatically. Clear cell tumors After establishing probable etiology, staging
tend to be heterogeneously hypervascular and issues deserve attention (see Fig. 4-5). The
fluid-rich with hyperintensity on fluid-sensitive multiplanar capabilities of MRI render size
sequences. Papillary tumors tend to be hypovas- assessment simple and accurate. The sensitivity
cular and homogeneously hypointense on fluid- of perinephric space extension is limited—
sensitive sequences. approximately 60% to 70%. The most specific
Clear cell RCC tumors, like other subtypes, CT finding—likely shared with MRI—is the pres-
arise from renal tubular epithelium in the ence of a discrete mass measuring at least 1 cm
226  •  Fundamentals of Body MRI

A B
FIGURE 4-32.  Clear cell RCC enhancement. A and B, Arterial (corticomedullary) phase postcontrast images in different patients with
right-sided (thin arrow in A) and left-sided (thin arrow in B) clear cell RCCs, respectively, show lesion enhancement less than adjacent
parenchyma (thick arrow in A) and approximating renal cortex (thick arrow in B).

A B

C D
FIGURE 4-33.  Clear cell RCC with intracytoplasmic lipid. An exophytic T2 hyperintense (A), heterogeneously enhancing (B) right renal
lesion (arrow), relatively hyperintense on the in-phase image (C), dramatically loses signal on the out-of-phase image (D), indicating
microscopic fat.

in the perinephric space.27 Linear strands infil- and slice thickness, and FOV and coronal
trating the perinephric space raise the suspicion plane orientation modifications) anecdotally
of perinephric invasion with low specificity increase sensitivity (Figs. 4-35 and 4-36). Unen-
(Fig. 4-34). hanced images supplement enhanced images
The sensitivity to enhancement and venous by showing vessel expansion and signal
patency versus occlusion and ability to detect alterations, including loss of the normal signal
tumor thrombus recommend MRI in the void (especially on T2-weighted images) and
staging of RCC.28 Whereas routine contrast- hypointense filling defects on steady-state
enhanced images often suffice to detect intra- images. To optimally differentiate tumor
luminal venous thrombus, dedicated magnetic thrombus from bland thrombus by detecting
resonance venography (MRV) images (with a enhancement, include and review subtracted
higher dose of gadolinium; a high flip angle images.
 B

FIGURE 4-34.  Clear cell RCC extending into the perinephric

space. The coronal T2-weighted image (A) shows an exophytic
mass (arrow) with mass effect on the renal collecting system
(open arrow), which is dilated. The postcontrast image
(B) shows the mass (arrow) with central necrosis and linear
enhancement in the perinephric space with focal thickening
and enhancement of Gerota’s fascia, seen to better advantage
on the magnified image (C) (open arrow in B and solid arrow
C
in C).

A B

FIGURE 4-35.  RCC with vascular invasion. The axial

T2-weighted image (A) reveals a complex mass arising
from the left kidney (arrows), which enhances on the
postcontrast image (B), illustrating typical features of
RCC. C, The delayed postcontrast image through the
renal hilum shows a filling defect in the left renal vein
(arrows) isointense to the enhancing mass, consistent with
C
tumor thrombus.
228  •  Fundamentals of Body MRI

A B

C
FIGURE 4-36.  RCC with tumor and bland thrombus. A, A large complex mass replacing the right kidney (thin arrows) on the postcontrast
image is associated with enhancing tumor thrombus in the IVC (thick arrow) and bland thrombus extending into the left renal vein
(open arrow). B, The coronal enhanced image shows the large right renal mass (thin arrows) with bland thrombus superior and inferior
to the renal vein (thick arrows). C, The coronal T2-weighted image catalogs the extent of retroperitoneal lymphadenopathy in the right
paracaval region (arrows).

Lymph node assessment is straightforward, Table 4-8). The papillary subtype owes its name
although relatively nonspecific. Although renal to the microscopic papillary growth pattern and
lymphatic drainage is variable, most detectable not to any macroscopically definable imaging
lymphatic metastases are (ipsilateral) para-aortic feature. The salient imaging features are the
nodes (see Fig. 4-36). Heavy reliance on size relative hypovascularity and signal charac­
criteria results in low specificity. Although the teristics occasionally simulating incidental
generally accepted threshold for normal retro- benign (hemorrhagic or proteinaceous) cystic
peritoneal nodes is 1.0 cm in short-axis diame- lesions. Papillary tumoral enhancement is
ter, reactive nodes often exceed this size. Direct modest; tumoral-to-aortic and/or tumoral-to-
invasion and distant spread to adjacent muscles, parenchymal enhancement of more than 0.25
the adrenal glands, the liver, the contralateral nearly effectively excludes papillary RCC.29 As
kidney, the pancreas, and osseous structures previously discussed, precontrast T1 hyperin-
must be addressed by your search pattern tensity confounds detection of enhancement,
(Fig. 4-37). which relies on perceiving an increase in signal.
Other subtypes follow different clinical and An increase in signal from a signal void is much
imaging patterns. The papillary subtype accounts easier to visually appreciate, justifying the use
for most of the remainder of RCC cases (see of subtracted images. Relative T2 hypointensity
 MRI of the Kidneys and Adrenal Glands   •  229

A B

C
FIGURE 4-37.  RCC with spread to other organs. A, The postcontrast image reveals a large heterogeneously enhancing mass in the right
kidney (arrow), typical of a clear cell RCC. T2-weighted (B) and postcontrast (C) images at the superior extent of the mass (thin arrow)
show extrarenal extension with neoplastic replacement of the right adrenal gland (thick arrow).

likely reflects the byproducts of hemorrhage RCC—relative hypovascularity and T2 hypo­

and/or necrosis (Fig. 4-38). Papillary tumors are intensity (Fig. 4-39).
generally homogeneous and usually lack micro- Multilocular cystic RCC technically belongs
scopic lipid. Although usually sporadic, papil- in the complex cystic section and bears consid-
lary RCC multifocality and bilaterality suggest an eration only because it simulates a benign
underlying inherited syndrome (see Fig. 4-31), lesion—MLCN. Although the multilocular cystic
prompting chromosomal analysis. Papillary RCC appearance is generally indistinguishable from
usually presents at a low stage—70% are intra- MLCN, unlike MLCN, multilocular cystic RCC
renal at diagnosis. spares children. Like MLCN, resection confers
Chromophobe RCC also exhibits fairly nonag- an excellent prognosis.
gressive biologic behavior and 86% present in
stage 1 or 2. The name refers to the fact that the Whereas malignant neoplasms of renal cell
cells fail to stain on histologic analysis. The inter- origin dominate the solid renal lesion category,
calated cell of the collecting tubule is the pos- a number of benign renal neoplasms exist,
tulated cell of origin (also for oncocytoma). including lesions of renal cell origin (Fig. 4-40).30
Shared ontogeny with oncocytoma is recapitu- Benign renal cell, or epithelial, neoplasms out-
lated in some of the imaging features. The occa- number other benign renal neoplasms by a wide
sional “spoke-wheel” enhancement pattern in margin. Although the renal papillary adenoma is
chromophobe RCC is the classic oncocytoma exceedingly common—40% of adults over 70
enhancement pattern. Chromophobe RCC according to autopsy series—very few are rec-
also shares imaging features with papillary ognized on imaging studies. According to the
230  •  Fundamentals of Body MRI

A B

C
FIGURE 4-38.  Papillary RCC with T2 hypointensity. A markedly hypointense lesion (arrow) arises from the lower pole of the right kidney
on the coronal T2-weighted image (A), which appears to mildly enhance based on mild relative hyperintensity after gadolinium admini­
stration from the precontrast (B) to the postcontrast (C) images—typical of papillary RCC.

A B
FIGURE 4-39.  Chromophobe RCC. A near-isointense lesion in the upper pole of the left kidney (arrow) on the T2-weighted image
(A) mildly enhances on the postcontrast image (B), simulating a papillary RCC.
 MRI of the Kidneys and Adrenal Glands   •  231

Renal Cell Metanephric Mesenchymal Mixed

tumors tumors tumors mesenchymal and
epithelial tumors

Oncocytoma Metanephric Angiomyolipoma Cystic nephroma

adenoma
Papillary adenoma Metanephric Leiomyoma Mixed epithelial
adenofibroma and stromal tumor
Metanephric Hemangioma
stromal tumor

Lymphangioma

Reninoma

Fibroma

Schwannoma

FIGURE 4-40.  Benign renal neoplasms. (Based on Eble JN, Sauter G, Epstein JI, Sesterhenn IA, eds. Pathology and Genetics of Tumours
of the Urinary and Genital Organs. World Health Organization Classification of Tumours. International Agency for Research on Cancer.
2004;12–43.)

World Health Organization (WHO) classification The MRI appearance depends on the relative
system, the renal papillary adenoma measures composition of the three tissue elements. Mac-
no more than 5 mm, which means that imaging roscopic fat diagnosed by signal suppression on
detection and characterization is essentially spectrally selective sequences (fat-saturated or
impossible. Interestingly, malignant transforma- short tau inversion recovery [STIR]) definitively
tion pathogenesis theories promote the papil- confirms the diagnosis and precludes further
lary adenoma as a precursor to RCC. investigation (Fig. 4-42). Solid, usually monoto-
nously enhancing smooth muscle elements
Oncocytoma cloud diagnostic certainty, especially when
The oncocytoma is a benign neoplasm account- present in large quantities at the expense of fat.
ing for 5% of adult primary renal epithelial neo- Avid enhancement of dysplastic vessels reflects
plasms. Occasionally present distinctive imaging the third tissue component—blood vessels.
features potentially suggest the diagnosis and These dysmorphic vessels predispose to aneu-
argue in favor of a partial nephrectomy instead rysmal dilatation and hemorrhage; large tumor
of a radical nephrectomy. A stellate central scar size (>4 cm) and tumoral aneurysms (>5 mm)
(one third of cases) and “spoke-wheel” enhance- positively correlate with hemorrhage.31 Because
ment (Fig. 4-41), although not pathognomonic, of this risk, partial nephrectomy is advocated
are specific enough to suggest partial instead for lesions over 4 cm in size. Lesions with spon-
of total nephrectomy. Otherwise, the imaging taneous bleeding are treated initially with
appearance is nonspecific in the form of embolization.
a relatively homogeneously enhancing, well- The problem of spontaneous hemorrhage,
demarcated solid cortical mass. otherwise known as Wunderlich’s syndrome
(defined as spontaneous extracapsular hemor-
Angiomyolipoma rhage contained within the perinephric fascia),
The AML is a benign hamartomatous lesion is diagnostically and therapeutically difficult.32
named for its histologic components—blood Management depends to some extent on the
vessels (angio-), smooth muscle (-myo-), and underlying etiology, which includes neoplasms
adipose tissue (-lipoma). Eighty percent of AMLs (AML and RCC), vascular disease (renal artery
occur sporadically and are usually solitary; the aneurysm and vasculitis), and hematologic dis-
remainder arise in the setting of inherited syn- orders. Whereas the hemorrhage presents little
dromes, such as TS, and are often multiple. diagnostic difficulty (see Fig. 4-29)—relying on
(AMLs are present in 80% of patients with TS.) T1 hyperintensity and absent enhancement—its
Although AMLs equate with benignity in clinical presence obscures the underlying etiology.
practice, the rare epithelioid subtype is poten- Management options range from conser­­
tially malignant. vative measures to embolization to emergent
232  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-41.  Oncocytoma. A, The axial image shows a lesion arising from the upper pole of the left kidney (arrow), which is hypointense
relative to the typical T2 appearance of oncocytoma. B, The corresponding arterial phase image shows a radiating enhancement pattern
(arrow), faintly reminiscent of the classic “spoke-wheel” pattern. The coronal T2-weighted image (C) in a different patient shows an
exophytic lesion (arrow), intensely enhancing in a loose “spoke-wheel” fashion on the arterial phase image (D).

nephrectomy depending on hemodynamic multiple bilateral renal masses, (2) diffuse infil-
considerations. tration, and (3) solitary mass. Predilection for
perinephric and renal sinus involvement results
The remaining focal solid renal lesions consti- from spread along the lymphatics. Metastases
tute an array of uncommon primary and malig- to the kidneys usually simulate metastases in
nant lesions—transitional cell carcinoma (TCC), other more commonly affected organs—
squamous cell carcinoma (SCC), metastases, and multiple small randomly scattered bilateral
lymphoma. Although lacking pathognomonic lesions—infiltrative spread is rare.
imaging features, distinctive findings usually
prompt diagnostic consideration. These lesions Urothelial Neoplasms
more frequently exhibit the “bean” morpho- Urothelial neoplasms—TCC and SCC among
logic growth pattern. Although exhibiting papil- others—arise from urothelial epithelium extend-
lary, expansile growth within the collecting ing from the renal collecting system through the
system, when involving the renal parenchyma, bladder. TCC accounts for most (90%), followed
TCC and SCC always conform to an infiltrative by SCC. When arising from the intrarenal col-
growth pattern. Protean manifestations of lym- lecting system, TCC and SCC infiltrate the renal
phoma include three parenchymal patterns: (1) parenchyma in 25% of cases. Imaging findings
 MRI of the Kidneys and Adrenal Glands   •  233

A B

C D

E F
FIGURE 4-42.  Macroscopic fat in AML. A partially exophytic lesion in the lower pole of the left kidney (arrow in A-D) blends impercep-
tibly with the retroperitoneal fat on the T2-weighted image (A) and on the out-of-phase image (B)—note the phase cancellation artifact
at the interface with the water-rich kidney. Complete loss of signal on the fat-suppressed postcontrast (C) and T2-weighted (D) images
confirms macroscopic fat. In a different patient, near isointense T2 signal compared with retroperitoneal fat in an exophytic lesion
(arrow) extending from the lower pole of the right kidney (E) is suppressed on the corresponding T2-weighted fat-saturated image (F).

when involving the intrarenal collecting system hyperintense lumen of the renal collecting
and kidney split into two major categories: system and/or the associated findings, such as
primary mass-related findings and secondary col- the curvilinear rim of fluid along the proximal
lecting system changes (Fig. 4-43). The primary margin of the mass, the oncocalyx (abnormally
collecting system mass typically grows in a papi­ dilated, tumor-distended calyx), phantom or
llary, expansile fashion; invasion of the renal amputated calyx (isolation of a calyx from the
parenchyma follows an infiltrative pattern (Figs. collecting system by the invading tumor), and
4-44 and 4-45). Heavily T2-weighted and MRU calyceal obliteration (see Fig. 4-45).
images identify the primary urothelial mass by Contrast-enhanced images are supplemented
depicting the lesion as a filling defect within the by T2-weighted images in detecting the primary
234  •  Fundamentals of Body MRI

Primary findings Secondary findings

Sessile, flat or polypoid mass Phantom calyx

Hypovascular infiltrative mass Oncocalyx

Intraluminal pelvic mass Nonfunctioning parenchymal

segments
Compression or invasion of Curvilinear collecting system
renal sinus fat rim at tumor margin

IVC invasion

Lymphadenopathy

FIGURE 4-43.  Urothelial neoplastic findings. IVC, infe- Stippled contrast within
interstices of tumor
rior vena cava.

A B

C D
FIGURE 4-44.  TCC. A, Severe left-sided hydronephrosis is apparent on the delayed, pyelographic phase postcontrast image due to dilata-
tion of the collecting system with absent enhancement and thinning of the overlying renal parenchyma. B, The axial T2-weighted image
suggests the presence of a sessile, mildly hyperintense lesion (arrows) arising from the anterior aspect of the renal pelvis, possibly simulated
by urinary flow artifact. C and D, Adjacent axial postcontrast images confirm the presence of an enhancing, papillary mass involving
the renal pelvis (arrows).

tumor and parenchymal invasion. Nonspecific displacement of renal sinus fat and/or parenchy-
T2 hyperintensity and hypovascularity relative mal invasion ensues. Infiltrative parenchymal
to renal parenchyma are the common denomi- infiltration preserves the “bean” shape of the
nator urothelial tumor imaging features. Eccen- kidney and blends subtly with the surrounding
tric urothelial thickening and enhancement renal parenchyma. Eventual loss of the normal
conform to either sessile, polypoid, or plaque- renal parenchymal architecture has been dubbed
like morphology. Associated invasion and/or the “faceless kidney,” with obliteration of the
 MRI of the Kidneys and Adrenal Glands   •  235

A B

C D
FIGURE 4-45.  Calyceal findings of TCC. A, The sagittal steady-state image reveals an ill-defined mass (thin arrows) surrounded by dilated
calyces; a thin rim of fluid hyperintensity (thick arrows) encircles tumor protruding into a lower polar calyx. B, The axial T2-weighted
image portrays the infiltrative intrarenal mass (thin arrows) inducing oncocalyces (thick arrows). C and D, The postcontrast pyelographic
phase images better depict the infiltrative nature of the hypovascular mass (thin arrows), encircled by a thin rim of excreted contrast
(thick arrows in C) in a dilated calyx, which also contains hypointense debris or hemorrhage.

Stage Findings

Stage 1 Limited to urothelial mucosa

and lamina propria

Stage 2 Invasion of pelvic or ureteral

muscularis

Stage 3 Invasion beyond muscularis

into adventitial fat or renal FIGURE 4-46.  TCC staging. (Based on Greene FL, Page
parenchyma DL, Fleming ID, eds. Renal pelvis and ureter. In: Ameri-
can Joint Committee on Cancer: AJCC Cancer Staging
Stage 4 Distant metastasis
Manual. 6th ed. New York: Springer, 2002;329–334.)

corticomedullary pattern. TCC spreads locally, Limited data on MRI staging TCC of the upper
invading within or along the inferior vena cava urinary tract suggests at least moderate success
(IVC) and/or along the lymphatics reflected by (Fig. 4-46).33 Staging deficiencies hinge on the
lymphadenopathy. Because of the high inci- potential to miss renal parenchymal invasion.
dence of multifocality (30%–50%) and bilateral- Surgical management entails total nephroureter-
ity (15%–25%), imaging the entire urothelial ectomy and bladder cuff excision. Metastatic
axis (collecting system through bladder) is disease is treated with chemotherapy and/or
warranted. radiation therapy.
236  •  Fundamentals of Body MRI

Although TCC is the paradigm infiltrative, or and melanoma. The propensity for multifocality
“bean,” mass, other less common lesions and bilaterality and the association with a
generate similar imaging features. Other urothe- primary tumor usually seal the diagnosis. The
lial tumors, such as SCC, mimic the appearance imaging appearance of nonneoplastic etiologies,
of TCC and are generally indistinguishable such as pyelonephritis, infarction, and papillary
(although TCC accounts for 90% of urothelial necrosis, also overlaps with the infiltrative
tumors). RCC rarely manifests infiltrative growth pattern of TCC. The clinical scenario hopefully
pattern. Rare subtypes, including collecting suggests these lesions, which fail to progress on
duct and medullary RCCs, exhibit infiltrative follow-up imaging (and are discussed in greater
growth. Both of these lesions arise from the detail).
renal parenchyma centrally and grow into the
renal sinus and collecting system (the opposite Renal Lymphoma
progression of TCC). Both of these lesions Although detected commonly postmortem
follow an aggressive clinical course; renal med- (approximately half of lymphoma patients),
ullary carcinoma is distinguished by its unique renal lymphoma is rarely seen on imaging studies
association with sickle cell trait and usually (<10% of patients). Renal involvement more fre-
afflicts patients younger than 40 years old. quently occurs in (B-cell) non-Hodgkin’s lym-
Secondary tumors also mimic the infiltrative phoma and usually indicates widely disseminated
appearance of TCC, including lymphoma and disease and a poor prognosis. As previously
metastases. Relative homogeneity of the primary mentioned, renal lymphoma presents three
mass(es) and disproportionately enlarged lymph growth patterns: (1) multiple bilateral renal
nodes characterize lymphoma. Extrarenal masses, (2) diffuse infiltration, and (3) solitary
tumors that metastasize to the kidneys include mass (Fig. 4-47). The renal parenchyma lacks
lung, breast, and gastrointestinal malignancies lymphoid tissue, and the pathogenesis of

A B

C
FIGURE 4-47.  Renal lymphoma. A, The axial T2-weighted image reveals a large left-sided lesion (arrow) that exhibits multiple features
typical of lymphoma: (1) T2 hypointensity, (2) involvement of the perinephric space, and (3) lack of necrosis despite large size. B, Note
the relative hyperintensity (arrow) on the fat-suppressed T2-weighted image, benefiting from increased dynamic range. C, The early
postcontrast image shows characteristic minimal enhancement (arrow).
 MRI of the Kidneys and Adrenal Glands   •  237

development of renal lymphoma has not been Segmental and diffuse lesions generally respect
elucidated. The frequent bilateral involvement the “bean” pattern, altering the renal signal
(50%) and multifocality of parenchymal masses intensity and/or enhancement pattern rather
conjure hematogenous spread. The lymphatic than the renal morphology. Whether segmental
origin is illustrated by the propensity to involve or diffuse, detection relies on comparison with
the renal sinus and perinephric space where the normal renal tissue. Segmental lesions deviate in
lymphatics reside. signal and/or enhancement from adjacent paren-
Lymphomatous masses tend to be monoto- chyma; diffuse lesions (unless bilateral) deviate
nously homogenously nearly isointense on T1- in signal and/or enhancement from the contra-
weighted and T2-weighted images with modest lateral kidney. The degree of renal involvement,
homogeneous enhancement, even when large ranging from segmental to diffuse to bilateral,
(in contradistinction to RCC, which typically hints at the diagnosis. Segmental lesions include
undergoes necrosis with increasing size). mainly neoplasms, infarcts (i.e., embolic and
Another characteristically unique feature is the vasculitic etiologies), pyelonephritis, and trau-
relative lack of mass effect on adjacent struc- matic injury. Diffuse lesions include vascular
tures. To summarize, a number of unique fea- lesions—such as RVT and renal artery stenosis
tures distinguish lymphoma from RCC and other (RAS)—and xanthogranulomatous pyelone­
solid lesions, such as homogeneity, lack of phritis (XGP). Bilateral lesions include intravas-
necrosis, lack of mass effect, central/medullary cular hemolysis, human immunodeficiency virus
involvement and/or centering outside the renal (HIV) nephropathy, and medical renal disease.
contour, lack of vascular invasion, massive Whereas previously discussed neoplasms—
lymphadenopathy, and bilaterality/multifocality. such as TCC, SCC, RCC medullary type, and
lymphoma—occasionally manifest with segmen-
Renal Metastases tal imaging features, ill-defined margins, some
Renal metastases usually occur in the setting of degree of mass effect, and/or a superimposed
widespread, end-stage disease from primary discrete mass distinguish these lesions from
melanoma or breast, lung, or gastrointestinal nonneoplastic segmental lesions. The other seg-
malignancies. Unlike lymphoma, metastases mental lesions—pyelonephritis, renal infarct,
arise within the renal parenchyma, rarely and renal trauma—often include sharply margin-
deforming the renal contour. Most metastatic ated triangular lesions pointing to the renal
lesions enhance minimally—hypervascular mel- hilum. Associated imaging and clinical features
anoma is the notable exception. help suggest the diagnosis.

Pyelonephritis
Segmental/Diffuse Lesions
Pyelonephritis—ascending infection of the renal
Segmental and diffuse lesions include mostly pelvis, tubules, and surrounding interstitium—
nonneoplastic etiologies—some previously dis- reiterates the pyramidal morphology of the col-
cussed neoplastic lesions straddle the line lecting system unit (Fig. 4-49). Actually, although
between solid/focal and segmental or diffuse, pyelonephritis spreads segmentally along the
such as TCC and lymphoma (Fig. 4-48). collecting system scaffolding accounting for

Infectious Vascular Neoplastic

Pyelonephritis Renal vein thrombosis Transitional cell

Xanthogranulomatous Renal artery stenosis Lymphoma

pyelonephritis

HIV nephropathy Renal infarction Renal medullary

Intravascular hemolysis

Usually segmental
Usually diffuse (unilateral) FIGURE 4-48.  Segmental and diffuse lesions. HIV,
Usually bilateral human immunodeficiency virus.
238  •  Fundamentals of Body MRI

segmental features, diffuse involvement often enhancement radiating from the papillary tip to
eventually ensues. Three basic patterns typify the peripheral cortex reflect poorly functioning
acute pyelonephritis: (1) hypoperfused, edema- tissue with interstitial edema, vasospasm, and
tous segment(s), (2) diffusely edematous, tubular obstruction (Fig. 4-50).35 The striated
hypoperfused enlargement, and (3) the striated nephrogram appearance of alternating parallel
nephrogram appearance. Wedge-shaped T2 enhancing and nonenhancing bands of renal
hyperintense segments with decreased parenchyma arranged centripetally toward the
renal hilum represent intermingled normal
and obstructed tubules, respectively. Diffuse
Renal cortex Renal papilla involvement results in renal enlargement, hyper-
Renal medulla
intensity, and decreased perfusion. Secondary
findings include infiltration of the perinephric
fat, perinephric fluid, and thickening and
Renal capsule
enhancement of the ipsilateral urothelial collect-
Renal pelvis
Minor calyx ing system wall (see Fig. 4-50).
In the setting of renal infection, pyonephrosis
Major calyx
and pyogenic abscess are the feared complica-
Renal column Ureter tions. Ongoing liquefaction without adequate
treatment leads to pyogenic abscess, potentially
Renal pyramid necessitating percutaneous drainage (in addi-
FIGURE 4-49.  Anatomy of the renal collecting system. tion to antibiotic treatment). Pyonephrosis

A B

C D
FIGURE 4-50.  Acute pyelonephritis. The axial postcontrast image (A) shows infiltration of the left renal sinus fat and urothelial thickening
and enhancement. The fat-suppressed T2-weighted image through the upper pole of the left kidney (B) shows perinephric edema (arrow).
The early (C) and delayed (D) postcontrast images show an evolving pyogenic abscess (thin arrow) with perinephric inflammation (thick
arrow in C) and dilated tubules with the striated nephrogram appearance.
 MRI of the Kidneys and Adrenal Glands   •  239

signifies obstruction plus infection and necessi- infiltration and fluid and urothelial thickening
tates prompt intervention because of the poten- and enhancement), and (3) clinical signs of
tial for rapid clinical deterioration, shock, and infection. The “cortical rim” sign of preserved
irreversible kidney damage. Pyonephrosis devel- capsular/subcapsular enhancement overlying
ops from either infection of an obstructed hypoperfused parenchyma reliably indicates
kidney or suppurative impaction inducing
obstruction and hydronephrosis. In addition to
findings of pyelonephritis, findings suggesting
pyonephrosis include obstruction, collecting Interlobar artery
system fluid complexity with debris and fluid-
fluid levels, and urothelial thickening and Interlobular
artery
enhancement.
Renal medulla
Renal Infarct
Renal infarcts are usually embolic and rigidly Renal artery
observe segmental morphology as a function of Segmental artery
renal arterial anatomy (Fig. 4-51). The wedge-
shaped region(s) of decreased enhancement,
Renal cortex
representing the renal tissue deprived of blood
flow subtending the occluded renal artery Arcuate artery
branch, mimics hypoperfused segments in
pyelonephritis with sharper linear margins (Fig.
4-52). Findings that favor infarction over infec-
tion include (1) absence of the striated nephro- FIGURE 4-51.  Renal arterial anatomy. (From Fox SI. Human
gram, (2) secondary findings (perinephric Physiology, 6th ed. New York: William C. Brown, 1998:529.)

A B

C D
FIGURE 4-52.  Renal infarct. The precontrast T1-weighted image (A) shows a sharply demarcated wedge-shaped lesion in the anterior
interpolar aspect of the left kidney (arrows), clearly delineated by adjacent enhancing renal tissue on the postcontrast image (B) due to
the lack of enhancement. Similar features (thin arrows in C) on adjacent sections (precontrast [C] and postcontrast [D]) with the cortical
rim sign on the enhanced image (thick arrows in D).
240  •  Fundamentals of Body MRI

small kidney. Except for RVT, other etiologies

TABLE 4-9.  Diffuse Unilateral Renal Disorders
distinguish themselves through other easily
Unilaterally Small discernible primary imaging features: hydrone-
Chronic renal artery stenosis
Chronic renal venous thrombosis
phrosis (postobstructive uropathy), normal
Renal hypoplasia signal and enhancement characteristics (renal
Longstanding subcapsular collection hypoplasia), and subcapsular collection (Page’s
Longstanding obstructive uropathy
kidney). Except for the primary renal versus
Unilaterally Enlarged arterial lesion, no imaging features distinguish
Acute renal vein thrombosis chronic RVT from RAS.
Acute renal artery occlusion
Acute obstructive uropathy
Pyelonephritis Renal Vein Thrombosis
Infiltrative neoplasms Acutely, both RVT (more common) and renal
Xanthogranulomatous pyelonephritis
artery occlusion enlarge the kidney as a conse-
quence of diffuse parenchymal edema (and the
appearance potentially simulates diffuse pyelo-
nephritis). Other etiologies of unilateral renal
enlargement result from acute obstructive urop-
ischemia over infarction and other etiologies athy and infiltrative processes, such as pyelone-
(see Fig. 4-52). The cortical rim sign reflects phritis, infiltrating neoplasm, and XGP. The
patent collateral circulation and develops 6 to 8 renal venous filling defect is best visualized on
hours after onset. delayed contrast-enhanced images and steady-
In addition to embolism, etiologies of isch- state images (Fig. 4-54), usually accompanying
emia include vasculitis and renal trauma. edematous renal enlargement and other nonspe-
Bilateral diffuse involvement and arterial micro- cific findings, including delayed nephrographic
aneurysms characterize vasculitis (i.e., systemic and pyelographic phases. When suspected, RVT
lupus erythematosis and polyarteritis nodosa) benefits from targeted MRV technique, sharing
and effectively exclude isolated embolic infarcts. parameters with renal magnetic resonance angi-
Blunt trauma usually fails to respect anatomic ography (MRA)—higher dose of gadolinium,
boundaries, resulting in irregular linear or seg- higher flip angle, and thinner slices—and includ-
mental devitalized renal tissue with or without ing focused steady-state images targeted to the
parenchymal disruption or subcapsular or peri- renal veins.
nephric hematoma.
Nonvascular etiologies of unilaterally enlarged
Diffuse unilateral renal disorders separate into kidney show their colors by directly altering
two major categories: unilaterally small kidney the renal parenchymal and/or collecting
and unilaterally enlarged kidney (Table 4-9). In system appearance. Hydronephrosis indicates
routine clinical practice, chronic RAS accounts obstructive uropathy; signal and enhancement
for most cases of unilaterally small kidney. derangement attend infiltrative neoplasms and
inflammatory etiologies, such as pyelonephritis
Chronic Renal Artery Stenosis and XGP. XGP represents chronic renal paren-
Chronic RAS results in a unilaterally globally chymal inflammation usually by Proteus or Esch-
atrophic kidney (as opposed to segmental erichia coli in patients with renal calculi.
infarction—previously discussed—resulting in Lipid-laden macrophages replace normal renal
focal atrophy). Other causes of a unilateral small parenchyma, leading to grossly reniform non-
kidney include chronic RVT, renal hypoplasia, functioning renal enlargement.36 The classic
longstanding subcapsular hematoma (Page’s XGP triad includes (1) nephrolithiasis, (2) renal
kidney), and postobstructive uropathy. Delayed enlargement, and (3) diminished or absent func-
nephrographic and urographic phases in chronic tion. Visible fat accumulation increases diagnos-
RAS are nonspecific—seen in other etiologies of tic confidence, although other lesions, such as
unilaterally small kidney, such as obstruction RCC and AML, also contain fat.37 “The fractured
and RVT (Fig. 4-53), except for renal hypoplasia. stone” sign is another unique XGP finding his-
Although best visualized on a dedicated angio- torically described as a CT finding, not practi-
graphic study, direct visualization of the arterial cally transferable to MRI, given the relative
stenosis excludes other etiologies of unilateral insensitivity of renal calculi.
 MRI of the Kidneys and Adrenal Glands   •  241

A B

C D
FIGURE 4-53.  Renal artery stenosis. The coronal (A) and axial (B) T2-weighted images reveal marked asymmetrical left-sided renal atrophy
and lack of corticomedullary differentiation. Early (C) and delayed (D) postcontrast coronal images show a corresponding delayed left-
sided nephrographic phase compared with the normal right kidney.

Diffuse bilateral renal disorders include a long

list of diseases rarely seen on MR images (Table TABLE 4-10.  Diffuse Bilateral Renal Disorders
4-10). These lesions divide into generic “medical Diabetic nephropathy
Acute glomerulonephitis
renal disease,” diffuse infiltrative neoplastic Collagen vascular diseases
etiologies, and signal-based diseases. Bilateral AIDS nephropathy
renal disorders under the medical renal disease Lymphoma/leukemia
Acute interstitial nephritis
umbrella are associated with renal insufficiency Hemoglobinopathy
by definition with variably sized kidneys. The Acromegaly
etiology is rarely forthcoming at MRI and usually Acute urate nephropathy
Amyloidosis
evades diagnosis in routine clinical practice. Fabry’s disease
Diffuse bilateral diseases inducing signal Von Gierke’s disease
derangement feature exclusive, distinctive MRI Intravascular hemolysis
findings. Although rare, these lesions are worth AIDS, acquired immunodeficiency syndrome.
discussing because of the ability to render
242  •  Fundamentals of Body MRI

A
B

C
FIGURE 4-54.  Renal vein thrombosis. The early (A) and delayed (B) postcontrast images demonstrate an at least nearly complete occlusive
filling defect in the left renal vein (arrow). The coronal T2-weighted image (C) shows subtle left renal enlargement.

specific diagnoses. Parenchymal signal disorders Although the renal findings in etiologies of intra-
are synonymous with parenchymal T2 hypoin- vascular hemolysis are identical, splenic hypoin-
tensity, for the most part, and the vast majority tensity implicates SCD. Few, if any, disorders
arises from hemorrhagic etiologies.38 Hemolytic simulate this appearance. Whereas other disor-
etiologies—paroxysmal nocturnal hemoglobin- ders, such as acute hemorrhage from trauma,
uria (PNH), mechanical hemolysis, and sickle amyloidosis, or acute cortical necrosis, poten-
cell disease (SCD)—dominate this category. tially mimic the MR appearance of intravascular
Other rare etiologies include hemorrhagic fever hemolysis, the pattern of involvement and clini-
with renal syndrome (HFRS) and vascular etiolo- cal features differ.
gies (often not bilateral), such as acute cortical
necrosis, acute RVT, and arterial ischemia and
infarction. PNH results from an acquired sensi- ADRENAL GLANDS
tivity to complement, ultimately inducing
Normal Features
intravascular hemolysis. Mechanical hemolysis—
exemplified by malfunctioning prosthetic The adrenal glands are Y-shaped structures
cardiac valves—generates an identical imaging inhabiting the superior extent of the retroperi-
appearance with marked hypointensity restricted toneum. The adrenal body measures approxi-
to the cortex (Fig. 4-55). Hypointensity is most mately 10 to 12 mm in length and the medial
dramatically apparent on T2-weighted images and lateral limb measures 5 to 6 mm.39,40 As a
and gradient-echo sequences (see Fig. 4-55), general rule of thumb, adrenal limbs measure
owing to the sensitivity to susceptibility artifact. 5 mm or less in thickness.41 The right adrenal
 MRI of the Kidneys and Adrenal Glands   •  243

A B

C D
FIGURE 4-55.  Mechanical hemolysis. Coronal T2-weighted (A) and axial T2-weighted fat-suppressed (B) images reveal marked hypoin-
tensity restricted to the renal cortex, not apparent on the out-of-phase image (C). D, Pronounced cortical signal loss on the in-phase
image connotes susceptibility artifact due to hemosiderin deposition.

gland sits 1 to 2 cm above the upper pole of the Adrenal lesion differential diagnosis hinges on
right kidney, and the left adrenal gland rests cystic (or nonsolid because hemorrhage is
ventral to the upper pole of the left kidney). included in this category) versus solid tissue
Adrenal gland dimensions vary, precluding the composition (Fig. 4-56). Lack of enhancement
use of specific normal size criteria. Dual parallel versus enhancement classifies adrenal lesions
adrenal embryology explains adrenal micro­ into the respective categories. With the excep-
anatomy and physiology, imaging appearance, tion of hemorrhage, nonsolid etiologies exhibit
and the spectrum of adrenal lesions. The outer nonspecific free water imaging features. Solid
cortex develops from coelomic mesoderm and lesion tissue composition often demonstrates
accounts for most of the bulk of adrenal tissue, specific imaging features suggesting the
responsible for synthesizing cholesterol-derived underlying diagnosis. Microscopic fat connotes
hormones—glucocorticoids and mineralocorti- adenoma, and macrosopic fat equals myeloli-
coids. The cholesterol compounds constituting poma. High fluid content and hypervascularity
the building blocks of the adrenal hormones explain the T2 hyperintensity and avid enhance-
account for the loss of signal on out-of-phase ment of pheochromocytoma, respectively.
images. The inner adrenal medulla derives from Other solid lesions, such as lipid-poor adenoma,
neural crest cells and produces catecholamines— metastasis, and adrenal cortical carcinoma are
mostly epinephrine. less specific.
244  •  Fundamentals of Body MRI

Cystic Solid

Endothelial cyst Adenoma

OOP IP
Epithelial cyst Myelolipoma

Pseudocyst Pheochromocytoma

Parasitic cyst Metastasis

Hemorrhage Adrenal cortical carcinoma

Adrenal adenoma
Adrenal hyperplasia
T1WI FS

T2WI T1WI Hemorrhage Adrenal

hyperplasia

Cysts
Myelolipoma

T2WI PG

Metastasis

Adrenal
cortical
carcinoma
Pheochromocytoma
FIGURE 4-56.  Adrenal differential diagnosis. FS, fast spin-echo; IP, in-phase; OOP, out-of-phase; PG, postgadolinium.

Unilateral Bilaterals

Blunt trauma Stress

Liver transplant (right-sided) Hemorrhagic diatheses

Primary or metastatic tumors Thromboembolic disease

Uncomplicated pregnancy Complicated pregnancy

FIGURE 4-57.  Differential diagnosis of adrenal
Spontaneous/idiopathic Meningococcal septicemia
hemorrhage.

Cystic (Nonsolid) Lesions

Adrenal Cysts
Adrenal cystic lesions are rare, with an inci- Adrenal cystic lesions are almost always asymp-
dence of less than 1%.42 Adrenal cystic lesions tomatic and virtually always detected inciden-
divide into two main categories: (1) true endo- tally on imaging studies. Symptoms manifest
thelial (lymphatic—lymphangiomatous and only with large size through mass effect on
vascular—hemangiomatous) and epithelial cysts adjacent organs. Nonspecific imaging features
(40%–45%) and (2) pseudocysts (40%)—usually usually fail to discriminate among the different
represents the sequela of previous hemorrhage cystic types.43 Most lesions share features of
but also includes infectious (parasitic) cysts and typical cysts, with internal free water signal
other rare cystic lesions. Hemorrhage consti- with absent central enhancement and a thin or
tutes a third nonsolid category (although meta­ imperceptible wall (Fig. 4-58). Internal contents
stases are included in the differential diagnosis in pseudocysts from previous hemorrhage
of adrenal hemorrhage, technically belying the exhibit a greater degree of heterogeneity (see
term nonsolid) (Fig. 4-57). Fig. 4-58).
 MRI of the Kidneys and Adrenal Glands   •  245

A B

E
FIGURE 4-58.  Adrenal cyst. Coronal T2-weighted (A) and enhanced (B) images show a right-sided true adrenal cyst (arrow) with simple
cystic features. C, The sagittal postcontrast image confirms the extrarenal origin with reciprocally convex margins (arrow). A more
complex left-sided adrenal pseudocyst (arrow in D and E) in a different patient demonstrates internal complexity on the T2-weighted
image (D), but no enhancement on the postcontrast image (E).
246  •  Fundamentals of Body MRI

Mimickers of adrenal cysts and pseudocysts, of two clinically important features: (1) hor-
which are not incidental, include parasitic (echi- monal activity (as a functional adenoma) and (2)
nococcal) cysts, pheochromocytoma, and cystic malignant histology (usually metastatic from
neoplasms. Adrenal echinococcal cysts share nonadrenal primary). Luckily, 70% of adrenal
imaging features with echinococcal cysts infest- adenomas are “lipid-rich,” facilitating diagnosis
ing other body parts, such as the liver (see through signal loss on out-of-phase images (if
Chapter 2).44 At the early stages of development, not detected on unenhanced CT). Endocrino-
the hydatid cyst simulates adrenal pseudocysts logically functional lesions manifest characteris-
and true cysts. With continued development, tic clinical findings (e.g., Conn’s syndrome,
characteristic features corroborate the diagnosis Cushing’s syndrome). Among the remaining
(e.g., daughter cysts, floating membrane). lesions—lipid-poor adenomas, myelolipoma,
The extreme T2 hyperintensity of the pheo­ pheochromocytomas, metastases, and adrenal
chromocytoma conjures cystic etiology on cortical carcinomas—some specific imaging
T2-weighted images, but avid enhancement con- features help establish the correct diagnosis
firms solid tissue, excluding fluid contents. Solid (Fig. 4-60).
tumors—such as metastases and adrenal cortical
carcinoma—with cystic degeneration and necro- Adrenal Adenoma
sis harbor solid neoplastic, occasionally subtle, Adrenal adenomas are benign tumors of the
components. Subtracted images improve solid adrenal cortex with no malignant potential. The
tissue conspicuity. vast majority is nonhyperfunctioning; a small
minority induces Cushing’s syndrome, Conn’s
Adrenal Hemorrhage syndrome, or virilization, depending on the
Although not exactly cystic, adrenal hormone synthesized—cortisol, aldosterone,
hemorrhage—except when induced by underly- and angrogens, respectively. Nonhyperfunction-
ing adrenal metastases—is nonsolid. Lack of ing adenomas usually measure less than 2 cm
enhancement best establishes the absence of and almost always less than 3 or 4 cm, whereas
solid tissue, which benefits from the incorpora- hyperfunctioning adenomas more likely measure
tion of subtracted images, given the precontrast greater than 2 cm. Other than size differences,
T1 hyperintensity of hemorrhage. Rich adrenal no difference in imaging features is observed.
arterial supply—hormonally enhanced under High intracellular lipid content accounts for loss
certain conditions—with limited venous drain- of signal on out-of-phase imaging in most adeno-
age through a single adrenal vein (prone to mas (Fig. 4-61). If small lesions are anticipated,
spasm induced by catecholamines) predisposes a 3-D sequence (without fat suppression) sup-
to hemorrhage. plements routine 2-D in- and out-of-phase images
Distortion of the adreniform shape depends in potentially detecting intracytoplasmic lipid.
on the degree of hemorrhage. Methemoglobin The lower slice thickness and potentially higher
T1 hyperintensity in acute/subacute hemor- matrix improve conspicuity to microscopic fat
rhage signals the diagnosis (Fig. 4-59). Follow-up in small lesions.
imaging shows involution and confirms the diag- Identifying microscopic fat is paramount—
nosis, while potentially identifying or excluding unique to adenomas and excluding all poten-
underlying lesions. tially sinister lesions, especially metastases.
Subjective signal loss on out-of-phase images
usually suffices. In equivocal cases, objective
Solid Lesions
measurement relies on comparison with a refer-
Solid lesions much more commonly affect the ence standard—the spleen.46 A relative drop in
adrenal gland than do cystic lesions. In fact, lesion signal on out-of-phase images compared
adrenal lesion evaluation is the most common with the spleen establishes the presence of
adrenal indication for MRI—dubbed the adrenal microscopic fat, according to the following
“incidentaloma.”45 Adrenal adenomas account equation:
for the vast majority of these lesions— Adrenal lesion IP Adrenal lesion OOP
approximately 90%. In the setting of the adrenal ÷
Spleen IP Spleen OOP
incidentaloma, the clinical mandate is to exclude
nonadenoma etiologies (especially metastasis). when the ratio is less than 0.7 (IP = in-phase;
Adrenal incidentalomas potentially harbor one OOP = out-of-phase).47,48 In the setting of iron
 A B

C D
FIGURE 4-59.  Adrenal hemorrhage. The T2-weighted image (A) shows bilateral adrenal lesions (arrows), which are hypointense relative
to adenomas or other adrenal lesions with marked hyperintensity on the in-phase image (B). C, Preservation of signal and peripheral
phase cancellation artifact (arrows) on the out-of-phase image excludes microscopic fat. D, Preservation of signal on the T1-weighted
fat-suppressed image excludes macroscopic fat and the signal characteristics typify hemorrhage (arrows).

Lipid-poor adenoma
Metastasis
Adrenal lesion Adrenal cortical carcinoma

Lack of
Cystic Solid specific
features

T1 hyperintensity Microscopic fat Macroscopic fat Cystic appearance

catecholamines

Endothelial cyst Hemorrhage Adenoma Myelolipoma Pheochromocytoma

Epithelial cyst
Pseudocyst
Parasitic cyst

FIGURE 4-60.  Solid adrenal lesions.

248  •  Fundamentals of Body MRI

A B
FIGURE 4-61.  Adrenal adenoma. The mildly hyperintense lesion (arrow) on the in-phase image (A) loses signal on the out-of-phase image
(B), indicating microscopic fat, diagnostic of an adenoma. Note the parallel loss of signal in the liver consistent with steatosis.

A B
FIGURE 4-62.  Lipid-poor adenoma with enhancement. There is modest signal drop in the right adrenal lesion (arrow) from the in-phase
(A) to the out-of-phase (B) image illustrating the potential diagnostic uncertainty in the case of a lipid-poor adenoma.

deposition (with signal loss on in-phase images), adenoma and probably malignant lesions.49
the renal cortex or muscle serves as a reference These features—homogenous T2 iso- or hypoin-
standard alternative. tensity and homogeneous enhancement—help
Homogenous signal characteristics and to suggest the diagnosis of lipid-poor adenoma
enhancement typify adenomas. Adenomas are over alternative lesions, such as metastases (Fig.
usually iso- to hypointense on T2-weighted 4-62). However, ultimately follow-up imaging
images. Prompt adenoma enhancement and excludes metastasis by establishing size stability
washout on CT has been observed and substan- (correlative studies, such as positron-emission
tiated on multiple studies. Adenoma CT enhance- tomography, are another option).
ment parameters range from a drop of 40% at
15 minutes to 50% at 10 minutes. The MR Adrenal Hyperplasia
enhancement pattern typically parallels the CT Signal characteristics of adrenal hyperplasia
enhancement pattern, and a relatively early peak (AH) mirror adrenal adenoma. AH respects
to enhancement—within 52 seconds—has been adreniform morphology, either diffusely or
proposed as a discriminating feature between asymmetrically enlarging the adrenal glands.
 MRI of the Kidneys and Adrenal Glands   •  249

Adrenal gland limb width over 10 mm suggests with adenoma or myelolipoma. Potential con-
AH and limb thickening may be smooth or founders include cystic lesions and cystic neo-
nodular. AH signal intensity follows the signal plasms. The presence of solid, enhancing tissue
intensity of normal adrenal glands—mild subjec- excludes cystic lesions, and clinical features
tive signal loss on out-of-phase images. Adreni- (paroxysmal hypertension, headaches and
form shape and signal characteristics generally tremors) suggest the correct diagnosis.
exclude other bilateral lesions from consider-
ation, such as metastases, lymphoma, and Metastases
hemorrhage. Adrenal metastases constitute the greatest malig-
nant threat to the adrenal glands. The adrenal
Myelolipoma glands are the fourth most common site of meta-
Myelolipoma shares one common feature with static involvement (following lungs, liver, and
adenoma—the presence of fat. Unlike adrenal bone). Primary malignancies usually responsible
adenoma fat, myelolipoma fat is macroscopic. for adrenal metastases include lung, breast, skin
The myelolipoma is a “metaplasia-choristoma,” (melanoma), kidney, thyroid, and colon cancers.
which means that it is composed of a mass of When discovered in the setting of known malig-
histologically normal tissue—in this case, bone nancy, adrenal incidentalomas incur a risk of
marrow—in an abnormal location. Intralesional metastasis ranging from 33% to 75%. Because
fat signal follows normal macroscopic fat of the high prevalence, the adrenal adenoma is
signal—loss of signal on fat suppressed and STIR the chief differential consideration. Without
sequences. Hematopoietic elements demon- microscopic lipid, diagnostic ambiguity ensues.
strate nonspecific imaging features with relative Growth based on size increase between suc­
T2 hyperintensity and enhancement. The typical cessive studies effectively eliminates benign
appearance of a well-circumscribed suprarenal etiologies. Other imaging features favoring
lesion with a relatively higher proportion of metastasis include T2 hyperintensity compared
mature adipose tissue mixed with strands and/ with adenoma, irregular margins, heterogeneity,
or swirls of hematopoietic is pathognomonic and the presence of widespread (metastatic)
(Fig. 4-63). Rarely, relative preponderance of lesions (Fig. 4-65).
hematopoietic tissue and paucity of adipose
tissue precludes signal loss on fat-suppressed Other Adrenal Malignancies
sequences and out-of-phase images potentially Other adrenal malignancies are exceedingly
show signal loss, reflecting lipid content. rare, such as adrenal lymphoma and adrenal
cortical carcinoma. Adrenal lymphoma usually
Pheochromocytoma represents spread of ipsilateral renal or retro-
The pheochromoctoma is a paraganglioma peritoneal lymphoma—usually non-Hodgkin’s
arising from the adrenal medulla, composed of lymphoma. Adrenal lymphoma manifests either
chromaffin cells synthesizing, storing, and as diffuse adrenal enlargement or as a discrete
releasing catecholamines. As an aside, the para- mass(es)—frequently bilateral (50%). Adrenal
ganglioma follows the “rule of 10s”: 10% bilat- cortical carcinoma usually raises the prospect of
eral adrenal, 10% malignant, 10% extra-adrenal. malignancy based on its large size and pro-
Most are sporadic, but 5% are inherited: in the nounced heterogeneity (despite occasional
form of multiple endocrine neoplasia type IIa intralesional lipid) (Fig. 4-66). These lesions
and type IIb, VHL, or neurofibromatosis type 1. usually measure at least 5 cm in diameter, and
Although the classic “lightbulb bright” T2 often much more. Cystic and necrotic dege­
appearance of pheochromocytoma occurs in neration figures prominently in the imaging
fewer than half of patients, T2 signal intensity appearance.
always exceeds the T2 signal of adrenal adeno-
mas (Fig. 4-64). Avid enhancement occurs either
RETROPERITONEUM
immediately or progressively and may demon-
strate a “salt-and-pepper” texture reflecting Although this entire chapter is devoted to the
enhancing tissue with intervening signal voids retroperitoneum, inhabited by the kidneys and
corresponding to vessels. Lack of intralesional adrenal glands, this particular section specifi-
lipid precludes signal loss on out-of-phase images cally focuses on extraparenchymal lesions of the
and fat-suppressed images, avoiding confusion retroperitoneum. Because the retroperitoneum
 A B

C D

E F
FIGURE 4-63.  Adrenal myelolipoma. A, On the T2-weighted image, a lesion occupying the right suprarenal space (arrows) blends with
retroperitoneal fat—inconspicuous, despite its large size. Signal loss on the T2-weighted fat-suppressed (B) image and hyperintense
signal on the in-phase image (C), maintained on the out-of-phase image (D), characterize macroscopic fat (arrows). Expected signal loss
on the T1-weighted fat-suppressed image (E) and lack of enhancement on the postcontrast image (F) is observed in an AML (arrows)
mostly composed of fat.

FIGURE 4-64.  Pheochromocytoma. Compared with relative T2 hypointensity of the adrenal adenoma (arrow in A), a large, partially cystic
pheochromocytoma exhibits relative T2 hyperintensity (arrow in B). Note the lack of signal loss (arrow in C and D) when comparing
the in-phase (C) with the out-of-phase (D) image. E, Avid enhancement (arrow) is clear on the postcontrast image. F, The “lightbulb
bright” appearance is apparent on the heavily T2-weighted image in a different patient with a right-sided pheochromocytoma (arrow).
Absent microscopic fat results in lack of signal change (arrow in G) between the in-phase (left in G) and the out-of phase (right in G)
images, and the solid nature of the mass (arrow in H) is reflected by avid enhancement on the postcontrast image (H).
 MRI of the Kidneys and Adrenal Glands   •  251

A B

C D

E F

G H
252  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-65.  Adrenal metastasis. A, Note the heterogeneously hyperintense right adrenal lesion (thin arrow) on the T2-weighted fat-
suppressed image harboring a central cystic necrotic focus (thick arrow) in a patient with metastatic lung cancer. No perceptible signal
loss (arrow in B and C) on the out-of-phase image (B) compared with the in-phase image (C) indicates a lack of microscopic lipid.
D, A corresponding image from a positron-emission tomography–computed tomography (PET-CT) scan reveals the hypermetabolic
activity typical of a metastasis (arrow).

is a space, by definition, in which organs happen

to reside,50 primary lesions of the retroperito- TABLE 4-11.  Inferior Vena Cava Anomalies
IVC duplication
neum are few and far between (Fig. 4-67). Left-sided IVC
Fascial planes divide the retroperitoneum into Azygous continuation of the IVC
three compartments: (1) the anterior pararenal Absent (infrarenal) IVC
space, (2) the perinephric space, and (3) the IVC, inferior vena cava.
posterior pararenal space (Fig. 4-68). Although
lesions arise in all three compartments, our
objective is to focus on those relegated to the
space between the perinephric spaces around Avoiding procedural complications arising from
the great vessels (discussion of lesions in the failure to acknowledge these anomalies is the
anterior pararenal space related to the pancreas main objective. For example, unilateral right-
appears in Chapter 3). sided IVC filter placement in IVC duplication
leaves the left-sided IVC untreated. Planning
abdominal surgical procedures, liver or kidney
IVC Anomalies
transplant, and interventional procedures ben-
Anomalies of the IVC (Table 4-11) speak for efits from preprocedural recognition of these
themselves and harbor no direct complications. anomalies.
 MRI of the Kidneys and Adrenal Glands   •  253

E F

G
FIGURE 4-65, cont’d  A large right adrenal mass (arrow in E and F) demonstrates even more heterogeneous signal and enhancement
with cystic necrosis on the T2-weighted fat-suppressed (E) and postcontrast (F) images in a different patient with metastatic RCC.
G, The primary mass is shown on the postcontrast image through the kidneys (arrow).

spine,” which is a feature of retroperitoneal lym-

Retroperitoneal Fibrosis
phoma (RL). The MR appearance evolves with
Inflammatory retroperitoneal etiologies— chronicity, initially appearing hyperintense on
retroperitoneal fibrosis (RF) and inflammatory fluid-sensitive sequences with avid enhance-
abdominal aortic aneurysm (IAAA) share ment and ill-defined margins. Over time, T2
common imaging features. In fact, etiologic signal and enhancement wane and margins
and histologic features also overlap. Although sharpen (see Fig. 4-69). Ureteral encasement
precise mechanisms are incompletely under- occurs frequently, leading to functional obstruc-
stood, both conditions involve autoimmune- tion due to suppression of peristalsis. RF is typi-
mediated fibrosis. Imaging features diverge cally centered in the retroperitoneum (L3–5),
significantly, however. but potentially extends caudally into the pelvis
RF represents a common inflammatory or cephalad into the mediastinum. Suggesting
pathway induced by a number of potential the diagnosis facilitates treatment, which is rela-
pathogens, such as drugs (methysergide, beta tively specific to RF—withdrawal of the inciting
blockers, hydralazine, ergotamine, and lysergic agent, corticosteroids, and relief of ureteral
acid diethylamide [LSD]), irradiation, autoim- obstruction.
mune diseases, retroperitoneal hemorrhage, and Potential confounders include RL, IAAA, and
malignancies (gastrointestinal, breast, prostate, retroperitoneal hemorrhage. As previously men-
lung, cervical, and renal malignancies). However, tioned, RL more commonly extends along the
two thirds of cases are idiopathic and referred posterior margin of the aorta, lifting it off the
to as Ormond’s disease. A rind of soft tissue spine, whereas RF relatively spares the posterior
envelops the aorta, IVC, and ureters in RF (Fig. aortic perimeter. Lymphoma—a relatively soft,
4-69), without “lifting the aorta away from the pliable neoplasm—rarely obstructs the ureters
254  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-66.  Adrenal cortical carcinoma. A, The coronal T2-weighted image reveals a large, complex mass (thin arrows) with central
necrosis (thick arrows) flattening the upper pole of the right kidney. B, The corresponding axial T2-weighted fat-suppressed image shows
the large size of the lesion (arrows). C, Signal preservation on the out-of-phase image excludes microscopic lipid and hyperintensity
suggests hemorrhage (thin arrows) and hemorrhagic necrosis (thick arrows). D, The postcontrast image discloses the hypovascularity of
the large, necrotic mass.

Normal variant Inflammation Trauma Neoplasm

IVC anomalies Retroperitoneal Retroperitoneal Lymphoma

fibrosis hemorrhage

Inflammatory Metastases
aneurysm

Sarcoma

FIGURE 4-67.  Retroperitoneal lesions. IVC, inferior vena cava.

 MRI of the Kidneys and Adrenal Glands   •  255

ARF = Anterior renal fascia

PRF = Posterior renal fascia

Peritoneal
cavity
ARF

Asc Pancreas Desc

colon colon

IVC Ao
Anterior
pararenal
space Spine

Perinephric
Perinephric (perirenal)
(perirenal) space
PRF
space
Posterior
pararenal FIGURE 4-68.  Retroperitoneal anatomy. Ao,
space aorta; asc, ascending; desc, descending.

A B

FIGURE 4-69.  Retroperitoneal fibrosis. A, A markedly hypoin-

tense confluent, rind of tissue (thin arrows) envelopes the
aorta and IVC without “lifting the aorta away from the spine”
(in contradistinction to lymphoma) on the T2-weighted
image—note the hydronephrosis (thick arrows) due to the
ureteral involvement and suppression of peristalsis. B, The
axial postcontrast image shows the modest enhancement (thin
arrows) and susceptibility artifact (thick arrow) corresponding
to an IVC filter. C, The coronal delayed enhanced image
better depicts the craniocaudal extent of involvement (thin
C
arrows) and the IVC filter (thick arrow).
256  •  Fundamentals of Body MRI

A B

FIGURE 4-70.  Inflammatory abdominal aortic aneurysm. The

coronal (A) and axial (B) T2-weighted images show a dilated
abdominal aorta (thin arrows) with a thickened hypointense
rim (thick arrows). C, The postcontrast magnetic resonance
angiography (MRA) sequence reveals the irregular luminal
contour (arrows) due to eccentric mural thrombus, with no
C
perceptible enhancement of the periaortic rind.

and discrete nodes are usually discernible. IAAA

Inflammatory Aortic Aneurysm
is essentially the same process as RF owing to
inciting antigen in the wall of the aorta, thought In IAAA, dense connective tissue infiltrated by
to reside in atheromatous plaque. The extent of inflammatory cells extends beyond the normal
involvement is generally restricted focally to the confines of the aneurysmal aortic adventitia,
aortic aneurysm. Retroperitoneal hemorrhage resulting in a periaortic enhancing rind of tissue
fails to enhance and exhibits signal characteri­ (Fig. 4-70). The periaortic tissue mantle mea-
stics expected of hemorrhage rather than sures up to 2 cm in thickness, and signal char-
fibrosis. acteristics seem to be less predictable than the
 MRI of the Kidneys and Adrenal Glands   •  257

D E
FIGURE 4-70, cont’d  Delayed coronal (D) and axial (E) postcontrast images show prominent enhancement of the periaortic mantle (arrows).

predictably prominent enhancement.51 Prompt a confluent nodal mass encircles the aorta
diagnosis and discrimination from uncompli- and IVC, displacing the aorta from the spine
cated abdominal aortic aneurysm ensure appro- (Fig. 4-71). Monotonous features with mild
priate treatment. The presence of perianeurysmal homogeneous hyperintensity on fluid-sensitive
inflammation prompts consideration of presur- sequences, mild enhancement with relative lack
gical treatment with corticosteroids to minimize of mass effect (even despite large size), and
inflammation and operative technical modifica- extensive retroperitoneal involvement typify
tions to minimize duodenal and ureteral dissec- lymphoma.
tion and improve surgical outcomes. RF and metastases from primary malignancies,
such as testicular and prostate carcinoma, figure
most prominently in the differential diagnosis.
Retroperitoneal Lymphoma
RF and metastatic disease fail to lift the aorta
Retroperitoneal neoplasms encompass a wide from the spine and RF frequently obstructs the
range of lesions (including a variety of sarco- ureters, unlike RL. Extension along lymphatic
mas), many of which are beyond the scope drainage pathways from the pelvis points to
of this text. RL is the most common retro­ genitourinary metastasis, such as testicular or
peritoneal malignancy, with either Hodgkin’s prostate carcinoma.
or non-Hodgkin’s lymphoma invading the
retroperitoneal lymph nodes. Hodgkin’s lym-
Retroperitoneal Metastases
phoma tends to involve the spleen and retro-
peritoneum with a contiguous spread pattern. Retroperitoneal metastases originate from hema-
Non-Hodgkin’s lymphoma more often involves togenous or lymphatic spread or from direct
a variety of nodal groups, with a predilection extension (Fig. 4-72). Metastatic lymphadeno­
for mesenteric nodes and extranodal sites. pathy is best appreciated as either (1) a con-
Overall, RL most commonly involves para-aortic, glomerate hyperintense mass on fat-suppressed
aortocaval, and retrocaval nodal groups. Nodes enhanced or T2-weighted sequences against the
tend to measure greater than 1.5 cm in short- signal void of signal-suppressed retroperitoneal
axis diameter with bilateral involvement. Often, fat or (2) on T1-weighted sequences without fat
258  •  Fundamentals of Body MRI

A B

C D
FIGURE 4-71.  Retroperitoneal lymphoma. The T2-weighted fat-suppressed (A) and postcontrast (B) images depict nearly coalescent lymph
nodes throughout the retroperitoneum, including retroaortic extension (thin arrows), with monotonous features—homogeneous T2
hyperintensity and modest homogeneous enhancement. Encirclement of the superior mesenteric artery (SMA; thick arrow) denotes
concurrent mesenteric involvement. C and D, The coronal steady-state images show the extent of craniocaudal involvement (arrows).

Lymphatic spread Hematogenous spread Direct Invasion

Testicular carcinoma Lung carcinoma Pancreatic carcinoma
Prostate carcinoma Breast carcinoma Gastrointestinal carcinoma
Bladder carcinoma Melanoma
Ovarian carcinoma
Endometrial carcinoma
Colorectal carcinoma

FIGURE 4-72.  Primary malignancies in retroperitoneal metastasis.

 MRI of the Kidneys and Adrenal Glands   •  259

saturation as a conglomerate mass against the 14. Meier P, Farres MT, Mougenot B, et al. Imaging medul-
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mate primary tumor enhancement. Generally obstruction. Clin Radiol 52:445–450, 1997.
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 chapter five 

Magnetic Resonance Imaging of

the Female Pelvis
region of interest and not the upper thighs or
INTRODUCTION
lower abdomen). Single-shot fast spin-echo
Magnetic resonance imaging (MRI) serves as the T2-weighted images or balanced gradient echo
most comprehensive and conclusive modality sequences yield the most diagnostic informa-
available to image the female pelvis. The inher- tion. Configure the localizer sequence to include
ent zonal anatomy of the uterus is exquisitely the kidneys because of the association of renal
depicted as a function of the different water anomalies with müllerian duct (fallopian tubes,
content and histology of each mural layer. The uterus, and proximal vagina) anomalies. The
predictable MRI appearance of the uterus remainder of the examination demands a
renders identification of abnormalities straight- focused approach with a higher spatial resolu-
forward (Fig. 5-1). tion and a field of view in the range of 24 cm.
The evaluation of the adnexa hinges on the A combination of T1-weighted, T2-weighted,
unique spectroscopic capability of MRI to dif- and fat-saturated sequences suffices to solve
ferentiate between lesions of different tissue most problems encountered in the pelvis (Table
composition, such as lipid (dermoid cyst), water 5-2). T2-weighted images are the mainstay of
(functional ovarian cyst), and hemorrhage (endo- pelvic imaging. T2-weighted images display the
metrioma). Improved tissue contrast elevates trilaminar anatomy of the uterus—the inner
the sensitivity for neoplastic and malignant fea- endometrium, the central inner myometrium
tures compared with other modalities. The most (junctional zone), and the outer myometrium
common indications for MRI of the female pelvis (see Fig. 5-1)—and confer conspicuity to the
include characterization of adnexal lesions, iden- ovaries and most adnexal lesions, especially
tification and characterization of fibroids, assess- cystic lesions. Oblique coronal and axial images
ment of fibroid treatment response, problem orthogonal to the axis of the uterus supplement
solving inconclusive ultrasound or computed the examination to characterize potential mül-
tomography (CT) findings, and adjunctive staging lerian duct anomalies, if suspected (Figs. 5-3
of malignancies (Table 5-1). and 5-4). T2-weighted images highlight cystic
adnexal lesions and any potential septa, mural
nodules, or other complex features. T1-weighted
TECHNIQUE
images depict hemorrhage and lipid, and the
Given the potentially small size of ovarian, cervi- addition of fat-saturated sequences allows for
cal, and uterine lesions and the need for high- differentiating between blood and fat (which
resolution imaging, the examination justifies the both appear hyperintense on T1-weighted
use of a high-field-strength system (≥1.0 T). images without fat suppression). In-phase and
Nonetheless, diagnostic images can be obtained out-of-phase images serve as a time-saving alter-
on systems of lower field strength (Fig. 5-2). A native to spin-echo T1-weighted images (~20 sec
dedicated phased array coil guarantees optimal compared with 3–5 min) with sensitivity to
signal to noise. An antiperistaltic agent to elimi- both intracellular fat and susceptibility artifact,
nate motion artifacts from bowel activity (such although potentially degraded by low signal-to-
as glucagons or hyoscyamine) ensures minimiza- noise on low-field-strength systems.
tion of motion artifact. Consider the application Gadolinium-enhanced images provide addi-
of vaginal gel to facilitate evaluating vaginal and tional information regarding the complexity
cervical lesions.1 and/or blood supply of a lesion and its tissue
Start off viewing a localizer sequence with a content and often increase lesion conspicuity.
large field of view to assess coil placement Enhancement of an ovarian lesion confirms
(ensuring maximal signal emanating from the its neoplastic etiology. Enhancement patterns
261
262  •  Fundamentals of Body MRI

provide diagnostic information.2 For example,

arterial enhancement characterizes an arteriove-
nous fistula and delayed enhancement charac-
terizes fibrous lesions (Table 5-3), such as an
ovarian fibroma. Dynamic imaging provides a
reliable timeframe to assess enhancement pat-
terns, whereas static pregadolinium and postg-
adolinium images yield only binary information
(enhancement vs. no enhancement). Quantita-
tive evaluation of fibroid vascularity demands
dynamic images.
Three-dimensional fat-saturated gradient echo
images offer the best spatial resolution and
tissue contrast. Approximately 20 mL of gado-
linium (0.1 mmol/kg) is administered intrave-
nously at approximately 1 to 2 mL/sec. A timing
bolus or timing sequence triggers the arterial
phase of the acquisition and one or two addi-
FIGURE 5-1.  Normal uterine mural stratification. Fat-suppressed
sagittal T2-weighted image through the uterus shows the normal
tional phases obtained in succession suffice. A
trilaminar appearance with the central hyperintense zone (the delayed T1-weighted (preferably fat-saturated)
endometrium—thin arrows), the middle hypointense zone (the sequence detects delayed enhancement, if
junctional zone—thick arrows), and the outer isointense zone present.
(outer myometrium—open arrow).

TABLE 5-1.  Female Pelvis Magnetic Resonance Imaging Indications

Clinical Presentation Imaging Objective Details

Pelvic pain Nonspecific

Dysmenorrhea (painful menstruation) Exclude endometrial and/or cervical lesions (polyp, fibroid, neoplasm) Standard protocol
Exclude adenomyosis and endometriosis
Menorrhagia (>80 mL/cycle) Same as above
Metrorrhagia (light bleed, irregular intervals) Same as above
Menometrorrhagia (heavy bleed > 80 mL, Same as above
irregular intervals)
Abnormal pelvic examination Exclude endometrial or cervical cancer or polyp Standard protocol
Delayed menses or precocious puberty
Postmenopausal bleeding
Evaluation of pelvic pain or mass
Pain or fever after pelvic surgery or delivery Exclude endometritis, hematoma Review gradient echo images for
susceptibility
Localization of intrauterine device Nonanatomic susceptibility artifact (usually linear or curvilinear) Review gradient echo images for
susceptibility
Evaluation infertility Müllerian duct anomalies ± Dedicated imaging planes
Congenital anomalies Müllerian duct anomalies ± Dedicated imaging planes
Uterine fibroid evaluation Location (submucosal vs. intramural vs. subserosal), vascularity ± Dedicated imaging planes
degeneration (cystic, hemorrhagic)
Assessment for pelvic floor defects Cystocele, enterocele, vagocele, rectocele abnormal pelvic floor descent ± Dynamic maneuvers
Clarification of indeterminate imaging findings Follow-up previously detected abnormality (i.e., hemorrhagic cyst)
Further characterization abnormality detected on another imaging study
Known or risk of malignancy Screening for malignancy in patients with increased risk Consider vaginal gel if cervical
Detection and staging of gynecologic malignancies or vaginal involvement
Tumor recurrence assessment
Presurgical/laparoscopic evaluation
Cervical and endometrial carcinoma staging
Cervical: Violation of fibrous stroma (intact 1A-B, disrupted 2B),
parametrial invasion (2B), vaginal invasion (upper vagina 2A, lower
one third 3A), spread to adjacent structures, spread to pelvic sidewall
(3B), spread to bladder/rectum (4A), pelvic lymphadenopathy
Endometrial: Depth of myometrial invasion (1A-C), cervical extension
(2A-B), spread to ovary/adnexa (3A), evidence of peritoneal spread
(3A), vaginal extension (3B), pelvic lymphadenopathy (3C), bladder/
bowel invasion (4A)
 Magnetic Resonance Imaging of the Female Pelvis  •  263

A B

C D
FIGURE 5-2.  0.3-Tesla images. A, Sagittal T2-weighted image through the uterus obtained on a 0.3-Tesla system reveals an isointense
endometrial mass with no deep myometrial invasion corresponding to endometrial carcinoma. B, The corresponding axial T2-weighted
image shows normal endometrium (thin arrow) abutting the distal aspect of the mass and an intramural fibroid (thick arrow). Sagittal
(C) and axial (D) T2-weighted images through the uterus obtained on a 0.3-Tesla system in a different patient show a tubular mildly
hyperintense lesion with a hypointense core within the endometrial cavity found to be an endometrial polyp. Also note the partially
subserosal fibroid arising from the posterior uterine body (arrow in D).

TABLE 5-2.  Female Pelvis Magnetic Resonance Imaging Protocol

Pulse Sequence Details Field of View Slice Thickness

Localizing sequence (coronal) SSFSE (5000/180) 32 cm 5 mm

b-FFE (min/min) 32 cm 5 mm
Axial T2 ± Fat saturated (4000/100) 24 cm 4 mm
Axial T1 FSE (5/200) 24 cm 4 mm
In-/out-of-phase (2.3, 4.6/200) 24 cm 7 mm
Sagittal T2 ± Fat saturated (80/2500)* 24 cm 6 mm
Dynamic Sagittal or axial (min/min) with fat suppression* 24 cm 4 mm (interpolated ⇒ 2 mm)
Delayed postgadolinium Three-dimensional GRE (min/min) 24 cm 4 mm (interpolated ⇒ 2 mm)
Two-dimensional SPGR (min/22) 24 cm 5 mm
*At least one fat-suppressed sequence is necessary to identify dermoid cyst and discriminate between hemorrhage and lipid.
FFE = fecal fat extraction; FSE = fast spin echo; GRE = gradient-recalled echo; SPGR = spoiled gradient echo; SSFSE = single-shot fast
spin-echo.
 TABLE 5-3.  Adnexal Lesion Enhancement
Patterns
Lack of enhancement Simple/functional ovarian cyst
Parovarian cyst
Ovarian torsion
Mild rim enhancement Corpus luteal cyst
Endometrioma
Some cystadenomas
± Ovarian torsion
Marked rim enhancement Some cystadenomas/
cystadenocarcinomas
Tubo-ovarian abscess
Solid enhancement
Arterial Arteriovenous malformation
Early Malignant > benign epithelial ovarian
neoplasms
Delayed Fibroma
Benign > malignant epithelial
ovarian neoplasms

FIGURE 5-3.  Oblique coronal imaging of the uterus. The full

extent of a fibrous septum (arrow) of a septate uterus (and other
congenital anomalies) is well delineated by orienting the imaging
plane along the long axis of the uterus to obtain an oblique
coronal image.

R L

A B

C D
FIGURE 5-4.  T-shaped uterus. A, Obliquely coronally reformatted T2-weighted image in a 47-year-old woman with a history of fetal
diethylstilbestrol exposure elegantly portrays the aberrant anatomy that is less clearly rendered with coronal (B), sagittal (C), and axial
(D) planes prescribed orthogonally to the axes of the body.
 Magnetic Resonance Imaging of the Female Pelvis  •  265

Look at the uterus, keeping in mind the age

INTERPRETATION
and menstrual status of the patient and any rel-
If pictures are worth a thousand words, imagine evant history, such as endometrial or cervical
how much the hundreds of images in the multi- carcinoma, cesarean section, or treated or
image sets in a female pelvis MRI study are untreated fibroids. Measuring the uterus in three
worth. This much information compels the use orthogonal planes is standard and helps objec-
of a directed search pattern (Table 5-4). First of tively assess overall uterine size. Observe uterine
all, assess the technical adequacy of the exami- zonal anatomy (central endometrium, middle
nation. Review the localizer sequence, which junctional zone, and outer myometrium) and
usually includes large field-of-view coronal measure the thickness of each. Identify any
images, and ensure that coil placement is ade- fibroids or other uterine lesions and record
quately reflected by the highest signal emanat- sizes. Comment on whether the uterus is ante-
ing from the region of interest (and not the verted or retroverted or retroflexed. In the
abdomen or subpelvic region) (Fig. 5-5). Note setting of hysterectomy, record the presence
whether gadolinium was administered and and status of the vaginal cuff and residual cervi-
whether enhancement is perceptible. Assess the cal or uterine tissue. Look for susceptibility arti-
degree of motion artifact and any other artifact fact on gradient echo images corresponding to
that degrades image quality (Fig. 5-6). surgical clips, if present.

TABLE 5-4.  Female Pelvis Checklist

Technical Vagina
Magnetic field strength Cystic lesions (upper vs. lower)
Coil position Vaginal wall
Signal ⇒ optimal signal corresponding to pelvis Focal vs. diffuse thickening
Kidneys ⇒ at least one large field-of-view coronal should include kidneys Invasion from adjacent structures
Enhancement ⇒ note amount and type of contrast agent Tampon
Inspect vessels for adequate enhancement
Artifacts Adnexa
Bowel peristalsis (see Fig. 5-6D-F) Ovaries
Susceptibility ⇒ surgical hardware, gas (e.g., bowel) Dimensions
Motion ⇒ bulk motion, respiratory motion, vascular flow artifacts Cystic lesions
Conductivity/dielectric effects ⇒ focal signal loss (⇑ at 3T) Size
Hemorrhage
Uterus Shading
Size (height × width × length) Lipid
Position Rim enhancement
Anteverted vs. retroverted Solid component/complexity
Anteverted vs. retroflexed Solid lesions
Endometrium T2 signal
Thickness Unilateral vs. bilateral involvement
Homogeneity Parovarian region
Focal lesions Cystic lesions
Presence of intraluminal fluid or susceptibility (e.g., gas, IUD) Vascular lesions
Inner myometrium (junctional zone) Lymphadenopathy
Thickness
Sharpness of border Other Anatomy
Intramyometrial hyperintensities Bladder
Cesarean section defect Bowel
Fibroids Musculoskeletal structures
Size(s) Bony pelvis
Submucosal vs. intramural vs. subserosal Lower lumbar spine
Degeneration: cystic vs. hemorrhagic vs. other Muscles
Vascularity: necrotic vs. hypovascular vs. hypervascular Gluteal
Adductor
Cervix Hip flexor
Mucosa Piriformis
Naboth’s cysts Tendons
Thickness Iliopsoas
Luminal fluid Rectus femoris
Stroma Hamstring
Integrity
Parametrial infiltration
IUD = intrauterine device.
266  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-5.  Poor coil placement. A and B, Coronal T2-weighted images of the pelvis show maximal signal centered at the level of the
pubic symphysis rather than the region of interest—the uterus and adnexa—and remember that the kidneys should be visualized in all
cases. Note the homogeneously hyperintense mass in the right hemipelvis in this patient with pelvic lymphoma (arrow). C, Coronal
T2-weighted image in a different patient demonstrates maximal signal arising from the region of the uterus with visualization of the
kidneys (thin arrows) in a patient with cervical carcinoma (thick arrow). D, The kidneys (thin arrows) are conspicuously well visualized
on this coronal T2-weighted image with maximal signal emanating from the abdominopelvic junction in this patient with a right-sided
cystadenofibroma (thick arrow).

Confirm the integrity of the fibrous stroma of older women and to their variable location.
the cervix and exclude the presence of any The presence of ovarian cysts often attracts the
cystic or solid cervical lesions. Inspect the examiner’s attention to their location. In the
vagina and vulva and keep in mind the preva- absence of an easily identifiable ovariform struc-
lence of benign developmental and acquired ture, remember the relevant anatomy tethering
cystic lesions. Exclude vaginal focal or diffuse the ovaries in the pelvis (Fig. 5-7). The suspen-
vaginal wall thickening and note intraluminal sory ligament contains the vascular structures
fluid if present. and originates from the pelvic sidewall in the
Look for the ovaries, often a difficult task region of the iliac bifurcation connecting to the
owing to their small size in prepubertal and ovary. The round “ligament” (actually composed
 Magnetic Resonance Imaging of the Female Pelvis  •  267

A B

C D
FIGURE 5-6.  Image degradation due to artifacts. A and B, Coronal T2-weighted (A) and axial T1-weighted fat-saturated gradient echo
(B) images depict wraparound artifact along the phase encoding axis (arrows in A and B), which do not obscure underlying anatomy
and reflect selection of a small field of view resulting in aliasing of subcutaneous fat. C, Sagittal T2-weighted image mildly degraded by
breathing motion artifact along the phase encoding axis (arrow). D, A combination of susceptibility artifact (thin arrows) and failure of
fat suppression (thick arrows) degrades this sagittal T2-weighted fat saturated image in a patient with a focal fundal adenomyoma (open
arrow).

largely of smooth muscle) is the female equiva-

lent of the spermatic cord and courses from the TABLE 5-5.  Acute Adnexal Pathology
uterine cornua into the inguinal canal through Ectopic pregnancy
the deep inguinal ring in an effort to maintain Ovarian torsion
Tubo-ovarian abscess
anteversion. The proper ovarian ligament origi- Ruptured cystic lesion (e.g., ruptured dermoid cyst)
nates adjacent to the round ligament but, unfor- Fibroid degeneration
tunately, usually averts detection as a discrete
structure. Measure the ovaries in three planes
and record measurements of any associated (Table 5-5). Pay particular attention to fluid-
ovarian lesions. sensitive sequences (such as T2-weighted fat-
Parenthetically, MRI occasionally supple- saturated and inversion recovery sequences),
ments ultrasound in detecting acute ovarian/ which most vividly portray the edema, inflam-
adnexal pathology. Under acute circumstances, mation, and/or fluid almost always associated
consider the possibility of (ectopic) pregnancy, with acute pathology.
tubo-ovarian abscess (TOA), torsion, and rupture Assess the quantity of free fluid in the pelvis
of a preexisting ovarian lesion (such as dermoid) and remember that a small quantity is
268  •  Fundamentals of Body MRI

E F

G
FIGURE 5-6, cont’d  E-G, Artifact arising from bowel peristalsis blurs and obscures normal pelvic anatomy with no evidence of gross patient
motion.

physiologic in reproductive-age females. Espe- peritoneal cavity as possible. View sagittal and
cially if there is a history of (ovarian) carcinoma, coronal images to assess for pelvic floor laxity.
exclude the presence of peritoneal thickening, Finally, use T1-weighted and fluid-sensitive
enhancement, or nodularity/implants. Look for sequences to exclude osseous lesions. Sagittal
pelvic lymph nodes and record any enlarged images are useful to detect disk pathology in the
nodes. lower lumbar spine. Evaluate muscles and
Although the bladder is often not optimally tendons (such as the gluteal, adductor, and hip
evaluated because of incomplete distention flexor muscles and iliopsoas, rectus femoris, and
(usually patients are instructed to void in order hamstring tendons) on T2-weighted axial and
to promote comfort and obviate motion for the coronal sequences.
duration of examination), do not ignore it.
Observe any focal lesions, filling defects/stones,
wall thickening, or diverticula. Check the UTERUS
urethra for diverticula.
Normal Features
Trace the bowel from the anus proximally as
far as possible. Look at the coronal images, In medical parlance, “uterus” signifies the uterus
which are often performed with the largest field body or corpus and “cervix” refers to the uterine
of view to visualize as much of the bowel and cervix. Before you can intelligently comment on
 Magnetic Resonance Imaging of the Female Pelvis  •  269

Symphysis pubis

Common iliac
vein and
Bladder artery

Round
ligament

Ovarian
ligament
Uterus
Fallopian
tube

Ovary

Rectum Suspensory
ligament

Broad ligament

Ureter

Uterosacral
ligaments

FIGURE 5-7.  Adnexal ligamentous anatomy.

Try to appreciate the zonal anatomy or mural

TABLE 5-6.  Normal Dimensions of the Ovaries stratification of the uterus, which is most devel-
and Uterus oped in reproductive-age females (Fig. 5-9;
Uterus reproductive age: 8 × 5 cm see also Fig. 5-1) and fades during menopause.
Uterus premenarchal and postmenopausal: 5 × 2 cm Endometrial cyclical changes occur only in men-
Endometrium
Proliferative: 3–8 mm struating females; in premenopausal and post-
Secretory: 5–16 cm menopausal females, the endometrial changes
Postmenopausal (no bleeding): ≤8 mm are only incurred by pathologic or iatrogenic
Postmenopausal (bleeding): ≤5 mm
Ovaries (volume = 0.523 × length × width × thickness) phenomena and normally measure up to 4 to
Premenstrual: 3.0 mL 5 mm in maximal thickness. In menstruating
Reproductive age: 9.8 mL females, endometrial thickness is variable.6 From
2.5–5.0 × 1.5–3.0 × 1.0–2.0 cm
Postmenopausal: 5.8 mL the proliferative phase, the endometrium thick-
ens from a minimum of 3 to 8 mm to 5 to 16 mm
during the secretory phase. Notwithstanding
age and menstrual status, normal endometrium
the status of the (body of the) uterus you need demonstrates uniformly homogeneously near-
to know the age and menstrual status of the fluid hyperintensity on T2-weighted images.
patient and any relevant surgical history. The If the appearance and/or thickness falls
size of the uterus is a function of age and outside the normal range, try to characterize
reproductive/menstrual history (Table 5-6).3–5 the abnormality as intracavitary fluid or gas
Without the stimulating effects of female hor- versus a focal or diffuse process. Fluid is a fre-
mones before puberty, cervical stature exceeds quent and generally nonpathologic finding in
uterine size. Measure the uterus in three menstruating females. Prepubertal endometrial
orthogonal dimensions along its axis and fluid generally indicates an obstructing
comment on uterine positioning or flexion lesion (hydrometrocolpos or hydrocolpos).
(anteversion, retroversion, anteflexure, or retro- Postmenopausal patients with endometrial fluid
flexure) (Fig. 5-8). often harbor an underlying endometrial or
270  •  Fundamentals of Body MRI

A B
FIGURE 5-8.  Uterine measurement technique and assessment of anteversion/retroversion/anteflexure/retroflexure. Sagittal (A) and axial
(B) T2-weighted images of a retroverted uterus illustrate the measurement technique for obtaining the longitudinal (solid line), height
(dashed line) and width (dotted line) measurements. Note the focal adenomyoma (arrow).

Uterine (T2-Weighted) Zonal Anatomy homogeneity of the T2 hyperintense endome-

Endometrium trial layer is the common denominator.
Outer
myometrium Junctional zone Endometritis
Endometritis falls into two main categories—
postpartum and non-postpartum. Endometritis
Uterus
most commonly follows vaginal delivery, espe-
cially with prolonged rupture of membranes,
chorioamnionitis, prolonged labor, and retained
products of conception. Risk factors for non-
Inner postpartum endometritis include uterine artery
myometrium Cervix
embolization (UAE), venereal disease, and pres-
(Junctional zone)
ence of an intrauterine device (IUD). Whereas
Vagina endometritis usually relies on clinical findings
for diagnosis, imaging studies exclude additional
abnormalities in patients with refractory symp-
FIGURE 5-9.  Zonal anatomy/mural stratification of the uterus.
toms. Typical findings include diffuse uterine
enlargement, intracavitary gas and (often
cervical lesion (such as endometrial atrophy, complex) fluid, and a thickened, heterogeneous
hyperplasia, polyp or carcinoma, and cervical endometrium.8 Look for edematous, relatively
stenosis), but fluid has not been conclusively hypovascular foci subjacent to the abnormal
proved to be pathologic.7 Gas may be present endometrium.
postprocedurally, postpartum, or in the context
of infection (endometritis). Gas induces suscep- Hormonal Factors
tibility artifact and is most conspicuous on gra- Hormonal (endogenous and iatrogenic) etiolo-
dient echo sequences. gies account for another major cause of diffuse
endometrial abnormality. Endometrial hyperpla-
sia generally arises from unopposed estrogen, a
Endometrial Pathology
potential etiology of diffuse endometrial thick-
Diffuse Abnormalities ening and heterogeneity without associated gas
Diffuse endometrial abnormalities include pre- (and less likely) intracavitary fluid. Remember
dominantly endocrinologic/proliferative, infec- that hormonal stimulation due to pregnancy
tious, iatrogenic, and neoplastic etiologies (including ectopic pregnancy) results in endo-
(Fig. 5-10). Global alteration in thickness or metrial thickening.
 Magnetic Resonance Imaging of the Female Pelvis  •  271

DIFFUSE ENDOMETRIAL ABNORMALITIES

Endocrinologic/ Infectious Iatrogenic Neoplastic

proliferative
Polycystic ovarian Postpartum Exogenous Endometrial
syndrome endometritis estrogen carcinoma
Pregnancy Non-postpartum Tamoxifen Cervical
endometritis carcinoma
Obesity
FIGURE 5-10.  Diffuse endometrial abnormalities.

either iatrogenic, neoplastic (benign and malig-

nant), or pregnancy-related (Fig. 5-12). Focal
iatrogenic lesions—intrauterine adhesions
(Asherman’s syndrome) and intrauterine devices
(IUDs)—do not pose a diagnostic dilemma.
Pregnancy-related lesions, such as retained
products of conception, GTD, and the gesta-
tional sac itself, rarely provoke MRI and fall
outside the scope of this text. Neoplastic
lesions encompass primary endometrial lesions,
such as endometrial polyps and endometrial car-
cinoma, and myometrial-derived lesions with
endometrial extension, such as submucosal
fibroids.

Intrauterine Adhesions
FIGURE 5-11.  Endometrial tamoxifen changes. The sagittal
Intrauterine adhesions, also known as Asher-
T2-weighted fat-suppressed image in a patient on tamoxifen
man’s syndrome, manifests as multiple linear
shows the typical cystic endometrial thickening.
intracavitary enhancing hypointensities, bridg-
ing the normal hyperintense endometrium (Fig.
Tamoxifen 5-13). These endometrial adhesions reflect the
Tamoxifen (adjunctive treatment for metastatic sequela of endometrial trauma from curettage,
breast cancer) possesses estrogenic activity, cesarean section, myomectomy, irradiation,
stimulating the endometrium. In addition to IUD, or endometritis. Patients may be asymp-
endometrial hyperplasia, tamoxifen engenders a tomatic or present with menstrual disorders,
number of endometrial abnormalities, including such as secondary amenorrhea, or infertility.
polyps, cystic atrophy, and endometrial carci- Few lesions simulate the appearance of intra-
noma. The presence of multiple cystic foci asso- uterine adhesions and their common denomina-
ciated with diffuse heterogeneous endometrial tor is T2 hypointensity—submucosal fibroids,
thickening typifies tamoxifen change (Fig. 5-11). endometrial polyps, IUDs, and occasionally
The definition of endometrial thickening in the blood clots. The central fibrous core of a polyp
setting of tamoxifen defies precise limits. The and the susceptibility artifact–inducing linear/
general consensus suggests an upper limit of 8 tubular shape of IUDs simulate the linear hypo­
to 9 mm.9 If vaginal bleeding coexists, hysteros- intensity of intrauterine synechiae but lack the
copy and biopsy are pursued. Remember the perpendicular orientation spanning the endo-
increased risk of nonendometrial abnormalities, metrial cavity. Fibroids and blood clots lack
such as endometriosis and adenomyosis, with the linear morphology and the predictable
tamoxifen use.10 orientation.

Focal Abnormalities Intrauterine Device

Focal endometrial abnormalities include a wide IUDs do not present diagnostic difficulty. Endo-
range of pathology most of which manifests spe- cavitary linear hypointensity on all pulse
cific MRI features. Most of these lesions are sequences signals the presence of an IUD (Fig.
272  •  Fundamentals of Body MRI

Focal Endometrial Lesions

2
4
Benign Malignant

3
1. Submucosal fibroid 5 6
2. Intrauterine device 7
3. Adhesions
4. Endometrial polyp
5. Cesarean section defect
6. Endometrial carcinoma
7. Cervical carcinoma spread
FIGURE 5-12.  Differential diagnosis of focal endometrial abnormalities.

A B
FIGURE 5-13.  Intrauterine adhesions. Sagittal T2-weighted fat-saturated (A) and T1-weighted fat-saturated postgadolinium gradient echo
(B) images show fluid distention of the endometrial canal proximal to an adhesion at the level of the internal cervical os (arrow).

5-14). The perfect linearity virtually excludes adenomyosis—which might exhibit intralesional
organic etiologies. hyperintensities, but not myometrial thinning—
and myometrial cysts, which also do not exhibit
Cesarean Section Defect myometrial thinning and are generally spherical
The most common lesion in the category of in morphology. Extreme uterine anteflexion
iatrogenic lesions is the cesarean section defect. simulates the defect at the point of flexion with
Because of its ubiquity, an awareness of the maintenance of the integrity of the myometrial
typical appearance of the cesarean section scar layer (Fig. 5-16).
is essential. The changes are best appreciated on
sagittal T2-weighted images as focal thinning of Endometrial Polyp
the anterior myometrium in the lower uterine The endometrial polyp is among the most
segment just above the internal cervical os with common focal endometrial abnormalities. Endo-
or without a fluid triangular hyperintensity metrial polyps conceptually represent focal
projecting into the defect continuous with glandular and stromal hyperplasia covered
adjacent endometrium (Fig. 5-15). Alternative by endometrium and come in different
etiologies are easily excluded, such as varieties (hyperplastic, atrophic, functional, and
 Magnetic Resonance Imaging of the Female Pelvis  •  273

A B

FIGURE 5-14.  Intrauterine device (IUD). A slender, linear

T-shaped hypointensity within the endometrial cavity
(arrow) on axial T2-weighted (A), T1-weighted (B), and
C
sagittal T2 fat-saturated (C) images corresponds to an IUD.

adenomyomatous). Discrimination from endo- ultimately, discrimination from endometrial car-

metrial carcinoma, let alone between the differ- cinoma requires tissue sampling.
ent types of polyps, is academic. Despite the
accuracy of MRI, definitive exclusion of endo- Endometrial Carcinoma
metrial carcinoma defies imaging capabilities Unfortunately, research has not substantiated
and excision is always recommended. None­ the ability of MRI (or other imaging modalities)
theless, certain features suggest the diagnosis, to differentiate endometrial carcinoma from
including pedunculated (occasionally sessile) endometrial polyps (or other benign endome-
morphology, a cornual or fundal point of endo- trial pathology) with enough confidence to
metrial attachment, intralesional cystic foci, a T2 obviate biopsy. Nonetheless, practically speak-
hypointense central fibrovascular core, and lacy ing, endometrial carcinoma is unlikely to simu-
enhancement (Fig. 5-17; see also Fig. 5-2C and late the pedunculated morphology of a polyp
D). These features render the endometrial polyp and is usually infiltrative and does not contain
conspicuous against the hyperintense, hypovas- a central hypovascular core or intralesional
cular endometrium and, when present, suggest cystic foci. Endometrial carcinoma more
the diagnosis, but not at the expense of biopsy— closely approximates the appearance of diffuse
274  •  Fundamentals of Body MRI

A B

FIGURE 5-15.  Cesarean section defect. A, Cesarean section

characteristically leaves a focal invagination of the hyper­
intense endometrium in the lower uterine segment best
appreciated on sagittal T2-weighted images (arrow).
B, Occasionally, susceptibility artifact (arrow) in the lower
anterior abdominal wall confirms prior surgical interven-
tion as illustrated in the axial in-phase gradient echo image.
C, On a sagittally fat-suppressed T2-weighted image in a
different patient with a history of cesarean section, uterine
C
retroversion lends conspicuity to the defect (arrow).

FIGURE 5-16.  Extreme uterine anteflexion and anteflexion simulate cesarean section. The apparent defect in the lower anterior myome-
trium (arrow) on the sagittal T2-weighted fat-suppressed image is a consequence of anteflexion superimposed on anteversion. The lack
of associated endometrial protrusion confirms the artifactual nature of this finding.
 Magnetic Resonance Imaging of the Female Pelvis  •  275

A B

C
FIGURE 5-17.  Endometrial polyp. Sagittal (A) and axial (B) T2-weighted images reveal a tubular isointense structure with cystic foci
within the endometrial canal (arrow). C, On the axial T1-weighted fat saturated postgadolinium image, the lesion is not clearly dis-
criminated from the adjacent myometrium, indicating moderate enhancement.
276  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-18.  Endometrial carcinoma (pedunculated type). A, Sagittal T2-weighted image reveals an isointense lesion indenting the
anterior endometrial contour (arrow). B, Coronal T2-weighted fat-saturated image corroborates distortion of the endometrium (arrow).
The appearance simulates an endometrial polyp (see Fig. 5-17). C-G, Compare the appearance with the endometrial polyp in a different
patient.

thickening due to hyperplasia (or tamoxifen TABLE 5-7.  Clinical and Histologic Features of
use), and even then, clinical factors may suggest Endometrial Carcinoma
the diagnosis. Notwithstanding, whenever a Endometrioid adenocarcinoma (75–80%)
focal lesion or diffuse thickening is noted and Vary from well-differentiated to undifferentiated (grade 1–3)
Low-grade ⇒ estrogen-related endometrial hyperplasia (younger
unless the abnormality conforms to a short list perimenopausal)
of obvious benign and/or incidental lesions, Serous papillary carcinoma (5–10%)
such as submucosal fibroid, IUD, or simple fluid, Older women
Atrophic endometrium
tissue sampling follows. Aggressive
The variable MRI features of endometrial car- Predilection for myometrial and vascular invasion
cinoma reflect its protean growth patterns, Clear cell carcinoma (3–5%)
Older patients
degree of myometrial invasion, and stage. Dismal prognosis
Whereas many subtypes of endometrial carci- Mucinous adenocarcinoma
noma exist, adenocarcinoma prevails, account- Squamous cell carcinoma
Miscellaneous rare
ing for 90% of cases and histologic subtype has Mixed cell type carcinoma
not been shown to correspond to specific Choriocarcinoma
imaging features (Table 5-7). Endodermal sinus tumor
Small cell carcinoma
A few generalities typify the MRI appear­­ Metastatic carcinoma
ance of endometrial carcinoma. Endometrial
 Magnetic Resonance Imaging of the Female Pelvis  •  277

E F

G
FIGURE 5-18, cont’d  The sagittal fat-suppressed (C) and axial (D and E) T2-weighted images reveal a more hyperintense tubular lesion
(thin arrow in C and D) with a well-defined stalk with a hypointense core (thick arrow in E). Early (F) and delayed (G) enhanced images
show clear delineation of the mass and lacy or textured and more avid enhancement compared with endometrial carcinoma. Note the
T2 hypointense (shading) right adnexal lesion—an endometrioma—abutting the anterior uterine fundus (thick arrow in D).

carcinoma begins as a mass arising from the relatively hypovascular lesion with gradual
endometrium ultimately expanding the endo- enhancement. Hypovascularity is best depicted
metrial cavity. Growth patterns generally on the early/arterial phase of the dynamic
conform to either infiltrative or sessile polypoid sequence; the avidly enhancing normal
(Figs. 5-18 and 5-19; see also Fig. 5-2A and B) myometrium highlights the relatively hypoin-
types, which is why biopsy ensues whenever tense lesion and the discrepancy in intensity
endometrial thickening or focal pedunculated generally fades over time (Fig. 5-20). Margins are
lesion is identified. The lesion evades detection generally indistinct and the lesion expands the
on (unenhanced) T1-weighted images and is endometrial cavity with continued growth
more conspicuous on T2-weighted images. (Table 5-8). Whereas the location strongly sug-
Endometrial carcinoma is usually heteroge- gests endometrial origin, keep in mind the
neously isointense to mildly hyperintense on overlap in imaging features with cervical carci-
T2-weighted images, rendering it visible com- noma, which occasionally extends into the
pared with hypointense inner myometrium endometrial cavity, simulating endometrial
(junctional zone). Endometrial carcinoma is a carcinoma.
278  •  Fundamentals of Body MRI

A B

C
FIGURE 5-19.  Endometrial carcinoma (sessile type). Sagittal T2-weighted fat-suppressed (A) and axial T2-weighted (B) images depict a
mildly hyperintense endometrial mass (arrow) within the hypointense junctional zone, indicating lack of deep myometrial invasion.
C, Relative hypointensity of the mass after gadolinium administration indicates hypovascularity. Note susceptibility artifact arising from
a tampon (arrow).
 Magnetic Resonance Imaging of the Female Pelvis  •  279

A B

C D
FIGURE 5-20.  Endometrial carcinoma with myometrial invasion. Sagittal (A) and axial (B) T2-weighted images show a heterogeneous
mass (arrows) centered in the anterior myometrium nearly reaching the serosal surface indicating deep myometrial invasion. Sagittal
pregadolinium (C) and postgadolinium (D) T1-weighted fat saturated gradient echo images show marked lesion hypovascularity com-
pared with enhancing myometrium (which exceeds the more commonly observed milder hypovascularity). The enhanced image vividly
portrays the deep myometrial invasion (predicting distant metastatic spread).

and bilateral salpingo-oophorectomy, peritoneal

TABLE 5-8.  Imaging Features of Endometrial washings and/or pelvic lymphadenectomy). The
Carcinoma depth of myometrial invasion and cervical
Early ⇒ exophytic, spreading pattern extension predicts the likelihood of pelvic
Later ⇒ myometrial invasion, cervical extension and para-aortic lymph node metastases. Presur-
Distant spread ⇒ direct (majority of local extrauterine spread)
lymphatic (pelvic, para-aortic nodes)
gical knowledge of these factors potentially
hematologic (lungs, liver, bones, brain) influences surgical technique, encouraging
peritoneal/transtubal (intraperitoneal implants) lymphadenectomy and adjuvant radiation and
chemotherapy. Remember that endometrial
cancer spreads by various pathways—direct
invasion of the cervix, vagina, and myometrium;
However, staging rather than diagnosis of lymphatic dissemination to pelvic and para-
endometrial carcinoma is often the objective of aortic nodes; transluminal spread through the
MRI (Table 5-9). FIGO (International Federation fallopian tubes into the peritoneal cavity; and
of Gynecology and Obstetrics) recommends hematogenous spread predominantly to the
surgical staging (total abdominal hysterectomy lungs, liver, and bone.
280  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-21.  Endometrial carcinoma without and with myometrial invasion. Axial (A) and coronal (B) T2-weighted images show a
mostly well-defined endometrial mass (thin arrow in A) focally invading the inner myometrium (junctional zone; thick arrow in B).
Precontrast (C) and postcontrast (D) images reflect lesion hypovascularity and render exquisite tissue contrast, confirming absence of
deep myometrial invasion.

myometrial extension.11,12 Scrutinize the junc-

TABLE 5-9.  Staging of Endometrial Carcinoma tional zone; preservation of the junctional zone
Stage IA: Tumor is limited to the endometrium. precludes deep myometrial invasion (>50%, or
Stage IB: Invasion of less than half the myometrium. IC disease) and the concomitant likelihood of
Stage IC: Invasion of more than half the myometrium.
Stage IIA: Endocervical glandular involvement only.
metastasis. Inspect the outer contour of the
Stage IIB: Cervical stromal invasion. uterus to detect blurring of the normal sharp
Stage IIIA: Tumor invades serosa or adnexa, or malignant peritoneal serosal margin. Wherever growth of tumor abuts
cytology.
Stage IIIB: Vaginal metastasis.
an adjacent organ, such as the bladder or rectum,
Stage IIIC: Metastasis to pelvic or para-aortic lymph nodes. ensure that the tissue planes are preserved—the
Stage IVA: Invasion of bladder or bowel. margins of each organ should be clearly identifi-
Stage IVB: Distant metastasis, including intra-abdominal or inguinal lymph
nodes.
able. Do not forget to look for lymph nodes—
nodes as small as 4 mm in short-axis diameter in
the pelvis may potentially be pathologic.13
Other malignant endometrial lesions are
extremely rare and beyond the scope of this
As a predictor of metastatic probability, the text. Among these neoplasms are lesions such
depth of myometrial invasion is of paramount as metastases from direct extension of cervical
importance (Fig. 5-21; see also Fig. 5-20). (or vaginal) carcinoma (Fig. 5-22), endometrial
T2-weighted images and (early phase) postgado- stromal sarcomas, and mixed müllerian tumors.14
linium images exceed all others in assessing Gestational trophoblastic disease (GTD) is
 Magnetic Resonance Imaging of the Female Pelvis  •  281

E F
S

G
FIGURE 5-21, cont’d  Sagittal T2-weighted image (E) in a different patient degraded by motion artifact poorly depicts uterine zonal anatomy,
which is seen to be due to an infiltrative mass on the axial image (arrows in F). G, Coronal enhanced image demonstrates deep invasion
of the enhanced myometrium by the hypovascular mass.

A B
FIGURE 5-22.  Cervical carcinoma extending cephalad to endometrium/uterus. A, Sagittal midline T2-weighted image depicts loss of the
normal cervical and lower uterine mural stratification pattern as a consequence of an infiltrative mass (thin arrows) obscuring both the
cervical fibrous stroma and the inner myometrium. The mass also extends into the upper vagina (thick arrow in A). B, Axial T2-weighted
image through the level of the uterine body shows the infiltrative mass (arrow) obliterating the junctional zone and invading the
myometrium.
282  •  Fundamentals of Body MRI

hardly more common (0.5–2 per 1000 pregnan- Fibroid Classification by Location
cies) and rarely proceeds to MRI, given the char-
2
acteristic sonographic appearance, suggestive
clinical scenario, and unpredictable behavior 4
and less clearly defined staging methods.
3 1
Pregnancy
Pregnancy is a rare unanticipated finding. Paren-
thetically, known pregnancy merits informed
consent, not because of any known complica- 1. Intracavitary 5
tions, but rather to acknowledge our limits. The 2. Submucosal
3. Intramural
patient deserves to understand that, although no 4. Subserosal
known fetal complications of static and time- 5. Pedunculated
varying magnetic fields exist or have been FIGURE 5-23.  Fibroid classification by location.
observed, absolute certainty has not been estab-
lished and the risk to the patient (and/or fetus)
justifies the (infinitesimal) risk. The same holds decreased signal on T2-weighted images. The
true for gadolinium, but current recommen­ inner myometrium normally measures no more
dations discourage the use of gadolinium in than 8 mm in thickness.
pregnancy.15,16
By approximately 7 weeks, an embryo is Fibroids
usually visible and the diagnosis is clear; Fibroids (otherwise known as leiomyomas) rep-
however, obstetric imaging is beyond the scope resent benign proliferations of smooth muscle
of this text. Aberrations in pregnancy constitute cells interspersed with collagen, explaining
a category of lesions known collectively as ges- the uniform hypointensity to myometrium
tational trophoblastic disease (GTD). Hydatidi- on all pulse sequences—especially T2-weighted
form mole (partial, complete, and invasive), sequences. Although occasionally solitary, they
choriocarcinoma, and placental site trophoblas- are often multiple and are present in approxi-
tic tumor compose this neoplastic disease of mately 20% of reproductive-age females. Symp-
pregnancy. The common denominator is preg- toms depend on the size and location of the
nancy and clinical course generally mirrors fibroid(s) and manifest approximately 50% of
postevacuation serum human chorionic gonado- the time.17 Submucosal fibroids abut and dis-
tropin (hCG) levels. hCG levels fall in 80% of place the adjacent endometrial mucosal surface,
postevacuation (partial and complete) hydatidi- projecting into the endometrial cavity and pre-
form moles, indicating benign disease. All other disposing to menorrhagia, infertility, miscar-
lesions are malignant. riage, menstrual dysfunction, dyspareunia, and/
or pelvic discomfort. Submucosal fibroids mostly
within the endometrial canal with a relatively
Myometrial Disease
smaller myometrial point of attachment are
Focal and Diffuse Lesions subclassified as intracavitary and potentially
Myometrial disorders are headlined by benign, decrease fertility rates. Intramural fibroids are
but frequently symptomatic conditions— confined to the myometrium and rarely provoke
fibroids and adenomyosis. To detect these symptoms. Subserosal fibroids protrude out-
lesions, remember the normal appearance of the wardly from the external surface of the uterus
myometrium. The myometrium is a bilaminar under the serosal surface (Figs. 5-23 to 5-28)
structure with an inner myometrium, referred infrequently inciting symptoms (pressure effects
to as the junctional zone, and an outer myome- and pain). Subserosal fibroids are substratified as
trial layer. The inner myometrium is hypoin- pedunculated when predominantly extramural
tense relative to the hyperintense endometrium with a (sometimes imperceptible) stalk or point
and mildly hyperintense outer myometrium (see of myometrial attachment. Pedunculation pre-
Figs. 5-1 and 5-9). An increased density of disposes to torsion and diagnostic confusion by
smooth muscle with a commensurate increase simulating adnexal masses.
in nuclear-to-cytoplasmic ratio and decreased The main indications for imaging fibroids
extracellular matrix accounts for the relatively include (1) explaining pelvic/menstrual symptoms
 Magnetic Resonance Imaging of the Female Pelvis  •  283

A B

C D
FIGURE 5-24.  Submucosal fibroid. A, T2-weighted fat-saturated image reveals an ovoid hypointense lesion arising from the anterior fundal
myometrium protruding into the endometrial cavity consistent with a submucosal fibroid (arrow). The axial T2-weighted (B) and
enhanced T1-weighted fat-suppressed (C) images show a second small submucosal fibroid arising from the right lateral myometrium
(thin arrow in B and C). D, A large hypointense right adnexal lesion mimics the appearance of a fibroid on the T2-weighted image
(thick arrow)—in combination with the marked T1 hyperintensity on the T1-weighted unenhanced image (thick arrow)—the constel-
lation of signal characteristics is most typical of chronic or concentrated blood products and diagnostic of an endometrioma.
284  •  Fundamentals of Body MRI

A C

B
FIGURE 5-25.  Intramural fibroid. The myometrium completely contains the hypointense, hypovascular fibroid (thin arrow in A-C) seen
to be distinct from the endometrium (thick arrow in B and C) on axial T2-weighted (A), sagittal T2-weighted fat-saturated (B), and
axial enhanced T1-weighted fat-saturated gradient echo (C) images.
 Magnetic Resonance Imaging of the Female Pelvis  •  285

A B

C D

E
FIGURE 5-26.  Intramural and subserosal fibroids. A-E, Multiple fibroids—some completely contained within the myometrium (thin
arrows) and some protruding into the endometrial canal (thick arrow)—indicate a combination of intramural and submucosal fibroids,
respectively.
286  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-27.  Subserosal fibroid. Sagittal T2-weighted (A and B) and T1-weighted fat-saturated gradient echo unenhanced (C)
and enhanced (D) images depict myometrium encircling the caudal aspect of a large subserosal pedunculated fibroid (arrows in A, B,
and D).

and detecting (if not known) and/or classifying Individual fibroids are generally round to oval
fibroids, (2) establishing uterine origin in the well-circumscribed hypointense lesions, ranging
case of subserosal pedunculated fibroids, which in size from a few millimeters to over 10 cm.
are often difficult to characterize with other Growth is mediated by sex steroids—especially
modalities (vs. primary ovarian lesion), (3) pre- estrogen—generally growing during pregnancy
treatment planning, and (4) assessing the and shrinking in menopause. Vascularity varies
response to treatment (UAE).18 The imaging and enhancement ranges from virtually absent
objectives include (1) identification of fibroid(s), (avascular) to marked enhancement (hypervas-
(2) spatial localization of fibroid(s) (submucosal, cular) (compared with adjacent myometrium)
intramural, subserosal), and (3) characterization (Figs. 5-29 and 5-30). Despite the degree of early
of fibroid(s) (i.e., degeneration, degree of enhancement (which defines fibroid vascular-
vascularity). ity), hypointensity on delayed images compared
 Magnetic Resonance Imaging of the Female Pelvis  •  287

A B

C D

E
FIGURE 5-28.  Subserosal fibroids simulating adnexal masses. Axial (A) and sagittal (B) T2-weighted images reveal a large hypointense
lesion in the cul-de-sac (thin arrow in A-C) of uncertain origin with hypovascularity depicted on the enhanced axial image (C); an
anterior intramural fibroid is incidentally noted (thick arrow in A and B). D and E, A stalk (arrow) connecting the lesion to the uterus
confirms uterine origin and the diagnosis of a fibroid in a different patient.
288  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 5-29.  Hypovascular fibroids. Axial T2-weighted (A and B) and T1-weighted (C) images reveal multiple hypointense intramural
fibroids (thin arrows in A-C) and a large hyperintense (hemorrhagic) fibroid arising from the right lateral myometrium (thick arrow in
B and C). Comparing the precontrast (D) with the enhanced images (E and F) indicates a relative lack of enhancement.
 Magnetic Resonance Imaging of the Female Pelvis  •  289

A B

FIGURE 5-30.  Hypervascular fibroids. Sagittal T2-

weighted fat-suppressed image (A) shows multiple
uterine fibroids, most of which enhance more than the
adjacent myometrium (thin arrows in B, postcontrast
image), except for a large hypovascular fibroid (thick
arrow). Note the Bartholin cyst on the sagittal image
(arrow in A). C, In a different patient, a hypervascular
submucosal fibroid (thin arrow) is hyperintense com-
pared with hypovascular (thick arrow) and avascular—
C
likely degenerating (open arrow)—intramural fibroids.

with myometrium is essentially unanimous. subserosal fibroid from a primary adnexal mass
With relatively increased smooth muscle (and (such as a fibroma). Marked hypointensity, sharp
less collagen) content, fibroids appear relatively margins, spherical to ovoid morphology, and
T2 hyperintense with greater enhancement. enhancement patterns usually differentiate an
Diagnostic uncertainty arises in the case of intracavitary submucosal fibroid from chiefly dif-
pedunculated subserosal fibroids, which simu- ferential considerations (Table 5-10). Adeno­
late adnexal lesions (see Fig. 5-28), and occa- myosis, when focal, often mimics an intramural
sionally in the case of an intracavitary submucosal fibroid, and differential features are deferred to
fibroid, which must be discriminated from an the upcoming discussion of adenomyosis.
endometrial polyp and endometrial carcinoma. Aberration in the otherwise monotonous
The presence of enhancement differentiates a appearance of fibroids is usually explained by
subserosal fibroid from a dark (shading) degeneration. Fibroids often exhibit different
endometrioma, and a stalk connecting the manifestations of involution, which is usually
fibroid with the parent uterus differentiates a asymptomatic. Types of degeneration are
290  •  Fundamentals of Body MRI

TABLE 5-10.  Intracavitary Fibroid Differential Diagnosis Scheme

Lesion T2 Signal Morphology Margins Enhancement

Intracavitary fibroid ⇓⇓ Ovoid-round Sharp Often hypovascular,

homogeneous unless
degenerating
Endometrial polyp Isointense ⇑, cystic foci Tubular Sharp Moderate, lacy
Endometrial carcinoma ⇓ Sessile-pedunculated Ill-defined Hypovascular

A B

C D
FIGURE 5-31.  Fibroid with myxoid degeneration. Sagittal fat-saturated (A) and axial (B) T2-weighted images show heterogeneous hyper-
intensity throughout the large fibroid undergoing myxoid degeneration. Pregadolinium (C) and postgadolinium enhanced
(D) T1-weighted fat-saturated gradient echo images document an absence of enhancement indicating absent perfusion and
degeneration.
 Magnetic Resonance Imaging of the Female Pelvis  •  291

TABLE 5-11.  Fibroid Degeneration Table

Magnetic Resonance Signal Characteristics
Type T1 T2 Gadolinium

Cystic ⇓⇓⇓ ⇑⇑⇑ –

Hyaline ⇑/⇓ ⇓ –
Myxoid ⇓ ⇑⇑ ±
Hemorrhagic ⇑⇑ ⇑/⇓, ± ⇓ rim –

E F
FIGURE 5-31, cont’d  E and F, In a different patient, an intramural fibroid undergoing myxoid degeneration in the anterior lower uterine
segment (thin arrow in E) demonstrates much greater T2 hyperintensity than the adjacent adenomyoma (thick arrow in E) on the sagittal
T2-weighted fat-suppressed image (E) and minimal enhancement (arrow in F).

described: hyaline, myxoid, cystic, and hemor- MRI postembolization often reveals hemor-
rhagic (Table 5-11).19 Fibroids undergoing rhagic transformation and decreased or absent
hyaline degeneration exhibit T2 hypointensity enhancement, which indicates successful treat-
similar to nondegenerating fibroids. Associated ment. Look for these features and an overall
calcification occasionally induces susceptibility decrease in uterine size postembolization (Fig.
artifact. Myxoid degeneration appears T2 hyper- 5-34). Hypervascularity, submucosal location,
intense with minimal enhancement (Fig. 5-31); and smaller size predict higher likelihood of
cystic degeneration corresponds to T2 hyperin- embolization treatment success. Expected MRI
tensity and absence of enhancement (Fig. 5-32). features of successfully embolized fibroids
Hemorrhagic transformation corresponds to T1 include T1 hyperintensity with corresponding
hyperintensity, which is often peripheral or T2 hypointensity and an absence of
diffuse (Fig. 5-33; see also Fig. 5-29B and C). enhancement.
292  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-32.  Fibroid with cystic degeneration. Axial (A) and sagittal (B) T2-weighted images of a uterus with a large heterogeneously
hyperintense fibroid (thin arrow in A and B) with submucosal extension (thick arrows in A and B) reveal multiple fluid intensity foci
(open arrows), which do not enhance (arrows in C and D), as seen on the axial (C) and sagittal (D) fat-suppressed T1-weighted images
after gadolinium administration.
 Magnetic Resonance Imaging of the Female Pelvis  •  293

A B

C D

E
FIGURE 5-33.  Fibroid with hemorrhagic degeneration. A mostly intramural fibroid with focal submucosal extension hyperintense on a
T1-weighted (in-phase) image without fat suppression (A) maintains hyperintensity on the corresponding T1-weighted fat saturated
image (B), confirming hemorrhage. C, The absence of enhancement on the postcontrast image confirms degeneration. Axial (D) and
coronal (E) T2-weighted images reveal mild relative hyperintensity compared with uncomplicated fibroids.
294  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-34.  Fibroid hypovascularity postembolization. Axial T1-weighted (A) and sagittal T2-weighted (B) images of a large intramural
fibroid with the typical homogeneous hypointensity before embolization contrast with signal characteristics indicating hemorrhagic
degeneration after embolization—marked T2 hypointensity as seen on sagittal T2-weighted fat-suppressed (C) and axial T2-weighted
(D) images and T1 hyperintensity on axial gradient echo T1-weighted (E) and fat-suppressed gradient echo T1-weighted (F) images
and absence of enhancement—compare pregadolinium (E) with postgadolinium (G) images.

Despite the rising popularity, UAE involves regrowth and inadvertent treatment of a degen-
the risk of complications (Table 5-12).8 If treated erated fibroid (leiomyosarcoma).
with embolization, pedunculated subserosal Malignant degeneration of fibroids (leiomyo-
fibroids tethered to the uterus with a thin sarcoma) is very rare—approximately 0.1%.
pedicle risk detachment and expulsion into the Features of malignant degeneration include a
peritoneal cavity with infarction. Expulsion of marked increase in size (compared with prior
submucosal fibroids also leads to potential com- examinations), indistinct margins, and invasion
plications. Detachment connotes infarction of adjacent structures (Fig. 5-35). Although rela-
with the attendant MRI findings; additional find- tively little established criteria exist for discrimi-
ings may coexist, such as migration and an nating these lesions from fibroids, suggestive
absence of a point of attachment. Poor collateral features based on more recent work include
circulation, among other factors, predisposes to greater than 50% T2 hyperintensity, small T1
uterine necrosis—a life-threatening complica- hyperintense foci, and pockets of avascularity.20
tion of UAE. Relative T2 hyperintensity, isoin-
tensity to hyperintensity on T1-weighted images, Adenomyosis
and an absence of enhancement with or without Other benign myometrial lesions include adeno-
signal voids indicating gas signify uterine necro- myosis (or focal adenomyoma) and focal myo-
sis. Other uterine complications include fibroid metrial contraction—both of which occasionally
 Magnetic Resonance Imaging of the Female Pelvis  •  295

E F

G
FIGURE 5-34, cont’d 

simulate fibroids. Adenomyosis is the intrau­

TABLE 5-12.  Uterine Artery Embolization terine counterpart to endometriosis—abnormal
Complications implantation of endometrial cells into the myo-
Major Complications metrium. Adenomyosis is either diffuse or focal
Fibroid passage (adenomyoma)—either type manifests the same
Infectious complications
Endometritis
features (Figs. 5-36 and 5-37). Unlike fibroids,
PID-TOA adenomyosis generally lacks distinct margins
Pyomyoma and exerts no mass effect. Instead of displacing
DVT
PE
or distorting the adjacent endometrium, adeno-
Malignant leiomyosarcoma (inadvertently embolized) myosis abuts the endometrium without dis-
Ovarian dysfunction placement. Whereas fibroids maintain acute
Fibroid regrowth
Uterine necrosis
margins with the endometrium, the interface
Death between adenomyosis and endometrium is
usually convex. Adenomyosis signal intensity
Minor Complications
Hematoma
approximates junctional zone hypointensity
UTI with possible intralesional T1 and/or T2 hyper-
Urinary retention intensities. A junctional zone measurement of
Transient pain
Nerve/vessel injury
12 mm or greater confirms the diagnosis of ade-
nomyosis; between 8 and 12 mm is indetermi-
DVT = deep venous thrombosis; PE = pulmonary embolism;
PID = pelvic inflammatory disease; TOA = tubo-ovarian abscess;
nate (Table 5-13). Cyclical menstrual uterine
UTI = urinary tract infection. changes suppress the zonal anatomy during the
From Kitamura Y, Ascher SM, Cooper C, et al. Imaging manifesta-
tions of complications associated with uterine artery embolization.
late secretory phase extending into the men-
Radiographics 25:S119–S132, 2005. strual phase as the outer myometrium fades
296  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-35.  Malignant degeneration of a fibroid. Axial (A) and coronal (B) T2-weighted images show a moderately heterogeneously
hyperintense ovoid lesion adjacent to the uterine fundus attached to the uterus with ill-defined margins in contradistinction to the
normally sharply defined stalk seen with a benign leiomyoma, indicating invasion of the adjacent myometrium (arrow). Differential
enhancement between the enhancing myometrium (thick arrow in D) and hypovascular mass (thin arrow in D) is evident when compar-
ing the precontrast image (C) with the postcontrast image (D).

from its peak hyperintensity from the midsecre-

TABLE 5-13.  Adenomyosis Features tory phase to near isointensity with the dark
Inner inner myometrium.21
Myometrial
Features Thickness Diagnosis
Myometrial Contractions
Sharply defined <8 mm Normal junctional zone Myometrial contractions manifest as regional
Uniformly hypointense
Indistinct margins 8–12 mm Indeterminate
myometrial low signal, which may be confused
adenomyosis with adenomyosis or fibroids.22 Focal buckling
Indistinct margins ≥12 mm Adenomyosis or folding or thickening of the junctional zone
Intralesional T1/T2
hyperintensities and/or myometrium is an occasional associated
finding. The key to this diagnosis is
changeability—a contraction is an ephemeral
phenomenon and most examinations span 30
minutes or more. Check each sequence for
interval change or resolution to confirm a myo-
metrial contraction.
 Magnetic Resonance Imaging of the Female Pelvis  •  297

A B

C D
FIGURE 5-36.  Diffuse adenomyosis. Sagittal (A) and axial (B) T2-weighted images of a grossly enlarged uterus fail to demonstrate the
normal discrimination between the inner and the outer myometrium with multiple myometrial hyperintensities in a patient with severe
diffuse adenomyosis (arrow, endometrium). C, T1-weighted fat-saturated image shows scattered T1 hyperintensities reflecting hemor-
rhagic foci. D, The corresponding enhanced T1-weighted fat-saturated gradient echo image shows diffuse heterogeneous enhancement
throughout the myometrium without evidence of an underlying focal lesion (arrow, endometrium).

Malignant Lesions invasiveness discriminate fibroids from sarco-

I have virtually excluded malignant myometrial mas. Lack of mass effect, thickening of the junc-
lesions from this discussion because they are tional zone, and the characteristic appearance
exceedingly rare. This category includes uterine of heterotopic endometrial tissue differentiates
sarcomas—leiomyosarcoma, stromal sarcoma, adenomyosis from these lesions. Differentiating
and carcinosarcoma (formerly mixed mesoder- sarcomas from endometrial cancer is less impor-
mal/müllerian tumor)—and lymphoma. When- tant because both will eventually require tissue
ever you see a large, heterogenous mass sampling for treatment. Confinement to the
with necrosis and evidence of rapid growth, endometrium or primary involvement of the
think about the possibility of a sarcoma (Fig. endometrium with myometrial invasion favors
5-38). Differentiating these lesions from endometrial carcinoma. The final lesion in this
benign disease—fibroids—and adenomyosis is category, lymphoma, more characteristically
critical. Signal characteristics (T2 hypointen- manifests with multiple lesions—although
sity), margins (sharply defined), and lack of solitary lesions do occur—a monotonous
298  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-37.  Focal adenomyoma. Sagittal (A) and axial (B) T2-weighted images reveal a lesion isointense to and blending with adjacent
junctional zone with indistinct margins and exerting no significant mass effect on the underlying endometrium (arrow). Sagittal (C) and
axial (D) enhanced T1-weighted gradient echo images with fat saturation confirm the inner myometrial origin.

appearance with relative isointensity to muscle channel. The unfused proximal segments consti-
on T1-weighted images and possibly generalized tute the fallopian tubes.
lymphadenopathy. Although differentiating between the differ-
ent types of müllerian duct anomalies is impor-
Global Uterine Abnormalities tant and can be challenging, they usually do not
This category of global uterine abnormality is pose a diagnostic dilemma. The degree of
essentially restricted to congenital or embryo- absence or fusion of the ducts accounts for the
logic disorders, otherwise known as müllerian deficiency or abnormal configuration. Think
duct anomalies. The incidence of müllerian duct about these lesions along a spectrum from
anomalies is approximately 1%, and they account global deficiency—agenesis/hypoplasia to uni-
for approximately 3% of reproductive failures.23 lateral deficiency—unicornuate—to a range in
A detailed discussion of the embryology of the incomplete fusion from didelphys to arcuate
genitourinary system is beyond the scope of this (Fig. 5-39).
book, but a general understanding facilitates There is even a subclassification scheme for
remembering the spectrum of anomalies. type 1 müllerian anomalies, depending on the
The primordial paramesonephric (müllerian) degree of vagina/cervical/uterine/tubal involve-
ducts develop to constitute the upper vagina, ment. Type 2 (unicornuate) müllerian duct
uterus, and fallopian tubes. The distal ends of anomalies are also subdivided depending on the
the ducts grow caudally and medially and even- presence and patency of the aplastic/hypoplastic
tually fuse to become the uterine body, cervix, horn. The type 3 (didelphys) anomaly repre-
and upper two thirds of the vagina. After fusion, sents a greater degree of müllerian duct fusion.
a residual septum regresses, yielding a common Global duplication of structures from the
 Magnetic Resonance Imaging of the Female Pelvis  •  299

A B

C D

E
FIGURE 5-38.  Leiomyosarcoma. Axial T2-weighted (A) and enhanced (B) and sagittal T2-weighted fat-suppressed (C) and enhanced
(D) images show a large, necrotic, poorly defined mass essentially replacing the entire uterine corpus and associated with lung metastases
on the corresponding computed tomography (CT) scan (E).
 MÜLLERIAN DUCT ANOMALIES

Class I (hypoplasia/agenesis): uterovaginal hypoplasia/agenesis

Class II (unicornuate uterus): partial or complete unilateral hypoplasia

Class III (didelphys uterus): complete müllerian duct nonfusion

Class IV (bicornuate uterus): partial müllerian duct nonfusion

Class V (septate uterus): incomplete resorption of septum between müllerian ducts

Class VI (arcuate uterus): anatomic variation with flat or mildly convex outer uterine
fundus with shallow endometrial cleft

Class VII (diethylstilbestrol-related anomaly): dysmorphic abnormalities of the uterus,

cervix; and/or vagina, including T-shaped uterus, hypoplastic uterus and/or cervix; and
a variety of other derangements

Normal

Class I- Hyoplasia

Rudimentary
horn

Class II- Unicornuate

Class III- Didelphys

Class IV- Bicornuate

Class V- Septate

Class VI- Arcuate

FIGURE 5-39.  Classification of müllerian duct anomalies.

 Magnetic Resonance Imaging of the Female Pelvis  •  301

A B

C D

E
FIGURE 5-40.  Uterus didelphys. A, Coronal enhanced T1-weighted gradient echo image shows widely splayed uterine cornua (thin white
arrows) and separate endocervical (thick arrows) and vaginal canals (black arrows). Widely splayed uterine horns characterize uterus
didelphys (and bicornuate uterus), as illustrated on axial enhanced (B) and T2-weighted (C) images. Separate cervical canals (arrows in
D) are confirmed on axial enhanced (D) and T2-weighted (E) images.

cervices through the uterine cornua character- a septate uterus is approached hysteroscopically
izes this anomaly with a variable longitudinal for septoplasty, and a bicornuate uterus is
vaginal septum (Fig. 5-40). approached transabdominally. Hysteroscopic
The chief differential is between the bicornu- metroplasty of a bicornuate uterus may result
ate (type 4) and the septate (type 5) uterus in myometrial perforation (Figs. 5-41 and
because of the difference in surgical approach— 5-42).
302  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-41.  Septate uterus. A, Coronal T2-weighted image shows a hypointense fibrous septum (arrow) dividing the endometrial
hemicavities. Axial T2-weighted images show the fibrous septum extending from the uterine fundus (B) through the cervix (C) and into
the upper vagina (D) and confirming features consistent with septate uterus—convex outer fundal contour (open arrow in B), closely
apposed uterine horns (thick arrows in B), and relatively low intercornual angle (black lines in B).

The outer fundal contour is a major discrimi-

nating factor between the two entities. The
septate uterine fundal contour ranges from
normal (convex) to flat to minimally concave
(<1 cm), whereas the bicornuate features a
deeper fundal cleft (≥1 cm). Try to measure the
intercornual angle by approximating the medial
margins of the endometrial hemicavities—105°
or greater suggests bicornuate, 75° or less sug-
gests septate.24 Wider splaying between the
apices of the cornua—or intercornual distance—
of 4 cm or more is a finding that potentially
discriminates between the two entities, suggest-
ing bicornuate uterus.25 Comparing the relative
positioning of the apices of the cornua with the
apex of the external fundal contour informs the
(sonographic) differentiation between the two
FIGURE 5-42.  Bicornuate uterus. Note the wider displacement and (Fig. 5-43)—greater than 5 mm cephalad posi-
more obtuse angulation between uterine horns compared with tioning of the intercornual line above the fundal
Figure 5-41. indentation purportedly separates the septate
 Magnetic Resonance Imaging of the Female Pelvis  •  303

Fundal apex

Line indicating
tubal ostia

Apex below tubal ostia → bicornuate BICORNUATE VERSUS

SEPTATE UTERUS

Features Bicornuate Septate

Fundal >10 mm ≤10 mm
contour indentation indentation
Fundal apex <5 mm above ≥5 mm above
interostial line
Apex <5 mm above tubal
Fundal contour Concave Flat or convex
ostia → bicornuate
Uterine horn >105° <75°
angulation
Intercornual >4 cm <4 cm
distance

Apex <5 mm above tubal

A ostia → septate

ARCUATE UTERUS RATIO

Length

Height
Cornual Cornual
apex apex

Fundal indentation

Height/length <0.1 → arcuate

Height/length >0.1 → bicornuate

B
FIGURE 5-43.  Bicornuate versus septate uterus and arcuate uterus ratio. Bicornuate versus septate uterus. Modified from references
24-28.

from the bicornuate (and didelphys) uterus 5-44). “Arcuate” refers to the minimal indenta-
(according to ultrasound-generated data, which tion of the external fundal contour and fertility
have not been substantiated with MRI).26,27 Of rates approximate normal. The arcuate uterus
course, do not forget to assess the intercornual also approximates the bicornuate uterus, and a
tissue; intervening myometrial tissue indicates measurement scheme has been proposed to dif-
bicornuate uterus; a thin linear uniform hypoin- ferentiate the two based on hysterosalpingogra-
tensity (typical of fibrous tissue) suggests septate phy findings—the arcuate uterus ratio (see Fig.
uterus. 5-43).28,29 A ratio of fundal indentation height to
Arcuate uterus (type 6 müllerian duct anomaly) intercornual length of less than 10% favors
is the forme fruste of this disorder—essentially arcuate uterus.
an anatomic variant, representing near-complete Remember that urinary tract anomalies such
resorption of the uterovaginal septum (Fig. as renal agenesis, horseshoe kidney, pelvic
304  •  Fundamentals of Body MRI

A B
FIGURE 5-44.  Arcuate uterus. A and B, Myometrial tissue (thick arrow) separating relatively closely apposed uterine cornua (thin arrows)
associated with a convex fundal contour (broken arrow) defines the arcuate uterus, as seen on these axial T2-weighted images.

kidney, and collecting system duplication often

Cystic Lesions
coexist with müllerian duct anomalies. For this
reason, large field-of-view coronal localizing Nabothian Cyst
images including the kidneys are recommended. The pivotal question in evaluating a cervical
Finally, a separate subtype addresses a terato- lesion is “cystic or solid?” The answer is usually
genic anomaly rather than a congenital one— straightforward. Courtesy of the ubiquitous
diethylstilbesterol-induced anomalies. The T- Nabothian cyst, cystic lesions are far more
shaped uterus (see Fig. 5-4) is the most widely common. A Nabothian cyst is a benign retention
recognized form, and most reflect some degree cyst reflecting an obstructed mucin-secreting
of hypoplasia. endocervical gland. They are often multiple,
usually measure less than 2 cm, and exhibit
simple fluid signal (T1 hypointensity and T2
hyperintensity)—but may be mildly hyper­
CERVIX AND VAGINA intense on T1-weighted images—and do not
enhance (Fig. 5-45).
Normal Features
The cervix is the cylindrically shaped lowest Other Benign Cystic Lesions
segment of the uterus—sort of a trunk or ped- Less common cervical cystic lesions include pre-
estal supporting the uterine corpus. The lower dominantly benign lesions, such as endocervical
half of the cervix protrudes into the upper or glandular hyperplasia, chronic cervicitis,
segment of the vagina and is known as the cervical adenomyosis, and Gartner’s duct cysts
portio. The overall dimensions of the cervix (Table 5-14).30 Glandular hyperplasia usually
average 3.5 cm in length and 2 cm in diameter. accompanies oral (progestational) contracep-
Prolapse, postmenopausal status, or cerclage tive agents, pregnancy, and postpartum status.
elongates the cervix. The uterine trilaminar MRI features of glandular hyperplasia include
mural stratification pattern is (less graphically) well-circumscribed, nonenhancing lesions in
recapitulated in the cervix dominated by a thick the endocervical mucosal layer exhibiting T1
central hypointense fibromuscular stromal layer, and T2 hyperintensity (Fig. 5-46).
an inner epithelial layer that generally measures Features of adenomyosis of the cervix simu-
less than 10 mm in thickness, and an outer thin late uterine adenomyosis and are difficult to per-
fibromuscular layer. The same T2 signal inten- ceive in the cervix. Aberrant cervical signal
sity pattern is demonstrated by the cervix: inner changes, such as T1 hyperintensity or T2 hypo­
hyperintensity, central hypointensity, and outer intensity, are the only clues, suggesting the pres-
intermediate intensity. ence of hemorrhage.
 Magnetic Resonance Imaging of the Female Pelvis  •  305

A B

C
FIGURE 5-45.  Nabothian cysts. Sagittal T2-weighted fat-saturated (A) and axial T2-weighted (B) images show a cluster of simple Nabo-
thian cysts (thin arrow in A and B) apposed to the endocervical canal in a patient with multiple fibroids, including a submucosal fibroid
(thick arrow in A). C, Sagittal enhanced T1-weighted fat-saturated image confirms an absence of enhancement.

TABLE 5-14.  Differential Diagnosis of Cystic Cervical Lesions

Lesion Etiology Magnetic Resonance Features

Cystic Lesions
Nabothian cyst Obstructed duct/retention cyst Usually simple cyst
Endocervical hyperplasia Hormonal stimulation Multiple small simple cysts
Chronic cervicitis Inflammation Thickened mucosal layer
Possible cysts
Adenomyosis Ectopic islands of endometrial tissue Hemorrhage

Complex Cystic Lesions

Adenoma malignum Mucinous adenocarcinoma subtype Complex cystic mass

Extravaginal Lesions
Gartner’s duct cyst Congenital—mesonephric duct Simple cyst
Anterolateral upper vagina
306  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-46.  Cervical glandular hyperplasia. A-D, The cervical endothelium appears uniformly thickened and redundant with preserva-
tion of the hypointense fibrous stroma.
 Magnetic Resonance Imaging of the Female Pelvis  •  307

E F

G
FIGURE 5-46, cont’d  E-G, A more florid example of endocervical hyperplasia simulates Nabothian cysts on the sagittal T2-weighted fat-
suppressed image (E). Note the mild hyperintensity on the axial T1-weighted image (F) and the lack of enhancement on the fat-suppressed
T1-weighted postcontrast image (G)—only thin septal enhancement of intervening tissue is noted.
308  •  Fundamentals of Body MRI

A B

C
FIGURE 5-47.  Chronic cervicitis. Axial T2-weighted (A), T1-weighted (B), and enhanced fat-suppressed T1-weighted (C) images reveal
mildly hyperintense cystic cervical lesions with an absence of masslike enhancement.

Cervicitis is a very common gynecologic of the pubic symphysis and usually contain
disease and is probably most commonly not simple fluid (Fig. 5-48). Occasionally, higher
detectable on imaging studies. The disease protein content results in mildly decreased T2
involves the inner mucosal layer, which may and increased T1 signal compared with simple
thicken and contain small (often T1-hyperintense) fluid. Cystic lesions of the female genital tract
cystic lesions (Fig. 5-47). In the absence of cystic are easily differentiated based on their charac-
lesions, the only clue may be an absence of teristic locations but frequently provoke confu-
zonal anatomy with diffuse intermediate signal sion because of their multiplicity.
throughout the cervix. Various cystic lesions inhabit the female
Gartner’s duct cysts represent remnants of the genital tract (Table 5-15). Unless large lesion size
mesonephric (or wolffian) duct that involutes in induces symptoms, diagnosis is academic. For
the absence of a Y chromosome. Gartner’s duct the most part, location dictates diagnosis. Mül-
cysts rarely present a diagnostic dilemma lerian and Gartner’s duct cysts are embryologic
because of their simple features and character- remnants of the müllerian or paramesonephric
istic location. Gartner’s duct cysts arise from the or wolffian or mesonephric ducts, respectively,
anterolateral wall of the vagina above the level arising from the anterolateral wall of the upper
 Magnetic Resonance Imaging of the Female Pelvis  •  309

A B

C D

E F
FIGURE 5-48.  Gartner’s duct cyst. Sagittal (A), axial (B), and coronal (C) T2-weighted images reveal a uniformly hyperintense lesion in
the upper vagina seen to be anteriorly located on the sagittal image (arrow). Mild hyperintensity indicates proteinaceous content on the
T1-weighted image (D), and lack of enhancement is reflected on the precontrast (E) and postcontrast (F) images.
310  •  Fundamentals of Body MRI

TABLE 5-15.  Cystic Lesions of the Female Solid Lesions

Genital Tract
Cervical Carcinoma
Magnetic The vast majority (85%) of cervical carcinomas
Resonance
Lesion Etiology Features are of the squamous cell histopathologic type
and exhibit solid morphology. Cervical carci-
Gartner’s duct cyst Congenital— Simple cyst noma originates from the mucosal layer at
mesonephric duct Anterolateral upper
vagina the squamocolumnar junction—the boundary
Müllerian duct cyst Congenital— Anywhere in vagina, between the squamous mucosa of the vagina
Müllerian duct usually large and the columnar mucosa of the uterus. The
simple cyst
Vaginal inclusion cyst Postsurgical or Simple cyst tumor is intermediate in signal on T2-weighted
traumatic Lower posterior or images—darker than normal cervical mucosa
lateral vagina and brighter than inner fibromuscular stroma
Bartholin’s gland cyst Dilated Batholin’s Posterolateral vaginal
gland introitus (Fig. 5-54). Enhancement is variable but present
Skene’s gland cyst Dilated periurethral Adjacent to distal and should be confirmed with careful compari-
gland urethra son between pregadolinium and postgadolinium
Urethral diverticulum Infection/ Arise from posterior
inflammation urethra images and/or subtracted images. A bimodal
Often encircle growth pattern is explained by age-related
urethra
changes; more caudal growth in younger
patients and cephalad extension toward the
uterus in older patients are a function of cepha-
vagina above the level of the pubic symphysis lad migration of the squamocolumnar junction
(Fig. 5-49). Bartholin’s gland cysts are abnor- with aging.
mally dilated Bartholin’s glands in the postero- Although staging is usually the primary objec-
lateral vaginal introitus seen medial to the labia tive because the diagnosis is often already estab-
minora (Figs. 5-50 and 5-51). Skene’s gland cysts lished, always consider alternative etiologies.
represent abnormal dilatation of the periure- If the diagnosis is still in doubt, other potential
thral glands adjacent to the distal urethra (Fig. etiologies include endometrial carcinoma,
5-52). Vaginal inclusion cysts are the most lymphoma/metastasis, benign cervical polyp,
common acquired vaginal cysts, usually located and cervical fibroid (Table 5-16). The features of
within the lower posterior or lateral vaginal endometrial and cervical carcinoma overlap,
wall, often postsurgical or traumatic in and the chief distinguishing characteristic is
etiology. endometrial versus endocervical origin (if this
can be ascertained). In the end, establishing an
Adenoma Malignum etiology with precision is moot. Unless a fibroid
Cervical neoplasms—dominated by cervical is confidently diagnosed, biopsy or excision is
cancer—are rarely cystic. An infamous subtype the next step.
of mucinous adenocarcinoma of the cervix, Start with identifying the endocervical canal—
known as adenoma malignum (or “minimal if still identifiable. Assess the location of the
deviation adenocarcinoma”) has a deceptively tumor with respect to the canal and assess the
benign, cystic appearance. Despite its deceptive integrity of the hypointense fibrous cervical
well-differentiated histopathologic features, stroma (Fig. 5-55)—the key issue in MRI of cervi-
adenoma malignum disseminates promptly into cal carcinoma. Violation of the hypointense
the peritoneal cavity and to distant sites.31 The fibrous cervical stroma separates stage IB from
classic morphologic description of adenoma stage IIB disease and surgical disease from non-
malignum is a botryoidal (grapelike) cluster of surgical disease treated with radiation therapy
cysts within background stroma. Whereas (Table 5-17). Look for tumor extending into the
cysts dominate, relatively understated complex vagina (best assessed on axial and sagittal
features—thick septae, irregular margins, and T2-weighted and T1-weighted postgadolinium
enhancing solid components—at least suggest images)—IIA and IIIA disease. Next, inspect the
the possibility of malignancy (Fig. 5-53). The parametrial tissues for extracervical extension
characteristic presentation of vaginal discharge of tumor. T1-weighted images without fat satu-
occasionally correlates with fluid within the ration and T2-weighted and T1-weighted
uterine/cervical or vaginal canal on MRI. Text continued on p. 317
 Magnetic Resonance Imaging of the Female Pelvis  •  311

A B

C D

E
FIGURE 5-49.  Müllerian duct cyst. The sagittal T2-weighted fat-suppressed image (A) demonstrates a large cystic lesion in the upper
vagina (arrow). In a different patient (B), the sagittal fat-suppressed (B) and axial (C) images shows a large septated cystic lesion (arrow)
also in the upper vagina. The fat-saturated T1-weighted image (D) demonstrates hyperintensity due to mucinous/proteinaceous content
and the subtracted postcontrast image (E) confirms cystic nature with lack of enhancement.
312  •  Fundamentals of Body MRI

A B
FIGURE 5-50.  Bartholin’s gland cysts. A, Axial T2-weighted image reveals two small cystic lesions inhabiting the vaginal introitus, located
posteriorly and caudally, as illustrated on the coronal enhanced T1-weighted image (B), revealing the cystic nature of the lesions (arrows).

TABLE 5-16.  Differential Diagnosis of Cervical Carcinoma

Solid Lesions
Benign
Cervical fibroid Usually small (5–10 mm)
Well-circumscribed

Cervical Polyp
Malignant
Endometrial carcinoma with cervical spread Endometrial origin
Myometrial invasion
Vaginal carcinoma with cervical spread Vaginal origin
Far less common
Lymphoma No mucosal involvement
Disseminated lymphadenopathy
Uterine sarcoma (leiomyosarcoma, endometrial sarcoma, hemorrhage, cystic necrosis, Larger size
malignant mixed müllerian tumor) Far less common

Complex Cystic Lesions

Cervicitis Absence of solid component
No enhancement
Preservation of mural
stratification
Glandular hyperplasia Absence of solid component
No enhancement
Preservation of mural
stratification
 Magnetic Resonance Imaging of the Female Pelvis  •  313

A B

C D
FIGURE 5-51.  Large complex Bartholin’s gland cyst. A large T2 hypointense and T1 hyperintense lesion (arrow) on axial T2- (A) and
T1-weighted in-phase gradient echo (B) images in the lateral aspect of the vagina with preserved hyperintensity on the corresponding
fat-suppressed image (C) is localized to the lower vaginal introitus below the level of the symphysis pubis as seen on the sagittal
T2-weighted fat-suppressed image (D).

FIGURE 5-52.  Skene’s gland cyst. A small cystic structure abutting the
distal urethra represents a dilated periurethral (or Skene’s) gland cyst
(arrow).
314  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-53.  Adenoma malignum. A, Axial T2-weighted image depicts a hyperintense cervical lesion (arrows) within the fibrous stroma
with a botrioidal, or grapelike, morphology. B, The signal-starved T2-weighted fat-saturated image shows the lesion expanding the cervix
(arrows) and the appearance simulates Nabothian cysts. C and D, T1-weighted images after intravenous gadolinium administration
reveal multifocal solid linear and nodular enhancing foci (arrows) not present in benign cervical lesions, such as Nabothian cysts or
cervicitis (compare with Figs. 5-45 to 5-47).
 Magnetic Resonance Imaging of the Female Pelvis  •  315

A B

C D
FIGURE 5-54.  Cervical carcinoma. An ill-defined mildly hyperintense lesion (arrow; hypointense to endometrium and hyperintense com-
pared with fibrous stroma) invades anteriorly on sagittal (A) and axial (B) T2-weighted images. Comparing precontrast (C) with post-
contrast (D) images confirms enhancement and relative hypovascularity.
316  •  Fundamentals of Body MRI

A B

C D

FIGURE 5-55.  Cervical carcinoma within the fibrous stroma.

Precontrast (A) and postcontrast (B) enhanced T1-weighted
fat-suppressed sagittal images depict a hypovascular lesion
(arrow in B) centered at the cervix. C and D, Axial
T2-weighted images confirm confinement of the lesion
within the hypointense fibrous cervical stroma (arrows).
E, Note the lack of tissue contrast on the corresponding
E
T1-weighted image.
 Magnetic Resonance Imaging of the Female Pelvis  •  317

TABLE 5-17.  Staging of Cervical Carcinoma

International Federation of Gynecology Magnetic Resonance
and Obstetrics Staging Imaging Findings Treatments

0. Carcinoma in situ Not visible

I. Confined to cervix
• IA.  Microscopic
 IA-1.  Stromal invasion <3 mm Not visible Surgery
 IA-2.  >3-mm, <5-mm invasion Small enhancing tumor Surgery
• IB.  Clinically visible (>5 mm) Tumor visible (intact stroma) Surgery
 IB-1.  <4 cm Surgery
 IB-2.  >4 cm X-ray therapy
II. Extends beyond uterus but not to pelvic wall or lower third
of vagina Vaginal wall disruption Surgery (<4 cm), x-ray therapy (>4 cm)
• IIA.  Vaginal extension, no parametrial invasion Stromal, parametrial invasion X-ray therapy
• IIB.  Parametrial invasion
III. Extension to lower third of vagina or pelvic wall invasion
with hydronephrosis Invasion lower vagina X-ray therapy
• IIIA.  Extension to lower third of vagina Pelvic muscle or dilated ureter X-ray therapy
• IIIB.  Pelvic wall invasion with hydronephrosis
IV. Located outside true pelvis
• IVA.  Bladder or rectal mucosa Loss low signal bladder/rectal wall X-ray therapy
• IVB.  Distant metastasis X-ray therapy
From Nicolet V, Carignan L, Bourdon F, Prosmanne O. MR imaging of cervical carcinoma: A practical staging approach. Radiographics 20:1539–
1549, 2000.

postgadolinium images with fat saturation are OVARIES AND ADNEXA

most sensitive for parametrial spread—IIB
Normal Anatomy
disease. Look for ill-defined hypointensity infil-
trating the hyperintense parametrial fat or The adnexa includes the ovaries and everything
hyperintensity infiltrating the saturated parame- else—paired fallopian tubes, broad and other
trial fat, respectively (Fig. 5-56). Assess the status parametrial ligaments, and the associated vascu-
of the ureters on axial and/or coronal T2-weighted lar structures. Only the ovaries are consistently
images for abnormal dilatation conceivably due well visualized and of clinical relevance—
to neoplastic involvement—IIIB. Check the disorders of the supporting structures are
axial and sagittal T2-weighted and T1-weighted beyond the scope of this text. The size and
postgadolinium images for obliteration of tissue appearance of the normal ovary depend on men-
planes separating the cervix and bladder and/or strual status (Fig. 5-58). Female hormones induce
rectum (Fig. 5-57)—IVA. Do not forget to inspect growth, and functional cyst development in the
the pelvic sidewall—not only for direct exten- ovary and normal ovarian features are listed in
sion of tumor but also for lymphadenopathy. Figure 5-59.
The pivotal findings are parametrial invasion The first task is to find the ovaries, usually
and violation of the fibrous stroma, which gen- located in proximity to the iliac vessels near the
erally preclude surgical treatment. Keep in mind bifurcation. However, the ovaries are not rigidly
that the accuracy of MRI staging ranges between tethered. Medially, they are adherent to the fal-
76% and 92%.33,34 lopian tubes, caudally to the broad ligament,
Occasionally, vaginal carcinoma simulates medially to the proper ovarian ligament, and
cervical carcinoma depending on its location superolaterally to the suspensory ligament,
and extent. The MRI appearance is basically which contains the ovarian vessels (Fig. 5-60).
indistinguishable—the tumor usually appears as Usually, T2-weighted images provide the best
a relatively T2 hyperintense, infiltrative, indis- anatomic roadmap and chance of finding the
tinct mass. Only when clearly confined to the ovaries. First, scan the adnexa for an ovariform
vagina should vagina carcinoma be considered structure with or without cysts. Next, trace
because of its low incidence compared with the ovarian vein caudally over the iliac vessels
cervical carcinoma. Combined vaginal and cervi- into the suspensory ligament, hopefully into a
cal involvement implicates cervical carcinoma recognizable ovary. If that fails, try to find the
over vaginal carcinoma proportional to the rela- round ligament entering the internal inguinal
tively higher prevalence. os and follow it posteromedially—proximally,
318  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-56.  Cervical carcinoma with parametrial invasion. Sagittal fat-suppressed (A) and axial (B) T2-weighted images reveal a mildly
hyperintense mass arising from the uterine cervix replacing normal anatomy (arrow) and obliterating the fibrous stroma, extending into
the parametrium. C, Parametrial spread is better depicted on the axial enhanced image (arrows). D, The corresponding sagittal delayed
postcontrast image illustrates the hypovascular, gradual enhancement of the mass (arrow).
 Magnetic Resonance Imaging of the Female Pelvis  •  319

E F

G H

FIGURE 5-56, cont’d  E-I, A sagittal T2-weighted fat-

suppressed image (E) in a different patient shows a
poorly defined mildly hyperintense mass (arrows) cen-
tered at the cervix. F and G, The axial T2-weighted
images at the level of the cervix show the infiltrative
mass extending into the parametrium (thin arrows) with
a remnant of the fibrous stroma (thick arrows) still
visible. H, The axial T2-weighted image at the level of
the upper vagina shows vagina involvement and evi-
dence of rectal (r) extension, rectovaginal fistula, and an
air-fluid level in the upper vagina (arrow). I, Note the
I
metastatic left iliac lymph node (arrow).
320  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-57.  Cervical carcinoma with local invasion of rectum and/or bladder. A large, heterogeneous mass displaces the bladder anteriorly
on the axial T2-weighted image (A), virtually replaces the entire uterus on the sagittal T2-weighted image (B), and invades the bladder,
which features endoluminal irregularity indicating transmural extension (arrow in B). C, Gadolinium enhancement shows central necro-
sis. D, The delayed image shows near-occlusive (thin arrow) and nonocclusive (thick arrow) thrombus in the common femoral veins.

A B
FIGURE 5-58.  Normal ovaries. Normal ovaries averaging 10 cc in size with subcentimeter ovoid, peripheral subcentimeter follicle cysts
(thin arrows), and central stroma (thick arrows) are easily identified when noting these typical characteristics, as exemplified on the axial
(A) and coronal (B) T2-weighted images. A small, partially subserosal fibroid protrudes from the anterior uterine body (open arrow
in B).
 Magnetic Resonance Imaging of the Female Pelvis  •  321

NORMAL OVARIAN FEATURES

Normal ovarian volume

Width
(reproductive age)
1.5–3 cm
L × W × T × 0.523
5–15 mL (≈cc3)

Type Size T1 signal T2 signal

Follicles ≤2.5 cm Low High
Length Thickness
3–5 cm 0.5–1.5 cm
Follicular 3–8 cm Low-high High
cyst

Corpus Variable Low-high High

luteal — up to (peripheral
cyst 2.5 cm enhancement)
or
greater
T2-hyperintense T2-hypointense
medulla cortex
FIGURE 5-59.  Normal ovarian features.

it courses along the anterior edge of the broad

ligament in the vicinity of the ovary and abutting TABLE 5-18.  Differential Diagnosis of Cystic
the proper ovarian ligament (see Figs. 5-7 and Ovarian Lesions
5-60). Inevitably, loops of (usually small) bowel Lesion Tissue Content
occupy the adnexal regions and complicate the
T2-Hypointense Adnexal Lesions
process. As long as you exclude the presence of Subserosal pedunculated fibroids Collagen
an underlying adnexal mass, you have accom- Endometrioma (shading) Concentrated blood products
plished your mission. Ovarian torsion Hemorrhage
Ectopic pregnancy Hemorrhage
Ovarian lesion characterization and diagnosis Vascular lesions Signal voids
figure prominently among the major indications Cystadenofibroma (cystic components Fibrous tissue
for pelvic MRI and boast a high probability of dominate)
Fibroma/fibrothecoma Fibrous stroma
success. A major discriminator is solid (or at Brenner tumor Fibrous stroma
least partially solid) versus cystic. Cystic lesions
are far more common and the approach should T1-Hyperintense Adnexal Lesions
Hemorrhagic cyst Hemorrhage
focus on two things—cyst content and com- Endometrioma Hemorrhage
plexity (differentiating neoplastic from non- Subserosal pedunculated fibroid with Hemorrhage
hemorrhagic degeneration
neoplastic cysts) (Tables 5-18 and 5-19). Ovarian torsion (peripheral hyperintensity) Hemorrhage
Dermoid cyst (hypointense with fat Fat
saturation)
Cystic Lesions
Bilateral Adnexal Lesions
First of all, to call a lesion “cystic,” you must Functional ovarian cysts
exclude a change in intensity between Ovarian epithelial neoplasms
Metastatic lesions (Krukenberg’s tumors)
T1-weighted pregadolinium and postgadolinium Endometriomas
images (which is an analog to perfusion, imply-
ing solid tissue). Catalog the signal intensity on Estrogenic Adnexal Masses
Granulosa cell tumor (most common)
the various pulse sequences. Using these data, Thecoma/fibrothecoma
almost all cysts fall into one of three broad
categories based on their content: (1) water, Virilizing Adnexal Masses
Sertoli-Leydig tumor
(2), lipid, and (3) hemorrhage. Cystic teratoma
Cystic ovarian lesions cannot be assessed on Metastatic tumors
one pulse sequence alone. Accurate classifica-
tion requires binary information from various
pulse sequence. The T2-weighted axial sequence
portrays cystic lesions consistently as round
hyperintense foci—albeit mildly variable
322  •  Fundamentals of Body MRI

Iliac vessels

Ovarian
vessles
Round ligament Mesosalpinx
(anterior course
to inguinal canal)

Suspensory
ligament

Uterus

Proper
ovarian
ligament Ovary

Broad ligament

Uterosacral
ligament
FIGURE 5-60.  Ovarian attachments.

TABLE 5-19.  Age-Predictive Probability Scheme Water Content

for Cystic Ovarian Lesions Of course, to equate “water” with ovarian cyst
content of any etiology is an oversimplification.
Prepubertal Reproductive Menopausal Nonetheless, this construct serves its purpose
Germ cell 80% Functional 70% Malignant 50% to identify a population of ovarian cysts that
Malignant 10% Endometrioma 10%
Neoplastic 20%
are further subclassified. “Water” defines the
  Benign 85% upper limit of hyperintensity on T2-weighted
  Malignant 15% images with commensurate hypointensity on
From Gant NF, Cunningham FG. Basic Gynecology and Obstetrics. T1-weighted images. Enhancement is absent
Norwalk, CT: Appleton and Lange, 1993. (Fig. 5-61). Under these circumstances, as long
as the size of the lesion does not violate physio­
logic limits and there is no evidence of wall
depending on cyst content (water > blood and thickening, septation, or mural nodularity to
fat). Next, note the signal intensity on a suggest underlying neoplasm, no further analy-
T1-weighted sequence without fat saturation— sis is necessary.
hypointensity connotes water and hyperinten-
sity indicates lipid or blood. Finally, review Functional Ovarian Cysts
T1-weighted fat-saturated images to distinguish The normal menstrual cycle involves the recruit-
between fat and blood; signal cancellation ment of a cohort of functional (or follicular)
indicates fat. Although this seems redundant, cysts that are generally smaller than 1 cm. A
following this scheme avoids errors in charac- single dominant cyst enlarges up to 2.5 cm and
terization. Some common errors include desig- usually undergoes ovulation, evolving into the
nating a T1-hyperintense lesion as a hemorrhagic corpus luteal cyst. Hemorrhagic cysts join the
cyst or endometrioma without noting signal sup- other two categories of functional cysts (follicu-
pression on fat-saturated images, or misclassify- lar and corpus luteal) and reflect blood from a
ing a T2-hyperintense lesion with no signal on ruptured vessel in the wall of a follicular cyst
T1-weighted fat saturated images as a dermoid (see “Blood Content” under “Cystic Lesions”).
without considering the possibility of a simple Even the postmenopausal ovary often continues
cyst with no signal on T1-weighted images to produce cysts that are usually spherical,
without fat saturation. simple, and unilocular. Therefore, regardless of
 Magnetic Resonance Imaging of the Female Pelvis  •  323

T1

T2

A B

C D

E
FIGURE 5-61.  Simple ovarian cyst. Axial T2-weighted (A), T1-weighted (B), precontrast (C), and postcontrast (D) T1-weighted fat-
saturated images show a small, simple right-sided ovarian cyst (thin arrow in A-D) exhibiting simple fluid characteristics with no
complexity or enhancement coexisting with a probable left ovarian corpus luteal cyst (thick arrow in A-C) with a thin rim of T1 hyper-
intensity (blood) and otherwise simple cystic features. With increased size (especially > 5 cm) and complexity, the probability of neoplasm
escalates, as illustrated in the axial T2-weighted image of a different patient (E) with a benign ovarian cystic epithelial neoplasm with
sepatation (thin arrows) and mild eccentric wall thickening (thick arrow).
324  •  Fundamentals of Body MRI

considered only when a history of pelvic surgery

TABLE 5-20.  Ovarian Cyst Management
or trauma (or possibly endometriosis) is con-
<2.5 cm ⇒ no follow-up necessary (regardless of age)
2.5–5 cm ⇒ imaging (ultrasound) follow-up different phase of menstrual firmed. The necessary precursors to a peritoneal
cycle (6 wk) inclusion cyst are adhesions and active ovarian
>5 cm ⇒ suggest surgical management (risk of torsion) tissue. Ovarian secretions gradually accumulate
as traumatized, reactive mesothelial tissue
absorbs fluid less freely, forming locules between
age, simple ovarian cysts up to 2.5 cm in diam- leaves of peritoneum and/or adhesions. As a
eter require no follow-up (Table 5-20). This consequence of this pathogenesis and growth
includes corpus luteal cysts, which characteristi- pattern, peritoneal inclusion cyst margins are at
cally exhibit a rim of enhancement and a nons- least partially spatially defined by anatomic
pherical shape (Fig. 5-62). Whereas the internal structures; they fill (potential) spaces rather
contents often approximate simple fluid, hemor- than creating their own space like tumors or
rhage occasionally may coexist resulting in T1 endothelially derived cystic lesions. Obtusely
hyperintensity (without T2 hypointensity—or angulated margins with adjacent structures are
shading—which indicates concentrated, or observed, because they insinuate around instead
long-standing blood products characteristic of of displacing structures. They are usually located
endometriomas, to be considered later). around (occasionally surrounding) or in proxim-
ity to the ovary. The contents usually approxi-
Ovarian Inclusion Cyst mate simple fluid (T1 hypointense and T2
An ovarian inclusion cyst is an equally benign, hyperintense) with no enhancement (Fig. 5-63).
incidental lesion common in menopause and The problem with this diagnosis is the protean
during the reproductive years. Imagine the appearance of peritoneal inclusion cysts, which
ovarian surface epithelium invaginating, forming overlaps with the appearance of multiple other
a self-enclosed cavity and losing its connection lesions, including ovarian neoplasms, hydrosal-
with the surface from which it arose (which pinx or pyosalpinx, and parovarian cysts.36 First
likely occurs during ovulation)—that is the of all, this diagnosis should not be con­sidered
etiology of an ovarian inclusion cyst. Whereas without the appropriate preexisting condition—
ovarian inclusion cysts may be a precursor to history of peritoneal injury/manipulation.
ovarian epithelial neoplasms, they exhibit simple Second, an extraovarian location must be estab-
features indistinguishable from a follicle cyst, lished. With septation or other evidence of com-
usually measuring no more than 1.5 cm. Because plexity (which is usually relatively sparse and
of the absence of physiologic ovarian cysts and often attributable to envelopment of adjacent
the relative prevalence of postmenopausal cystic structures), stability on prior or follow-up exam-
ovarian neoplasms, surveillance of postmeno- inations is confirmatory. Finally, margins that
pausal ovarian cysts has been observed histo­ conform to extralesional structures, such as the
rically, according to different, often institutionally pelvic sidewall, loops of bowel, or uterus, are
driven, guidelines. Follow-up algorithms in­ characteristic of peritoneal inclusion cysts.
formed by the features of inclusion cysts and the
risk of torsion with increasingly large lesion size Parovarian Cysts
generally conformed to the following guideline: True parovarian cysts are uncommon, usually
(1) less than 16 mm, no follow-up; (2) 16 mm simple, water-containing cysts and occasionally
to 5 cm, 4-month follow-up, and (3) 5 cm or simulate simple ovarian cysts. They arise in
larger, surgical resection. However, the burden the mesosalpinx between the ovary and the
of evidence indicates an exceedingly low likeli- fallopian tube. Parovarian cysts are usually
hood of neoplasm associated with cystic lesions meso­thelial or embryologic remnants (usually
regardless of age. Consequently, cystic ovarian paramesonephric vs. mesonephric). Their clini-
lesions up to 2.5 cm generally require no cal importance lies in their frequent symptom-
surveillance. atic nature and diagnostic confusion with
primary ovarian pathology.
Peritoneal Inclusion Cyst
Another variety of inclusion cysts developing in Lipid Content
the appropriate clinical setting is actually extra- In addition to simple fluid—or water—ovarian
ovarian. The peritoneal inclusion cyst should be cysts may contain hemorrhage or lipid (in
 Magnetic Resonance Imaging of the Female Pelvis  •  325

A B

C D
FIGURE 5-62.  Corpus luteal cyst. Coronal T2-weighted (A) and axial fat-saturated enhanced T1-weighted (B) images show a small cystic
lesion (thin arrow in A) with a thin peripheral rim of enhancement (thick arrows in B) and no other evidence of complexity. C-F, In a
different patient, a thicker rim of enhancement delineates a right-sided corpus luteal cyst (arrow) on T2-weighted (C), T1-weighted
(D), enhanced T1-weighted unsuppressed (E), and fat-suppressed (F) images. G, An irregular—collapsed or deflated—morphology often
characterizes corpus luteal cysts, as seen in a different patient (arrow).
326  •  Fundamentals of Body MRI

E F

G
FIGURE 5-62, cont’d 
 Magnetic Resonance Imaging of the Female Pelvis  •  327

A B

C D

E
FIGURE 5-63.  Peritoneal inclusion cyst. A and B, The lateral margin (thin arrows in A) of a fluid collection encircling the right ovary
(thick arrow in A and B) is bounded by the pelvic sidewall. Minimal wall thickening (thin arrows in B) and internal septation (open
arrow in B) are observed—seen to better advantage on the enhanced image (A) compared with the T2-weighted image (B)—and the
features are characteristic of a peritoneal inclusion cyst. Axial (C) and coronal (D) T2-weighted and axial enhanced T1-weighted (E)
images in a different patient reveal bilateral cystic lesions abutting the ovaries (arrows in C and D) and at least partially spatially defined
by anatomic borders—namely, the pelvic sidewalls. The left-sided lesion appears more masslike and an appropriate clinical history (i.e.,
surgery), stability, and an absence of neoplastic features should be confirmed.
328  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-64.  T1 hyperintense ovarian cysts—hemorrhagic cyst and dermoid cyst. The hemorrhagic cyst (thin arrow in A-C) exhibits
hyperintense signal on all pulse sequences—T2-weighted (A), T1-weighted (B), and T1-weighted fat-suppressed (C) images. Dependent
clot (thick arrow in A) and/or wall thickening occasionally complicate the appearance of hemorrhagic cysts. D-H, A biloculated dermoid
cyst in a different patient contains water (thin arrow) and sebaceous or fatty (thick arrow) components. Although the sebaceous locule
maintains signal on T2-weighted (D), T1-weighted out-of-phase (E), and in-phase (F) images, in contradistinction to the hemorrhagic
cyst, signal is nullified with fat suppression (G). H, After gadolinium administration, no enhancement is observed in either lesion.

the case of a dermoid cyst). Both of these short tau inversion recovery (STIR) or spectrally
types of cysts are differentiated from water- fat-saturated images (documenting signal sup-
containing cysts by their hyperintensity on pression from the inversion pulse or frequency-
(non–fat-saturated) T1-weighted images. The specific pulse targeted to fat).
key to differentiating between the hemorrhagic
and the lipid-containing cyst is the loss of signal Dermoid Cyst (Mature Cystic Teratoma)
on fat-suppressed images in the case of a dermoid Once fat signal is identified, the diagnosis is
(fat-containing) cyst (Fig. 5-64). Avoid the sealed—dermoid cyst. Additional findings, such
mistake of assuming that hypointensity on as multilocularity or internal complexity, such
T1-weighted fat saturated images alone con- as linear strands, septa, and debris, are common
notes lipid—this appearance indicates either a findings and do not suggest alternative diagno-
long T1 value (i.e., water) or a suppressed signal ses (Figs. 5-65 to 5-68). Dermoid cysts are
from fat. T1 hyperintensity plus evidence of fat protean, but the common thread and the (practi-
suppression equals fat—confirming this requires cally speaking) MRI sine qua non diagnostic
inspecting unsuppressed T1-weighted images feature is intralesional lipid signal. Rarely, fat
(look for isointensity to subcutaneous fat) and signal is subtle to absent and the dermoid
 Magnetic Resonance Imaging of the Female Pelvis  •  329

E F

G H
FIGURE 5-64, cont’d 

simulates a neoplastic lesion (although careful Blood Content

inspection should exclude enhancement and Endometrioma.  If hemorrhage is confirmed
evidence of a solid component). by T1 hyperintensity and no loss of signal on
Even though we call it a “dermoid cyst,” this fat-suppressed images, the next step is to
lesion is actually a benign neoplasm. The assess signal intensity on T2-weighted images.
dermoid cyst is more appropriately termed Hemorrhage exhibiting relatively low signal on
“mature cystic teratoma,” and is the benign T2-weighted images (called “shading”) harbors
counterpart to its malignant cousin, the imma- concentrated iron products, which is a sign of
ture teratoma (to be discussed in the Complex chronicity implying endometriosis (Fig. 5-69).
Cystic and Solid Lesions section). The mature This is in contradistinction to other hemorrhagic
cystic teratoma arises from a single pluripoten- lesions, the functional lesions—the hemorrhagic
tial germ cell and is composed of tissues from and corpus luteal cysts, which are ephemeral
at least two of the three germ cell layers (ecto- lesions. Additional supporting findings include a
derm, mesoderm and endoderm). In the case of nonspherical shape and multiplicity (Figs. 5-70
the mature cystic teratoma, these tissues are to 5-72).
mature and not aggressive in contradistinction
to the immature teratoma. Text continued on p. 338
330  •  Fundamentals of Body MRI

A B

C
FIGURE 5-65.  Dermoid cyst. A, The sagittal T2-weighted image reveals a relatively nonspecific moderately hyperintense lesion (arrow).
B, Axial T1-weighted image reiterates isointensity to fat (arrow) and reveals mild complexity—wall thickening and septation. C, The
addition of fat saturation (and intravenous gadolinium) confirms predominantly lipid content (arrow), an absence of enhancement and
the diagnosis of a dermoid cyst.
 Magnetic Resonance Imaging of the Female Pelvis  •  331

A B

C D

E
FIGURE 5-66.  Dermoid cyst, Rokitansky’s nodule. T1-weighted out-of-phase (A) and in-phase (B) images demonstrate a bilobed hyper-
intense lesion (thin arrows in A-D) with a peripheral nodule—the Rokitansky nodule (thick arrow in A-E). Exaggerated hypointensity
surrounding internal debris within the locules on the out-of-phase image (open arrows in A) shows the effects of phase cancellation when
the water-rich debris and surrounding fat exist in the same voxel. C, Axial T2-weighted image reveals signal isointense to subcutaneous
fat and relatively hypointense to simple fluid. The application of fat saturation to T1-weighted (D) and T2-weighted (E) images results
in complete signal suppression, indicating gross fat content.
332  •  Fundamentals of Body MRI

A B

C
FIGURE 5-67.  Dermoid cyst, fluid-fluid level. A, T2-weighted coronal localizing image in a pregnant patient (note the vertex presentation
and fundal placentation) also show a large left adnexal, at least biloculated cystic lesion (thin arrow) with internal debris and/or nodular-
ity (thick arrow). B, The axial T2-weighted image through the level of the fetal bladder (thick arrow) shows a fluid-fluid level (thin
arrow) with dependent fluid isointense to amniotic fluid (open arrow). C, The fluid-fluid level signal intensities are reversed on the
out-of-phase T1-weighted image with the nondependent fluid isointense to subcutaneous fat. The signal void at the fluid-fluid level
suggests destructive interference between the water (dependent) and the lipid (nondependent) protons—phase cancellation artifact—
additional evidence of fat composition and the diagnosis of a dermoid cyst.
 Magnetic Resonance Imaging of the Female Pelvis  •  333

A B

C D

E
FIGURE 5-68.  Dermoid cyst, minimal to no lipid. Axial T2-weighted (A) and T1-weighted (B) images show a hyperintense lesion with
internal debris. The addition of fat suppression to the sagittal T2-weighted (C) and T1-weighted (D) images confers slightly greater
conspicuity to the internal globules without convincing fat saturation. E, Subtracted image after gadolinium administration shows a
corresponding signal void (circle), excluding enhancement. Although this strongly suggests a benign cystic etiology and minimal fat
content may be suggested by the slight loss of signal in the relatively nondependent internal globules, the signal characteristics do not
allow for a definitive diagnosis of any of the dominant cystic lesions and surgery should be considered (as in this case—the final diagnosis
was “mature cystic teratoma”).
 A B
2002 2003

C D
2004 2006

E F
2008 2008
FIGURE 5-69.  Shading in an endometrioma. A-E, Sequential T2-weighted images of an evolving endometrioma (arrow) over a 6-year time
course showcase the phenomenon of shading—progressive T2 shortening due to ongoing concentration of blood products over time,
which results in gradually decreasing T2 signal over time. F, Axial T1-weighted fat-suppressed image obtained at the last timepoint
confirms the presence of hemorrhage (arrow).
 Magnetic Resonance Imaging of the Female Pelvis  •  335

A B

C D
FIGURE 5-70.  Endometrioma. Sagittal scout (A) and axial (B) T2-weighted images display a large moderately hypointense right adnexal
lesion (arrow) dwarfing the adjacent uterus. C, The corresponding T1-weighted image confers hyperintensity and discloses mild wall
thickening (arrows), an occasional feature seen in endometriomas. D, Preservation of hyperintensity on the T1-weighted fat-saturated
image excludes the possibility of lipid and confirms the presence of blood.
336  •  Fundamentals of Body MRI

A B

C
FIGURE 5-71.  Endometriosis. A, Axial T2-weighted image. The left ovary appears mildly heterogeneously enlarged with distortion of the
normal ovarian architecture with a few hypointense lesions (thin arrows) and a paucity of functional cysts (thick arrow). B, In-phase
T1-weighted image. Corresponding hyperintensity (arrows) in the T2 hypointense irregularly shaped left ovarian lesions indicates either
blood or lipid. C, Failure of signal suppression on the T1-weighted fat saturated image excludes fat and confirms hemorrhage. The
combination of nonsuppressing T1-hyperintensity, T2-shortening, multiplicity, ovarian location, and irregular morphology typifies
endometriosis.
 Magnetic Resonance Imaging of the Female Pelvis  •  337

A B

C D

E
FIGURE 5-72.  Endometriomas. Another typical case of endometriosis reveals an ill-defined left adnexal lesion with marked T2-shortening
(arrow in A) combined with corresponding hyperintensity on T1-weighted fat-saturated image (B)—signifying concentrated hemorrhage—
lesion multiplicity, and nonspherical morphology. C-E, In a different patient, multiple irregular lesions (arrows in C and E) with similar
signal characteristics on the T1-weighted fat-suppressed image (C) with shading—albeit less profound—on the T2-weighted image
(arrows in D) typify endometriosis. E, The T1-weighted in-phase gradient echo image reveals additional bilateral hyperintense lesions
in the iliac fossa (thick arrows) not to be confused with endometriomas (or other hemorrhagic or fatty lesions). Flow-related enhance-
ment accounts for hyperintensity in the iliac veins, in this case. Remember that gradient echo images are time-of-flight images (without
the parameter modifications of dedicated vascular sequences) and prone to the in-flow effect (especially in two-dimensional sequences
in the case of the entry slice with respect to the vessel).
338  •  Fundamentals of Body MRI

TABLE 5-21.  Hemorrhagic Adnexal Lesion Features

Lesion T1 Signal T2 Signal Number Morphology

Corpus luteal cyst Usually ⇓⇓ ⇑⇑ 1 Flattened, “deflated”

(usually no hemorrhage)
Hemorrhagic cyst ⇑⇑ ⇑⇑ Usually 1 Usually round-oval
Endometrioma ⇑⇑ ⇑-⇓⇓ 1-many Ovoid-irregular

Functional Hemorrhagic Cyst Acute Lesions

The chief differential diagnostic hemorrhagic Acute adnexal pathology, such as tuboovarian
cystic lesions to distinguish from an endome- abscess (TOA), ovarian torsion, and ectopic
trioma are functional hemorrhagic and corpus pregnancy (Table 5-22),37 may mimic endome-
luteal cysts (Table 5-21)—assuming acute patho­ triomas, functional cysts, or cystic neoplasms,
logy is excluded (i.e., ectopic pregnancy and but these usually distinguish themselves by their
torsion). The hemorrhagic cyst reveals none of abrupt clinical presentation (and/or pregnant
the complex features of the endometrioma; status). The equalizing factor is rupture, result-
except for the T1 hyperintensity indicating ing in pelvic fluid, which is present (especially)
hemorrhage, it approximates a simple cyst in in TOA/pelvic inflammatory disease (PID) and
all other respects. When complicated by ectopic pregnancy and torsion (to a lesser
hemorrhage—which is infrequent—the corpus extent). Edema is the sentinel finding of acute
luteal cyst may simulate an endometrioma. The adnexal pathology and is really the hallmark of
corpus luteal cyst’s inner lining of luteinized TOA/PID (Fig. 5-75).
cells corresponds to a mildly thickened wall
exhibiting mild enhancement (Fig. 5-73). The Tubovarian Abscess
nonspherical shape, deflated shape, communi- PID spans the spectrum from endometritis/
cates recent rupture. myometritis (which we have already discussed)
to pyosalpinx to a TOA. Pyosalpinx and TOA
Hematosalpinx manifest as complex cystic masses with thick-
The fallopian tube is essentially the innocent ened walls. Generally, the contents are nearly
bystander of the adnexa and contributes an item identical to simple fluid. Compared with urine,
to the list of hemorrhagic adnexal lesions— the contents are mildly T1 hyperintense and
hematosalpinx. Blood in the fallopian tube mildly T2 hypointense owing to the presence of
usually reflects secondary accumulation of debris and/or hemorrhage. Morphologically,
hemorrhage from pathology arising elsewhere: pyosalpinx is characteristically a tortuous,
endometriosis, infection, müllerian duct anoma- tubular structure, and confirmation of this
lies, ectopic pregnancy, cervical stenosis, and feature usually requires reviewing images in all
even tubal ligation and IUDs. Consider hemato- planes (Fig. 5-76). TOA is most often multilocu-
salpinx to be a clue to potential associated lated and both lesions are occasionally difficult
pathology, such as endometriosis or ectopic to differentiate from adjacent bowel loops
pregnancy. Tubular morphology and T1 hyper- (Fig. 5-77).
intensity go without saying. Relatively central Before such a diagnosis of pyosalpinx or TOA
(periuterine) location, tubular/tortuous mor- (or any other diagnosis of extraintestinal origin)
phology, and consideration of presence or is confirmed, exclusion from bowel loops is
exclusion of primary etiologies summarize the essential. Follow the bowel retrograde from the
imaging approach to hematosalpinx (Fig. 5-74). anus and rectum and antegrade from the cecum,
Other hemorrhagic lesions distinguish them- ileocecal valve, and terminal ileum if possible.
selves with an acute clinical presentation and Changeable appearance over time favors bowel
evidence of localizing inflammation—ectopic loops undergoing peristalsis. Internal foci of gas
pregnancy and ovarian torsion. Along with TOA, have been promoted as specific for an abscess,
these lesions deserve special mention and a which is self-evident when discriminating
topic of their own—acute adnexal lesions. between different adnexal lesions, but not
 Magnetic Resonance Imaging of the Female Pelvis  •  339

TABLE 5-22.  Acute Adnexal Pathology

Ectopic pregnancy β-hCG Evidence of blood
Ovarian torsion Nonspecific Evidence of blood
Ovarian enlargement
Enlarged follicles
Traction adjacent structures
Tubo-ovarian abscess Signs of infection Edema/inflammatory changes
⇑ Fluid
Ruptured dermoid cyst Nonspecific Signs of lipid (extracystic)
Evidence of peritonitis
Hemorrhagic ovarian cyst Midcycle Hemorrhage without shading
β-hCG = β-human chorionic gonadotropin.

A B

C
FIGURE 5-73.  Corpus luteal cyst. Axial T2-weighted (A) and T1-weighted (B) images show a simple-appearing right ovarian cystic lesion
(thin arrow) adjacent to a punctate lesion with inverted signal characteristics most typical of an endometrioma (thick arrow). C, Thin
rim enhancement (arrows) clinches the diagnosis of corpus luteal cyst, assuming the appropriate attendant features (menstrual status,
size ≤ 2.5 cm, and lack of obvious complexity).
340  •  Fundamentals of Body MRI

A B

C D

E F
FIGURE 5-74.  Hematosalpinx. Tubular morphology, T1 hyperintensity, and periuterine location are all easily appreciated in this case of
hematosalpinx (thin arrows in A and B) showcased on axial T1-weighted fat-suppressed (A) and T2-weighted (B) images. C and D, An
adjacent endometrioma in the cul-de-sac (arrow) demonstrates the typical signal characteristics—T1 hyperintensity (C) and shading, or
T2 hypointensity (D). Note the multiple incidental intramural fibroids (thick arrows in B and D). E and F, Tubular morphology is even
better demonstrated in a different patient with dependent-lying concentrated blood products (arrows) exhibiting shading on the
T2-weighted image (E) and hyperintensity on the T1-weighted fat-suppressed image (F).
 Magnetic Resonance Imaging of the Female Pelvis  •  341

A B

C
FIGURE 5-75.  Edema associated with tubo-ovarian abscess (TOA) or acute adnexal pathology. A, Coronal T2-weighted image. Unilateral
edema (arrows) in a young female with acute symptomatology practically limits diagnostic consideration to acute inflammatory patho­
logy, including appendicitis and other gastrointestinal conditions and acute adnexal conditions. B and C, Axial T2-weighted images
showing asymmetrical edema (thin arrows in B) emanating from a complex cystic fluid collection in the right adnexa (thick arrows in
C), in the absence of bowel pathology (and the appropriate clinical findings), which indicates pelvic inflammatory disease.
342  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-76.  Pyosalpinx. A, Sagittal T2-weighted fat-suppressed image shows edema (thin arrows) surrounding a dilated fallopian tube
(thick arrows), which indicates inflammation, further supported by the complex, heterogeneous fluid collection (open arrow). B, The
subtracted image after gadolinium administration reveals a greater degree of wall thickening and enhancement (arrows) than would be
expected in the absence of inflammation. Coronal T2-weighted (C) and axial enhanced T1-weighted fat-suppressed (D) images disclose
the full extent of the TOA (arrows).

necessarily helpful when trying to differentiate are often helpful. Third, interstitial hemorrhage
from bowel. In any event, gas bubbles are signal (reflecting vascular congestion) is common and
voids that are the least confluent on multiecho virtually diagnostic, especially in a suggestive
sequences, progressively blooming with single- clinical setting (Figs. 5-78 and 5-79). Trace the
echo technique to T1-weighted gradient echo vascular pedicle, if possible, to identify abnor-
images to T2*-weighted images. mal twisting. Occasionally, none of these fea-
tures is evident and the only clue is an abnormally
enlarged ovary with proliferation of the central
Ovarian Torsion stoma and peripheral displacement of enlarged
Ovarian torsion has a protean imaging appear- follicles (Fig. 5-80). This appearance reflects
ance, exhibiting a few common themes. First of relatively mild and gradual and/or intermittent
all, there is often an underlying adnexal lesion development of torsion with relative compensa-
leading to torsion. Dermoid cysts and ovarian tion. This phenomenon is referred to as “massive
cysts are common offenders. Second, the ovarian edema.” A curious feature of this disor-
symptom generator is the vascular occlusion der is the predilection for the right ovary, which
that theoretically manifests as an absence of is explained by the higher pressure in the left
enhancement. At least near-complete absence of ovarian vein, conferring a higher tolerance to
enhancement is the rule and subtraction images torsion.
 Magnetic Resonance Imaging of the Female Pelvis  •  343

A B

u u

C D

E
FIGURE 5-77.  TOA. A, The sagittal T2-weighted fat-suppressed image demonstrates a complex cystic lesion (thin arrows) with surround-
ing edema (thick arrows) in the cul-de-sac displacing and compressing the uterus (u). The axial T2-weighted image (B) reveals the extent
of the multiloculated inflammatory process, and the corresponding T1-weighted image (C) excludes hemorrhage. D, After gadolinium
administration, the T1-weighted fat-suppressed image shows the degree of wall thickening and enhancement. E, An ultrasound performed
immediately before the magnetic resonance imaging (MRI) corroborates the complexity of the collection.
344  •  Fundamentals of Body MRI

A B

C D

FIGURE 5-78.  Ovarian torsion. A, A heterogeneously

hypointense adnexal lesion (arrows) is shown on the
sagittal T2-weighted fat-saturated image. B, Persis-
tently dark signal (arrows) on the T2-weighted image
without fat suppression excludes the presence of fat
and a normal left ovary. C, Central isointensity (thin
arrows) on the T1-weighted image is noted and the
signal characteristics are most typical of acute hemor-
rhage. Peripheral hyperintensity (thick arrows) is
occasionally associated with ovarian torsion. Compar-
ing the unenhanced (D) with the enhanced (E)
T1-weighted fat-saturated image demonstrates essen-
tially no enhancement (arrows), confirming the diag-
E
nosis of ovarian torsion.
 Magnetic Resonance Imaging of the Female Pelvis  •  345

A B

C D
FIGURE 5-79.  Bilateral ovarian torsion. A, Sagittal T2-weighted fat-suppressed image reveals a large unilocular cystic lesion with a mildly
irregular wall thickening (arrow) shown to be a serous cystadenoma after surgical resection. B, Axial T2-weighted image shows diffusely
abnormal right ovarian hypointensity (thick arrow) and diffusely abnormal left ovarian hyperintensity (thin arrow). C–E, Axial
T2-weighted images through the caudal aspect of the lesion demonstrate the spatial relationship to bilaterally heterogeneously abnormal
ovaries (right ovary, thin arrow in C and E; left ovary, thick arrow in D and E). The diffusely hypointense enlarged right ovary appears
directly adherent with a tapering rind of tissue extending along the lateral aspect of the mass (open arrow in C), indicating right ovarian
origin. The markedly hyperintense left ovary is enlarged to a lesser degree. T1-weighted images without (E) and with (F) fat suppression
reveal ovarian hypointensity, particularly on the left (right ovary, thin arrow in E and F; left ovary, thick arrow in E and F), with a
minimal peripheral rim of hyperintensity seen to better advantage on the fat-suppressed image (open arrow in F). G, Lack of enhance-
ment is more definitively identified (arrow). H, Mild relative ovarian enhancement (thick arrow) and a focal serpiginous lesion (open
arrow) likely representing the sequela of an involuted corpus luteal cyst are discernible. Surgical resection confirmed right ovarian hemor-
rhagic ischemia; the left ovary was described as edematous, but not ischemic—probably the effects of intermittent low-grade ischemia/
partial torsion.
346  •  Fundamentals of Body MRI

E F

G H
FIGURE 5-79, cont’d 

Ectopic Pregnancy epithelial type) to solid. Management of cystic

In the presence of blood (and pregnancy), keep lesions pivots on the identification of complex
ectopic pregnancy in mind, because of its features. Simple cysts can be ignored or fol-
life-threatening potential. The only potentially lowed, whereas cysts with evidence of solid
specific, pathognomonic finding is a gestational tissue demand surgical resection. Acknowledg-
sac. Other findings overlap with other acute ment of this fact and accurate discrimination
gynecologic diseases—especially torsion—and from simple cysts is more important than spe-
include hematosalpinx/adnexal hematoma, hem- cific diagnosis of complex cystic or solid lesions.
orrhagic ascites, and a complex hemorrhagic
adnexal mass (Fig. 5-81).15 Always consider Epithelial Neoplasms
ectopic pregnancy in a reproductive-age female Almost invariably, cystic ovarian neoplasms
presenting acutely with a complex adnexal mass derive from the ovarian epithelial cell line with
and edema and/or hemorrhage and encourage two major subtypes dominating: serous cystad-
correlation with pregnancy status and β-hCG. enoma (or cystadenocarcinoma) or mucinous
cystadenoma (or cystadenocarcinoma)—among
the five total subtypes. For the sake of maintain-
Complex Cystic and Solid Lesions
ing perspective on the issue of ovarian neo-
Primary plasms, there are four major categories:
Outside the acute adnexal lesions, complexity epithelial, germ cell, sex cord–stromal, and met-
confers solid tissue or neoplasm. Ovarian neo- astatic (Table 5-23). Epithelial tumors account
plasms range from nearly entirely cystic (usually for 60% of all ovarian neoplasms and the vast
 Magnetic Resonance Imaging of the Female Pelvis  •  347

A B

FIGURE 5-80.  Ovarian torsion manifesting as an

enlarged ovary. A and B, Axial T2-weighted
images in a patient with an early intrauterine
pregnancy show a small gestational sac (arrow in
A) and a massively enlarged ovary (thick arrows
in B) with multiple enlarged cysts (open arrows
in B). C, The coronal T1-weighted gradient echo
localizing image lends a sense of scale to the ovary
(thin arrows), which dwarfs the bladder (thick
arrow) and spans more than half the width of the
C
abdomen.

majority of malignant ovarian neoplasms

TABLE 5-23.  Classification Scheme for (~85%).39
Ovarian Neoplasms Epithelial ovarian neoplasms are a disease of
Epithelial Sex Cord–Stromal Tumor older women, peaking in the sixth and seventh
Serous Granulosa–stromal cell tumor decades of life. They are classified as benign
Mucinous Granulosa cell tumor
Endometrioid Fibrothecoma (60%), borderline or low-grade (5%), or malig-
Clear cell Sclerosing stromal tumor nant (35%), depending on the histologic and
Brenner Sertoli-Leydig cell tumor clinical behavior. Our job is to detect features
Undifferentiated Steroid cell tumors
that suggest malignancy—such as an obvious
Germ Cell Tumors Metastatic Tumors solid component, large size (>4 cm), wall
Teratoma thickening, papillary projections—or meta­­­
Mature
Immature
static spread—ascites, adenopathy or peritoneal
Dysgerminoma implants, and pelvic sidewall invasion (Tables
Endodermal sinus tumor 5-24 and 5-25 and Fig. 5-82). Clinical manage-
Embryonal cell carcinoma
Choriocarcinoma
ment depends less on local spread compared
with cervical (and endometrial) carcinoma. Dis-
From Jung SE, Lee JM, Rha SE, et al. CT and MR imaging of ovarian
tumors with emphasis on differential diagnosis. Radiographics criminating benign from malignant and identify-
22;1305–1325, 2002. ing metastatic spread constitute the chief
348  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-81.  Ectopic pregnancy. Axial T2-weighted (A), T1-weighted out-of-phase (B) and T1-weighted in-phase (C) images. The right
cornual region has a small complex cystic lesion (circle) with central fluid signal, a thin peripheral rim of hemorrhage, and an adjacent,
lateral hypointense focus (presumably blood). Precontrast (D) and postcontrast (E and F) T1-weighted fat-suppressed images reveal
enhancement around the lesion indicating inflammation (arrow in E and F). G, Corresponding CT image shows the right lower quadrant
inflammation (arrows) adjacent to the lesion (circle). The α-fetoprotein measured approximately 35, and no intrauterine pregnancy was
identified.
 Magnetic Resonance Imaging of the Female Pelvis  •  349

E F

G
FIGURE 5-81, cont’d 

TABLE 5-24.  Ovarian Carcinoma Staging TABLE 5-25.  Features Suggesting Malignancy
Stage Description in Ovarian Epithelial Neoplasms
Feature Benign Malignant
I Grossly confined to one or both ovaries
IA: Intracapsular and unilateral Size
IB: Intracapsular and bilateral Component Entirely cystic Solid tissue
IC: Actual or potential peritoneal contamination* Papillary projections
II Local extension; grossly confined to the true pelvis Wall Thin (<3 mm) Thick
IIA: Involvement of Fallopian tubes or uterus Ascites None With possible implants
IIB: Involvement of other pelvic tissues, e.g. sigmoid, pelvic Other Adenopathy
implants Invasion
IIC: Actual or potential peritoneal contamination*
III Nodal metastases, or peritoneal implants outside the pelvis From Jung SE, Lee JM, Rha SE, et al. CT and MR imaging of ovarian
IIIA: Microscopic abdominal implants tumors with emphasis on differential diagnosis. Radiographics
IIIB: <2 cm abdominal implants 22;1305–1325, 2002.
IIIC: >2 cm abdominal implants or positive nodes
IV Distant spread (e.g., malignant pleural effusion, intrahepatic
metastases)
*Based on the presence of surface tumor, tumor rupture, ascites
containing malignant cells, or positive washings.
350  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-82.  Malignant features of ovarian epithelial neoplasm. Axial (A) and coronal (B) T2-weighted images show gross mural papillary
excrescences (arrows) virtually filling the contents of the mildly thick-walled unilocular cystic adnexal mass. Precontrast (C) and post-
contrast (D) fat-suppressed T1-weighted sagittal images show enhancement of the mural excrescences (thick arrow in D) signifying solid,
viable tissue in a serous cystadenocarcinoma. A low-grade seromucinous adenocarcinoma in a different patient (axial T2-weighted [E],
axial T1-weighted [F], sagittal T2-weighted fat-suppressed [G], and sagittal T2-weighted enhanced [H] images) manifests similar—albeit
less complex—features with a smaller, more confined papillary excrescence (thin arrow in E-G) exhibiting mild enhancement (thick
arrow in H).

imaging objectives. Ultimately, staging is accom- important objective is to identify or exclude

plished surgically. malignant features.40 Even relatively indolent
Whereas differentiating between the different lesions may harbor malignancy and your thresh-
epithelial subtypes is largely academic, progno- old should be low in suggesting the possibility
sis and malignant potential differ. Approximately (Fig. 5-85).
40% of serous tumors are low-grade or malig- The other subtypes of ovarian epithelial neo-
nant compared with only 20% of mucinous neo- plasms are far less common. Endometrioid
plasms. MRI features of the two main histologic and clear cell types are usually malignant and
subtypes largely overlap, but there are some are the most common malignant neoplasms
important discriminating characteristics (Table arising from endometriosis (endometrioid is
5-26 and Figs. 5-83 and 5-84). Keep in mind that first). There are few suggestive, although not
serous tumors are more likely to be malignant entirely reliable, features of the less common
and that mucinous tumors have a propensity epithelial neoplasms. Endometrioid carcinoma
for low-grade mucinous intraperitoneal appears as a large complex cystic mass with
spread (pseudomyxoma peritonei). The most solid components with frequent bilaterality
 Magnetic Resonance Imaging of the Female Pelvis  •  351

E F

G H
FIGURE 5-82, cont’d 

(30–50%). Clear cell carcinoma commonly mani- tissue in the form of nodules, plaques, or septa
fests as a unilocular cyst with solid protrusions. (Fig. 5-86).
Brenner’s tumors, which are rarely malignant,
are usually small (T2) hypointense solid or mul- Other Primary Ovarian Neoplasms
tiloculated cystic lesions with solid components Other ovarian neoplastic varieties are fairly
(which may exhibit exuberant calcifications); uncommon, constituting between 8% (sex
the uniform hypointensity reflects the fibrous cord–stromal) and 15% to 20% (germ cell) of
stroma and generally limits the scope of diagnos- ovarian neoplasms. Germ cell tumors include
tic possibilities (Table 5-27). An association with the (mature and immature) teratoma, dysgermi-
endometriosis suggests endometrioid or clear noma, endodermal sinus tumor, embryonal cell
cell carcinoma. carcinoma, and choriocarcinoma; a comprehen-
Cystadenofibroma is another subtype of sive discussion of these mostly rare tumors is
ovarian epithelial neoplasm. Usually benign, beyond the scope of this text. As previously
these tumors often express a multiloculated discussed, the mature teratoma—or dermoid
morphology and contain intralesional fibrous cyst—is the most common benign ovarian
 A B

C D

E F
FIGURE 5-83.  Serous cystadenoma. Axial T2-weighted (A) and enhanced (B) and sagittal T2-weighted (C) and enhanced (D) images.
A large unilocular cystic lesion is virtually indistinguishable from a simple (functional) cyst except for the relatively large size 
and few inconspicuous mural nodules (arrows in A, B, C, and D) underscoring the importance of closely scrutinizing these lesions,
especially when large. Although more often unilocular than its mucinous counterpart, the serous cystadenoma also expresses multilocular
morphology (arrows in E and F), as seen in a different patient (coronal T2-weighted [E] and sagittal [F] enhanced images).
 Magnetic Resonance Imaging of the Female Pelvis  •  353

A B

C D
FIGURE 5-84.  Mucinous cystadenoma. Axial T2-weighted (A) and sagittal fat-suppressed T2-weighted (B) images of a left ovarian muci-
nous cystadenoma (arrow) show multilocularity with thin septation and no other evidence of complexity. Precontrast (C) and postcontrast
(D) images confirm the lack of malignant features.

TABLE 5-26.  Features of Serous versus TABLE 5-27.  Differential Diagnosis of T2

Mucinous Epithelial Ovarian Neoplasms Hypointense Ovarian Lesions
Feature Serous Mucinous Lesion Tissue Composition

Clinical Non-neoplastic
Benign 25% 20% Endometrioma Concentrated blood products
Malignant 50% 10% Ovarian torsion Acute blood
Ratio 60% benign 80% benign
15% low-grade 10–15% low-grade Neoplastic
25% malignant 5–10% malignant Cystadenofibroma Dense collagenous stromal
proliferations
Imaging Fibroma Fibrous stromal tissue
Size Smaller Larger Brenner’s tumor Abundant fibrous stroma
Morphology Unilocular Multilocular Krukenberg’s tumor Reactive stromal proliferation
Thin-walled Small locules
Signal intensity Uniform Variable Extra-ovarian
Papillary projections Common Rare Subserosal pedunculated fibroid Dense collagen
Calcification Psammomatous Linear
Bilaterality Frequent Rare
Carcinomatosis More common Pseudomyxoma
peritonei
From Jung SE, Lee JM, Rha SE, et al. CT and MR imaging of ovarian
tumors with emphasis on differential diagnosis. Radiographics
22;1305–1325, 2002.
354  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-85.  Mucinous cystadenocarcinoma. Axial T2-weighted (A) and sagittal T2-weighted fat-suppressed (B) images demonstrate a
moderate-sized multiloculated cystic lesion with mildly thickened septa. T1-weighted precontrast (C) and postcontrast (D) images fail
to detect any additional potential malignant features. Based on imaging findings, the likelihood of neoplasm is definite and the likelihood
of malignancy is indeterminate. Surgery was recommended and a mucinous cystadenocarcinoma without evidence of invasion was
resected.

tumor in young women. The imaging appear- tumors (and the other even rarer germ cell
ance of a mature teratoma ranges from entirely tumors) are in the differential diagnosis of a
cystic to a largely fat-containing mass, corre- complex solid adnexal mass in a young woman
sponding to T1 hyperintensity that is suppressed (Fig. 5-87).
on fat-saturated sequences (see Figs. 5-65 to Sex cord–stromal tumors derive from the mes-
5-68). Mural nodules are common and may enchyme of the embryonic gonads, which
exhibit hypointensity or susceptibility artifact means that they arise from the ovarian cells sur-
due to calcium or hair (see Figs. 5-65 and 5-66). rounding the oocytes.41,42 Among these nongerm
Although the immature teratoma may also cell and nonepithelial cell types are granulosa
harbor small foci of fat, its complexity, poor cells, thecal cells, Sertoli cells, Leydig cells, and
definition, internal necrosis and/or hemorrhage, fibroblasts. Granulosa and theca cells participate
and solid components belie its malignant nature. in the production of estrogen, and Leydig cells
The endodermal sinus tumor (yolk sac tumor) secrete androgens and tumors of these cell
and dysgerminoma are probably most character- types—granulosa cell tumors, thecomas, and
istic for the associated hormonal secretions and Leydig cell tumors, respectively—are often asso-
their predilection for young women. Endoder- ciated with elevations in these hormone levels.
mal sinus tumors often elicit α-fetoprotein, These lesions may be benign or malignant.
and dysgerminomas occasionally produce hCG. Fibroblasts and thecal cells often collaborate
Both have a variable appearance and exhibit to form a spectrum of benign tumors named
complexity and solid components. Both of these according to the relative contribution of fibrous
 Magnetic Resonance Imaging of the Female Pelvis  •  355

A B

C D
FIGURE 5-86.  Cystadenofibroma. Coronal (A) and axial (B) T2-weighted and sagittal fat-suppressed (C) images of a right ovarian cyst-
adenofibroma (circle) show at least two dark clumps of fibrous tissue (arrows). D, There is mild enhancement of the septa and fibrous
plaque (arrow).

tissue and hormonally active thecal cells. Fibro- condition that resolves after resection of the
mas are the most common stromal tumors and tumor that is postulated to arise from the fric-
usually occur in postmenopausal females. They tional effects of a hard mass stimulating perito-
are usually unilateral and are not hormonally neal fluid production.
active. Fibromas are usually monotonous Thecomas and fibrothecomas, although lipid-
uniformly hypointense lesions on all pulse containing and hormonally active, generally do
sequences and exhibit mild enhancement, not contain enough lipid to be detected on MRI
which may be difficult to visually perceive (Figs. (or microscopically, for that matter). Only in
5-88 and 5-89). Review subtracted images or postmenopausal women in whom no uterine
measure intensity values compared with a estrogenic stimulation is expected is a thecoma/
control, such as muscle, which enhances fibrothecoma distinguished from a fibroma.
approximately 15%. Check for the presence of Granulosa cell tumors are the most common
ascites (and pleural effusion) constituting the malignant sex cord–stromal ovarian tumor, con-
triad of Meigs’ syndrome (benign ovarian tumor, stituting less than 5% of all malignant ovarian
pleural effusion, and ascites). This is an odd neoplasms. Granulosa cell tumors are also the
356  •  Fundamentals of Body MRI

A B

C D

E
FIGURE 5-87.  Dysgerminona. Axial gradient echo T1-weighted in-phase (A) and axial (B) and coronal (C) T2-weighted images. A non-
specific monotonous solid mass exerts marked mass effect on surrounding structures of the pelvis (note the uterus ventrally flattened
against the abdominal wall—arrow in C). Precontrast (D) and postcontrast (E) images show diffuse enhancement.
 Magnetic Resonance Imaging of the Female Pelvis  •  357

A B

C D
FIGURE 5-88.  Bilateral fibromas. Serpiginous hypointensity (arrows) distorts the appearance of the ovaries bilaterally on axial (A) and
coronal (B) T2-weighted images. C, Axial T1-weighted in-phase gradient echo image shows monotonous mild hypointensity to isoin-
tensity (circles), and signal characteristics most strongly suggest fibrous tissue. D, Mild bilateral enhancement (circles) is noted on the
subtracted postcontrast image.

A B
FIGURE 5-89.  Ovarian fibroma. Axial T2-weighted image (A) shows a small left ovarian fibroma (arrow in A) with very low signal and
mild enhancement (circle in B) on the T1-weighted fat-suppressed enhanced image (B).
358  •  Fundamentals of Body MRI

A B

C D
FIGURE 5-90.  Granulosa cell tumor. A, In this case, the tumor is mostly solid with punctate hyperintense cystic foci on the axial
T2-weighted image. The monotonous isointensity on the out-of-phase (B) and fat suppressed T1-weighted (C) images excludes hemor-
rhage. D, After intravenous gadolinium, moderate enhancement is noted.

most common estrogenic ovarian tumor, and a most common virilizing ovarian tumor, the
small subset occurs in prepubescent girls (unlike Sertoli-Leydig cell tumor is very rare, represent-
the thecoma/fibrothecoma). Following a macro- ing less than 0.5% of ovarian tumors. The appear-
follicular growth pattern with multilocular ance is nonspecific, ranging from solid to cystic,
cystic spaces, the imaging appearance is often and variable T2 hypointensity reflects fibrous
complicated by hemorrhage, fibrous degenera- stroma; the most characteristic feature is the
tion, irregular growth, or necrosis. Conse- androgenic hormone secretion.
quently, the granulosa cell tumor appearance Sclerosing stromal tumors are rare sex cord–
ranges from largely solid to largely cystic possi- stromal tumors usually occurring in the second
bly with hemorrhagic foci (Fig. 5-90). or third decade of life. The imaging appearance
Sertoli-Leydig cell tumors represent a spec- has been described as a “pseudolobular pattern”
trum of lesions composed of Sertoli and Leydig with hypointense, mildly enhancing nodules
cells that secrete androgenic hormones. As the surrounded by T2 hyperintense stroma. A
 Magnetic Resonance Imaging of the Female Pelvis  •  359

A B
FIGURE 5-91.  Metastatic ovarian lesions. A and B, Axial T2-weighted images. An amorphous solid mass replaces the left ovary (circle in
A) and a smaller, more hypointense lesion mildly expands and distorts the right ovary (arrow in B).

combination of rapidly enhancing cellular and

gradually enhancing collagenous hypocellular TABLE 5-28.  Miscellaneous Pelvic Lesions
components exhibiting peripheral enhance- Uterus Gastrointestinal Neoplasms
ment with centripetal progression characterizes Endometrial stromal sarcoma Rectal carcinoma
Adenosarcoma GIST
the imaging appearance. Carcinosarcoma
Soft Tissue Tumors
Secondary Fallopian Tube Hemangiopericytoma
Fallopian tube adenocarcinoma Liposarcoma
Secondary ovarian tumors are predominantly Aggressive angiomyxoma
composed of metastatic gastric, breast, and Ovary
colon carcinoma. When arising from a primary Clear cell adenocarcinoma
Metastatic disease
gastrointestinal malignancy, the eponym
“Krukenberg’s tumor” is applied. Although the Peritoneal Neoplasms
appearance is nonspecific, the process is usually Multicystic mesothelioma
Pseudomyxoma peritonei
bilateral and ovarian tissue has a tendency Desmoid tumor
to form desmoplastic tissue in response to GIST = gastrointestinal stromal tumor.
the metastases resulting in T2 hypointense From Szklaruk J, Tamm EP, Choi H, Varavithya V. MR imaging of
solid components. Bilateral (hypointense) solid common and uncommon large pelvic masses. Radiographics
23:403–434, 2003.
ovarian lesions in elderly patients—especially
with a known primary (gastric, breast, or
colonic) malignancy—strongly suggest meta-
static disease (Fig. 5-91).

Miscellaneous female genital tract is the cervix. To keep it in

The final category is composed of miscellaneous perspective, cervical lymphoma constitutes less
lesions not belonging to any of the other catego- than 1% of cervical malignancies. Compared
ries. These are entities to keep in the back of with cervical carcinoma, lymphoma is more
your mind to use whenever another, more likely homogeneous and undergoes less necrosis.
diagnosis is not forthcoming. Among these Perhaps the only definitive findings are the lack
lesions are pelvic lymphoma, aggressive angio- of mucosal involvement and sparing of the cervi-
myxoma, peritoneal carcinomatosis, fallopian cal stroma and uterine junctional zone.44 The
tube carcinoma, and other rare primary lesions imaging features are otherwise nonspecific with
of the peritoneum, such as multicystic mesothe- mild T2 hyperintensity and mild enhancement.
lioma (Table 5-28).43 The term “monotonous” is often applied to
describe the imaging appearance of lymphoma-
Pelvic Lymphoma tous masses, referring to the relatively homoge-
Primary lymphoma of the pelvis is a rare entity neous uniformly solid, mildly enhancing mass
and the most common site of origin in the with no unique identifiers.
360  •  Fundamentals of Body MRI

Aggressive Angiomyxoma of FSH induces mild global changes in the

Aggressive angiomyxoma is an unusual uncom- ovaries. Ovarian size ranges from normal to
mon tumor almost exclusively arising from the slightly enlarged and numerous small follicles
female perineum. They are composed of mesen- (≤10 mm) are observed. The findings are gener-
chymal stellate or spindle cells with a loose ally less dramatic than in polycystic ovaries.
myxoid background of collagen with small
thick-walled vessels. Despite the name, these Ovarian Hyperstimulation Syndrome
tumors are deceptively aggressive in appear- Ovarian hyperstimulation syndrome (OHSS) is a
ance; actually these tumors displace and/or rare iatrogenic phenomenon induced by fertility
grow around adjacent structures, rather than drugs, particularly gonadotropin therapy. The
invading (Fig. 5-92). These uniformly solid clinical manifestations run the gamut from
lesions exhibit an enhancement pattern that has mild discomfort to life-threatening multiorgan
been described as “whorled.” derangements (including hemoconcentration,
decreased blood volume, clotting disorders,
abnormal renal function, and respiratory dis-
Globally Abnormal Ovaries
tress). The main clinical categories—mild, mod-
Bilaterally globally abnormal ovaries usually erate, and severe—stratify patients based on
derive from hormonal imbalances (unless clinical and imaging data. Patients with mild
involved with an extrinsic process, such as met- OHSS experience mild abdominal discomfort
astatic disease). Consider this category to extend and the ovaries usually measure less than 5 cm
from nearly normal ovaries to massively enlarged, in diameter. In moderate OHSS, the ovaries
cystic ovaries, or from multifollicular ovaries measure between 5 and 10 cm and weight gain,
(which is a forme fruste of polycystic ovary vomiting, ascites develop. The ovaries enlarge
syndrome [PCOS] seen in puberty associated to over 10 cm in severe OHSS with worsening
with mildly reduced follicle-stimulating hor­­ clinical manifestations including gross intraperi-
mone [FSH] levels) at the nearly normal end toneal fluid, pleural effusions, hypotension,
of the spectrum to ovarian hyperstimulation and electrolyte imbalances. Multiple enlarged
syndrome. ovarian cysts are also typically observed and the
MRI appearance overlaps with massive ovarian
Polycystic Ovary Syndrome edema and PCOS (Fig. 5-94). Whereas the
Multifollicular ovaries and polycystic ovaries imaging features may be indistinguishable in
differ mainly in their clinical context. PCOS (or some cases, the clinical presentations diverge
Stein-Leventhal syndrome) is a clinical entity significantly, allowing for a precise diagnosis
defined as hyperandrogenism with chronic (although with ovarian enlargement in OHSS,
anovulation without underlying adrenal or pitu- the possibility of torsion increases).
itary etiology. The ovaries in these patients
enlarge (usually bilaterally) and classically
Vascular Lesions
contain multiple, mildly enlarged, peripherally
distributed follicles (Fig. 5-93). Imaging criteria Although vascular lesions bear little conceptual
have been generated to assist in the diagnostic resemblance to other adnexal lesions, some
process and include (1) ovarian volume greater imaging features overlap. Whereas flowing
than 10 cm3, (2) 12 or more follicles per ovary, blood often induces signal voids on spin-echo
(3) no dominant follicle of 10 mm or larger, and images, dilated pelvic veins occasionally appear
(4) peripheral follicular distribution; at least two hyperintense on T2-weighted images, mimick-
or three of these items should be present to ing other tubular structures, such as hydro­
entertain the diagnosis.45 Be advised that these salpinx (Fig. 5-95). Intraluminal enhancement
criteria were designed as a sonographic diagnos- matching venous enhancement obviates poten-
tic tool, and consider them as a general guide- tial misdiagnosis.
line for MRI. Polycystic ovaries differ from PCOS The three dominant vascular disorders are
ovaries only in the absence of the clinical syn- pelvic arteriovenous malformation (AVM),
drome, not in the imaging appearance. pelvic congestion syndrome or pelvic varices,
Multifollicular ovaries are essentially polycys- and ovarian vein thrombosis (Table 5-29).
tic ovaries in mid to late puberty. Incomplete Reviewing the normal anatomy of the pelvis is
pulsatile gonadotropin with relatively low levels a good starting point for a discussion of these
 Magnetic Resonance Imaging of the Female Pelvis  •  361

A B

C D

FIGURE 5-92.  Aggressive angiomyxoma.

A, The sagittal T2-weighted image reveals a
large mass (arrows) replacing the native uterus
posthysterectomy. B and C, Axial T2-weighted
images show the lesion displacing regional
structures, insinuating around the colon
(arrow in B) and extending into the left
ischiorectal fossa. D, Monotonous hypointen-
sity on the axial T1-weighted image is replaced
by a “swirled, or whorled” enhancement
pattern on the postcontrast image (E). The
unrestricted growth without invasion is char-
E
acteristic of aggressive angiomyxoma.
362  •  Fundamentals of Body MRI

B: 28.9 mm
A: 25.5 mm

A: 40.9 mm

A B

C D
FIGURE 5-93.  Polycystic ovaries. The axial (A) and sagittal fat-suppressed (B) T2-weighted images in a patient clinically presenting with
polycystic ovary syndrome (PCOS) show an enlarged right ovary with multiple subcentimeter peripheral follicles and hypertrophic central
stromal tissue (arrow in A), supporting the clinical diagnosis. The left ovary (not shown) exhibited similar features. The complex cystic
mass anteriorly demonstrates central signal cancellation (arrows in B) on the fat-suppressed image, indicating fat in a dermoid cyst. In
a second patient without the clinical stigmata of PCOS (coronal [C] and axial [D] T2-weighted images), bilaterally mildly enlarged
ovaries contain multiple peripherally distributed follicles with no dominant cyst.
 Magnetic Resonance Imaging of the Female Pelvis  •  363

C: 46.3 mm D: 50.0 mm

A: 74.2 mm B: 70.5 mm

A B

C
FIGURE 5-94.  Ovarian hyperstimulation syndrome. A, The coronal localizer steady-state image in a patient undergoing fertility treatment
shows bilaterally enlarged cystic ovaries (arrows). B, Measurements obtained on the axial T2-weighted image far exceed normal parameters
and the increased size and number of ovarian cysts obliterates ovarian architecture and stromal tissue. C, Axial enhanced fat-suppressed
T1-weighted image reveals enhancing tissue centrifugally compressed around the peripheral margins of the enlarged cysts (arrows).

TABLE 5-29.  Vascular Lesions

Lesion Clinical Features Imaging Findings

Pelvic arteriovenous malformation Preexisting trauma Early enhancement

Dilated vessels
Tangled, tortuous vessels
Pelvic congestion syndrome Physiologic factors Dilated veins
⇑ Prominent veins
Ovarian vein thrombosis Nonspecific triad Lack of enhancement
Lack of signal void
364  •  Fundamentals of Body MRI

A B

C
FIGURE 5-95.  Normal pelvic veins simulating hydrosalpinx/fluid-filled tubular structures. Axial T2-weighted (A and B) and T1-weighted
postcontrast fat-suppressed (C) images through the lower pelvis at the level of the cul-de-sac. Multiple tubular hyperintense lesions (less
intense than the bladder) enhance avidly (arrows), more than the iliac veins, probably as a consequence of arteriovenous shunting.

lesions (Fig. 5-96). The arterial supply of the venous drainage. The common features of all
pelvic viscera is derived from the paired ovarian AVMs are serpiginous, tubular structures exhib-
arteries (arising from the aorta caudal to the iting flow and enhancement with early enhance-
renal arteries) and paired branches of the inter- ment of the draining vein (Fig. 5-97). On
nal iliac arteries—primarily the uterine and spin-echo sequences, the AVM appears as a
vaginal arteries. These vessels form paired signal void. Blood protons are a moving target
arcades anastamosing with one another along and flow out of the region of interest too rapidly
the lateral aspects of the pelvic viscera. Venous to be exposed to the 90° excitation and 180°
drainage essentially mirrors the arterial supply, refocusing pulses necessary to generate signal.
except that the left ovarian vein drains into the As a vascular structure, the AVM enhances
left renal vein instead of the inferior vena cava. avidly—equivalent to an artery—maintaining
hyperintensity on T1-weighted postgadolinium
Pelvic Arteriovenous Malformation images matching vascular structures. In the case
The main categories of AVMs are uterine, of uterine AVMs, the lesion is centered in the
vaginal, and pelvic. The underlying abnormality myometrium with consequential disruption of
is an abnormal connection between arteries and the normal uterine zonal anatomy.
veins. The result is a nest of dilated vascular Acquired AVMs are more common than
channels promoting increased arterial flow and congenital AVMs and commonly arise from
 Magnetic Resonance Imaging of the Female Pelvis  •  365

IVC Left renal Renal

vein artery

Left ovarian
vein

Left ovarian
Right artery
ovarian
vein

Internal
iliac vein

Internal
iliac artery

Uterine artery

Uterine vein
Bladder

FIGURE 5-96.  Pelvic vascular anatomy.

traumatic and infectious etiologies, such as dila- puberty and pregnancy, hormonal vasodilata-
tation and curettage, IUDs, pelvic surgery, infec- tion, mechanical obstruction (left renal vein
tion, GTD, endometrial or cervical carcinoma, between the aorta and the superior mesenteric
and diethylstilbestrol exposure. Differential vein, the right common iliac vein under the
diagnostic considerations include GTD (which right common iliac artery, and the retroaortic
may coexist with uterine AVMs), retained left renal vein behind the aorta), and primary
products of conception (associated with recent valvular insufficiency. Although the disorder is
pregnancy and elevated β-hCG), and pelvic con- defined as noncyclical chronic pelvic pain
gestion syndrome. caused by dilated pelvic veins, there is proba-
bly overlap in the imaging appearance between
Pelvic Congestion Syndrome afflicted and unafflicted women. In the appro-
Synonyms for pelvic congestion syndrome are priate clinical setting, the imaging criteria of
pelvic varices, pelvic venous incompetence, pelvic congestion syndrome include four ipsi-
and pelvic vein syndrome. This disorder is not lateral tortuous parauterine veins, at least one
well understood and multiple etiologic factors which measures at least 4 mm in diameter or
have been proposed. Among these factors are an ovarian vein diameter of greater than
physiologic increase in pelvic blood flow during 8 mm.46
366  •  Fundamentals of Body MRI

A B

D E
FIGURE 5-97.  Pelvic arteriovenous malformation (AVM). A hypointense pelvic AVM with ovoid and serpiginous morphology (circle in A
and B) coexisting on adjacent slices of a coronal T2-weighted sequence (A and B) lacks signal voids on the companion T1-weighted
in-phase gradient echo image (circle in C). (Adjacent blooming hypointensities arise from gas in sigmoid diverticula.) D and E, The
reformatted maximal intensity projection images (D) from the arterial phase of the pelvic magnetic resonance angiography (MRA)
demonstrates pronounced enhancement (thin arrow) with early draining into the internal iliac vein (thick arrow)—compare with the
contralateral side (E).
 Magnetic Resonance Imaging of the Female Pelvis  •  367

A B

C D
FIGURE 5-98.  Ovarian vein thrombosis. A, A circular hyperintensity (arrow) corresponding to the distal ovarian vein abuts the inferior
vena cava near the right kidney on the T2-weighted image. B, Corresponding hyperintensity on the in-phase T1-weighted gradient echo
image indicates acute clot (circle). C and D, Coronal images from a gadolinium-enhanced three-dimensional magnetic resonance veno­
graphy (MRV) display filling defect (arrows) within the upper (C) and lower (D) ovarian vein.

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Index
Note: Page numbers followed by f refer to figures; page numbers followed by t refer to tables.

A Adrenal glands (Continued) Biliary tract (Continued)

Abdominal aortic aneurysm, 256–257, lymphoma of, 249 carcinoma of, 188–193, 190f–195f
256f–257f metastatic disease of, 229f, 249, congenital communicating
Abscess 252f–253f cavernous ectasia of, 54–56,
gallbladder, 173, 175f myelolipoma of, 249, 250f 184
hepatic, 64 normal, 203f, 242–243 congenital dilatation of, 182–184,
amebic, 61t, 64–66 pheochromocytoma of, 249, 182f–185f
fungal, 61t, 64 250f–251f hamartoma of, 54, 56f, 66
vs. metastatic disease, 87 solid lesions of, 244f, 246–249, imaging techniques for, 181–182
mycobacterial, 61t 247f infection of, 187–188
pyogenic, 61t, 64, 64f–65f Amebiasis, 61t, 64–66 inflammation of, 187–188,
renal, 218–221, 221f, 238–239 Amniotic fluid, 332f 188f–189f
tuboovarian, 338–342, 339t, Ampere’s Law, 2–3, 4f normal, 178–179
341f–343f Angiomyolipoma obstruction of, 186
Accident prevention, 28–29, 32f hepatic, 97–98, 98f benign, 186, 187f
Acinar cell, 129 renal, 216f, 231–232, 233f infectious, 187–188
Acinar cell carcinoma, 160 Angiomyxoma, 360, 361f inflammatory, 187–188,
Acoustic noise, 29–32 Angular momentum (spin), 1, 3f 188f–189f
Acquired cystic kidney disease, 215, Annular pancreas, 130–131, 132f malignant, 188–196, 195f.
217t Aorta, aneurysm of, 52f, 256–257, See also Cholangiocarcinoma
Acquisition time, 22–23 256f–257f postoperative strictures of, 186
Adenocarcinoma, pancreatic. See Arteriovenous malformation, 363t, rupture of, 66–67, 67f, 123
Pancreas, adenocarcinoma of 364–365, 366f Biloma, 66–67, 67f, 123
Adenoma Artifact Birt-Hogg-Dube syndrome, 225f
adrenal, 48f, 246–248, 248f India ink, 15f, 17 Bladder, 268
gallbladder, 177, 179f motion. See Motion artifact fetal, 332f
hepatic, 68–70, 69f phase cancellation, 332f metastatic disease of, 320f
vs. focal nodular hyperplasia, prohibitive, 36f–37f Blooming, 17, 18f
70–71 susceptibility. See Susceptibility Bowel, 18f, 26f, 44f, 47f, 267f–268f,
vs. metastatic disease, 86–87 artifact 268
Adenoma malignum, 305t, 310, 314f wraparound, 23, 25f, 267f–268f Breast implants, 56f
Adenomyoma, 267f–268f, 270f, Ascites, 112–113, 114f Brenner’s tumor, 350–351, 353t
290f–291f, 298f Asherman’s syndrome, 271, 272f Budd-Chiari syndrome, 117–120, 118t,
Adenomyomatosis, gallbladder, 176, Autoimmune hepatitis, 115 119f
178f Autoimmune pancreatitis, 135–144, vs. cirrhosis, 120
Adenomyosis 143f nodules in, 118–120
cervical, 304, 305t Burn injury, 29
myometrial, 294–296, 296t, 297f B
Adhesions, intrauterine, 271, 272f Bartholin’s gland cyst, 289f, 308–310, C
Adnexa, 317–367. See also Fallopian 310t, 312f–313f CA 19-9, in pancreatic
tube(s); Ovary (ovaries) Beaded appearance, in primary adenocarcinoma, 150
imaging of, 261–262 sclerosing cholangitis, 42f–43f, Calcification
coil placement in, 265, 266f 115–116, 116f in chronic pancreatitis, 135, 142f
dynamic, 261–262, 264t Bile duct(s). See also Biliary tract in hepatic hemangioma, 58–60
interpretation of, 265–268, 265t, common, 133f in hereditary pancreatitis, 144, 146f
267t calculi of, 185–186, 185f in pancreatic solid-cystic papillary
normal, 317–321 stricture of, 186, 187f epithelial neoplasm, 171f–172f
Adrenal glands, 242–249, 244f cyst of, 54, 54f Calculi
adenoma of, 48f, 246–248, 248f cystadenocarcinoma of, 61 biliary, 185–186, 185f–186f
carcinoma of, 249, 254f cystadenoma of, 61, 62f gallbladder, 47f, 173, 174f
cystic lesions of, 244–246, hamartoma of, 54, 56f, 66 renal, 218, 220f
244f–245f Bile salts, 171–172, 179 Candidiasis, 66
echinococcal cysts of, 246 Biliary tract, 178–186. See also Bile Carcinoma
hemorrhage of, 243, 244f, 246, duct(s) adrenal, 249, 254f
247f ampullary carcinoma of, 193–196, biliary. See Cholangiocarcinoma
hyperplasia of, 248–249 194f–195f cervical. See Cervical carcinoma
imaging of, 199–200, 200f anatomy of, 178–179 endometrial. See Endometrial
indications for, 199, 200t benign strictures of, 186, 187f carcinoma
interpretation of, 200–201 calculi of, 185–186, 185f–186f gallbladder, 177–178, 179f–180f

369
370  •  Index

Carcinoma (Continued) Cholestasis, intrahepatic, 103–104, Cyst(s) (Continued)

hepatic. See Hepatocellular 104f vaginal
carcinoma Cholesterosis, 176–177 Bartholin’s gland, 289f, 308–310,
ovarian. See Ovarian carcinoma Choriocarcinoma, 282 310t, 312f–313f
pancreatic. See Pancreas, Cirrhosis, 110–115 Gartner’s duct, 308, 309f, 310t
adenocarcinoma of ascites in, 112–113, 114f inclusion, 308–310, 310t
renal. See Renal cell carcinoma atrophy-hypertrophy pattern in, Müllerian duct, 311f
vaginal, 317 108f, 110–111, 110f, 112f water in, 21f, 322, 323f, 325f–327f
Caroli’s disease, 54–56, 184 vs. Budd-Chiari syndrome, 120 Cystadenocarcinoma
Cerebrospinal fluid (CSF), 21f, 47f caudate–to–right lobe ratio in, 111, biliary, 61
Cervical carcinoma, 266f, 310–317, 111f ovarian, 347–350, 350f–351f, 354f
315f etiology of, 113–115, 113t Cystadenofibroma, 266f, 351, 355f
bladder invasion in, 320f fibrosis in, 111–112 Cystadenoma
differential diagnosis of, 310, 312t hepatocellular carcinoma and, biliary, 61, 62f
endometrial metastases from, 112–113 ovarian, 350, 352f–353f
280–282, 281f imaging signs in, 110–111, 110f pancreatic, 164f, 166, 167f–168f
fibrous stroma in, 310–317, 316f portal venous thrombus in, 114f Cystic fibrosis, 145, 147f
parametrial invasion in, 318f–319f portosystemic collaterals in, 47f,
rectal invasion in, 318f–320f 108f, 112–113, 112f–114f D
staging of, 310–317, 317t regenerative nodules in, 73, Dermoid cyst, 328–329, 328f–333f,
Cervicitis, 305t, 308, 308f 74f–75f, 111–112, 111f 339t
Cervix, 304–317 Column of Bertin, 207, 208f Diagmagnetic substances, 16
adenoma malignum of, 305t, 310, Corpus luteal cyst, 322–324, 323f, Diethylstilbestrol, fetal exposure to,
314f 325f–326f, 338, 339f 264f, 303–304
adenomyosis of, 304, 305t Cortical rim sign, 239–240 Diffusion-weighted imaging, 10
carcinoma of. See Cervical Cyst(s) Double duct sign, 150–151,
carcinoma of adenoma malignum, 305t, 310, 153f–154f
cystic lesions of, 304–310, 305f, 314f Doughnut sign, 85–86, 87f
305t adrenal, 244–246, 244f–245f Dysgerminoma, 354, 356f
glandular hyperplasia of, 304, 305t, cervical, 304–310, 305t
306f–307f Nabothian, 304, 305f, 305t E
imaging of, 261–262 choledochal, 182–184, 182f–185f Echinococcal cysts
interpretation of, 265t, 266 hepatic, 53, 54f adrenal, 246
inflammation of, 305t, 308, 308f echinococcal, 61–63, 61t, 63f hepatic, 61–63, 61t, 63f
lymphoma of, 359 vs. metastatic disease, 88f, 89 Echo, 9
Nabothian cyst of, 304, 305f, 305t ovarian, 266–267, 321–346, Edema
normal, 304 321t–322t, 324t. See also fallopian tube, 342f
Cesarean section defect, 272, 274f Dermoid cyst gallbladder, 176, 177f
Chain of lakes appearance, in chronic complex, 346 ovarian, 338, 341f, 342, 347f
pancreatitis, 135, 141f hemorrhagic, 324–328, 328f– pancreatic, 134, 137f–138f
Chelation, in hemochromatosis, 107 329f, 338, 338t–339t Embryo, 282
Chemical shift imaging, 14–15, 15f lipid content in, 324–328, Endodermal sinus tumor, 354
Chemoembolization, hepatic 328f–333f Endometrial carcinoma, 263f,
complications of, 91, 93f water content in, 322, 323f, 273–282, 279t
Chemotherapy, hepatic complications 325f–327f classification of, 276, 276t
of, 91 pancreatic, 145, 149f, 161–170, invasive, 276–277, 279f–281f, 280
Cholangiocarcinoma, 188–193, 189f, 164f pedunculated, 276f–277f
191f–192f parovarian, 324 vs. polyps, 272–273
extrahepatic, 91–92, 92t, 188, 193f renal, 207, 208f, 209 sessile, 276–277, 278f
hilar (Klatskin’s tumor), 91–92, 92t, acquired, 215, 217t staging of, 279, 280t
102f, 188, 190f classification of, 207, 209t, 210, Endometrioma, 19f, 276f–277f, 283f,
peripheral, 91–95, 92t, 188 211f 329, 338, 338t, 353t
capsular retraction in, 92–93, complex, 207, 210–212, shading in, 334f, 337f, 340f
95f–96f, 97t 212f–213f, 218, 220f wall thickening in, 335f
infiltrating, 92–93, 94f differential diagnosis of, 209f Endometriosis, 329, 336f–337f, 338
intraductal papillary, 92–93, 94f exophytic, 210, 210f–211f Endometritis, 270
mass-forming, 92–93, 94f hemorrhagic, 201, 208f, Endometrium, 270–282, 270f
staging of, 97t 209–211, 212f–213f carcinoma of. See Endometrial
Cholangitis, 187–188, 188f–189f infection of, 221 carcinoma
Cholecystitis, 173–176 infectious, 218–221, 220f–221f diffuse abnormalities of, 270, 271f
acute, 173, 174f–175f lithium-induced, 214f, 215, 217f, fluid in, 269–270
chronic, 176, 176f 220f focal abnormalities of, 271, 272f.
gangrenous, 176 neoplastic. See Multilocular See also specific abnormalities
Cholecystoses, hyperplastic, 176–177 cystic nephroma; Renal cell gas in, 269–270
Choledochal cyst, 182–184 carcinoma, cystic hormonal effects on, 270
classification of, 182f parapelvic, 210, 211f hyperplasia of, 270
type I, 182–183, 182f–183f parenchymal, 210, 211f metastatic disease of, 280–282, 281f
type II, 183, 184f septated, 213f polyps of, 263f, 272–273,
type III, 183, 184f simple, 207, 208f, 209–212, 275f–277f
type IV, 184, 185f 210f–211f, 213f tamoxifen-related changes in, 271,
Choledocholithiasis, 185–186, 185f site of, 210, 211f 271f
Cholelithiasis, 47f, 173, 174f Skene’s gland, 308–310, 310t, 313f thickness of, 269–270
 Index  •  371

Endoscopic retrograde Gartner’s duct cyst, 305t, 308, 309f, Hepatocellular carcinoma (Continued)
cholangiopancreatography, 181 310t cirrhosis and, 112–113
Entamoeba histolytica infection, 61t, Gas, endometrial, 269–270 classic imaging features of, 78,
64–66 Gastrinoma, 156, 156f 80f–82f
Gastrointestinal system, free water in, differential diagnosis of, 79–83,
F 21f 83t–84t
Fallopian tube(s), 269f Germ cell tumor, 347t, 351–354 diffuse, 78, 79f
blood in, 338, 340f Gerota’s fascia, 203 extrahepatic spread of, 79, 83f
inflammation of, 338–342, 342f Gestational trophoblastic disease, fat in, 78, 79f–80f
Fat, 15–16, 15f–16f 280–282 fibrolamellar, 70–71, 83–84, 85f
Fat-water chemical shift imaging, Ghosting, 21, 22f. See also Motion vs. focal nodular hyperplasia,
14–15, 15f artifact 70–71
Femoral vein thrombus, 320f Glucagonoma, 156–158, 156f vs. high-grade dysplastic nodules,
Ferromagnetic substances/objects, Gradient moment nulling, 27, 27f 75–76
28–29 Gradient system, 4–6, 5f hyperintensity in, 78, 79f–82f
Fertility treatment, ovarian X (frequency-encoding), 4–5, 5f hypointensity in, 78
hyperstimulation syndrome with, Y (phase-encoding), 4–5, 5f–6f lymphadenopathy in, 79, 83f
360, 363f Z (slice-select), 4, 5f vs. metastatic disease, 86–87
Fetus Granulosa cell tumor, 354–358, 358f nodular, 78
bladder of, 332f Groove pancreatitis, 144, 144f–145f nodule-within-nodule appearance
diethylstilbestrol exposure and, Gyromagnetic ratio, 1 in, 76, 77f
264f, 303–304 pathogenesis of, 72–73, 74f,
MRI effects on, 33 H 76–77
Fibroids, uterine. See Uterine Halo sign, 115, 116f pseudocapsule in, 78, 80f–81f
fibroid(s) Hamartoma, biliary, 54, 56f vs. regenerative nodules, 73–75
Fibroma, ovarian, 354–355, 357f vs. candidiasis, 66 screening for, 77–78, 78t
Field of view (FOV), 22–23, 24f–25f Hazards, 28–33, 29f–31f solitary, 78
Five-gauss line, 28–29, 32f screening for, 30f–31f staging of, 78t
Flip angle (FA), 13 Helium, risk of, 32 vs. steatosis, 99
Focal nodular hyperplasia, 52f–53f, Hemangioma thrombus in, 78–79, 79f, 82f
70–71, 70f–72f free water in, 21f vascular invasion in, 78–79, 81f–82f
vs. adenoma, 69–70 hepatic, 56–61, 57f–58f washout in, 53f, 68, 68f, 78,
vs. hemangioma, 70–71 calcification in, 58–60 80f–81f, 85f
vs. hepatocellular carcinoma, complex, 58–60, 59f Hepatoma. See Hepatocellular
69–71 vs. focal nodular hyperplasia, carcinoma
vs. metastatic disease, 86–87 70–71 Hydatid disease, 61–63, 61t, 63f
vs. transient intensity differences, giant, 58, 59f Hydatidiform mole, 282
72 malignant transformation of, 60 Hydrogen, 1, 2f
Fourier transform, 7–8 small, 57, 58f Hydronephrosis, 215–218, 218t, 219f,
Fractional echo sampling, 27–28, STIR image of, 26f 234f, 240
28f Hemangiomatosis, 60–61, 60f
Fringe field, 28–29, 32f Hematoma I
Fungal infection, hepatic, 61t, 64, 66 hepatic, 66, 67f Image blur, 23–24
intervention-related, 91, 94f In-phase imaging, 14–15, 15f–16f, 17,
G renal, 222–223 18f
Gadolinium Hematosalpinx, 338, 340f Inclusion cyst
adverse reactions to, 32–33, 33f Hemochromatosis ovarian, 324
formulations of, 32, 33f hepatic, 106–107, 107f–108f, 109t peritoneal, 324, 327f
pregnancy-related administration of, pancreatic, 107, 145, 148f vaginal, 308–310, 310t
33 splenic, 108f India ink artifact, 15f, 17
pulse sequences with, 17, 19f–20f Hemolysis, renal, 241–242, 243f Infarction
Gallbladder, 170–178 Hemorrhage hepatic, 101, 102f
abscess of, 173, 175f adrenal, 243, 244f, 246, 247f intervention-related, 91, 93f
accessory, 172 hepatic, 86 post-transplantation, 122–123,
adenoma of, 177, 179f pancreatic, 134, 136f 124f
adenomyomatosis of, 176, 178f precontrast imaging of, 17, 19f renal, 239–240, 239f
agenesis of, 172 renal, 222–223, 224f, 241–242 Inferior vena cava, anomalies of, 252,
anatomy of, 170–171 retroperitoneal, 253–256 252t
calculi of, 47f, 173, 174f Hemosiderosis, 48f, 106–107, Inflammatory abdominal aortic
carcinoma of, 177–178, 179f–180f 107f–108f aneurysm, 256–257, 256f–257f
ectopic, 172, 173f Hepatic adenoma, 68–70, 69f Informed consent, pregnancy and,
edema of, 176, 177f vs. focal nodular hyperplasia, 282
free water in, 21f 70–71 Insulinoma, 156, 156f, 158f
imaging technique for, 172 vs. metastatic disease, 86–87 Intraductal papillary mucinous
inflammation of, 173–176 Hepatic artery thrombosis, 121–122 neoplasms, 149f, 153f, 162–166
acute, 173, 174f–175f Hepatitis branch duct, 164f, 166, 166f,
chronic, 176, 176f acute, 105f, 105t 168f
gangrenous, 176 autoimmune, 115 main duct, 162, 164f–165f, 166
metastatic disease of, 178, 181f chronic, 113–115 Intrauterine adhesions, 271, 272f
normal, 171–172 Hepatocellular carcinoma, 42f–43f, Intrauterine device (IUD), 271–272,
polyps of, 176–177 77–83 273f
Gallstones, 47f, 173, 174f vs. adenoma, 69–70 Inversion time (TI), 14, 14f
372  •  Index

Iron Kidney(s) (Continued) Liver (Continued)

hepatic deposition of, 48f, 102, region of interest measurements chemotherapy-related lesions of, 91
106–107, 107f–108f, 109t in, 201, 202f–203f cholestasis of, 103–104, 104f
pancreatic deposition of, 107, 145, lymphoma of, 232, 236–237, 236f cirrhosis of. See Cirrhosis
148f malrotation of, 206f confluent fibrosis of, 103, 103f
Islet cell tumors. See Pancreas, mechanical hemolysis of, 241–242, cystic lesions of, 53, 54f
neuroendocrine tumors of 243f infection of, 54
Islets of Langerhans, 129 medullary cystic disease of, 214, vs. metastatic disease, 88f, 89
214f, 220f developmental lesions of, 54–61
J metastatic disease of, 232, 237 diffuse abnormalities of, 104–125,
Johanson-Blizzard syndrome, 145–148 multilocular cystic nephroma of, 104t
220f, 222, 223f occult, 104–105, 105t
K normal, 201f, 203, 203f echinococcal cysts of, 61–63, 61t,
K space, 7–8, 7f–8f oncocytoma of, 225f, 231, 232f 63f
Kasabach-Merritt syndrome, 60 pancake, 205–206 fatty (steatosis), 38f, 48f, 100f,
Kidney(s), 199–260, 266f polycystic disease of, 214–218, 105–106, 106f
abscess of, 218–221, 221f, 238–239 214f geographic, 36f–37f, 102, 103f
agenesis of, 204–205 autosomal dominant, 214, micro- vs. macrovesicular, 99
angiomyolipoma of, 216f, 231–232, 214f–215f, 214t, 217t, 220f nodular, 99
233f autosomal recessive, 214, 214f, fibrocystic ductal plate diseases of,
“bean” vs. “ball” lesions of, 223, 217t, 220f 54–55, 55t
224f positional anomalies of, 204–205, focal fatty sparing in, 99, 100f
benign neoplasms of, 229–232, 205f–206f focal lesions of, 51–99. See also
231f–232f pseudolesions of, 204–207, 204t, specific cystic and solid
calculi of, 218, 220f 223, 224f lesions
column of Bertin of, 207, 208f ptotic, 204–205, 205f focal nodular hyperplasia of,
corticomedullary differentiation of, segmental lesions of, 237–242, 237f 52f–53f, 70–71, 70f–72f
201, 201f, 203 solid lesions of, 207–209, 209t, vs. adenoma, 69–70
cysts of, 207, 208f, 209 223. See also Renal cell vs. hemangioma, 70–71
acquired, 215, 217t carcinoma vs. hepatocellular carcinoma,
classification of, 207, 209t, 210, vs. cyst, 208f 69–71
211f squamous cell carcinoma of, vs. metastatic disease, 86–87
complex, 207, 210–212, 232–236 vs. transient intensity differences,
212f–213f, 218, 220f structural anomalies of, 207 72
differential diagnosis of, 209f transitional cell carcinoma of, 220f, geographic lesions of, 99–104,
exophytic, 210, 210f–211f 232–236, 234f–235f 101f
hemorrhagic, 19f, 201, 208f, in tuberous sclerosis, 214, 214f, hemangioma of, 56–61, 57f–58f
209–211, 212f–213f 216f, 217t, 220f hemangiomatosis of, 60–61, 60f
infection of, 221 Klatskin’s tumor, 91–92, 92t, 102f, hematoma of, 66, 67f
infectious, 218–221, 220f–221f 188, 190f intervention-related, 91, 94f
lithium-induced, 214f, 215, 217f, Krukenberg’s tumor, 353t, 359 hemorrhagic cysts of, 54
220f imaging of, 35–45
neoplastic. See Multilocular L BolusTrack, 39f, 40
cystic nephroma; Renal cell Larmor equation, 3 coils in, 35, 40, 41f
carcinoma Leiomyomas. See Uterine fibroid(s) dynamic, 35, 39f, 41, 47–51,
parapelvic, 210, 211f Leiomyosarcoma, 294, 297–298, 299f 49f–50f, 52f–53f
parenchymal, 210, 211f Leydig cell tumor, 354, 358 fading on, 68, 68f
septated, 213f Lightbulb sign, 85–86, 87f field-of-view in, 40, 42f–43f
simple, 207, 208f, 209–212, Lipoma, hepatic, 98 gadolinium for, 35, 39f, 39t, 41,
210f–211f, 213f Lipomatosis, pancreatic, 133 51, 52f
site of, 210, 211f Lithium, renal cysts with, 214f, 215, heavily T2-weighted, 40–41, 46,
unilateral, 215–218 217f, 220f 50, 50f
developmental anomalies of, Liver, 35–128. See also Bile duct(s); indications for, 35, 37t
204–207, 204t, 205f–207f Biliary tract interpretation of, 45–50, 45t–46t,
diffuse lesions of, 237–242, 237f ablated-lesion imaging in, 90–91, 84t
bilateral, 241–242, 241t 91f–92f, 91t moderately T2-weighted, 41–46,
unilateral, 240, 240t, 241f abscess of, 64 49–50, 50f
faceless, 233–235 amebic, 61t, 64–66 protocol for, 40–45, 40t
fetal lobulation of, 207 fungal, 61t, 64, 66 signal-to-noise ratio in, 35,
focal lesions of, 207–237, 208f mycobacterial, 61t 36f–38f
fusion anomalies of, 205–206, 206f pyogenic, 61t, 64, 64f–65f SSFSE (single-shot fast spin-echo),
hematoma of, 222–223, 224f vs. metastatic disease, 87 38f, 40–41, 41f, 44f, 46, 47f,
hemolysis of, 241–242, 243f adenoma of, 68–70, 69f 50f
hemorrhage in, 222–223, 224f, vs. focal nodular hyperplasia, steady-state, 46, 47f
241–242 70–71 T1-weighted, 41, 41t, 46–50, 46t,
spontaneous, 231–232 vs. metastatic disease, 86–87 48f
horseshoe, 205–206, 207f angiomyolipoma of, 97–98, 98f three-dimensional pulse
imaging of, 199–200 candidiasis of, 66 sequences in, 45
indications for, 199, 200t carcinoma of. See Hepatocellular washout on, 53f, 68, 68f, 78,
interpretation of, 200–201, 201f carcinoma 80f–81f, 85f
protocols for, 199–200, 200f chemoembolization-related lesions infarction of, 101, 102f
reference standard for, 201 of, 91, 93f intervention-related, 91, 93f
 Index  •  373

Liver (Continued) Lumbar spine, 268 Metastatic disease (Continued)

post-transplantation, 122–123, Lungs, metastatic disease of, 299f hypovascular, 88–89, 88f–89f,
124f Lymphadenopathy 88t
infectious lesions of, 61–66, 61t in hepatocellular carcinoma, 79, stratification of, 88, 89t
inflammation of, 104–105, 105f, 83f lymph node, 79, 83f
105t, 115 periportal, 20f ovarian, 359, 359f
iron deposition in, 48f, 102, Lymphoma pancreatic, 158–160, 160f–162f
106–107, 107f–108f, 109t adrenal, 249 pulmonary, 299f
lipid-based lesions of, 97–99 cervical, 359 rectal, 318f–320f
lipoma of, 98 hepatic, 89–90, 90f renal, 232, 237
lymphoma of, 89–90, 90f myometrial, 297–298 retroperitoneal, 257–259, 258f
metastatic disease of, 48f pancreatic, 160–161, 162f–163f vaginal, 281f, 318f–319f
hemorrhage and, 86 pelvic, 266f, 359 Mirizzi’s syndrome, 185–186, 186f
vs. hepatocellular carcinoma, 79 periportal lymphadenopathy in, Motion artifact, 21–27, 22f
hypervascular, 84–87, 84t, 20f acceleration factor and, 22–24
86f–87f renal, 232, 236–237, 236f echo train length and, 22–24
hypovascular, 88–89, 88f–89f, 88t retroperitoneal, 257, 258f field of view and, 22–23, 24f–25f
stratification of, 88, 89t Lymphoplasmacytic sclerosing geometry factor in, 24
neoplastic lesions of, 61. See also pancreatitis, 135–144, 143f gradient moment nulling and, 27,
Hepatocellular carcinoma 27f
nodules of, 72–76, 74f M in liver imaging, 35, 36f–37f
dysplastic, 72–73, 74f, 75–76, Magnet, 1–3, 4f, 8f minimization of, 22–23, 23f, 26, 26f
76f–77f Magnetic alignment, 1, 2f number of excitations and, 22–23,
nodule within a nodule of, 76, Magnetic resonance 26
77f cholangiopancreatography in pelvic imaging, 267f–268f,
prehypervascular, 72–73, 75 (MRCP) 280f–281f
regenerative, 72–73, 74f–75f, in ampullary carcinoma, 194f–195f physiologic monitoring and, 24–26,
111–112, 111f in biliary hamartoma, 56f 26f
siderotic, 72–73 in biliary stricture, 186, 187f spatial resolution and, 24
normal, 50–51, 51f in cholangiocarcinoma, 190f, 193f tissue-specific signal intensity and,
passive congestion of, 120, 120f in choledocholithiasis, 185f 26
PEComa of, 49f in chronic pancreatitis, 141f view-to-view, 21, 22f
polycystic disease of, 54, 55f in ectopic gallbladder, 173f within-view, 21, 22f, 27
primarily enhancement lesions of, in groove pancreatitic, 144, 145f Mucinous cystic neoplasm, 166,
100–102 in hereditary pancreatitis, 146f 168f–170f
schwannoma of, 20f in infectious cholangitis, 187–188 Müllerian duct anomalies, 298–304,
segments of, 51f in intraductal papillary mucinous 300f
simple cysts of, 54, 54f neoplasm, 164f, 166f class II (unicornate uterus),
solid lesions of, 67–88. See also in lithium nephropathy, 217f 298–301, 300f
specific solid lesions in Mirizzi’s syndrome, 186f class III (didelphys uterus),
cystic components of, 67 in mucinous cystic neoplasm, 298–301, 300f–301f
hypervascular, 68, 68f, 84t 169f–170f class IV (bicornuate uterus), 300f,
hypovascular, 87–88, 88f, 88t in pancreas divisum, 133f 301–303, 302f–303f
transient intensity differences of, in pancreatic adenocarcinoma, class V (septate uterus), 264f, 300f,
72, 101, 101f 154f–155f 301–303, 302f–303f
vs. focal nodular hyperplasia, 72 in pancreatic serous cystadenoma, class VI (arcuate uterus), 303, 304f
geographic, 73f 167f–168f imaging of, 261, 264f
pseudoglobular, 72, 74f in primary sclerosing cholangitis, Müllerian duct cyst, 311f
transplantation of. See Liver 42f–43f, 116f–117f, 188f–189f Myelolipoma, adrenal, 249, 250f
transplantation in septated renal cyst, 213f Myometrium, 282–304
traumatic lesions of, 66–67 Magnetic spin, 3, 3f adenomyosis of, 294–296, 296t,
von Meyenburg complex of, 54, Magnetic susceptibility, 16 297f
56f Magnetically active nuclei, 1, 2f anatomy of, 262f, 270f, 282
Liver transplantation, 120–125, 121f Magnetism, 1, 2f–3f, 16 contractions of, 296
biliary complications of, 123–125 Medullary sponge kidney, 214–215, malignant disease of, 297–298, 299f
biloma after, 123 220f
complications of, 121f Melanoma N
hepatic artery thrombosis after, hepatic metastases from, 48f, 86, Nabothian cyst, 304, 305f, 305t
121–122 86f Navigatory pulse, 26
infarction after, 122–123, 124f pancreatic metastases from, Necrosis, pancreatic, 134, 139f
inferior vena cava stenosis after, 160f–161f Nephrogenic fibrosing dermopathy,
122, 124f uveal, 19f, 48f, 86f 32–33
lymphoproliferative disorder Menstrual cycle, 322–324 Nephroma, cystic, multilocular, 220f,
syndromes after, 125, 125t Metastatic disease 222, 223f
malignancy after, 125 adrenal, 229f, 249, 252f–253f Nephropathy, contrast-induced, 32
perihepatic fluid after, 120–121, bladder, 320f Net magnetic vector, 1–4, 3f–4f
121f, 123 endometrial, 280–282, 281f Neuroendocrine (islet cell) tumors,
periportal fluid after, 120–121, 122f gallbladder, 178, 181f 151–158, 156f–157f
portal venous complications of, hepatic, 48f cystic, 157f, 159f, 166
122, 123f vs. hepatocellular carcinoma, 79 gastrin-secreting, 156, 156f
rejection after, 121–122 hypervascular, 84–87, 84t, glucagon-secreting, 156–158, 156f
stenosis after, 121–122 86f–87f insulin-secreting, 156, 156f, 158f
374  •  Index

Neuroendocrine (islet cell) tumors Ovary (ovaries) (Continued) Pancreas (Continued)

(Continued) fibroblastic, 354–355, 357f neuroendocrine tumors of,
nonfunctioning, 156f, 158, 159f germ cell, 347t, 351–354 151–158, 157f
somatostatin-secreting, 156–158, granulosa cell, 354–358, 358f cystic, 166
156f Leydig cell, 354, 358 gastrin-secreting, 156, 156f
VIP-secreting, 156–158, 156f metastatic, 359, 359f glucagon-secreting, 156–158,
Nonalcoholic fatty liver disease, Sertoli cell, 354, 358 156f
105–106, 106f sex cord–stromal, 347t, 351–354, insulin-secreting, 156, 156f, 158f
Notch sign, 110f 358–359 nonfunctioning, 156f, 158, 159f
Nuclei, 1, 2f thecal cell, 354–355 somatostatin-secreting, 156–158,
normal, 269f, 317–321, 320f–322f 156f
O polycystic, 360, 362f VIP-secreting, 156–158, 156f
Ohmic heating, 29 postmenopausal cysts of, 322–324 normal, 129, 130f–131f
Oncocalyx, 232–233 teratoma of, 351–354. See also pseudocysts of, 138f, 161
Oncocytoma, 225f, 231, 232f Dermoid cyst in Schwachman-Diamond
Operator’s console, 8, 8f torsion of, 339t, 342, 344f–347f, syndrome, 145
Ormond’s disease, 253 353t serous cystadenoma of, 164f, 166,
Out-of-phase imaging, 14–15, 15f–16f, 167f–168f
17, 18f P solid-cystic papillary epithelial
Ovarian carcinoma, 346–351, 347t, Pancreas, 129–170 neoplasm of, 170, 171f–172f
353t acinar cell carcinoma of, 160 in von Hippel–Lindau disease, 145,
classification of, 347t, 349t acinar cell of, 129 149f, 161
clear cell, 350–351 adenocarcinoma of, 149f–150f, Pancreas divisum, 132, 133f–134f
endometrioid, 350–351 150–151 Pancreatic ducts, 130, 131f
mucinous, 350, 350f–351f, 353t, arterial phase imaging in, anatomic variants of, 132, 134f
354f 150–151, 152f–153f failed fusion of, 132, 134f
serous, 350, 350f–351f, 353t duct obstruction in, 150–151, Pancreatitis, 134–144
staging of, 349t 153f–154f acute, 131f, 134–135
Ovarian hyperstimulation syndrome, hypointensity in, 151f fluid collection in, 134,
360, 363f vs. metastatic disease, 158–160 137f–138f
Ovarian vein thrombosis, 363t, 367, vs. pancreatitis, 150f, 151 hemorrhagic, 134, 136f
367f spread of, 151, 154f–155f necrotic, 134, 139f
Ovary (ovaries), 317–367 unresectability of, 151, 154f pseudoaneurysm formation with,
corpus luteal cyst of, 322–324, 323f, agenesis of, 132–133 134, 140f
325f–326f, 338, 338t, 339f anatomy of, 129, 130f venous thrombosis in, 134–135
cystadenocarcinoma of, 347–350, annular, 130–131, 132f autoimmune, 135–144, 143f
350f–351f, 354f congenital/developmental chronic, 131f, 135, 141f–142f
cystadenofibroma of, 266f, 351, anomalies of, 130–133, vs. intraductal papillary mucinous
353t, 355f 132f–134f neoplasm, 162
cystadenoma of, 350, 352f–353f in cystic fibrosis, 145, 147f etiology of, 134, 135f
cystic lesions of, 266–267, cysts of, 145, 149f, 161–170, groove, 144, 144f–145f
321–346, 321t–322t, 324t 164f hereditary, 144, 146f
complex, 346 edema of, 134, 137f–138f Parallel imaging, 24, 25f
hemorrhagic, 324–328, embryology of, 130, 131f Paramagnetic substances, 16, 16f, 19f
328f–329f, 338, 338t–339t focal lesions of, 148–170, 149f Parovarian cyst, 324
lipid content in, 324–328, cystic, 149f, 161–170, 164f PEComa, 49f
328f–333f solid, 148–161, 149f–150f Pelvic arteries/veins, 364f–365f
water content in, 322, 323f, function of, 129 Pelvic congestion syndrome, 363t,
325f–327f hemochromatosis of, 107, 145, 365
dermoid cyst of, 328–329, 148f Pelvic inflammatory disease, 338, 341f
328f–333f, 339t imaging of, 129–130 Pelvic miscellaneous lesions, 359,
dimensions of, 269t dynamic, 129–130, 131f 359t
edema of, 338, 341f, 342, 347f fat-suppressed T1-weighted, 129, Pelvic vein, 360–364, 364f
follicle cyst of, 320f, 322–324 130f Pelvic vein syndrome, 365
functional cysts of, 322–324 fat-suppressed T2-weighted, 129, Pelvic venous incompetence, 365
globally abnormal, 360 134, 137f Pelvis, female, 261–368. See also at
hyperstimulation of, 360, 363f T1-weighted, 129, 130f Adnexa; Cervix; Ovary (ovaries);
imaging of, 261–262 T2-weighted, 129, 131f Uterus; Vagina
interpretation of, 266–267 inflammation of. See Pancreatitis imaging of, 261–262, 263t
inclusion cyst of, 324 intraductal papillary mucinous coil placement in, 265, 266f
massive edema of, 342, 347f neoplasms of, 149f, 153f, dynamic, 261–262, 264t
multifollicular, 360 162–166, 164f–166f, 168f indications for, 261, 262t
neoplasms of, 346–360 islet cell tumors of. See Pancreas, interpretation of, 265–268, 265t
classification of, 347t neuroendocrine tumors of vascular anatomy of, 360–364,
dysgerminoma, 354, 356f in Johanson-Blizzard syndrome, 364f–365f
endodermal sinus, 354 145–148 Perineum, angiomyxoma of, 360, 361f
epithelial, 323f, 346–351, 347t lipomatosis of, 133 Periportal halo sign, 115, 116f
benign, 346–351, 349t, lymphoma of, 160–161, 162f–163f Peritoneal inclusion cyst, 324, 327f
352f–353f, 353t, 355f metastatic disease of, 158–160, Phase cancellation artifact, 332f
classification of, 346–351 160f–162f Pheochromocytoma, 249, 250f–251f
malignant, 346–351, 349t, mucinous cystic neoplasm of, 166, Placental site trophoblastic tumor,
350f–351f, 353t, 354f 168f–170f 282
 Index  •  375

Polycystic kidney disease, 214–218, Pulse sequence (Continued) S

214f T2-weighted, 12, 13f, 14–21, 16f, Safety, 28–33, 29f, 32f
autosomal dominant, 214, 19f–21f Santorini, duct of, 130, 132,
214f–215f, 214t, 217t, 220f vascular (solid/viable tissue), 17 132f–133f
autosomal recessive, 214, 214f, water-only, 20–21 Sarcoma, retroperitoneal, 259
217t, 220f Pyelonephritis, 237–239, 237f–238f Schwachman-Diamond syndrome, 145
Polycystic liver disease, 54, 55f xanthogranulomatous, 240 Schwannoma, hepatic, 20f
Polycystic ovary disease, 360, 362f Pyonephrosis, 238–239 Screening form, 30f–31f
Polyps Pyosalpinx, 338–342, 342f Sertoli cell tumor, 354, 358
endometrial, 263f, 272–273, Sex cord–stromal tumor, 347t,
275f–277f Q 351–354, 358–359
gallbladder, 176–177 Quenching, 32 Signal-to-noise ratio, 28, 28f
Portal hypertension, 112–113, 114f Skene’s gland cyst, 308–310, 310t,
Portal vein thrombus, 102, 102f R 313f
in hepatocellular carcinoma, 78–79, Receiver system, 6–7, 8f Solid-cystic papillary epithelial
79f, 82f Rectangular field of view, 22–23, 24f neoplasm, 149f, 170, 171f–172f
Posttransplant lymphoproliferative Rectum, metastatic disease of, Somatostatinoma, 156–158, 156f
disorder syndromes, 125, 125t 318f–320f Spatial resolution, reduction in, 24
Pregnancy, 282 Recurrent pyogenic cholangitis, Specific absorption rate, 32
dermoid cyst in, 332f 55–56 Spin, 1, 3f
ectopic, 339t, 346, 348f–349f Renal artery (arteries), 239f Spin-spin relaxation, 12
gadolinium administration and, 33 infarction of, 239–240, 239f Spiral valves of Heister, 170–171
hydronephrosis and, 219f stenosis of, 237f, 240, 241f Squamous cell carcinoma, urothelial,
informed consent and, 282 Renal cell carcinoma, 25f, 220f, 232–236
ovarian torsion in, 347f 223–231 Stein-Leventhal syndrome, 360, 362f
Primary biliary cirrhosis, 115, acquired cystic kidney disease and, Stenosis, renal artery, 237f, 240, 241f
115f–116f 215, 217t Stent, 29
Primary sclerosing cholangitis, adrenal extension of, 229f Stones
42f–43f, 55–56, 115–117, chromophobe, 229, 230f biliary, 185–186, 185f–186f
116f–117f, 187, 188f–189f clear cell, 225, 225f–227f, 229f gallbladder, 47f, 173, 174f
differential diagnosis of, 117 collecting duct, 236 renal, 218, 220f
Proton density pulse sequence, cystic, 211–212, 216f, 221–222, String of pearls appearance, in
12–13, 13f 222f, 229 chronic pancreatitis, 135, 141f
Pseudoaneurysm, pancreatic, 134, in hereditary syndromes, 225f Superparamagnetic substances, 16
140f lymph node assessment in, 228 Surgical clips, 27
Pseudocyst medullary, 236 Susceptibility artifact, 27–28, 28f
adrenal, 244 vs. multilocular cystic nephroma, in gastrointestinal tract imaging, 18f
pancreatic, 138f, 161 222 in liver imaging, 40–41, 44f, 48f,
Pulsatile vascular flow, 21 pancreatic metastases from, 162f 69f, 108f, 111f
Pulse sequence, 6, 6f, 9–10 papillary, 225f, 228–229, 230f minimization of, 27–28, 27f–28f,
bound water, 17–18, 20f solid lesions of, 224f 40–41, 44f, 47f
chemical-shift, 14–15, 15f staging of, 204f, 225–226, 228f in pelvic imaging, 267f–268f, 274f,
dynamic, 17, 19f–20f subtypes of, 221–222, 221t 278f
susceptibility artifact and, 27–28, thrombus with, 226, 227f–228f in renal imaging, 220f
28f vascular invasion of, 227f
echo planar (EPI), 10 Renal collecting system, 238f T
fast spin-echo, 16f carcinoma of, 232–236, 234f–235f T2 contrast, 12
fat-saturation, 14 distention of, 218, 218t, 219f T2* contrast, 12
fat-suppression, 14 imaging of, 200, 200t, 203 T2* decay, 9, 12
susceptibility artifact and, 28 infection of, 237–239, 238f T1 relaxation, 11–12, 11f–12f
fluid attenuation inversion recovery Renal insufficiency, cystic disease in, Tamoxifen, 271, 271f
(FLAIR), 14 215 Tampon, 278f
free water, 18–20, 21f Renal vein thrombosis, 237f, TE (time to excitation), 12–13
gradient-echo, 6f, 9–10, 9f–10f 240–242, 242f Teratoma, ovarian, 351–354
gradient-recalled echo, 16f in renal cell carcinoma, 226, mature. See Dermoid cyst
heavily T2-weighted, 18–20, 21f 227f–228f Thecal cell tumor, 354–355
interstitial, 17, 20f Resonance, 1 Thumb rule, 2–3, 4f
inversion, 14, 14f Respiratory triggering, 26, 26f Time-varying magnetic fields, 29
lesion suppression, 18–20, 21f Retrograde pyelography, 208f Tissue contrast, 11–15
moderately T2-weighted, 17–18, Retroperitoneum, 249–259, T2 decay and, 11–12, 11f
20f 254f–255f. See also Adrenal T1 relaxation and, 11, 11f
paramagnetic, 17, 19f glands; Kidney(s) TR (time to repetition), 9
proton density, 12–13, 13f fibrosis of, 253–256, 255f Transient hepatic intensity
short tau inversion recovery (STIR), hemorrhage of, 253–256 differences, 72, 101
14, 24–26, 26f lymphoma of, 257, 258f vs. focal nodular hyperplasia, 72
single-shot fast spin-echo (SSFSE), metastatic disease of, 257–259, 258f pseudoglobular, 72
16f, 18f–19f neoplasms of, 257, 258f Transitional cell carcinoma, 220f,
spectrally selective, 14 sarcoma of, 259 232–236, 234f–235f
spin-echo, 6f, 9–10, 9f–10f Rf transmitter system, 3–4 Tuberous sclerosis, 214, 214f, 216f,
steady-state free precession (SSFP), Rokitansky-Aschoff sinuses, 176, 178f 217t, 220f, 225f
10 Rokitansky’s nodule, 331f Tuboovarian abscess, 338–342, 339t,
T1-weighted, 12–21, 12f–13f, 16f Round ligament, 266–267, 269f, 322f 341f–343f
376  •  Index

U Uterus (Continued) Vagina (Continued)

Ultrasonography, in tuboovarian bicornuate, 300f, 301–303, metastatic disease of, 281f,
abscess, 343f 302f–303f 318f–319f
Urethra, Skene’s gland cysts of, cesarean section defect of, 272, Müllerian duct cyst of, 311f
308–310, 310t, 313f 274f Varices, pelvic, 360–365, 363t
Uterine artery embolization, 291, 294, didelphys, 298–301, 300f–301f Vascular (solid/viable tissue) pulse
294f–295f, 295t endometrial disease of, 270–282. sequence, 17
Uterine fibroid(s), 282–294 See also at Endometrial Venous thrombosis
classification of, 282, 282f carcinoma; Endometriosis; femoral vein, 320f
cystic degeneration of, 289–291, Endometrium ovarian vein, 363t, 367, 367f
291t, 292f fibroids of. See Uterine fibroid(s) in pancreatitis, 134–135
degeneration of, 289–291, global abnormalities of, 298–304. portal vein, 78–79, 79f, 82f, 102,
290f–293f, 291t See also Müllerian duct 102f
differential diagnosis of, 286–289, anomalies renal vein, 226, 227f–228f, 237f,
290t gravid, hydronephrosis and, 219f 240–242, 242f
hemorrhagic degeneration of, imaging of, 261–262 VIPoma, 156–158, 156f
289–291, 291t, 293f coil placement in, 265, 266f Von Hippel–Lindau disease
hyaline degeneration of, 289–291, indications for, 262t pancreatic lesions in, 145, 149f, 161
291t interpretation of, 265–268, renal lesions in, 214, 214f, 216f,
identification of, 282–286 265t 217t, 225f
intracavitary, 282, 282f protocol for, 263t Von Meyenburg complex, 54, 56f
intramural, 263f, 282, 282f, myometrial disease of, 282–304.
284f–285f, 288f–289f, See also Adenomyosis; Uterine W
293f–295f, 340f fibroid(s) Water, 15–16, 16f, 20–21
malignant degeneration of, 294, normal, 262f, 268–270, 269t, 270f bound, 17–18, 20f
296f retroversion of, 270f, 274f free, 18–20, 21f
myxoid degeneration of, 289–291, septate, 264f, 300f, 301–303, Wraparound artifact, 23, 25f,
290f–291f, 291t 302f–303f 267f–268f
pedunculated, 282, 282f size of, 265, 268–269, 269t, 270f Wunderlich’s syndrome, 231–232
postembolization, 291, 294, T-shaped, 264f, 303–304
294f–295f, 295t unicornuate, 298–301, 300f X
submucosal, 282, 282f–283f, 289f X (frequency-encoding) gradient, 4–5,
subserosal, 263f, 282, 282f, V 5f
285f–287f, 286–289, 320f, Vagina, 304–317 Xanthogranulomatous pyelonephritis,
353t arteriovenous malformation of, 240
vascularity of, 286–289, 288f–289f 364–365
Uterus, 268–304 Bartholin’s gland cyst of, 289f, Y
anatomy of, 262f, 269f–270f, 365f 308–310, 310t, 312f–313f Y (phase-encoding) gradient, 4–5,
anteflexion of, 272, 274f carcinoma of, 317 5f–6f
anteversion of, 274f cystic lesions of, 304–310, 310t
arcuate, 300f, 303, 303f–304f Gartner’s duct cyst of, 308–310, Z
arteriovenous malformation of, 309f, 310t Z (slice-select) gradient, 4, 5f
364–365 inclusion cyst of, 308–310, 310t Zollinger-Ellison syndrome, 156